Escolar Documentos
Profissional Documentos
Cultura Documentos
ORAL MEDICINE
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DISCLAIMER NOTICE
The information in this book should not be used by unqualified personnel to do
any self diagnosis. All dental surgeons are requested to kindly verify the latest
prescribing practices prior to making decision. Most values are indicative and
have been checked against latest reliable sources, but the publisher and
author do not have any direct or indirect liability to the use or misuse of this
information.
Prior to prescribing any medication please check that they are from ethical
drug manufactures following sound quality control practice. Follow the
manufacture direction in most prescription and please confirm side effect, safety
in children and pregnancy.
Author
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Textbook of
ORAL MEDICINE
Second Edition
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Published by
Jitendar P Vij
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Textbook of Oral Medicine
2010, Anil Govindrao Ghom
All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any
means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the author and the publisher.
This book has been published in good faith that the material provided by author is original. Every effort is made to ensure
accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s). In case of any
dispute, all legal matters to be settled under Delhi jurisdiction only.
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To
My Mother,
My Daughter Milini,
My Son Sanvil,
My Wife Savita
and
My Family
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Contributors
Vikas Meshram
Reader,
Chhattisgarh
Dental College and
Research Institute,
Rajnandgaon,
Chhattisgarh
Ch 48: Emergency
Drugs used in
Dentistry
Sachin Manglekar
Reader, School of
Dental Science,
Krishna Institute of
Medical Science
University, Karad,
Maharashtra
Ch 46: Desensitizing
Agents, Gum Paints
and Mouthwashes
Savita Ghom
Lecturer,
Chhattisgarh
Dental College and
Research Institute,
Rajnandgaon,
Chhattisgarh
Ch 43: Anticancer
Drugs
Ch 47: Drugs used in
Pregnancy
Raghvendra Shetty
Reader,
Chhattisgarh
Dental College and
Research Institute,
Rajnandgaon,
Chhattisgarh
Ch 40: Antibiotics
Amit Parate
Lecturer,
Government Dental
College and
Hospital, Nagpur,
Maharashtra
Ch 20: Oral
Pigmentation
Vaishali Gawande
Lecturer,
Chhattisgarh
Dental College and
Research Institute,
Rajnandgaon,
Chhattisgarh
Ch 42: Antifungal
Drugs
Ch 44: Antiviral
Drugs
Abhishek Soni
Reader, VSPM
Dental College and
Research Institute,
Nagpur,
Maharashtra
Ch 24: Gingival and
Periodontal Diseases
Anjusha Ganar
Ex-lecturer,
Chhattisgarh
Dental College and
Research Institute,
Rajnandgaon,
Chhattisgarh
Ch 45: Corticosteroids
Neeta Wasnik
Lecturer,
Chhattisgarh
Dental College and
Research Institute,
Rajnandgaon,
Chhattisgarh
Ch 41: Analgesic and
Anti-inflammatory
Drugs
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Foreword
Enthusiasm is a driving force that overcomes all obstacles
It is my proud privilege to write a foreword for second edition of this book by Dr Anil Ghom. In
short time, this book has become most popular among undergraduates and postgraduates all over
the country.
In the second edition, numbers of chapters have been presented in a better organized manner.
This book carries updated information of the subject in this rapidly changing world of science. A
new chapter Controversial Diseases and Terminologies is incorporated, also there are large
number of new photographs, radiographs, MCQs and references. I am sure this new updated
second edition will be more beneficial for the undergraduate and postgraduate students for reference
and regular reading.
RN Mody
Professor and Head
Department of Oral Medicine and Radiology
Hitkarini Dental College
Jabalpur, MP
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You must not be discouraged if the world does not rush to you, demanding what you have; neither must
you quietly sit down to let world wonder and then seek you; you must be aggressive, you must carry your
truths to people and cause them to see them so clearly that they must accept them
The student looked for a reference on which to build an educational foundation with
regard to basic principle. A few years ago much of the information offered in this text was not
available.
Since the principle and treatment modalities offered herein will continue to evolve, it behooves
the student to be fully informed of the state-of-art to be able to critically evaluate the worthiness or
applicability of any future development.
I have endeavored to ensure that a consistent style has emerged and is in harmony where appropriate with the diseases
of oral region along with the differential diagnoses which are covered in detail.
The purpose of this book is to correlate the gross and microscopic pathological features with the radiographic appearance
of oral diseases and systemic diseases manifested in the jaw.
In our increasingly litigious society, it is vital that the dentist understands the law as it relates to dentistry. The Chapter
on Medicolegal Issue is Essential Reading, along with the Consumer Protection Act.
Diseases can be understood best when the interpreter understands not only the disease process but also the basic
science associated with it. For this reason, I have included separate section for basic science.
Recently, as exam pattern is changing and MCQs are getting importance, MCQs are added in separate chapter.
I tried my best, to cover all the aspects of oral diseases in my book. If this goal is achieved, then this textbook may
contribute, in a small way to better care of patients who suffer from these diseases.
Anil Govindrao Ghom
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Acknowledgements
The man who really wants to do something finds a way, the other finds an excuse
No work will be complete without help of your friends and well wishers and I am lucky to have them with me in this
venture.
First of all, I am immensely thankful to Dr Vaishali Gawande for her untiredly help in completion of this project. My
special thanks to Dr Neeta Wasnik and Dr Anjusha Ganar who helped me a lot.
I am also thankful to Dr Swapnil Diwakirti for her help in preparation of diagrams in the book. I am thankful to all the
contributors for their contribution in this book.
My sincere thanks to Dr Pravin Lambade, Dr Jitendra Sachdeo, Dr Vikas Meshram, Dr Bhaskar Patle, Dr Revant Chole,
Dr Amit Parate, Dr Sanjay Pincha, Dr Milind Chandurkar, Dr Ashok L, Dr Umaraji, Dr Tapasya Karemore, Dr Avinash
Kshar, Dr M Shimizu, Dr Fusun Yasar, Dr Iswar, Dr Bande, Dr Kadam, Dr R Kamikawa, Dr FM Debta and Dr Suwas
Darvekar for providing clinical and radiological photographs in the book.
Beauty is Gods gift but to utilize it in proper direction is in your hand. I am thankful to all those beautiful faces in
book Dr Gagandeep Chawala, Dr Smiriti Goswami, Dr Uma Rohra, Dr Swapnil Dewakirti, and Dr Pragya Jaiswal.
I would like to thank Dr Ranit Chhabra, Dr Priyanka Aggarwal, Dr Shaheen Hamdani, Dr Payal Tapadiya, and
Dr Vivek Lath for their help in proofreading.
I offer my humble gratitude to my guide Dr RN Mody for his guidance during my postgraduation and after postgraduation.
Friends are always big supporters so I am grateful to Dr Pravin Sundarkar, Dr Neeraj Alladwar and Dr Ravindra
Govindwar for heartily wishes. I am also thankful to my brothers and sisters especially elder brother Sadanand for their
moral support in my life.
I am thankful to Shri Jitendar P Vij (Chairman and Managing Director) and Mr Tarun Duneja (Director-Publishing) of
M/s Jaypee Brothers Medical Publishers (P) Ltd., for publishing this book. Commendable type setting, proofreading and
improvement in illustrations have been done respectively by Ms Sunita Katla, Md Shakiluzzaman & Ms Geeta Srivastava
and Mr Sumit Kumar.
Whenever I think who completely changes my life is my wife Savita, who is there in my thick and thin. Whenever I am
down, she is there to uplift me with her prayer and support. She is a person with generous heart and I am thankful to God
to give gift like her to me in my life.
Lastly, I offer my earnest prayers to the Almighty for endowing me the strength and confidence in accomplishing to the
best of my abilities.
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Contents
Section 1
Basics
1. Oral Diseases: An Introduction .....................................................................................................................3
2. Development and Eruption of Teeth ............................................................................................................5
3. Development and Anatomy of Craniofacial Region ................................................................................9
4. Immunity, Antigen-Antibody Reaction .................................................................................................... 18
5. Neoplasm ........................................................................................................................................................ 24
6. Infection Control in Dental Office ............................................................................................................. 35
Section 2
Diagnostic Procedures
7. Case History .................................................................................................................................................... 45
8. Investigation in Dentistry ............................................................................................................................ 86
Section 3
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Section 4
Systemic Diseases
Manifested in Jaw
30. Bacterial Infections ..................................................................................................................................... 733
31. Viral Infections ............................................................................................................................................ 757
32. Fungal Infections ......................................................................................................................................... 775
33. Specific System Disorders ......................................................................................................................... 784
34. Diseases of Bone Manifested in Jaw ...................................................................................................... 828
35. AIDS ................................................................................................................................................................ 859
36. Endocrine Disorders .................................................................................................................................... 874
37. Blood Disorders ............................................................................................................................................ 894
38. Vitamins ......................................................................................................................................................... 926
39. Metabolic Disorders .................................................................................................................................... 944
Section 5
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Contents xvii
Section 6
Miscellaneous
49. Professional Hazards of Dentistry ........................................................................................................ 1035
50. Forensic Dentistry ...................................................................................................................................... 1040
51. Controversial Diseases and Terminologies ........................................................................................ 1051
Appendices
Appendix 1: Causes and Classifications ............................................................................................... 1063
Appendix 2: Syndromes of Oral Cavity ................................................................................................. 1103
Appendix 3: Glossary ................................................................................................................................. 1114
Appendix 4: Multiple Choice Questions ............................................................................................... 1133
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Oral Diseases:
An Introduction
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Suggested Reading
1. Geis WJ. Dental education in the United States and Canada: A
report to the Carnegie Foundation for the Advancement of
Teaching. Carnegie Foundation: New York, Bulletin 19.1926.
2. Gnanasundaram N. Nine gems of the speciality and ten
commandments for specialists in oral medicine and radiology.
JIAOMR 2006:18(4):196-201.
3. Millard HD, Mason DK. Perspectives on 1988 World Workshop
in Oral Medicine. Chicago: Year Book Publishers, 1989.
4. Millard HD, Mason DK. Perspectives on 1993 World Workshop
in Oral Medicine. Ann Arbor: University of Michigan, 1995.
5. Knapp MI. Oral disease in 181,338 consecutive oral examinations.
J Am Dent Assoc 1971; 83:1288-93.
6. Pilot T. Trends in oral health care, a global perspective. World
Health Organization: Geneva, 6-23 November 1989.
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Development and
Eruption of Teeth
Introduction
Development of tooth is a result of complex process
occurring between oral epithelium and underlying
mesenchymal tissue. The primitive cavity is lined by
stratified squamous epithelium, i.e. oral ectoderm, which
contacts the endoderm of foregut to form the buccopharyngeal membrane. At 27th day of gestation, this
membrane ruptures and primitive oral cavity establishes a
connection with the foregut.
The scale of human tooth development:
42-48 daysdental lamina formation.
55-56 daysbud stage-deciduous incisor, canine and
molar.
14th weekbell stage for deciduous bud for permanent.
18th weekdentin and functional ameloblast.
32nd weekdentin and functional ameloblasts of
permanent 1st molar.
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Fig. 2-2: Diagram of bud stage showing dental lamina and dental
papilla formation (ectomesenchyme condensation).
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1
Fig. 2-5: Advanced bell stage showing root sheath of Hertwigs.
Eruption of Teeth
The axial or occlusal movement of tooth from its developmental position within the jaw to its functional position in
the occlusal plane is known as eruption of teeth. There are 3
types of movements which are described as follows:
Pre-eruptive
Crowding of teethwhen deciduous tooth germ first
differentiates, there is good deal of space between them.
But due to their rapid growth, this available space is
utilized and developing teeth become crowded together,
especially in incisor and canine region (Fig. 2-6).
Drifting of deciduous molarcrowding is relieved by
growth in length of infants jaws, which provides room
for second deciduous molars to drift backward and
anterior teeth to drift forward. At the same time, the tooth
germ also moves outward as jaw increases in width and
height (Fig. 2-6).
Movement of permanent teethpermanent teeth with
deciduous predecessors also undergo complete
movement before they reach the position from which
they will erupt (Fig. 2-6).
Eruption of deciduous predecessor teethas their deciduous
predecessors erupt, they move to a more apical position
and occupy their own bony crypt.
Permanent premolarspremolars begin their development lingual to their predecessors at the level of occlusal
surface. They are situated beneath the divergent roots of
deciduous molars.
Permanent molarthe permanent molars which do not
have predecessors also move from the site of their initial
differentiation.
Eruptive
Posteruptive
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Deciduous dentition
Tooth
Formation of enamel
matrix and dentin begins
Enamel completed
Eruption
Root completed
4 months in utero
4 months in utero
5 months in utero
5 months in utero
6 months in utero
1 months
2 months
9 months
6 months
11 months
7 months
9 months
18 months
14 months
24 months
1 years
2 years
3 years
2 years
3 years
4 months in utero
4 months in utero
5 months in utero
5 months in utero
6 months in utero
2 months
3 months
9 months
5 months
10 months
6 months
7 months
16 months
12 months
20 months
1 years
1 years
3 years
2 years
3 years
Upper
Central incisor
Lateral incisor
Cuspid
First molar
Second molar
Lower
Central incisor
Lateral incisor
Cuspid
First molar
Second molar
Permanent dentition
Tooth
First evidence of
calcification
Crown completed
Eruption
Root completed
3-4 months
10 months
3 years
1 - 1 years
2-2 years
At birth
2- 3years
7-9 years
4-5 years
4-5 years
6-7 years
5-6 years
6-7 years
2 -3 years
7-8 years
12-16 years
7-8 years
8-9 years
11-12 years
10-11 years
10-12 years
6-7 years
12-13 years
17-21 years
10 years
11years
13-15 years
12-13 years
12-14 years
9-10 years
14-16 years
18-25 years
3-4 months
3-4 months
4-5 months
1 - 2 years
2 - 2 years
At birth
2 -3 years
8-10 years
4-5 years
4-5 years
6-7 years
5-6 years
6-7 years
2 - 3 years
7-8 years
12-16 years
6-7 years
7-8 years
9-10 years
10-12 years
10-12 years
6-7 years
11-13 years
12-21 years
9 years
10 years
12-14 years
12-13 years
13-14 years
9-10 years
13-15 years
18-25 years
Upper
Central incisor
Lateral incisor
Canine
First premolar
Second premolar
1st molar
2nd molar
3rd molar
Lower
Central incisor
Lateral incisor
Canine
1st pre molar
2nd pre molar
1st molar
2nd molar
3rd molar
Suggested Reading
1. Avery JK.Oral Development and Histology (1st edn), BC Decker
Inc, Philadelphia, 1988.
2. Avery JK. Embryology of the Teeth. J Dental Research 1951;30:
490.
3. Bhaskar SN. Orabans Histology and Embryology (11th edn),
Mosby, 1997.
4. Johnson PL, Bevelander G. The Role of the Stratum Intermedium
in Tooth Development. Oral Surg 1957;10:437.
5. Mina M, Kollar E. The Induction of Odontogenesis in Non-dental
Mesenchymal Combine with Early Murine Mandibular Arch
Epithelium. Archive of Oral Biology 1987;32:123.
6. Thesleff I, Vaahtokari A. A Role of Growth Factors in the
Determination of Odontoblastic Cell Lineage. Proc Finn Dent Soc
1992;88:357-68.
7. Ten Cate A. Oral Histology Development: Structure and Function
(2nd edn), St. Louis CV Mosby, 1986.
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Development and
Anatomy of Craniofacial
Region
Vestibule
Lips
It is described in the Chapter 23: Disease of Lip.
Cheeks
Contentcheeks are the fleshy flaps, forming a large part
of the sides of the face. Mobile portion of cheeks is formed
by the buccinator muscle. Intraorally, it is covered by the
mucous membrane, and extraorally by the skin. The
mucous membrane of the cheeks is fixed to the inner
fascia of the buccinator muscle by tight strands of
connective tissue.
Posterior partposterior part consist of masseter muscle
and the parotid gland which are interposed between
the mucous membrane and buccinator muscle on one
side and the skin on the other side.
Nasolabial sulcuscheek are continuous infront with the
lips and the junction is indicated by the nasolabial sulcus
which extends from the side of nose to the angle of the
mouth.
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Hard Palate
Developmentthis is the tissue which is interposed
between oral and nasal cavity. Palate develops from
medial and lateral palatine process. Development of
palate starts in sixth week. It develops as intermaxillary
segment, between maxillary process of upper jaw. This
is called as primary palate. At the end of sixth week,
secondary palate develops from lateral palatine process.
Lateral palatine process grows medially downward or
vertically on either side of tongue.
Boundariesit is a partition between the nasal and oral
cavities. Anterolateral margins are limited by alveolar
arches and gingiva. Posterior margin is continuous
with the soft palate. Superior surface forms the floor of
the nose and inferior surface forms the roof of the oral
cavity.
Nerve supplyit is supplied by greater palatine nerves
from the greater palatine foramen and nasopalatine nerve
from the incisive foramen.
Blood supplyit is supplied by greater palatine branch
of the maxillary artery and nasopalatine artery.
Venous drainagepalatine vessels go to the pterygoid
plexus of veins.
Lymphatic drainageit drains mostly into the upper cervical and partly into the retropharyngeal groups of nodes.
Soft Palate
Gingiva
It is described in the Chapter 24: Gingival and Periodontal
Diseases.
Teeth
Structurethe teeth form a part of the masticatory
apparatus and are fixed to the jaws. In man, the teeth are
replaced only once (diphyodont) in contrast with nonmammalian vertebrates where teeth are constantly
replaced throughout life (polyphyodont). Each tooth has
three parts, i.e. crown (projection above the gums), root
(embedded in the jaw beneath the gum) and neck
(between the crown and root and surrounded by the
gums).
Nerve supplyit is supplied by anterior superior alveolar
(upper incisor and canine teeth), middle superior alveolar
(upper premolar teeth), posterior superior alveolar (molar
teeth) and inferior alveolar nerve (lower teeth).
Blood supplyit is supplied by posterior superior alveolar
artery (molar and premolar maxillary teeth), anterior
superior alveolar (It is branch of infraorbital artery and
supplies incisor and canine maxillary teeth) and inferior
alveolar artery (it enters the mandibular canal and gives
branches to the mandible and to the roots of each teeth
attached to the bone).
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Tongue
It is described in the Chapter 22: Diseases of Tongue.
Floor of Mouth
Contentit is a crescent shaped area between the lower
gingiva and undersurface of the tongue which composes
the inferior most portion of the oral cavity overlying the
mylohyoid and thyroglossal muscles.
Nerve supplyit is supplied by the branches of
trigeminal nerve.
Arterial supplyit is supplied by facial artery.
Venous drainagedrains into facial or lingual vein (Fig.
3-2).
Lymphatic drainagefrom the anterior portion of mouth,
lymphatics may pass into the deep cervical nodes or
laterally to the periosteal lymphatics and then to the
submandibular nodes and goes to the deep internal
jugular nodes.
11
cell of third and fourth arches. It forms the stylopharyngeal, cricothyroid, levator palatine and constrictor
muscle of the pharynx.
Contentit is a wide muscular tube situated behind the
nose, mouth and larynx. Clinically, it is a part of upper
respiratory tract. It is divided into three parts, i.e.
nasopharynx (nasal part of pharynx), laryngopharynx
(laryngeal part of pharynx) and oropharynx (oral part
of pharynx). Oropharynx is the middle part of the
pharynx situated behind the oral cavity.
Blood supplyit is supplied by ascending pharyngeal
branch of the external carotid artery, ascending palatine
and tonsillar branch of the facial artery, dorsal lingual
branch of lingual artery and greater palatine, pharyngeal
and pterygoid branch of the maxillary artery.
Venous drainageit is supplied by a plexus which
receives blood from the pharynx and soft palate and
prevertebral region and drains into the internal jugular
and facial veins.
Lymphatic drainageit drains into the retropharyngeal
and deep cervical lymph nodes.
Nerve supplyit is supplied by the pharyngeal plexus
of nerves which lies chiefly on the middle constrictor.
Muscles of Mastication
The muscles of mastication move the mandible
during mastication and speech. They are the masseter,
the temporalis, the lateral pterygoid and the medial
pterygoid.
Development
Maxillary Sinus
It is described in the Chapter 27: Disorders of Maxillary Sinus.
Salivary Glands
It is described in the Chapter 26: Disorders of Salivary Glands.
Pharynx
Developmentmuscles of pharynx are formed at about
7th week of intrauterine life. It forms from the muscle
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12
Masseter Muscle
Siteit is the most superficial to the masticatory muscle,
stretches as a rectangular plate from the zygomatic arch
to the outer surface of the mandible. It has three layers
i.e. superficial, middle and deep.
Superficial layerit arises by thick aponeurosis from the
zygomatic process of the maxilla and from the anterior
two-third of the lower border of zygomatic arch. Its fibers
pass downward and backward to be inserted into the
angle and lower half of lateral surface of ramus of
mandible (Fig. 3-4).
Middle layer it arises from the deep surface of the
anterior two-third of the zygomatic arch and posterior
one-third of lower border of zygomatic arch and is
inserted into middle of ramus of mandible.
Deep layerit arises from deep surface of the zygomatic
arch and is inserted into upper part of the ramus of the
mandible and into the coronoid process.
Nerve supplyit is supplied by masseteric nerve which
is a branch of anterior division of the mandibular nerve.
Blood supplythe masseteric artery which is a branch of
internal maxillary artery and the masseteric vein follow
the course of the nerve.
Lateral Pterygoid
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13
1
Fig. 3-7: Origin and insertion of medial pterygoid muscle.
Bones
The skull consists of the 22 bones. Out of which, 8 are paired
and 6 are unpaired. Paired bones are parietal, temporal,
maxilla, zygomatic, nasal, lacrimal, palatine and inferior
nasal concha. Unpaired bones are frontal, occipital,
sphenoid, ethmoid, mandible and vomer. From dental point
of view, maxilla and mandible are the most important and
they are described below:
Maxilla
Medial Pterygoid
Origin and insertionit is a thick quadrilateral muscle
attached to the medial surface of lateral pterygoid plate
and the grooved surface of the pyramidal process of the
palatine bone above. It has a superficial head which
originates from the tuberosity of the maxilla and
adjoining bone. Its deep head originates from the medial
surface of medial pterygoid plate and the lateral surfaces
of pyramidal process of palatine bone. Its fibers pass
downward, laterally and backward and are attached by
strong tendinous lamina to the posterior inferior part of
the medial surfaces of the ramus and the angle of
mandible as high as mandibular foramen and as forward
as mylohyoid groove (Fig. 3-7).
Nerve supplyit is supplied by branch of the mandibular
nerve.
Blood supplyit is supplied by the branch of maxillary
artery.
Functionsit helps in the elevation of mandible. Acting
with the lateral pterygoid, they protrude the mandible.
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Mandible
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Trigeminal Nerve
The trigeminal nerve is the 5th cranial nerve and is also
the largest. It has a large sensory root and a small motor
root. It is attached to lateral part of pons by its two roots. It
conveys both exteroceptive and proprioceptive impulses.
Exteroceptive impulses of touch, pain and thermal senses
are transmitted from skin of face, forehead, mucous
membrane of nasal and oral cavity, sinus, and floor of
mouth, teeth and anterior 2/3rd of tongue. Proprioceptive
impulses of deep pressure are conveyed from teeth,
periodontium, hard palate and temporomandibular joint
receptors.
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Maxillary division
It is intermediate division, and entirely sensory. It enters
the orbit through inferior orbital fissure. It is now named
infraorbital nerve and having traversed the infraorbital
groove and canal in floor of orbit, it appears on face through
infraorbital foramen. Branches are divided into 4 groups
Middle meningeal nervesupplies the dura with sensory
fibers.
Ganglionic branchesthey contain secretometer fibers for
the lacrimal gland and sensory fibers for orbital
periosteum and mucous membranes of the nose, palate
and pharynx.
Zygomatic nerveit is divided into two branches, i.e.
zygomaticofacial (supplies sensory fiber to skin over the
prominence of zygomatic bone) and zyomaticotemporal
(it supplies sensory fibers to skin over anterior temporal
fossa region).
Posterior superior alveolar nerveit gives sensory
branches to mucous membrane of sinus. It also supplies
the maxillary molars and their gingivae.
Middle superior alveolar nerveit supplies upper premolar
and mesiobuccal root of upper first molar.
Anterior superior alveolar nerveit supplies roots of
maxillary central and lateral incisors. They also send
branches to superior dental plexus of nerves within
maxilla. They also supply mucous membrane of anterior
part of maxillary sinus as well as labial gingivae of
incisors and cuspid teeth.
Inferior palpebral branchesthey supply sensory fibers to
skin of lower eyelid and its conjunctiva.
External or lateral nasal branchesthey supply skin of side
of nose.
Mandibular Nerve
It is the largest of the three divisions. It is divided into
following branches:
Nervus spinosusit supplies dura and mastoid cells.
Nerve to internal pterygoid muscleit supplies internal
pterygoid muscle.
Pterygoid nerveit enters medial side of external
pterygoid muscle to provide motor nerve supply.
Masseter nerveit supplies masseter muscle.
Anterior deep temporal nerveit ends in deep part of
anterior portion of temporal muscle.
Posterior deep temporal nerveit passes upward to deep
part of temporal muscle.
Long buccal nerveit supplies mandibular 2nd and 3rd
molars. It then sends fibers to mucous membrane and
skin of cheek, retromolar triangle, and buccal gingivae
of mandibular molars and mucous membrane of lower
part of buccal vestibule.
Auriculotemporal nerveit traverses upper deep part of
parotid gland and then crosses the posterior root of
zygomatic arch. It passes with superficial temporal artery
in its upward course and then divides with numerous
branches to tragus of external ear, to scalp, to the ear
and as for upward as vertex of skull.
Parotid branchesthey are sensory, secretory and
vasomotor fibers to the gland.
Articular branchesit enter the posterior part of the
temporomandibular joint.
Nodes
Sites
Occipital
Posterior auricular
Skin anterior to the temple, external meatus, lateral forehead, lateral eyelids, infraorbital
nodes, posterior cheek, part of the outer ear, parotid gland
Infra-orbital
Skin of inner corner of the eye, skin of anterior face, and superficial aspect of the nose
Buccal
Skin over the anterior face, mucous membrane of the lips and cheeks, occasionally
mandibular and maxillary teeth and gingivae
Submental
Tip of the tongue, midportion of the lower lips, chin, lower incisors and gingivae
Mandibular (supra-mandibular)
Skin over the mandible, mucous membrane of the lips and cheeks. Occasionally, maxillary
and mandibular teeth and gingivae.
Submandibular (sub-maxillary)
Upper and lower teeth and gingivae except mandibular incisor, anterior nasal cavity, palate,
body of tongue, upper lip, lateral angle of eye, submental nodes
Superficial cervical
Deep cervical
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Suggested Reading
1. Avery JK. Oral Development and Histology (1st edn), BC Decker
Inc, Philadelphia, 1988.
2. Bhaskar SN. Orabans Histology and Embryology (11th edn),
Mosby, 1997.
3. Gasser RF. The Development of Facial Muscle in Man. American
Journal of Anatomy 1967;120:357.
4. Grays Anatomy (38th edn), Churchill Livingstone, 1995.
5. Hall BK. The Embryonic Development of Bone. Amer Scientist
1988;76(2):174.
6. Poswillo D. The Pathogenesis of the First and Second Branchial
Arch Syndrome. Oral Surg 1973;35:302.
7. Ten Cate A. Oral Histology Development: Structure and Function
(2nd edn), St. Louis CV Mosby, 1986.
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Immunity
The word immunology derived from Latin word immunis
meaning free of burden. It is the resistance exhibited by
the host towards injury caused by microorganisms and
their products. It is a reaction of body against any foreign
antigens. Immunity against infectious diseases consists
of two main types, each with humoral and cellular
components and their effective cells. The importance of
immune system occurs in life-threatening infection suffer
by patient with immune defect.
Uses of Immunity
Understanding the diseaseit helps to understand the
etiology and pathogenesis of many diseases.
Vaccinedevelopment of vaccine can be done with the
help of immunity.
Treatmenttreatment of many diseases can be done
with antibodies.
Future susceptibilityit helps to find with future
susceptibility to disease with the help of HLA typing
system.
Innate Immunity
This is also called as natural immunity. This compromise
of preexisting non-specific defences. It is the resistance to
infection, which an individual possesses by virtue of his
genetic and constitutional make up. It does not depend
upon the prior contact with microorganisms or
immunization. Innate immunity can be considered at the
level of race, species or at individuals levels.
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Acquired Immunity
Active Immunity
It is resistance developed by an individual because of
antigenic stimulus. This involves active functioning of
hosts immune apparatus leading to synthesis of
antibodies or production of immunologically active cells.
Once the active immunity develops, it is long lasting. It is
also of two types.
Naturalit results from either a clinical or an
inapparent infection with the parasite, e.g. a person
who has recovered from an attack of smallpox develops
natural immunity to it. The immunity following
bacterial infection is generally less permanent than that
following a viral infection.
Artificialit is the resistance induced by vaccines,
which are preparations of live or killed microorganisms
or their product.
Passive Immunity
The resistance that is transmitted to a person in readymade
fashion is known as passive immunity. There is no
antigenic stimulant, instead preformed antibodies are
administered. There is no latent period, protection being
effective immediately after passive immunization. It is less
effective and inferior to active immunization, but it is
immediate in action and can be employed when instant
immunity is needed. It is also of two types.
Naturalit is the resistance passively transferred from
mother to baby. By active immunization of mothers
during pregnancy, it is possible to improve the quality
of passive immunity in the infants.
Artificialit is passively transferred to the recipient by
the administration of antibodies. The agent used is
hyperimmune sera of animal or human origin,
convalescent sera and pooled human gamma globulin.
Local Immunity
It is important in treatment of infection, which is either
localized or due to surgeries (postoperative infection), in
combating infections at the site of primary entry of the
pathogen. Natural infection or the live virus vaccine
administered provides local immunity.
Herd Immunity
This refers to the overall level of immunity in a community
and is relevant in the control of epidemic diseases. When
a large proportion of individuals in a community (herd)
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Antigen-Antibody Reaction
Antigen
Definitionany substance which when introduced
parenterally into a body stimulates the production of
an antibody, with which it reacts specifically and in an
observable manner. The immune system can respond
to antigen either by cell mediated immunity or by
humoral immunity.
Sizemost antigens are large molecules (over 1000
molecular weight). Smaller molecules do not provoke
an immune response unless bound to large carrier
molecules. The complete antigen is able to induce
antibody formation and produces a specific and
observable reaction with the antibody so produced.
Haptensthese are substances which are incapable of
inducing antibody formation by themselves, but can
react specifically with antibodies.
Epitopethe smallest unit to antigenicity is known as
an epitope or antigenic determinant.
IgM
It is formed by J chains into pentamers of the Ig molecules
and these attain very high molecular weight of 9000,000.
The large molecular size prevents it from leaving the
plasma, except when permitted by increased vascular
permeability in inflammatory lesions. As it has antigen
combining sites, it has good agglutinating and
complement fixing properties. It is the first class of
antibodies to be formed in immune response.
IgE
It binds selectively to mast cells and to basophils by its Fc
fragment. The binding of antigen to its Fab fragment
triggers reflex of histamine and other substances which
are important in anaphylactic type of hypersensitivity.
IgD
The function of IgD is largely unknown, but it may act as
an antigen receptor on the lymphocyte surface.
Antibody
Antibody is produced by plasma cells in the lymph nodes,
bone marrow and spleen. The cells are ovoid with an
eccentrically placed nucleus. The cytoplasm is basophilic.
One plasma cell produces antibody of one class, reactive
with only one antigen. There are five classes of
immunoglobulins which are as follows:
IgG
It is the most abundant immunoglobulin in the plasma
and extracellular fluid. It can cross placenta and is
important in passive transfer of immunity to the fetus. It
is capable of neutralizing toxins and may be cytolytic
through the activation of a complement. Polymorphs and
macrophages have surface receptors for Fc fragment of
IgG, thus binding of IgG to particular antigens promotes
adhesion of these cells and subsequent phagocytosis of
antigen.
IgA
It is secreted locally by plasma cells in the respiratory
passages, salivary and lacrimal glands and intestinal
mucosa. It is an important constituent of breast milk. IgA
occurs in two forms, serum IgA is principally a monomeric
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Fig. 4-3: Precipitation reactionA diagrammatic representation.
Precipitation Reaction
Formation of insoluble precipitatewhen a soluble antigen
combines with antibody in the presence of electrolyte
(NaCl) at a suitable temperature and pH, the antigenantibody complex forms an insoluble precipitate which
is greatly influenced by the relative proportions of
antigens or antibodies.
Resultsif into the same amount of antiserum in different tubes, increasing quantities of antigens are added,
precipitation will be found to occur most rapidly and
abundantly in one of the middle tubes in which Ag
and Ab are present in optimal or equivalent proportion.
The precipitation will be weak in proceeding or later
tubes (Fig. 4-3).
Mechanismcomplement takes part in many immunological reactions and is absorbed during the combination of antigens with their antibodies. The ability of
antigen-antibody complexes to fix complement is made
to use in the complement fixation test. This is a very
sensitive and a versatile test.
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Componentit consists of five reagents which are antigen, antibody, complement, sheep erythrocytes, and
amboceptor. Each of these has to be separately
standardized.
One unit or minimum hemolytic dose of complement
is defined as the highest dilution of guinea pig serum
that lyses one unit volume of washed sheep erythrocyte
in the presence of excess of hemolysin (amboceptor)
within a fixed time (usually 30 or 60 minutes) and at a
fixed temperature (37C) (Figs 4-5 and 4-6).
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Immunofluorescence
Mechanismfluorescence is a property of absorbing
light rays of one particular wavelength and emitting
rays with different wavelengths. Fluorescence dye
can be conjugated to antibodies and such labelled
antibodies can be used to locate and identify antigen
in tissue.
Suggested Reading
1. Gupte S. A Short Textbook of Medical Microbiology (9th edn), Jaypee
Brothers, New Delhi, 2006.
2. Roitt I, Brostoff J, Male D. Immunology (5th edn), Mosby, London,
1997.
3. Samaranayake LP. Essential Microbiology for Dentistry (2nd edn),
Churchill Livingstone, 2002.
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Neoplasm
Definition
It is an abnormal mass of tissue, growth of which exceeds
and is uncoordinated with that of normal tissues and
persists in the same excessive manner, after cessation of
the stimuli that evokes the changes.
Oncology is the study of neoplasm.
Nomenclature
There are mainly of two types neoplasm: benign and
malignant. Benign tumors are designated by attaching oma
to cell of the organ. Malignant tumors arising from
mesenchymal tissues are known as sarcomas, like
osteosarcoma. Malignant tumors of epithelial origin are
called carcinoma, like adenocarcinoma and squamous cell
carcinoma.
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Neoplasm
Carcinoma of stomach is five times higher in Japanese
than in Americans.
Nasopharyngeal cancer is common in south East Asians.
Age
Generally, it occurs in older individuals past 5th decade of
life but, there is variation in age groups. For example, acute
leukemia occurs in children, neuroblastoma in infancy.
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Sex
It is generally more common in men except cancer of breast,
gallbladder, and thyroid.
Acquired Preneoplastic
Conditions
These may be inflammatory, hyperplastic conditions or may
be certain benign tumors. It includes chronic atrophic glossitis, leukoplakia of oral cavity, vulva and penis, cirrhosis of
liver, chronic irritation and multiple neurofibromas.
Carcinogenesis
Carcinogenesis or oncogenesis or tumorigenesis means
induction of tumors; agents which can induce tumors are
called carcinogens. Carcinogens are broadly divided into
four groups (Fig. 5-3):
Chemical carcinogens
Physical carcinogens (radiation)
Hormonal carcinogens
Biologic carcinogens (virus)
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Chemical Carcinogenesis
Initiators of Carcinogenesis
Direct-acting carcinogensthese require no metabolic
conversion to become carcinogens.
Alkylating agents it includes, various chemotherapeutic
drugs that have successfully cured, controlled or delayed
recurrence of certain types of cancers only to later evoke
a second form of cancer usually leukemia. Various
agents used are cyclophosphamide, chlorambucil,
busulfan, melphalan, nitrosourea, -propiolactone and
epoxides. This tragic consequence is called as Pyrrhic
victory which becomes less of a victory when their initial
use has been converted to cause later on second form of
cancer.
Acylating agentssubstances like acetyl imidazole.
Indirect-acting carcinogens or procarcinogensthese are
chemical substances requiring metabolic activation for
becoming potent initial carcinogens.
Polycyclic aromatic hydrocarbons (in tobacco, smoke,
animal foods, industrial oil, and atmospheric
pollutants). Important chemical compounds included
are benzanthracene, benzapyrene, methylcholanthrene.
They may cause lung cancer, skin cancer, cancer of oral
cavity, and sarcoma.
Aromatic amines and azo dyesThese are -naphthylamine, benzidine, azo dyes used for coloring foods, and
acetyl aminofluorene. They may cause bladder cancer
and hepatocellular carcinoma.
Naturally occurring productAflatoxin, actinomycin-D,
mitomycin-C, safrole, and betel nut. It can cause hepatocellular carcinoma.
Miscellaneousnitroso compounds, vinyl chloride
monomer, asbestos, arsenical compounds, metals like
nickel, lead, chromium, and insecticides, fungicides can
cause gastric carcinoma, hemangiosarcoma of liver,
bronchogenic carcinoma, epidermal hyperplasia, basal
cell carcinoma, and lung cancer.
Promoters of Carcinogenesis
Physical Carcinogenesis
Mechanism of Action
Binding to DNA and RNAthe great majority of chemical
carcinogens are mutagens. They bind directly to DNA
and RNA or cytoplasmic proteins to specific sites within
Radiation Carcinogenesis
Forms of radiationradiation whenever in the form of
UV light from sunlight, UV lamp, welders arc, or
ionizing radiation like X-ray, , and ray, radioactive
isotopes, protons and neutrons are established
carcinogens.
Example of radiation induced cancersmost frequent
radiation induced cancers are leukemia, cancer of
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Neoplasm
thyroid, skin, breast, lung, and salivary gland.
Therapeutic irradiation can also induce carcinogenesis.
Facts about radiation causing cancerradiant energy have
potential of producing mutation and even killing cells.
It can affect carcinogenesis by the following facts:
Few tumors appear only after long latent period
during which successive generation of clones are
developed.
The radiation initiation is generally irreversible, but
at a low dosage level is amenable to repair.
The effect of radiation depends upon a number of
factors such as type of radiation, dose, length of
interval between the doses, capability of cells to repair
in intervals and various host factors such as age,
individual susceptibility, immune competence,
hormonal influence and type of cell irradiated.
Mechanismit induces cancer by following mechanism;
Radiation may directly alter the cellular DNA and it
may dislodge ions from water and other molecules of
cell and result in the formation of highly reactive free
radicals that may bring about the damage.
Radiation mutation may render cell vulnerable to
other carcinogenic influence, i.e. acting as cocarcinogen.
Inhibition of cell division and inactivation of enzymes.
Radiation might cause cell killing; permitting
survivors to proliferate and thereby, become
vulnerable to oncogenic influence.
Hormonal Carcinogenesis
Carcinoma is most likely to develop in organs and tissues
which undergo proliferation under influence of excessive
hormonal stimulation. Hormone sensitive tissues
developing tumors are breast, endometrium, myometrium,
vagina, thyroid, liver, prostate, and testis.
Estrogenin experimental animals, estrogen can cause
induction of breast cancer in mice. Other cancers which
can be induced in mice by estrogens are squamous cell
carcinoma of cervix, connective tissue tumor of myometrium, tumor of kidney in hamsters, and benign and
malignant tumors of liver in rats. In case of human
women receiving estrogen therapy and women with
estrogen secreting granulosa cell, tumor of the ovary have
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Biologic Carcinogenesis
The epidemiological studies on different types of cancer
indicate the involvement of transmissible biologic agents
in their development, chiefly viruses. It has been estimated
that about 20% of all cancers worldwide are virus
associated cancers. Therefore biological carcinogenesis is
largely viral oncogenesis. A large number of viruses have
been proved to be oncogenic in wide variety of animals
and in certain types of cancers in humans.
The association of oncogenic virus with neoplasia was
observed by an Italian physician Sanarelli in 1889 who
noted association between myxomatosis of rabbit with
poxvirus. Oncogenic viruses fall into 2 broad groups, i.e.
those containing ribonucleic acid are termed as RNA
oncogenic viruses and those containing deoxyribonucleic
acid are termed as DNA oncogenic viruses.
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Neoplasm
Encodingoncogenes may encode a defective receptor
that send stimulating signals to the cells, even in the
absence of growth factors.
Multiple mutationscancer is a genetic disease that
results when multiple mutations accumulate in the DNA
of a cell and specific chromosomal abnormalities
predispose to cancer.
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Theories of Carcinogenesis
The Epigenetic Theory
According to this theory, the carcinogenic agents act on the
activators or suppressors of genes and not on the genes
themselves and result in the abnormal expression of genes.
Genetic Theory
Conceptthis is the most popular theory which suggests
that cells become neoplastic because of alteration in the
DNA. It is suggested that, the secret of cancer lies within
the normal cells themselves in the form of protooncogenes (C-oncs). The mutated cells transmit their
characters to the next progeny of cells. Inappropriate
over expression of the gene or point mutation cause the
cell to produce stimulating growth factors or in some
way damages normal regulatory control. The qualitative
and quantitative changes in the expression of genome
may be brought about by carcinogenic influence, i.e.
chemical, viruses, radiation or spontaneous random
mutations.
OncogenesOncogenes are the transforming genes
present in many tumor cells. Closely related genes are
detected on normal animal and human cells and are
called as proto-oncogenes or cellular oncogenes,
abbreviated as c-oncs
Cellular oncogenes of the host cells can transcribe its
copies in the viral genome of acute transforming
oncogenic retroviruses called as viral oncogenes or
v-oncs. An alternate mechanism is by anti-oncogenes
in which, there is inactivation or deletion of genes that
normally perform the function of suppressing cell
proliferation, thus allowing them to proliferate.
Feedback deletionaccording to genetic regulatory
mechanism theory, primary change in the cell consists
of a modification of repressor molecule which controls
the functions of the gene. The repressor molecules are
either RNA or protein. The modification of repressor
molecules removes their orderly inhibitory control,
which is responsible for normal morphogenesis and
differentiation, and unearths the cell genetic potentiality
for unrestricted growth. This concept of loss of growth
control is described as feedback deletion.
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Virus Theory
Monoclonal Hypothesis
Currently, there is strong evidence on studies of human
and experimental animals that most of the cancers arise
from single clone of transformed cell.
The best documentation of monoclonal origin of cancer
cells come from the study of G6PD in women who are
heterozygous for its two isoenzymes A and B. It is observed
that all tumor cells in benign uterine tumor (leiomyoma)
contain either A or B genotype of G6PDi.e. the tumor cells
is derived from a single progenitor cell.
Multistep Theory
According to this theory, carcinogenesis is a multistep
process which is substantiated in vitro by changes in experimental animals as well as in vivo by changes in human
cancers.
In chemical carcinogenesis, there are two essential
features, i.e. initiation and promotion. Many tumors arise
from combination of activation or growth promoting
oncogenes and inactivation of growth suppressing antioncogenes. In some cancers, there is initial dysplastic
change that may progress into carcinoma in situ and then
into invasive carcinoma.
Metastasis
Metastasis is defined as spread of tumor by invasion in such a
way that discontinuous secondary tumor mass/masses are formed
at the site of lodgment. This metastasis is the transfer of the
disease from one organ or part to another not directly connected
with it.
If malignant cells did not metastasize, the surgical
removal of primary neoplasm would completely cure the
patient. Metastasis is fundamentally an embolic process.
The invasiveness of malignant cells involves motility,
which requires change in shape and adhesiveness and
ability to degrade the matrix in order to penetrate it.
Thus, a definition of the behavior of the metastatic tumor
cells is the tendency to cross the tissue compartment /
boundary and intermix with other cell types. The metastatic
process can be divided into several sequential steps
although these steps are interconnected.
Factors which control metastasis are proteolysis, cell
adhesion, tumor angiogenesis, cell mediated immunity and
genetic factor.
Steps of Metastasis
Breaking of cellsthe breaking of loose neoplastic cells
from the parent tumor.
Invasioninvasion of the matrix (sarcoma), penetration
of the basement membrane and invasion of connective
tissue (carcinoma).
Entering the blood vesselsit then entering the wall of
blood and lymphatic vessels.
Survivalsurvival of malignant cells in the bloodstream.
Survival in the compatible tissue environment and
induction of growth factor to stimulate new vessel
formation to obtain nutrition.
Emergence of cellsemergence of the malignant cells from
the blood vessels in the form of the emboli and lodgment
in other tissues.
Multiplicationmultiplication of neoplastic cells and
growth to form secondary neoplasm at the new site.
Control mechanismeach of these steps is probably
controlled by different molecular mechanism and this
may explain the differences in the behavior with
reference to tumor metastasis. Neoplastic cells within a
single tumor might differ in their ability to metastasize.
A sub-population of cells preexists within the heterogeneous primary tumor. The relative size of this subpopulation in the primary tumor may vary with time
between the neoplasms.
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Neoplasm
Routes of Metastasis (Fig. 5-6)
Lymphaticsparticularly for carcinoma and lymphosarcoma. For example, mouth-to-neck nodes and breastto-axillary nodes.
Bloodstreamparticularly veins from gut via portal
circulation to liver, from systemic sites through right
heart to lung, from left heart to any systemic sites.
Cavitiesalong epithelium lined cavities, for example:
respiratory tract, gut, urinogenital tract etc.
Otherstranscelomic spread, cerebrospinal fluid, tissue
planes and through nerve sheath.
Grading
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CIN Grading
Alternative classification for grading of dysplasia and
carcinoma in situ together is cervical intraepithelial
neoplasia (CIN). According to this grading, the criteria are
as follows:
CIN Iit represents less than 1/3rd involvement of the
thickness of the epithelium.
CIN IIin it, there is 1/3rd to 2/3rd involvement.
CIN IIIit is full thickness or equivalent to carcinoma in
situ.
Depending on thickness of squamous epithelium involved
by atypical cells
According to this, grading of dysplasia is as follows:
Mild
Moderate
Severe
Staging
It is the extent of spread of tumor within patients.
Assessment
It is assessed by following ways:
Clinical examinationstaging can be assessed clinically
by the size and extent of primary lesion.
Investigationinvestigation like radiology, sonography
can lead to staging of disease.
Pathological examinationthis is very important part
while staging of neoplastic process is done. Mainly
biopsy, cytology are used.
Infiltrationdegree of infiltration of primary lesion
should be carried out.
Metastasispresence or absence of metastasis to regional
lymph nodes. Presence and absence of distant metastasis. Involvement of contralateral or ipsilateral node.
Whether node are fixed or not.
Objectives
Treatment planningit aids clinician in the planning of
treatment.
Prognosisto give some indication of prognosis.
Evaluation of treatmentto assist in evaluation of the
result of treatment.
Exchange of informationto facilitate the exchange of
information between treatment centers.
Investigationto contribute to the continuing investigations of human cancer.
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Neoplasm
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TNM Staging
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Features
Benign tumors
Malignant tumors
Boundaries
Surrounding tissues
Often compressed
Usually invaded
Size
Usually small
Often large
Growth
Capsule
Present
Absent
Degeneration
Rare
Common
Recurrence
Not common
Common
Fixity
Absent
Present
Secondary changes
End of growth
Pattern
Basal polarity
Retained
Lost
Pleomorphism
Often present
Nucleo-cytoplasmic ratio
Normal
Increased
Anisonucleosis
Absent
Present
Hyperchromatism
Absent
Often present
Mitosis
Cytoplasm
Function
Well maintained
Growth rate
Usually slow
Usually rapid
Local invasion
Metastasis
Absent
Present frequently
Macroscopic Features
Microscopic features
Suggested Reading
1. Franks LM, Teich NM. Introduction to the Cellular and Molecular
Biology of Cancer (3rd edn), Oxford University Press, 1997.
2. Howaldt HP, Kainz M, et al. Proposal for Modification the TNM
Staging Classification for Caner of the Oral Cavity: DOSAK.
J Craniomaxillofac Surg 1999;27:275-88.
3. Underwood JCE. General and Systematic Pathology (3rd edn),
Churchill Livingstone, 2000.
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Infection Control in
Dental Office
Introduction
In dental practice, the risk of infection is a high priority
issue, considering the nature of oral environment which is
rich in diverse aerobic and anaerobic bacterial flora and
more hazardous viral pathogens. Dental personnel and
patients are at increased risk of acquiring many diseases
which can get transferred from patient to doctor and
vice versa. With changing times, risk associated with
viral pathogens such as herpes, hepatitis and HIV are
increased. The common goal of infection control is to
eliminate or reduce the number of microbes shared between
people.
Many objects in the dental office are potential source of
infection. These are called as vectors. For examples; saliva,
blood, nasal secretion, dust, hands, hair, clothing, films,
X-ray machine, dental instrument and dental chairs. Cross
infection occurs when these vectors transmit pathogenic
organisms from one patient to another or to dental
personnel.
All patients should be treated using universal
precaution. There should be no exception and no extra
precaution for specific patients. By practicing infection
control, patients as well as operator can be protected.
High standard of dental infection control and
occupational safety must be followed by dental personnel;
for the safety of patient and dental health care workers.
The word infection control does not mean total prevention
of iatrogenic, nosocomial or occupational exposure, but it
means to reduce the risk of disease transmission.
General Consideration
Every person working in hospital or general practitioner
has a legal duty to ensure that all necessary steps are taken
to prevent cross infection protect themselves, their
colleagues and the patients.
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Methods of Decontamination
Sanitizationthis is first level of decontamination. This
is process of physical cleaning to reduce quantity of
microbes. This is done by cleaning the surface with soap
and water or with detergent.
Disinfectionthis is next level of decontamination. It kills
all vegetative microorganisms, fungi. This uses chemical
germicides, radiation, ultraviolet rays or heat.
Sterilizationthis is third level. Sterilization kills all
bacteria, fungi, virus and bacterial endospores. It uses
chemical methods and physical methods.
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Working Area
Sterilization
Sterilization is the process of destroying all the microbial
life from an article or surface inclusive of bacterial spores.
It can be achieved by:-
Dry Heat
Moist Heat
Moist heat denatures and coagulates the proteins of a
microorganism and is a better method of sterilization due
to a higher efficiency of penetration than dry heat and a
faster killing rate. This is due to latent heat of vaporization
which is present in moist heat. This principle is used in the
autoclave (Fig. 6-3).
Various methods of autoclaving are available base on
the same principle. The temperature required for this is
121C with a minimum holding time of 20 minutes. For
practical consideration, vacuum models are operated at a
temperature of 139C, 332lb pressure and holding time of 5
minutes.
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The basis for infection control lies in the fact that, as dentist
are more prone to acquire many infectious diseases;
including blood borne diseases such as AIDS and hepatitis
B. The procedure for infection control can be grouped into
six major areas:
Training
All the staff members should be given training of
infection control procedure. They should be told about the
hazards due to infection which can occur to them or get
transferred from them to patients. Continued education
programme about infection control measures should be
held regularly.
Disinfection
This is the process by which pathogenic microorganisms
are removed from the surface without removing bacterial
spores. This process is used to treat articles which do not
penetrate mucous membrane or skin. Examples of
disinfectants are formaldehyde, halogens, phenols and
chlorhexidine.
Vaccination
This is very important in infection control procedure. All
clinical staff should be vaccinated against hepatitis B, etc.
and regularly get it checked.
Covering of Wound
Open wound on the hand should be covered with
waterproof dressing. Hand injuries during dental
procedure should be avoided.
Hand Washing
It provides protection to both the patients and the dental
team. Hand washing continues to be an important means
for personal protection and of disease prevention. Washing
hands before gloving reduces the skin microbial flora and
helps to prevent skin irritation by waste products of
bacterial growth under gloves.
Gloved hands should be washed under running water
before and after taking radiograph of patient and a
disinfectant like povidone iodine and 7.5% surgical scrubs
or chlorhexidine gluconate 4% surgical scrub should be
used.
Hand washing should be done at the start of treatment
and after removing the gloves. Hand washing after using
gloves is required to reduce the bacterial count that build
on the skin during glove used. Specific step should be taken
to hand wash. They are as follows (Fig. 6-5).
Wet hands with warm water.
Dispense an adequate amount of soap.
Thoroughly rub the hands including area around the
thumb and finger for 30 seconds.
Wash hand with warm water to remove the soap.
Dry hands with proper towel.
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Gloves
Gloves used for patient care protect the dental team
members from direct contact with patient microbes and
they protect patients from contact with microbes on the
hands of dental team member. Gloves need to be changed
between patients and are to be washed with detergent.
Gloves should be inspected periodically during patient care
and torn or punched gloves should be removed as soon as
possible and the hands should be washed.
Although some of these types, i.e. utility gloves can be
autoclaved (nitrile type) through washing with an
antimicrobial hand washing agent followed by rinsing and
towel drying is adequate between routine uses.
Exam gloves are made from latex, vinyl, nitrile and
polyurethane. While wearing the gloves, you should look
for breaches in the integrity of gloves. Gloves should never
be washed before use or disinfected for reuse. Grubby
gloves and cleaning swabs should be placed in suitable
disposable bags and sealed for incineration.
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Fig. 6-9: Complete face shield also help to protect from aerosols
from patient oral cavity.
Instrument Asepsis
You should provide instruments that are safe for patients
use. Pre-soaking of contaminated instruments keeps them
wet until thorough cleaning can occur. This procedure
prevents blood and saliva from drying on the instrument
which facilitate cleaning.
A cleaning solution manufactured for use in ultrasonic
cleaners should be used and it needs to be changed daily.
Protection against splashing and direct contact with this
contaminated solution is important. Usually 2 to 20 minutes
are needed to clean instruments ultrasonically as
determined by observing the cleanliness of the processed
instruments and making appropriate adjustments.
After cleaned instruments have been rinsed and dried,
they are to be packaged in functional sets before sterilization. Instrument packages sterilized in steam becomes
wet and must be allowed to dry before handling so that the
packing does not tear.
Surface Asepsis
It eliminates the involvement of surface in the spread of
diseased agents.
There are two general approaches to surface asepsis.
One is to clean and disinfect contaminated surface and the
other is to prevent the surface from becoming contaminated
by use of surface covers.
Disinfection of surfaces involves the cleaning of surface
after every patient and application of a disinfectant
chemical. These chemicals include alcohol, phenols,
glutaraldehyde, chlorine etc.
Spittoons should be flushed with water.
Aseptic Technique
Fig. 6-10: While examining the patient, dental professional should
wear mask, gloves.
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Suggested Reading
1. American Dental Association, infection control recommendation
for the dental office and dental laboratory. J American Dental
Association, 1992;123(8), suppl 1.
2. Bachman CE, White JM, Goodis HE, et al. Bacterial adherence
and contamination during radiolgic processing. Oral Surg Oral
Med Oral Pathol 1990;76;112-9.
3. Ciola B. A readily adaptable, cost effective method of infection
control for dental radiography. JADA 1988;117:349-52.
41
4. Kartz JO, Geist JR, Melanuria JA, et al. Potential for bacterial and
mycotic growth in developer and fixer solutions; J
Dentomaxillo-facial Radiol 1988; (suppl); 52.
5. Kohli A, Puttaiah R. Infection control and occupational safety
recommendation for oral health professional, Dental council of
India, 2007.
6. Miller CH. Sterilization and disinfection, why every dentist needs
to know; JADA 1992;123: 46.
7. Stranczyk DA, Paunovich ED Broome JC, et al. Microbiological
contamination drig dental radiographic film processing. Oral
Surg Oral Med Oral Pathol 1993;76;112-9.
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Case History
Introduction
Personal Information
Name
A patient usually likes to be called by name. This will help
to elicit the history properly, but it will also be of psychological benefit to the patients. In case of pediatric patients,
addressing the patient by his/her name or pet name will
encourage him/her to talk freely. Advantage of knowing
the patient names are identification, to maintain record,
communication and psychological benefit
Age
Knowing the patients age is beneficial to the clinician in
more ways than one.
Diagnosis
Certain diseases are more common at certain ages (Tables
7-1 to 7-4).
Treatment Planning
Fig. 7-1: Taking and recording history of the patient is important
part in diagnostic sequence.
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Case History
Table 7-1: Disease present at/since birth
DENTAL DISEASES
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Related to jaw
Agnathia
Facial hemihypertrophy
Macrognathia
Cleft palate
Facial hemiatrophy
Related to lip
Commissural pits and fistulae
Double lip
Cleft lip
Hereditary intestinal polyposis syndrome
Related to gingiva
Congenital epulis of the newborn
Fibromatosis gingiva
Related to rest of oral mucosa
Pigmented cellular nevus
Cystic hygroma
Fordyces granule
Systemic diseases
Congenital heart diseases
Bronchiectasis
Pneumonia
Related to tongue
Microglossia
Macroglossia
Aglossia
Ankyloglossia
Cleft tongue
Fissured tongue
Median rhomboidal glossitis
Lingual thyroid nodule
Child dose
Childs age
Young rule = adult dose
Age+12
Child age at next birth day
Clark rule = adult dose
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Age
Dilling rule = adult dose
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Related to teeth
Pre-deciduous dentition
Related to TMJ
Aplasia or congenital hypoplasia of the mandibular condyle
Others
Teratoma
Erythroblastosis fetalis
Hemophilia
SYSTEMIC DISEASES
Related to heart
Atrial septal defect
Patent ductus arteriosus
Ventricular septal defect
Pulmonary stenosis
Aortic stenosis
Tetralogy of Fallot
Related to respiratory system
Bronchiolitis
Cystic fibrosis
Related to CNS
Congenital myopathy
Aqueduct stenosis
Related to alimentary tract
Meckels diverticulum (it is common congenital anomaly. It is a
small hollow wide mouthed sac protruding from ileum)
Annular pancreas (pancreas encircle the 2nd and 3rd part of
duodenum leading to gastric outlet obstruction )
Sex
Diagnosiscertain diseases are more common in a
certain sex (Tables 7-5 and 7-6).
Giftingin case of pediatric patients, gifting varies
according to the sex of the child.
Estheticsfemales are much conscious about esthetics.
Emotionfemales are emotional and sensitive hence one
must be very careful during treatment. Failure to thrive,
educational and emotional abuse are most common in
case of female patients.
Child abusesexual abuse or exploitation is more
common in case of females.
Dosefemales have smaller body weight and require
lower dose as compare to males.
Drug interactionin females, consideration must be given
to menstruation, pregnancy and lactation. Drugs given
during pregnancy can affect the fetus. Antihypertensive
drugs interfere with sexual function in males but not in
females. Gynecomastia is a side effect of ketoconazole,
metronidazole, chlorpromazine and digitalis administrations that occur in males. Ketoconazole causes loss of
libido in men but not in women.
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Hypertension
Congestive cardiac failure
and myocardial infarction
Chronic valvular heart disease
Hepatitis
Asthma
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Caries
Pleomorphic adenoma
Adenoameloblastoma
Myasthenia gravis
Peripheral cemental dysplasia
Juvenile periodontitis
Recurrent aphthous stomatitis
Peripheral giant cell granuloma
Peripheral ossifying fibroma
Idiopathic thrombocytopenic
purpura
Case History
Table 7-6: Diseases more common in males
Attrition
Carcinoma in situ
Keratoacanthoma
Leukoplakia
Verrucous carcinoma
Liposarcoma
Hodgkins disease
Solitary plasma cell myeloma
Wegeners granulomatosis
Osteoid fibroma
Benign osteoblastoma
Reiters syndrome
Adenolymphoma
Pernicious anemia
Address (Residence)
Correspondenceit is necessary for future
correspondence. Full postal address of the patient should
be taken for future communication.
Geographical prevalence of dental/oral diseasesa few
diseases have got geographical distribution. Dental caries
and mottled enamel are dependent on the fluoride content
of the domestic water. In India, cancer of the lip is very rare
and cancer of tongue and buccal mucosa constitute the bulk
of oral cancers. In cancer patients from Mumbai, common
site affected is the tongue and in Chennai, it is the buccal
mucosa. Dental caries is more common in modern
industrialized areas while periodontal diseases are more
common in rural areas. Habits also vary according to
residence. Chutta, a form of tobacco, is common in
Tamilnadu, gutkha in Bihar, hukli in Bhavnagar district of
Gujarat. Bajjar is a dry snuff used by women in Gujarat.
Geographical prevalence of medical diseasethere are many
medical diseases which have got geographical
prevalence. For example filariasis (Orissa), leprosy
(Bankura district of West Bengal), gall bladder disease (West
Bengal and Bangladesh), peptic ulcer (North Western and
Southern parts of India), sleeping sickness (South Africa),
hydatid disease (Australia), tropical disease (tropical
countries), kangri cancer (Kashmir), anemia and
malnourishment (rural areas) obesity, arthrosclerosis (urban
area) and other industry related diseases (urban areas).
Registration Number
It is good to give each and every patient a unique registration
number and to maintain his/her records under that number
so that when the patient visits the doctor at a later date, the
doctor can know the details of the patient and the treatment
done before.
Occupation
Financial statustreatment varies according to the
financial status of the patient. Expensive treatment
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Religion
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Case History
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Trauma
Normal resorption of deciduous teeth
Pulpoperiodontal disease
Malignant tumor
Chondroma
Myxoma
Hemangioma
Histiocytosis X
Familial hypophosphatemia
Papillon-Lefvre syndrome
AIDS
Bad taste
Aging changes
Heavy smoking
Poor oral hygiene
Dental caries
Periodontal disease
ANUG
Diabetes
Hypertension
Medication
Psychosis
Neurological disorder
Decreased salivary flow
Uremia
Intraoral malignancy
Halitosis
Poor oral hygiene
Periodontal disease
Third molar opercula
Decayed tooth
ANUG
Oral cancer
Spicy foods
Tobacco use
Nasal infection
Tonsillitis
Pharyngeal infection and tumor
Gastric problems
Diabetes
Uremia
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Ulcer
Mode of onsetmode of onset and duration of the ulcer
should be asked and recorded.
Painulcers associated with inflammation are painful;
ulcers associated with epithelial or basal cell carcinoma
are painless.
Dischargeserum, blood and pus.
Associated diseasestuberculosis, nephritis, diabetes, and
syphilis.
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Case History
Past Dental History
Patient attitudein addition to chief complaint and
history of the present illness, it is necessary to elicit a
past dental history. It is necessary to obtain description
of the details of previous dental treatment and his
reaction to his dentist and the treatment. By noting this,
you may get accurate idea of the importance he gives to
good dental treatment and how conscious he has been
in pursuing a goal of good oral health.
Component of past dental historysignificant component
of past dental history include previous restorative,
periodontic, endodontic or oral surgical treatments,
reasons for loss of teeth, untoward complication of dental
treatment, experience with orthodontic appliance and
dental prostheses; and radiation or other treatment for
past oral and facial lesions.
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Consultation letter
Place
Date
Patient Name
Referral doctor name
To
Dr X
I am referring the patient who has to undergo
stressful procedure. We have to use local anesthesia for
this patient. Medical history of patient reveals that he is
suffering from . Please advice us about the status
of the patient whether he can undergo stressful dental
procedure, which type of local anesthesia should we use
and what precaution should we take.
Patient signature
Date
Doctor signature
Date
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Case History
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Family History
This is very important for many hereditary diseases. Many
diseases recur in families like hemophilia, diabetes mellitus,
hypertension and heart diseases.
Examination
Steps of Clinical Examination
Inspectionit is referred to as passive visualization of
the lesion. Intraorally mirror can be used for visualization of structure.
Palpationthis will help for evaluation of structure and
to know their consistency, fixity etc.
Bilateral palpationthis is done to differentiate
between symmetrical structures on both side of face
(Fig. 7-8).
Bidigital palpationin this, two fingers are used to
manipulate the tissue. It is used for thinner structure
(Fig. 7-9).
Bimanual palpationit is done by palms of both
hands. In this, one hand is used to support the
structure hand and another is used to manipulated
the structure. This type of palpation is used in floor of
mouth (Fig. 7-10).
Auscultationit is used to study the movement of TMJ
and also used for examination of venous malformation
(Fig. 7-11).
Probingthis is used to detect carious lesion.
Percussionthis is used to check whether patient is
having periapical infection.
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2
Fig. 7-11: Auscultation of TMJ is done to examine the
movement of TMJ.
General Examination
Build
It can be described as poorly built, moderately built and
well built.
Asthenicit appears as lean and underweight.
Sthenicthey are athletic in appearance.
Hypersthenicpersons have thick muscular and heavy
bone structure.
Pyknicthey appear as heavy and rounded.
Cachexiathere is abnormally low tissue mass, occur
due to malnutrition.
Pulse
Fig. 7-9: Bidigital palpation is done in case of thinner structure.
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Case History
Blood Pressure
Normal blood pressureSystolic 120140 mm Hg and
diastolic 80 mm Hg (any above 90 is abnormal). Normal
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Temperature
Procedurethis is normally taken in the mouth or in the
axilla by keeping mercury thermometer (Fig. 7-14) for a
minute. The temperature of mouth is about 1 degree
higher than that of axilla. The normal body temperature
varies from 36 degree Celsius to 37.5 degree Celsius. The
lowest temperature being between 2-4 am and highest
in the afternoon. The normal oral temperature is 37oC.
Fever or pyrexia is more than 1 degree or any rise above
the maximum normal temperature.
Conversion of Fahrenheit to Celsiustemperatures usually
taken in Fahrenheit and to convert Fahrenheit into
Celsius subtract 32 and multiply by 5/9.
Respiration
Significanceit is used to assess the condition of the
patient under anesthesia and in early postoperative days.
Procedureyou should always check the respiration
while checking the pulse of the patient. You should look
at the patient abdomen and see how many times he
breath. One complete cycle of inspiration and expiration
is counted as one. Normal rate14-18 cycles/minute
(Fig. 7-15).
Tachypnoea (fast breathing)it occurs in fever, shock,
hypoxia, cerebral disturbances, metabolic acidosis,
tetany, and hysteria.
Types of fever
Continuous feverthe temperature remains above
normal throughout the day and does not fluctuate
more than 1 degree in 24 hours. E.g. lobar pneumonia,
typhoid and infective endocarditis.
Remittent feverThe temperature remains above
normal throughout the day and fluctuates more than
1 degree in 24 hours e.g. typhoid.
Intermittent feverthe temperature is present only for
some hours in a day and remits to normal for the
remaining hours. When the spike occurs daily, it is
called as quotidian, when every alternate day it is
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Case History
Bradypnoeaslow and deep respiration is seen in
cerebral compression.
Snoring noiseparalysis of the soft palate causes an
inspiratory snoring noise.
Expiratory wheezingexpiratory wheezing is heard in
bronchitis and asthma.
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Clubbing
Definitionclubbing is bulbous enlargement of soft part
of the terminal phalanges of the nail (Figs 7-16 and
7-17).
Cyanosis
Definitioncyanosis is the bluish discoloration due to
increased amount of reduced Hb (more than 5 mg%) in
capillary blood.
Typesit can be central, peripheral, cyanosis due to
abnormal pigment or mixed.
Sites where peripheral cyanosis is looked fornailbed, tip
of the nose, skin of the palm and toes.
Sites where central cyanosis is looked fortongue and other
sites mentioned above. Tongue is unaffected in
peripheral cyanosis.
Causes
Centralcardiac causes like congenital cyanotic heart
disease and congestive cardiac failure, pulmonary
causes like chronic obstructive lung disease (Fig.
7-18), collapse and fibrosis of lung, pulmonary
obstruction, and high altitude due to low pressure of
O2.
Peripheralit includes cold, increased viscosity of
blood and shock.
Mixedit includes acute left ventricular failure, mitral
stenosis and cyanosis due to abnormal pigments like
sulfonamides and aniline dye.
Causesit includes:
Pulmonary causeslike bronchogenic carcinoma, lung
abscess, bronchiectasis, and tuberculosis with
secondary infection.
Cardiac causeslike infective endocarditis and
cyanotic congenital heart disease.
Alimentary causeslike ulcerative colitis, Crohns
disease and biliary cirrhosis.
Icterus
Definitionin jaundice, there is icteric tint of the skin,
due to presence of bilirubin, which varies from faint
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Head
Extraoral Examination
Skin
Appearancechanges in appearance, rashes, sores,
lumps or itching is looked for and history of sun
exposure is questioned.
Colorit is seen for anemia and jaundice.
Generalized pallorit is seen in severe anemia. Pallor
can be seen in hypopituitarism, shock, syncope, left
heart failure and Raynauds disease.
Lemon yellow tinta pale lemon yellow tint in
hemolytic jaundice and dark yellow or orange tint in
obstructive jaundice is seen.
Yellowness of skinyellowness of skin is seen in
carotenemia.
Textureit is thickened, greasy and loose in acromegaly.
In dehydration, skin is dry and inelastic so that it can be
pinched into ridge. Skin is atrophied with age and
sometimes after treatment with glucocorticoids.
Jaws
Normal landmarknormal anatomic landmarks to be
identified include mandibular border, angle of mandible,
condyle and coronoid process, maxillary bone, lingual
notch and maxillary sinus.
Tenderness over the jawsnote any tenderness over the
joint or masticatory muscles (temporalis, masseter) while
palpating externally over lateral pterygoid and
buccinator muscles (distal and lateral to upper molar
teeth) and medial pterygoid muscle (pterygomandibular
ligament and medial aspect of anterior faucial pillars)
with the mouth open.
Traumaany trauma to head and neck such as injury
from motor vehicle or bicycle accident, injury to the side
of face and chin should be looked for.
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Case History
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Temporomandibular Joint
The clinical examination for a patient with possible
temporomandibular disorder supplements the routine
regional head and neck examination. Following point
should be noted while examining the temporomandibular
joint.
Historymedical history about illness, particularly
rheumatoid arthritis, degenerative joint disease,
osteoarthritis should be asked. Before treatment of
temporomandibular joint disorder is initiated, it is
necessary to exclude other disorders that might present
with similar symptoms like trigeminal neuralgia,
multiple sclerosis, glossopharyngeal neuralgia,
temporal arteritis, migraine headache, angina pectoris,
pulpoperiodontal disease, salivary gland inflammation,
duct blockage, otitis, sinusitis and psychogenic pain.
Symmetry of facethe symmetry of the face should be
assessed. Gross asymmetry reflects growth disturbances.
Interincisal openingthe maximum interincisal opening
of the mouth should be determined, which is, normally,
in an adult, 35-50 mm. Measurement also should be
recorded for the degree of opening where pain begins.
Mandibular movementany deviation of the mandible
during opening should be noted, along with its severity.
The lateral mandibular range of motion is determined
by having the patient to occlude the teeth and then slide
the jaw in both directions. The range of movement from
the midline is measured in mm and any pain along with
location and severity is recorded. Normal lateral
movement is usually 8-10 mm.
Question to be asked to patientjaw and joint symptoms
should also be discussed with the patient:
Does the TMJ click or pop on opening or closing?
Has there been limitation in the movement or
deviation of the lower jaw on opening?
Has the jaw ever locked or dislocated on opening?
Has the patient experienced pain and dysfunction in
other joints of the body?
Palpation of jointpalpate the joint and listen for clicking
and crepitus during the opening and closing of the jaw.
Use stethoscope to characterize and locate this sound
accurately. Explore the anterior wall of external auditory
meatus for tenderness and pain that are usually
associated with arthritic changes.
Methods of palpation
Pretragus palpationthe patient should be requested
to slowly open and close the mouth while the doctor
bilaterally palpates the pretragus depression with
his/her index fingers (Fig. 7-20).
Intra-auricular palpationit is also performed by
inserting the small finger into the ear canal and
pressing anteriorly (Fig. 7-21).
2
Fig. 7-20: Examination of TMJ with pretragus palpation method.
Masticatory Muscle
Digital palpationregional muscles are examined for the
tenderness and trigger points using the digital palpation.
Masseter musclesthe masseter muscles are most
effectively examined by simultaneously pressing them
from inside and outside the mouth in the process of
bimanual palpation.
Lateral pterygoid musclethe lateral pterygoid muscles
are evaluated by inserting a finger each behind the
maxillary tuberosities, whereas the medial pterygoid is
checked by running a finger in an anteroposterior
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Lymph Nodes
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Case History
Examination of Other Parts
Nosesevere nasal obstruction leads to breathing
through mouth which leads to dryness of mouth which
results in persistent sore throat. Infection from nose may
spread to the orbit from the adjacent paranasal sinus.
Longstanding nasal obstruction suggests a deviated
nasal septum. Epistaxis (nasal bleeding) may indicate
life threatening conditions like cerebral hemorrhage.
Nasal discharge may be purulent, bloody, watery or
mucoid.
Paranasal sinusan apical tooth abscess of the upper
jaw may drain into the maxillary sinus causing acute
sinusitis.
Eyesvisual disturbances, color of the sclera and
conjunctivae are looked for anemia and liver diseases.
Ocular pain, diplopia and edema of eyelid etc. are also
looked for.
Earsimpaired hearing, loss of hearing, discharge from
ears, tinnitus.
Neckcheck for movement in neck, lump in the neck,
cervical lymphadenopathy. If thyroid enlargement is
suspected, check if the mass moves up and down with
trachea when the patient swallows.
External jugular veinobserve the external jugular vein
as it crosses the sternomastoid muscle and with the
patient at an angle, approximately 45 degree to the
horizontal, note any distension and/or pulsation in the
vein. Distension more than 2 cm above the sternal notch
is abnormal and is seen in severe right side heart failure.
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Doctors Position
Position of doctors is very important while intraoral
examination. As there are many professional hazards
which occur due to improper position of the doctors.
Basic positiondoctor should be either low seated or in
standing position. In cases of examining while doctors
in standing position, he should stand erect without
bending of spinal cord. Patient head should be at elbow
level of the doctor. The ideal position is 10 o clock or
11 o clock position.
Guideline for examinationyou should avoid resting arms
over patient shoulder, and maintain comfortable
distance from the patient. Eye contact should be
maintained with the patient. Drape the patient and avoid
keeping instrument on the patient chest.
Upper left posterior regionIn this case doctors should
stand behind the patient with his left hand going around
the patient head (Fig. 7-25).
Intraoral Examination
Intraoral examination is the most important part in dental
point of view.
Inspection
The volume of the tonguemassive tongue due to
lymphangioma, hemangioma and neurofibroma.
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2
Fig. 7-26: Doctors position for upper right posterior region.
Fig. 7-29: One should note the color of tongue. In this case, color is
white due to candidiasis
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Case History
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2
Fig. 7-31: Note for any cleft in the palate while examining.
In this case, cleft is due to cleft palate.
Fig. 7-30: Mobility of tongue can be checked by holding it with the hand.
Palate
Inspection
Point to look forcongenital cleft, perforation, ulceration,
swelling, fistulae, papillary hyperplasia, tori, recent
burns and hyperkeratinization.
Cleft examinationin case of congenital cleft, note the
extent of the cleft (involving only the uvula, only the soft
palate or part or whole of the hard palate). Whether the
nasal septum is hanging free or attached to one side of
the cleft (Fig. 7-31).
Perforationperforation of the hard palate is usually
caused by gumma.
Scar of operationany scar of the operation around or
history of operation, as sometime a hole may persist after
an operation for closure of congenital cleft.
Palpation
Point to look fortender, fluctuating swelling close to
alveolar process is an alveolar abscess. Soft swelling in
the midline of the hard palate is gumma.
Lip
Inspection
Point to be notednote lip color, texture and any surface
abnormalities, angular or vertical fissures.
Cleftcleft lip (Fig. 7-32), either complete or incomplete,
bilateral complete cleft lip in which there is also cleft
palate and protuberant pre-maxilla. Cleft between
maxilla and side of the nose.
Pigmentationpigmentation of lip and buccal mucosa
in Addisons disease. In Peutz Jeghers syndrome,
melanin pigmentation of the lip and oral mucosa occurs.
Chancrechancre on lip is a painless ulcer with dull
red color.
Ectopic salivary neoplasmectopic salivary neoplasm is
seen in upper lip as slow growing, lobulated tumor.
Macrocheliathickening of the lip which often involves
the upper lip.
Cheilitisin cheilitis glandularis, lower lip becomes
enlarged, firm and everted. In cheilitis granulomatosa,
there is diffuse swelling of the lower lip.
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Palpation
Point to be notedbenign neoplasm is firm and lobulated
while carcinoma of the lip is hard in consistency.
Chancre is rubbery hard whereas carcinoma is stony
hard. Mucous retention cyst is seen on the inner surface
of the lip. In cheilitis granulomatosa, the swelling is soft
usually exhibiting no pitting on pressure.
Floor of Mouth
Inspection
Procedureask the patient to open his mouth and to keep
the tip of tongue upward to touch the palate. This will
expose the floor of mouth.
Point to be notedany swelling, red-white patches in the
floor of mouth should be noted.
Color of swellingwhen a swelling is present note its
color. A ranula appears as a unilateral bluish translucent
cyst over which Whartons duct can be seen. In
hemangioma swelling is red in color (Fig. 7-33).
Site of lesiona sublingual dermoid lies exactly in the
midline and may extend into the submental region. A
deeper plunging ranula may have cervical prolongation
into the submandibular region.
Ankyloglossiain ankyloglossia there is fusion between
the tongue and floor of mouth.
Fig. 7-34: White patch seen on cheek
mucosa due to leukoplakia
Palpation
Point to be notedmucous cysts have smooth surface and
are movable over the deeper structures. Fluctuation can
be elicited by pressing on the top of the cyst while the
sides are palpated by other 2 fingers. Papilloma is a
solid tumor with irregular surface and is mobile over
the deeper structures. Carcinoma is fixed and indurated.
Palpate the muscles of cheek.
Palpation
Point to be notedRanula is a fluctuant swelling with
positive translucence. Sublingual dermoid which is not
translucent but tense and fluctuant swelling is seen on
the midline. Carcinoma of the floor of mouth is revealed
by its indurated base and probable fixation to the
underlying structures.
Cheek
Inspection
Point to be notedexamine the inside of the cheek for
aphthous ulcer, leukoplakia (Fig. 7-34), and mucous cyst,
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Mucobuccal Fold
Permanent teeth
87654321 12345678
87654321 12345678
Deciduous teeth
+05+04+03+02+01 +01+02+03+04+05
0504 0302 01 01 02030405
Point to look foryou should look for caries (pit and
fissure, smooth surface caries, cervical caries), defective
restoration or recurrent caries. You should also note
missing and supernumerary teeth (Mesiodens,
paramolar, distomolar). Presence of root piece of badly
carious fractured teeth. You should also look for overretained deciduous teeth, impacted teeth, ankylosed
teeth, fusion of teeth, Talons cusp, dens evaginatus,
taurodontism, and anodontia, enamel hypoplasia,
mottled enamel, neonatal teeth, eruption sequestra, delay
eruption, attrition, abrasion, erosion, sclerosis, pulp
calcification, resorption of teeth, hypercementosis,
plaque, calculus and stains.
Difference between deciduous and permanent teethit is
described in Table 7-8.
Stains and calculusstains and calculus should be
recorded in the finding. If calculus is present, there are
always chance that gingival inflammation is present as
calculus act as local irritant. Different grading for stains
and calculus is as follows
+stain and calculus involving only cervical portion
of teeth (Fig. 7-37).
++stains and calculus extending upto the middle
third of teeth (Fig. 7-38).
+++stains and calculus involving whole of the
facial or lingual surface (Fig. 7-39).
Deciduous teeth
A B C D E FG H I J
T S R Q P ON MLK
F.D.I (two digit system)in it first digit indicates the
quadrant as 1 to 4 of the permanent teeth and 5-8 for
primary teeth. The second digit indicates the tooth in
the quadrant. Thus, deciduous upper right second
molar is denoted as 55 and pronounced as five-five
and not fifty five and first mandibular left permanent
molar is denoted as 36.
Permanent teeth
18 17 16 15 14 13 12 11 21 22 23 24 25 26 27 28
48 47 46 45 44 43 42 41 31 32 33 34 35 36 37 38
Deciduous teeth
55 54 53 52 51 61 62 63 64 65
85 84 83 82 81 71 72 73 74 75
Dane system
Permanent teeth
+8+7+6+5+4+3+2+1 +1+2+3+4+5+6+7+8
8 765 432 1 12 34 5678
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Case History
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Fig. 7-38: Stains ++ showing involvement upto middle third of the
patient. In this patient there is also calculus + on the lingual surface.
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Permanent teeth
The crown of the primary teeth have prominent cervical ridge on the
buccal surface
The crown and roots of the primary teeth show marked cervical
constriction
The roots of the primary molar flare out from the cervical third
The furcation is close to the cervical line resulting is a short root
trunk
The primary teeth are lighter in color because of thinner enamel and
different refractive index of the enamel
Both enamel and dentin thickness is less as compared to the
permanent teeth
According to Glickman
Grade-Islightly more than normal.
Grade II-moderately more than normal.
Grade IIIsevere mobility faciolingually and/or
mesiodistally combined with vertical displacement.
According to Millar2nd method was developed by
Millar (1950) in which tooth is held firmly between 2
instruments and move back and forth and mobility
score is noted (Fig. 7-42) as follows
0it denotes no detectable movement when force
is applied other than what is considered normal
(physiologic) motion.
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Case History
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2
Fig. 7-43: Class I molar relationship showing mesiobuccal cusp of
maxillary permanent molar occlude in buccal groove of mandibular first
molar.
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2
Fig. 7-47: Probe should be inserted parallel to the vertical axis of
tooth in periodontal pocket examination.
Fig. 7-48B: Electric pulp tester is used for vitality testing of pulp.
Fig. 7-48A: Grade IV furcation involvement winch is associated with
gingival recession.
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Case History
ethyl chloride on the tooth being tested. Another
simple method is to wrap a sliver of ice in wet gauze,
and to place it against the facial surface of the tooth
and to compare to reaction of control tooth.
Anesthetic testing
When it is requiredthis test is restricted to patient
which is in pain at the time of the test, when the
usual test has failed to enable one to identify the
tooth. The objective is to anesthetize a single tooth
at a time until the pain disappears and is localized
to specific tooth.
Infiltration of teethusing either infiltration or the
intraligament injection injects the most posterior
tooth in the area suspected of being the cause of
pain. If pain persists when the tooth has been fully
anesthetized, anesthetize the next tooth mesial to
it and continue to do so until the pain disappear.
Inferior alveolar nerve blockif the source of the pain
cannot be determined, whether in maxillary or
mandibular teeth, an inferior alveolar injection
should be given.
Test cavityit is performed when other method of
diagnosis have failed. It is made by drilling
through the enamel and dentin junction of an unanesthetized tooth. The drilling should be done
at slow speed and without a water coolant.
Sensitivity and pain felt by the patient is an
indication of pulp vitality. Sedative cement is
placed in the cavity and search for the source of
infection continues. If no pain is felt, cavity
preparation continues until the pulp chamber is
reached. If the pulp is completely necrotic,
endodontic treatment can be continued in many
cases without anesthesia.
Gingiva
Colornormal is coral pink; physiological pigmentation
of melanin may be seen.
Sizeit corresponds to the sum total of the bulk of cellular
and intercellular elements and their vascular supply.
Alteration in size is a common feature of gingival disease.
Contourit depends upon shape of the teeth and their
alignment in the arch, location and size of the area of
proximal contact and dimension of the facial and lingual
gingival embrasures (Fig. 7-49).
Shapeit is governed by the contour of proximal tooth
surface and the location and shape of gingival
embrasures.
Consistencyfirm and resilient with exception of free
margin.
Surface textureorange peels appearance or stippled.
Positionthe level at which the gingival margin is placed
on the tooth.
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2
Fig. 7-49: Irregular shaped contour of gingiva in the patient who has
got misalignment of teeth. Gingiva is of normal color.
Examination of Swelling
Inspection
Situationa few swellings are peculiar in their position
such as dermoid swelling which is mostly seen in the
midline of the body or on the line of fusion of the
embryonic process. Nasopalatine cyst is common in
maxillary anterior region.
Colorthe color of swelling should be noted. Color of
swelling lead to some clue in the diagnosis.
Black colorit is of benign nevus and melanoma; red
purple color of hemangioma.
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Case History
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Palpation
Temperaturetemperature of the swelling is best felt by
the dorsal aspect of the hand. First, note systemic
temperature. Place finger of the hand on skin in the
area of concern and finger of other hand on skin on
contralateral part of body. It is increased in inflammation
as there is increased metabolic rate and increased
vascularity of area. It is increased in superficial
aneurysm, arteriovenous shunt and large recent
hematoma.
Tendernessinflammatory swellings are mostly tender
whereas neoplastic swellings are non-tender. When the
patient complains of pain due to the pressure exerted by
the clinician, the swelling is said to be tender.
Size, shape and extentdeeper dimensions of the swelling
remain unknown during inspection. The vertical and
horizontal dimensions are better clarified by palpation.
Tissue surrounding and underlying bases should be
carefully palpated to determine the maximum extension
of lesion into the surrounding tissue. Whether the mass
is poorly defined or moderately defined or well define
should be ascertained (Fig. 7-51).
Surfacewith the palmar surface of the fingers the
clinician should palpate the surface of the swelling. It
can be smooth (cyst), lobular with smooth bumps (lipoma),
nodular (matted lymph nodes) and irregular and rough
(carcinoma).
Edges and borderMargins are palpated with the help of
tip of the finger. Border of firm process in loose connective
tissue is readily determined than soft process in loose
connective tissue. If the surrounding normal tissue is of
same consistency as the pathological tissue, the border
cannot be determined.
Benign swellingsit has smooth margins whereas
malignant growth has irregular margins.
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Soft
Adipose tissue
Fascia
Veins
Loose connective tissue
Glandular connective tissue
Minor salivary gland
Sublingual salivary gland
Firm
Fibrous tissue
Tensed muscle
Large muscle
Cartilage
Cheesy
Brain tissue
Rubbery
Skin
Relaxed muscle
Glandular tissue with capsule
Arteries and arteriole
Liver
Bony hard
Bone
Enamel
Dentin
Cementum
Cartilage
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Aspiration
The preoperative aspiration of a fluid-filled mass is worthwhile precautionary procedure, as it should eliminate an
unpleasant surprise of opening of an innocuous lesion that
may be proved to be a dangerous vascular tumor. Usually
it should be carried out before surgery to avoid bacterial
infection.
Straw colored fluidit contain cholesterol crystals in wall
that are frequently seen as small shiny particles when
syringe is transilluminated. It is seen in some
odontogenic and fissural cyst.
Thick yellowish white and granular fluidit is seen in
epidermoid and keratocyst in which lamina is filled with
keratin.
Yellowish cheesy materialdermoid cyst contains most
of dermal appendage and the aspirate is thickest and
fills of yellowish cheesy substance.
Sebumsebaceous cyst yields sebum which is thick
homogenous and yellowish cheesy substance.
Amber colored fluiddark amber colored fluid of
thyroglossal duct cyst.
Lymph fluidit is colorless with high lipid content,
appears cloudy and frothy. It is seen in hygroma and
lymphoma.
Blue bloodit is seen in early hematoma, hemangioma
and varicosities.
Brighter red bloodaneurysm and arteriovenous fistula.
Pusaspiration of painful warm fluctuant swelling yield
pus.
Sulfur granulesin actinomycosis, it yield pus with few
yellow granule in it. These are sulfur granule.
Clear viscous fluidsticky clear viscous fluid yielded in
retention phenomenon.
Other Examination
Other examinations of swelling which are not frequently
done in dental office:
Percussionits role is to find gaseous content within the
swelling like resonant note over the hernia or to elicit
slight tenderness like Brodies abscess. Hydatid thrills
in case of hydatid cyst.
Auscultationall pulsatile swellings are auscultated to
exclude presence of any bruit or murmur.
Measurementit is done to find out increase in swelling
size at definite intervals but is also to find out if there is
any wasting distal to the swelling.
Examination of Ulcer
An ulcer is a break in continuity of the skin and epithelium.
Inspection
Size and shapethe size and shape of the ulcer should be
noted. This will yield in diagnosis of the ulcer. The size
of an ulcer is important in deciding the time which will
be required for healing. A bigger ulcer will definitely
take longer time to heal than smaller ulcer. To record
exactly the size and shape of an ulcer sterile gauze may
be pressed on to the ulcer to get measurement.
Tuberculosis ulcersthey are generally oval in shape
but their coalescence may give an irregular crescentic
border.
Syphilitic ulcerssyphilitic ulcers are similarly circular
or semilunar to start with but may unite to form
serpiginous ulcer.
Carcinomatous ulcerscarcinomatous ulcers are
irregular in size and shape.
Numbertuberculosis, gummatous, varicose and soft
chancre may be more than one in number.
Positionit is very important and often gives clue to the
diagnosis. Rodent ulcers are usually confined to the upper
part of the face above a line joining the angle of the mouth
to the lobule of the ear, occurring frequently near the inner
canthus of the eye. Malignant ulcers are more commonly
seen on the lips, tongue, breast and penis.
Edgesedges of the ulcer should be properly examined
(Fig. 7-55).
Spreading ulcerin a spreading ulcer the edges are
inflamed and edematous whereas in a healing ulcer
the edges, if traced from the red granulation tissue in
the center towards periphery, will show blue zone
(due to thin growing epithelium) and a white zone
(due to fibrosis of the scar).
Undermined edgeit is mostly seen in tuberculosis.
The disease causing the ulcer spreads in and destroys
the subcutaneous tissue faster than it destroys the
skin. The overhanging skin is thin friable, reddish
blue and unhealthy.
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Fig. 7-56: Edges, margins and floor of ulcer should be properly examined.
In this case, it has got rolled and everted edges of malignancy.
Palpation
Tendernessan acutely inflamed ulcer is always
exquisitely tender. Chronic ulcers are slightly tender.
Neoplastic ulcers are never tender.
Edgesin palpation different types of the edge of the
ulcer are corroborated with the finding of the inspection.
Marked induration of the edge is characteristic feature
of a carcinoma.
Basethe student must understand the difference
between the floor (exposed surface within the ulcer) and
base (on which ulcer rests and it is better felt than seen).
If an attempt is made to pick up the ulcer between thumb
and the index finger, the base will be felt. Marked
induration of the base is an important feature of
squamous cell carcinoma and hunterian chancre.
Depthyou should make assessment regarding depth
of the ulcer. It can be recorded in the examination sheet
in millimeters.
Bleedingwhether the ulcer bleeds on touch should be
checked as it is a common feature of malignant ulcer.
Relation with deeper structurethe ulcer is made to move
over the deeper structures to know whether it is fixed to
any of these structures. A gummatous ulcer over a
subcutaneous tissue or bone is often fixed to it. Malignant
ulcer will be fixed to the deeper structure by infiltration.
Palpation
Tendernessis the sinus tender? The sinus from
inflammatory source will be tender.
Wall of sinusit is palpated to note any thickening there.
Chronic sinus will have thick wall due to presence of
fibrosis surrounding the wall of the sinus.
Inspection
Numberthe majority of fistulae which occur in the body
are single. Actinomycosis has multiple sinuses and
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Case History
Mobilityis the sinus mobile over the deep structure?
Sinuses resulting from osteomyelitis are fixed to the bone,
which becomes irregular, thickened and tender.
Lumppresence of lump in the neighborhood of a sinus
often indicates tuberculosis lymphadenitis.
Probe examinationthis will inform the clinician about
the direction and the depth of the sinus. It will also detect
presence of any foreign body which will be movable at
the depth of the wound and whether fistula is
communicating with a hollow viscous or not and
whether fresh discharge comes out on withdrawal of
the probe or not.
Depth of sinusit is done with the help of radiograph. A
gutta percha point is inserted in the sinus and
radiograph is taken (Fig. 7-57). As gutta percha points
are radiopaque it will locate the exact direction and
depth of the sinus.
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Optic Nerve
Ophthalmoscopeit is tested by investigation of visual
acuity and the visual fields and those trained in the use
of the ophthalmoscope can use this instrument to
examine the ocular fundus directly for lesions.
Wall chartvisual activity can be tested with the familiar
wall chart but can also be evaluated by asking the patient
to read print of various sizes in a book or newspaper
held at various distance from the patient eye.
Trigeminal Nerve
Olfactory Nerve
Procedureit is traditionally tested by closing one of the
patient nostrils with a finger and asking him if he can
smell a strongly scented volatile substance such as coffee
or lemon extract. The test is then repeated with other
nostril. The patient should sniff strongly to draw the
volatile molecules well into the nose (Fig. 7-58).
Fig. 7-58: Smelling of volatile substance from nostril will test for
olfactory nerve.
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Facial Nerve
Significancethe facial nerve is tested for abnormalities
of motor function involving the mimetic muscle of facial
expression and also gustatory disorders. A gustosalivary
reflex involves facial nerve gustatory stimuli and increase
salivary function.
Lemon juice applicationAffected chorda tympani may
be associated with failure of salivary flow to increase
following application of lemon juice or citric acid to the
affected side of the mouth.
Motor function testmotor function of facial nerve is tested
by observing facial muscle function in response to request
to wrinkle (Fig. 7-60) the forehead, frown, close the eyelid
tightly, open the mouth, retract the mouth, blow out the
cheek, pucker the lips, screw up the nose, whistle and
speak.
Glossopharyngeal Nerve
It provides taste fibers to the posterior aspect of the tongue,
somatic sensory fibers to the same area of the tongue as
well as pharynx and soft palate and motor fibers to the
stylopharyngeal muscle that plays only minor role in
palatal function, preventing any accurate testing of 9th
cranial nerve functions.
Vagus Nerve
Significancethe vagus nerve is the chief motor nerve of
the pharynx and larynx and also provides sensory fibers
to the pharyngeal and faucial mucous membrane
Pharyngeal movement observationroutine testing is
carried out by observation of pharyngeal movements
i.e. symmetrical elevation of the soft palate and
shortening of the uvula when the patient says ah and
Hypoglossal Nerve
It provides motor supply to the tongue; hypoglossal
paralysis causes deviation of the tongue when patient
extrudes it. Atrophy of tongue musculature may be noted
on oral examination and its muscular tonus by the force
with which the patient can push the tongue against either
cheek or by evaluation of the tongue jerk.
Investigations
Laboratory investigations help to come to the final
diagnosis, e.g. in case of caries (proximal) the provisional
diagnosis will be mesial or distal caries. Radiograph will
confirm the diagnosis and help us to differentiate it into
incipient, moderate, advanced and severe. To confirm the
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Case History
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Clubbing
Cyanosis
Extra oral examination
Facial symmetry
Lip seal
TMJ movements
Lymph node
Ear
Nose
Intraoral examination
Hard tissue examination
Teeth present
Dental arch irregularities
Caries
Fractured tooth
Tenderness
Wasting disease
Discolored tooth
Calculus and stains
Occlusal facets
Mobility
Furcation involvement
Soft tissue examination
Tongue
Size
Dorsum
Ventral surface
Margin
Frenal attachment
Distribution of papilla
Final Diagnosis
The final diagnosis can usually be reached following
chronologic organization and critical evaluation of the
information obtained from the patient history, physical
examination and the result of radiological and laboratory
examination.
The final diagnosis usually identifies the diagnosis for
the patients primary complaint first, with subsidiary
diagnosis of concurrent problems. Previously diagnosed
conditions that remain as actual or potential problems are
also included, with comment by history previously
diagnosed.
In case of no definite diagnosis is made diagnosis should
be written as idiopathic, unexplained, functional and
symptomatic.
The patient should be informed of the diagnosis, results
of tests and examination.
Cheek
Color
Any ulcer
Lips
Color
Vermillion border
Commissures
Ulcer and lesion
Hard and soft palate
Discoloration
Papillary hyperplasia
Swelling
Ulcer
Any recent burns
Any lesion
Floor of mouth
Gingiva
Color
Contour
Consistency
Surface texture
Position
Size
Bleeding on probing
Exudate/suppuration
Frenal attachment
Provisional diagnosis
Investigation
Final diagnosis
Treatment planning :
Medical / emergency phase
Planned treatment
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System
Question to be asked
General
Cardiovascular system
Respiratory system
Dyspnea on exertion
Wheezing, coughing, excessive sputum production
Coughing up blood.
Blood disorders
Nervous system
Head-injury or concussion
Seizures/black-outs/fits
Frequent headaches
Experienced any pain, numbness, or tingling in your face , arms or legs
Had any paralysis.
Metabolic-endocrine system
Gastrointestinal,
hepatic, biliary tracts
Difficulty in swallowing
Heart-burn or belching
Episodes of nausea and vomiting
Vomited blood
Frequent stomach or abdominal pain
Recently had a change in bowel habits
Frequent episodes of diarrhea
Ever noticed bright-red, or black colored stools.
Genitourinary system
Urinate frequently
Difficulty or pain during urination
Ever passed brown or red urine
(for females) had abnormal or irregular menstrual period
Are you now or recently been under a physicians care? if so, what is the condition being treated?
Have you been hospitalized during past 2 years?
Do you take prescription or non-prescription medicines on a permanent or non-permanent basis?
Do you have any allergies, if so to what?
Aspirin
Sulphur containing drugs
Penicillin or any other antibiotics
Codeine or any narcotic
Dental anesthetic or
Any specific drug
Does dental treatment make you nervous?
Chest discomfort on exertion, when eating or at rest
Tightness of the chest
Palpitation
Fainting
Ankle edema
Shortness of breath
High or low blood pressure
Heart murmur.
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Case History
Inscriptionspecific information regarding the drug
(generic or proprietary name or both) and the dosage.
Subscriptiondirection to the pharmacist for filling
the inscription (number of capsules or tablets to be
dispensed or the volume of liquid), the number of
refills allowed and time constraints, directions to be
listed on the container label.
Transcriptioninstruction to the patient, to be listed
on the container label.
Signature and educational degree of prescribing doctor- a
signature is required by law only for certain controlled
substance (schedule II drug).
Guidelines for prescription writing
Obtain an accurate and complete patient history,
including whether the patient is taking any drugs
prescribed by other doctors or any over the counter
drugs; both can affect the dosage or effects of the drug
being prescribed.
Use separate prescription blank for each drug
ordered. Avoid using prescription blank with trade
names printed on them.
Never presign prescription blank and always store
blank prescription pads in a secure place.
Write out number than using digits so that
prescription cannot be altered.
Prescribe sufficient drug and at adequate dosing
intervals to maintain therapeutic blood level.
Keep the record of all drugs prescribed for each
patient.
Instruction listed on the drug container for the patient
must be specific. Full disclosure is verbally given
regarding the prescription before the patient leave
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Suggested Reading
1. Glick M. Did you take your medication? The dentist role in helping
patient adhere to their drug regimen. JADA 2006;137:1636-8.
2. Glick M. Screening for traditional risk factors for cardiovascular
disease. JADA 2002;133:291-300.
3. Greenberg, Glick, Ship. Burkets Oral Medicine: BC Decker Inc:
2008.
4. Kay E, Nuttal N. Clinical decision makingan art or a science.
Br Dental J 1995;190-3.
5. McCarthy FM, Malamad SF. Physical evaluation system to
determine medical risk and indicated dental therapy modification.
JADA 1979;99:181-4.
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Investigation in
Dentistry
Introduction
There are various important investigations which are
required for the diagnosis and treatment plan of various
disorders related to the oral cavity. Laboratory studies are
an extension of physical examination in which tissue,
blood, urine or other specimens are obtained from patients
and subjected to histological, bio-examination, microbiological or immunological examination. Information
obtained from these investigations help in identifying the
nature of the disease.
Molecular methods
Quantification of nuclear DNA content
Tumors markers
Microsatellite markers.
Clinical Method
Toluidine Blue Staining
The use of Toluidine blue (tolonium chloride) dye as a
mouthwash or topical application is currently receiving
much attention as an aid to the diagnosis of oral cancer
and potentially malignant lesions. The method has good
sensitivity with a very low false negative rate. The dorsum
of the tongue always stains positively, due to the retention
of dye in crevice between the papillae. It is effective in
demonstrating dysplasia and early malignant lesion which
is not clinically recognizable.
Mechanism
Classification
Clinical method
Vital stainingtoluidine blue method and Lugols
iodine method
Vizilite
Acridine binding method
Photodiagnosis
5-Aminolevulinic acid mediated fluorescence
endoscopic imaging
5-Aminolevulinic acid mediated digitized
fluorescence endoscopic imaging
Autofluorescence spectroscopy
Fluorescence photography
Histopathological methods
Biopsy
Exfoliative cytology
Oral CDx system
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Investigation in Dentistry 87
Availability
Contents
Toluidine blue1 gm
Acetic acid10 cc
Absolute alcohol4.19 cc
Distilled water86 cc
pH adjusted to 4.5
Contents
Technique
Rinsinginitially you ask the patient to rinse the mouth
twice with water (20 seconds each). After rinsing with
water, ask patient to rinse with 1% acetic acid (20
seconds).
Drying of areayou should gently dry suspicious
mucosal areas with gauze. You have to take care not to
abrade the tissue while drying.
Application of toluidine blue solutionapply 1% toluidine
blue solution to the lesion with a cotton swab.
Rinsingask patient to rinse again with acetic acid
(approximately 150 ml for one minute). After rinsing
with acetic acid, then ask patient to rinse with water.
Positive stainingif the mucosa is stained positive
(Fig. 8-1), you have to repeat the procedure in one to two
weeks. Biopsy of all sites is advised, which stain positive
on two successive visits.
Iodine2 gm
Potassium iodide4 gm
Distilled water100 cc
Mechanisms
Reaction with glycogenLugols iodine solution produces
a brown black stain by reaction of iodine with glycogen.
Iodine is removed by fixation in alcohol and
formaldehyde.
Effect on proliferating epitheliumglycogen content is
inversely related to the degree of keratosis, suggesting a
role of glycogen in keratinization. So when proliferating
epithelium is present it is usually poorly stained or
unstained.
Effect on inflammatory tissuethere is relationship
between the degree of inflammation and glycogen
content. So in this case, tissue will stain dark brown.
Vizilite
Vizilite is non-toxic chemiluminescent light that is shined
in the mouth. Tissue which are not normal, they glows
differently, as compared to normal tissue. This will make
them more visible. Vizilite will be more useful for the
detection of biopsy proven squamous cell dysplasia which
is not seen with naked eye.
Contents
Vizilite rinse1% acetic acid solution
Vizilite capsulechemiluminescent light stick
Vizilite retractorsheath and handle
Mechanism
Fig. 8-1: Positive toludine blue staining showing uptake toludine blue
by dysplastic mucosa (Courtesy Zila Pharmaceutical).
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Technique
Autofluorescence Spectroscopy
Useautofluorescence spectroscopy is non-invasive
method. It is used for detection for alteration in the
structural and chemical composition of cells. It is also
useful for optimal location of biopsy.
Mechanismautofluorescence occurs due to endogenous
fluorophores. It consists of fluorophores from tissue
matrix molecule, intercellular molecules like collagen,
elastin and nicotinamide adenine dinucleotide
phosphate.
Fluorescence Photography
Photodiagnosis
This optic method is used for the early diagnosis. It is based
on fluorescence measurement. Light induced fluorescence
(LIF) spectroscopy is useful for the early cancer detection
in oral cavity. The principle is that there is endogenous
tissue fluorescence of photosensitizer which is accumulated
in tumor tissue. Photosensitizer which can be used are
m-THPC and delta aminolevulinic acid.
Histopathological Examination
Biopsy
It is a process of surgically removing tissue from a patient
for histopathological examination. It is the removal of
sample tissue from living individuals. It provides valuable
information in determining the prognosis and type of
treatment required.
Indications
Undiagnosed clinical conditionafter careful clinical
examination, if any alteration from normal is seen and it
is not possible to identify the condition clinically, a
histopathological investigation is necessary.
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Investigation in Dentistry 89
Nature of lesionto evaluate the exact histological nature
of any soft tissue or intra-osseous lesion.
Screening testto screen abnormal tissues removed from
oral cavity including granuloma and cyst.
Detection of malignancyto confirm the existence and
nature of directly apparent malignancy so that the
treatment can be undertaken immediately.
Diagnostic testdiagnostic tests for evaluation of nonneoplastic lesions such as mucosal nodules, papilloma,
erosive lichen planus, erythema multiforme, lupus erythematosus, pemphigus, pemphigoid and desquamative
gingivitis.
Uses
Diagnosisbiopsy is useful for the diagnosis of pathologic lesions. It also helps in determining neoplastic and
non-neoplastic lesions of oral cavity.
Grading of tumorsit aid in determining the grading of
tumor.
Metastatic lesionit is also useful for the diagnosis of
metastatic lesions.
Recurrencefor the evaluation of recurrence.
Management assessmentit is useful for the therapeutic
assessment of the lesion by differentiating between
benign and malignant lesion.
Types of Biopsy
More commonly used biopsies are excisional, incisional,
fine needle, punch, scrape and trephine. Some biopsy like
bite, cone, core, endoscopic, irrigation, pressure, shave and
sponge are less commonly used.
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Incisional Biopsy
Fig. 8-4: Biopsy slide is prepared and stored properly.
Indications
Large lesionif the lesion is large and diffuse and extends
deeply into the surrounding tissue so that total removal
cannot be obtained easily with local anesthesia, an
incisional biopsy is indicated.
To determine nature of treatmentlesions in which
diagnosis will determine whether the treatment should
be conservative or radical.
Procedure
Excisional Biopsy
Total excision of a small lesion for microscopic examination
is called as excisional biopsy. It is a therapeutic as well as a
diagnostic procedure. Normal tissue on the margins of the
lesion should be included.
Indications
Small lesionit is the preferred treatment if, the size of
lesion is such that it may be removed along with the
margins of normal tissue and wound can be closed
primarily. It is usually done in case of lesion smaller
than 1 cm.
Sessile lesionwhen the lesion is sessile or pedunculated,
excisional biopsy can be done.
Movable tissuetissues which are freely movable and
located above the mucosa or just beneath the surface.
Procedure
Local anesthesiaanesthetize the lesion with 2% local
anesthetic containing vasoconstrictor. Care is taken not
to inject directly into the lesion that is to be removed.
Elliptical incisionwith the scalpel, make an elliptical
incision on either side of the base of the lesion so that
incision line intersected. The blade should be at an angle
of 45 towards the center of the lesion.
Pulling of tissueoutward tension is placed on the lesion
by means of suture or with the help of tissue forceps
Intraosseous Biopsy
It is less frequently performed. It may be in the form of
exploratory curettage in which the representative tissue is
obtained to determine the nature of large radiological
alterations.
Procedure
Selection of siteafter correlating the radiographs with
overlying anatomical structures, the site of which the
mucoperiosteal flap is to be raised is selected.
Local anesthesiaanesthesia to the area is accomplished
by block injection to the area and with local infiltration
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Investigation in Dentistry 91
Punch Biopsy
It is rarely necessary in the oral cavity as most of the oral
lesions are easily accessible. With this technique the surgical
defect that is produced is small and does not require
suturing.
In this technique, a sharpened hollow tube (Fig. 8-5);
several millimeters in diameter is rotated until underlying
bone or muscle is reached. The tissue is then removed in
the same manner as in incisional or excisional biopsy.
Advantages
Frozen Section Biopsy
It is performed in order to get an immediate histological
report of a lesion. It is done to determine whether a lesion is
malignant or not. It is also used to evaluate the margins of
an excised cancer, to ascertain that the entire lesion is
removed at the time of surgery.
The tissue is obtained from lesion and it is kept in deep
freeze and then frozen tissue is sectioned and stained to
get a prompt diagnosis. In this type of biopsy, the slides
cannot be preserved for future reference.
Exfoliative Cytology
In this, the surface of the lesion is either wiped with some
sponge material or scraped to make a smear. It is the
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Disadvantages
Firm tumorsfirm tumors may prevent a proper
cytodiagnosis due to paucity of cells in the aspirate.
False negative resultsoral cytology can give false ve
findings due to inadequate sampling. Another reason
for this is many lesion have a thick keratinized surface
layer and contain subtle change of dysplasia.
Non-assessmentsome specimens cannot be assessed due
to poor cellularity.
Indications
Patient preferenceas a compromise, when the patient
refuses for biopsy.
Follow-upas a means of follow-up for recurrence in
patients who had radiation therapy for the lesion that
was superficial or adjacent to bone, periodic recall of
high risk patient.
Debilitated patientsin place of biopsy, when dealing
with extremely debilitated patients possessing problems
to determine a suitable biopsy site.
Adjunct testas an aid to the diagnosis of some
dermatological diseases such as Pemphigus, White
sponge nevus, oral malignant and pre-malignant
lesions.
Periodic reviewperiodic review of oral lesion like
leukoplakia, lichen planus should be carried out by this
method.
Rapid evaluationfor rapid evaluation of an oral lesion
that on clinical grounds, is thought to be malignant or
pre-malignant and for which, the dentist is unable to
obtain permission for a biopsy.
Sequential laboratory evaluationfor sequential laboratory
evaluation of an area of the mucosa that has previously
been treated by radiation or by excisional biopsies to
remove malignancy.
Vesicular lesionfor evaluation of vesicular lesions
where facilities for rapid evaluation of Tzanck smears
are not available.
Population screeningwhen population screening is done
for the detection of oral caner exfoliative cytology is the
recommended method.
Instruments Used
Instrument which are used in exfoliative cytology are glass
microscopic slide, lead pencil, cement spatula or wax
carver, wooden tongue depressor, toothpick, canister of
cytospray and 95% isopropyl alcohol or ethyl alcohol.
Procedure
Information to written on slideuse of two slides for each
site to be sampled. With lead pencil print the patients
name, date when the slide is prepared and the site of the
lesion on frosted end of glass microscopic slide.
Instrumentthe instrument selected to remove the
superficial cell must have a square edge with a contour
sufficient to scrape off the superficial layer of cells.
When the lesion is very small, the edge of toothpick is
effective.
Clearing of surfaceclear the surface of oral lesions with
debris and mucus.
Scraping the tissuewhile the tissue is stretched, the
squared edge of the collection instrument is positioned
at the back of the lesion and is firmly held and brought
forward and pressure applied until visible material is
collected. Vigorous scraping of the entire surface of the
lesion several times is done with a metal cement spatula
or a moistened tongue blade.
Spreading of material on microscopic slidecollected
material is then quickly spread evenly over the
microscopic slide.
Fixing of tissuefix it in commercial preparation such
as spraycyte, 95% alcohol or equal part of alcohol and
ether, immediately before it dries. Then allow it to stand
for thirty minutes so that it air dried.
Repeatrepeat the procedure and prepare a second
smear.
Interpretation
It is reported by a cytologist as follows into one of the
following five classes:
Class I (normal)it indicates that only normal cells are
observed.
Class II (atypical)presence of minor atypia but no
evidence of malignant changes.
Class III (indeterminate)this is a stage in between that
of class II and IV and separates non-cancer cells from
cancer cells displaying wider atypia that may be
suggestive of cancer but they are not clear-cut and may
represent pre-cancerous lesion or carcinoma in situ and
a biopsy is recommended in such cases.
Class IV (suggestive of cancer)few cells with malignant
characteristic or many cells with borderline features.
Biopsy is mandatory in such cases.
Class V (positive of cancer)cells that are obviously
malignant. Biopsy is mandatory in such cases.
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Investigation in Dentistry 93
and a safe procedure for rapid diagnosis. First discovered
by Kun in 1847 and reintroduced in 1930 by Martin and
Ellis.
Indications
Interpretation
Procedure
Needle positioningfirst you have to position the needle
within the target tissue.
Application of negative pressureplunger is pulled to
apply negative pressure. Needle is moved back and forth
within the target tissue to obtain a greater field.
Releasing of negative pressurenegative pressure is then
released while the needle remains within the target
tissue.
Withdrawing the needleneedle is withdrawn and then
the defumed air drawn in the syringe and the aspirate is
blown onto the slide.
Fixingfixing is done in 95% alcohol for 1 hour for Pap
stain and a little prolonged for HE stain.
Molecular Methods
ORALCDX Test
It is highly specialized computer assists analysis of an oral
brush biopsy performed on oral tissue. It is the most recent
development in oral biopsy technique. This technique is
ideal for determining the need for scalpel biopsy in benignappearing oral mucosal leukoplakia.
Procedure
Collection of sample cellsthis technique utilizes a
disposable brush to collect a transepithelial sampling
of cells (Fig. 8-7).
Computer screeningthe sample is screened by computer
which is programmed to detect cytologic changes
associated with premalignancy and squamous cell
carcinoma. The computer consists of neural network
based image processing system specially designed to
detect oral epithelial precancerous and cancerous
cells.
Procedure
It is done by flow cytometer analysis. Flow cytometer is
automated, precise, reproducible, reliable and objective
measuring device of cellular DNA content. Limitation of
flow cytometer analysis is that it scans only severe
dysplasia of detectable oral premalignancy.
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Tumors Markers
Indirect Immunofluorescence
Microsatellite Markers
It is one of sensitive method for studying clonal changes in
tumors and premalignant lesion. This requires small
quantities of DNA. It is done by polymerase chain based
Microsatellite analysis.
In oral premalignant lesion loss of heterozygosity is seen.
Immunofluorescence Procedure
Fluorescent dyes such as fluorescein isothiocyanate
(FITC) and rhodamine can be chemically linked (conjugated)
with antibody globulin without destroying the specificity
of the antibody. Such fluorescent labeled antibodies used
to detect specific antigen-antibody reaction can be used to
locate either antigens or antibodies of known specificity in
tissue sections. When tissue sections labeled in this fashion
are illuminated with ultraviolet light in an ultraviolet
microscope, specific labeled tissue component can be
identified by their bright apple green fluorescence against
a dark or counter stained background. The technique is
used to identify a number of tissue structures and abnormal
deposits of antibody globulin and other macromolecules
as well as bacteria and viruses in infected tissues and
smears.
It is carried out in the following three ways.
Direct Immunofluorescence
Application of fluorescent labeled antiserumfluorescent
labeled antiserum directed against a particular tissue
component is applied directly to a thin, unfixed smear
or tissue section mounted on a slide.
Incubation of slidethe slide is incubated at 37C to allow
the antigen and the labeled antibody to react.
Washing of slide in buffered normal salinefollowing
incubation, the slide is washed in buffered normal saline
to remove un-reacted labeled antibody.
Examination under ultraviolet microscopethe slide is
examined in ultraviolet microscope.
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Investigation in Dentistry 95
Uses
Preventive measuresto determine the need and extent of
preventive measures.
Success of therapeutic measureto determine the success
of therapeutic measures.
Diet counseling and oral hygiene procedureto motivate
and monitor the effect of education programs related to
diet counseling and oral hygiene procedures.
Identification of high risk groupto identify high risk
groups and individuals.
Technique
Collection of salivastimulated saliva is collected before
breakfast by chewing paraffin.
Spreading on agar platethis is shaken and 1:10 and 1:100
dilutions are spread on the surface of agar plate.
Incubationthese are incubated at 37C for a period of
3-4 days. The number of colonies is then counted in a
Quebec counter.
Resultsthe count expressed as the average number of
colonies per milliliter of the original saliva sample.
Interpretation
Immuneif the count is less than 103 then the patient is
immune.
Slightif the count is between 103 5000, caries activity
is slight.
Mediumif the count is between 5000104 , caries
activity is medium.
Highif it is more than 104 then caries activity is high.
Snyder Test
This test measures the ability of microorganisms in saliva
responsible for formation of acids from carbohydrate media.
Technique
Collection of salivathe saliva sample is collected in a
manner similar to the Lactobacillus colony count test.
Snyder mediathe media contains bactopeptone (20 gm),
dextrose (20 gm), sodium chloride (5 gm), agar (16 gm)
and bromocresol green (0.02 gm).
Mixing of media with salivathen 0.2 cc of saliva is pipette
into the media which is incubated at 37C for a period of
72 hours.
Resultsbromocresol green, being an indicator, changes
the color from blue green to yellow in the range of pH of
5.4-3.8. The color change is then correlated with the caries
activity.
Interpretation
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Albans Test
Technique
Technique
Preparation of Alban medium60 gm of Snyder test agar
is placed in 1 liter of water and the suspension is brought
to boil over a low flame or a hot plate at medium heat
(excessive heating should be avoided to prevent
scorching of medium). When thoroughly melted, agar is
distributed, using about 5 ml per tube. The tube should
be autoclaved for 15 minutes, allowed to cool and stored
in a refrigerator.
Mixing and incubation of saliva with Alban mediumtwo
tubes of Alban medium are taken from the refrigerator
and saliva is drooled directly into the tubes and tubes
are incubated for 4 days at 37 Celsius.
Resultsthe tubes are observed daily for change in color.
The color change is noted from bluish green to yellow
and the depth to which change has occurred is noted.
Interpretation
Negativeno color changes.
+
beginning of color change (from top of the
medium towards bottom).
++
one-half color changes.
+++ three-fourth color changes.
++++ total color change.
Interpretation
Low buffer capacitysaliva sample requiring less than
0.45 ml of standard hydrochloride acid to reduce the pH
to 5 has low buffer capacity.
High buffering capacitysaliva sample requiring 0.45 ml
or more has high buffering capacity.
Interpretation
Streptococcus Mutans Level in Saliva
Saliva samples are obtained by using tongue blades (after
air drying the tooth for plaque samples). These are then
incubated on M.S.B. agar (Mitis Salivarius Bacitracin Agar).
The number of colonies is then used to estimate the caries
activity and more than 105 colonies per ml of saliva is
indicative of high caries activity.
Dewar Test
Technique
Collection of plaque sampleplaque samples are collected
from the gingival third of buccal tooth surfaces and
placed in Ringers solution.
Mitis Salivarius agar platethe sample is shaken until
homogenized. The plaque suspension is streaked across
a Mitis-Salivarius agar plate.
Incubationafter aerobic incubation at 37 C for 72 hours,
the culture is examined under a low power microscope
and the total colonies in 10 fields are recorded.
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Investigation in Dentistry 97
Interpretation
This test is an attempt to semi-quantitatively screens the
dental plaque for a specific group of caries causative
organisms including streptococci.
Swab Test
The swab test involves sampling of the oral flora by
swabbing the buccal surface of teeth and placing it in
Snyder media. This is incubated for 48 hours and the pH
changes are read and correlated with caries activity.
Reductase Test
This test measures the activity of salivary enzyme reductase.
Technique
Collection of saliva and mixing with diazoresorcinolsaliva
is collected and the sample is mixed with a diazoresorcinol, which colors the saliva blue.
Resultsthe change in color from blue to red is measured
after 30 seconds and 15 minutes and this is taken as
measure of caries activity.
Fig. 8-10: Collection of capillary blood specimen is
done by finger prinking.
Interpretation
Non-conductiveif it remains blue after 15 minutes it is
non-conductive.
Slightly conductiveif it changes to orchid after 15
minutes, it is slightly conductive.
Moderately conductiveif it changes to red after 15
minutes, moderately conductive.
Highly conductiveif it changes immediately to red, it is
highly conductive.
Extremely conductiveif it changes to pink or white
immediately, it is extremely conductive.
Hematological Investigation
Normal values are given in Table 8.1.
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Procedure
Office and chair sidethe test is performed manually
under a microscope by direct counting of the number of
cells in diluted sample of blood confined in a calibrated
chamber of special glass microscope slide (hemocytometer technique).
Automated procedurethe electronic counting of
erythrocyte is usually carried out with equipment such
as coulter counter model (Fig. 8-12). The sample of whole
Interpretation
Earliest signs and symptoms of hematological disease
affecting erythrocytes are anemia and polycythemia. It
is reduced in some anemia and increased in
polycythemia and dehydration.
Erythrocytes Indices
In evaluation of nature of anemia, assistance is obtained
by calculating standard indices relating to the size of RBCs.
By measuring these indices we can classify anemia as
microcytic, macrocytic and normocytic and hypochromic
and normochromic (Tables 8.1 and 8.2).
Types
MCHthe hemoglobin content of erythrocyte is referred
to as the mean corpuscular hemoglobin (MCH)
expressed in picograms of hemoglobin per cell.
MCHCthe concentration of hemoglobin in the
erythrocyte is referred to as the mean corpuscular
hemoglobin concentration (MCHC)
MCV- average red cell volume referred to as the mean
corpuscular volume (MCV) is expressed in cubic microns
per cell.
Table 8-1: Different erythrocytes indices
Indices
Calculation
MCH
10
RBC in million/mm 3
MCHC
MCV
Hematocrit
10
RBC in million/mm3
Types of anemia
MCV
MCH
MCHC
Microcytic
hypochromic
Decreased
Decreased
Decreased
Macrocytic
normochromic
Increased
Increased
Normal
Normocytic
normochromic
Normal
Normal
Normal
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Investigation in Dentistry 99
Hematocrit
Technique
Indications
Anemiathe classic signs and symptoms of anemia
indicate for the measurement of the hematocrit value.
History of blood losshistory of excessive blood loss,
pallor of oral mucous membrane, palate, conjunctiva,
nailbeds.
Evaluation of patient for general anesthesiaTo evaluate
patients ability to tolerate general anesthesia or oral
surgical procedures.
Othersunexplained syncope, excessive fatigue,
glossitis and atrophy of lingual papillae, recurrent and
persistent gingivitis and stomatitis.
Technique
Equipment2 heparinized microhematocrit capillary
tubes. A box of matches and microhematocrit centrifuge
equipped with reader and magnifier.
Collection of bloodblood is obtained by a finger prick or
venipuncture and is allowed to flow by capillary action
into two microhematocrit tubes, until each is about th
filled. The volume of blood should be free from air
bubbles.
Sealing of tubethe end of each tube away from the column
of blood is sealed by melting the glass in the flame of a
match or small gas jet without heating the blood.
Keeping tube in centrifugethe tubes are cooled and
placed opposite to each other in the slots of the head of
the centrifuge, with sealed ends pointing outward. The
centrifuge head covers are closed and the centrifuge timer
is set for 5 minutes.
Centrifugationthe centrifuge is started and it accelerates
to 12,500 rpm and stop automatically at the end of
required time.
Resultsthe centrifuge head covers are removed and
with the aid of magnifying lens for greater accuracy, the
hematocrit is read by means of scale incorporated in the
head of the instrument.
Interpretation
Increasedit is increase in primary and secondary
dehydration.
Decreasehemoglobin concentration decreased in
anemia.
WBC Count
In the management of dental patients total WBC count is
used as one of the index of presence of systemic infection
and to rule out possibility of leukemia and malignant
neutropenia (Table 8-3).
The total WBC count can be calculated manually with a
hemocytometer or with an automated cell counter. To count
WBCs in the presence of RBCs, RBCs are lysed by diluting
the blood sample with dilute acetic acid or equivalent
reagent supplied by the manufacture of the automated
equipment leaving the WBCs intact.
Table 8-3: Interpretation of WBC count
Increased in (leukocytosis)
Decreased in (leukopenia)
Aplastic anemia
Influenza, measles and
respiratory tract infection
Catarrhal jaundice
Early leukemia
Depression of bone
marrow due to certain drugs
Drug and chemical toxicity, shock
Interpretation
Increaseincrease in the value indicates primary and
secondary polycythemia and dehydration.
Decreasevalue is decreased in anemia.
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Technique
Increased in
Decreased in
Neutrophils
Pregnancy, exercise
Infection, inflammation
Neoplasm, severe
hemorrhage
Hemolysis and erythroblastosis fetalis
Intoxication by drugs and
poisons like corticosteroids
Aplastic anemia
Cyclic neutropenia
Malignant neutropenia
Drug induced
myelosuppression
Early leukemia
Lymphocytes
Lymphocytic leukemia
MumpsGerman measles
Whooping cough
Chronic infection
Convalescence from
acute infection
Aplastic anemia
Myelogenous anemia
Monocytes
Hodgkin disease
Monocytic anemia
Malariakala-azar
Sub-acute bacterial
endocarditis
Tuberculosis
Aplastic anemia
Acute leukemia
Eosinophils
Fig. 8-13: DLC count is calculated by instrument.
Interpretation
It is discussed in Table 8-4.
Platelets
Parasitic infection
Allergic disease
Drug reaction dermatoses
like pemphigus, pemphigoid,
atrophic dermatitis
Scarlet fever
Immune defect
Acute stress
Injection of adrenocorticotropic
hormone
Typhoid fever
Aplastic anemia
Basophils
Bleeding Time
It measures the time required for hemostatic plug to form.
Lack of any clotting factor and platelet abnormalities may
increase the bleeding time. It is a useful screening test in
patients with a history of prolonged bleeding following
previous surgery. It should be carried out in patients in
whom certain symptoms are with strongly suggestive of
bleeding disorders.
Technique Equipment
Equipmentsphygmomanometer, cuff, jar of sponges
soaked in 70% alcohol and jar of dry sponges, blood
lancet, 3 to 4 pieces of filter paper about 1 inch square,
stop watch (Fig. 8-14).
Patient positionthe patient is seated comfortably with
his arm supported on the chair arm or his own thigh.
Application of cuff to patientthe sphygmomanometer
cuff is applied to the patients upper arm and inflated to
40 mm pressure.
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Indications
Bleeding abnormalitiesit is used to screen for bleeding
abnormalities especially where there is suspicion of
platelet disorders.
Petechiae in oral cavitythe discovery of petechiae in the
oral cavity or on the skin is the most common indication
for the capillary fragility test; especially where the
petechiae are confined to the oral cavity and could also
conceivably have resulted from local trauma or denture
irritation.
Scurvyin dental practice, it is used as a screening test
for scurvy, which is an etiological factor in periodontal
disease.
Technique
Interpretation
An abnormal bleeding timeit is usually the result of
abnormalities in the structure or ability of the capillary
blood vessels to contract or abnormalities in the number
or functional integrity of the platelets.
Contributing factorsa bleeding time of 5 minutes
does not mean that a patient will stop bleeding from
any type of wound in 5 minutes. The time for bleeding
to stop is related to the way in which the wound is
produced, the caliber of the vessels involved in
the hemorrhage, the amount to tissue damage adjacent
to the wound and systemic factors such as blood
pressure and individual response to the type of
anesthesia.
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Technique
Mechanismthe rate is accelerated when there are
changes in the physicochemical properties of plasma or
the red cell surface or when the changes in plasma
protein cause the RBCs to aggregate.
Westergren methodin the Westergren method, a
graduated sedimentation tube is filled with oxalates
blood and placed in an absolutely vertical position (Fig.
8-16).
Resultsthe erythrocyte level is read at 10 minutes
intervals and at the end of an hour.
Clotting Time
Procedure
Feeling of blood in dry tubesone millimeter of venous
blood is placed in each of the four dry tubes of standard
size, maintained in a water bath.
Tilting of tubethe first tube is tilted at 30 seconds
interval, until the blood no longer flow. The next tube it
tilted until clotting occurs, after which the third and
fourth tubes are similarly treated.
Resultsthe average time between venipuncture and
clotting in the last three tubes is expressed in minutes as
the clotting time. The normal range is 10 to 25 minutes.
Interpretation
Increasesit is prolonged in diseases affecting stage II
and stage IV of coagulation. It is also increased in
cirrhosis, hemophilia A and B, factor XI deficiency,
hypofibringenemia and heparin and dicumarol
anticoagulant therapy.
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Blood Chemistry
Detection of Diabetes Mellitus
Diabetes mellitus is a disease of insidious onset that is not
infrequently complicated by serious tissue changes leading
Indications
Evaluation of patient suspected of diabetes mellitusfor
evaluation of a patient suspected of having diabetes
mellitus. Its presence should be suspected whenever
any of the following are found: history of weight loss in
the presence of adequate diet, history of excessive thirst
and attendant excessive and frequent urination, history
of repeated episodes of boils, skin infections and
periodontal abscesses and presence of severe
periodontitis with excessive bone loss.
Screening testas a screening test for diabetes mellitus,
where the dentist suspects the occurrence of disease in
the absence of characteristic signs and symptoms.
Family historytesting of the patient with a family
history of diabetes.
Known diabetes patientas a measure of degree of control
of disease in a patient who is known to be a diabetic but
who is not under regular medical care and is unwilling
to accept referral to a physician for reevaluation of the
disease.
Types
Urine glucose estimationmany diabetics excrete glucose
in their urine, testing the urine with commercial
available reagent strips (Tes-Tape, Clinistix, Chemstrip)
is the most convenient screening method of diabetes (Fig.
8-17). But in patient with mild diabetes urine may not
exhibits glycosuria. False positive urine sugar tests also
occur in individuals with renal glycosuria.
Blood glucose estimationthis is most accurate method
for detection of diabetes mellitus. Three schedules for
determination of blood glucose concentration are used:
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Technique
Two hour postprandial blood glucose
Diet instructionspatient may take serving of 1 fruit juice
plus 1 bowl of cereals with 2 tea spoonful of sugar plus
1 cup of milk plus coffee or tea with sugar plus anything
he desires at breakfast at 8 am. If the patient is to be
retested in the afternoon, he may eat 1 sandwich plus 1
piece of cake or pie plus coffee or tea with sugar or milk
plus anything else he wishes for lunch at 1 pm.
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Normal value
Test
Material
Normal value
Hemoglobin
Amylase
Serum
Bilirubin (total)
Serum
0.1 to 1 mg /dl
Cholesterol (total)
Serum
150-250 mg/dl
WBC
4000-11000 / mm3
Uric acid
Serum
Platelet count
Calcium
Serum
8.8-10.5 mg/dl
Hematocrit
At birth54
Adult males42-50%
Adult females36-45%
Chloride
Serum
98-108 mEq/L
Sodium
Serum
135-148 mEq/L
Potassium
Serum
3.5-5.5 mmol/l
Phosphorus
Serum
2.5-4.5 mg%
SgPT
Serum
5.40 IU/L
SgOT
Serum
5.40 IU/L
Creatinine
Serum
Folate
Serum
Erythrocyte
5-25 mg/ml
166-640 mg/ml
Glucose
Iron (total)
Iron binding capacity
Iron saturation
Serum
Serum
Serum
60-150 g/dl
250-400 g/dl
20-55%
Phosphatase acid
Alkaline phosphatase
Serum
Serum
Test
80-96 cu micron
27-31 pg
32-36 gm/dl
ESR
<15mm/hr
< 20 mm /hr
< 20 mm/hr
< 30 mm / hr
Absolute value
2500-7000/ul
50-500/ul
0-100/ul
Lymphocytes20-47%
Monocytes0-9 %
1000-4000/ul
200-800/ul
Reticulocyte count
0.5-2.5 %
Bleeding time
1-6 minutes
3-5 minutes
4-10 minutes
of original mass in 1 hr
Protein total
Albumin
Globulin
Serum
Clot retraction
6-7.8 gm/dl
3.2-4.5 gm/dl
2.3-3.5mg/dl
Prothrombin time
12-15 seconds
Triglyceride
Serum
4-150 mg/dl
Urea nitrogen
Serum
8-18 mg/dl
Thrombin time
10-12 seconds
Plasma fibrinogen
150-400 mg/dl
30-35 seconds
Magnesium
Serum
Thyroid hormones
Thyroxin
T4
T3
Serum (RIA)
Table 8-8: Comparison of calcium, phosphorus and alkaline phosphatase levels in common
disorders of bone and calcium metabolism
Disease
Serum calcium
Serum phosphorus
Normal
2 to 5 mg / dl of blood
Rickets
Increased 20 to 40 X normal
Osteomalacia
Decreased
Decreased
Hyperparathyroidism
Marked increased
Usually decreased
Increased 2 to 50 X normal
Pagets disease
Usually normal
Usually normal
Occasionally elevated
Osteogenesis imperfecta
Usually normal
Usually normal
Usually normal
Normal
Normal
Normal
Normal
Tetany
Normal or elevated
Normal
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Fig. 8-18: Intraoral periapical radiograph is backbone of dentistry.
Radiological Investigations
Intraoral Projection
It is the backbone of dental radiography.
Intraoral periapicalit shows all the teeth including
surrounding bone and mainly the periapical area (Fig.
8-18).
Occlusalit shows more areas of teeth and bone than
seen in an IOPA radiograph.
Bite wingit only shows crowns of teeth and adjacent
alveolar crests.
Figs 8-20A and B: Specialized technique like OPG (A) and Computed
tomography (B) is also act as valuable aid in making diagnosis of the
lesion in oral cavity.
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Extraoral Projection
4.
7.
5.
6.
8.
9.
10.
Suggested Reading
1. Brickley M, Cowpe J, Shepherd J. Performance of computer
stimulated neural network trained to categorized normal,
premalignant and malignant oral smears. J Oral Patho Med
1996;25:424:8.
2. Dinkar A, Satoskar S. Diagnostic aids in early oral cancer
detection, a review, IIAOMR, 2006;18(2):82-9.
3. Epstein JR, Scully C, Spinelli. Toludine Blue and Lugol Iodine
11.
12.
13.
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9
Classification
Developmental Tooth Alteration
Size of Teeth
Microdontia
Macrodontia
Shape of Teeth
Gemination
Twinning
Fusion
Concrescence
Talon cusp
Dilaceration
Dens in dente
Dens evaginatus
Hypercementosis
Supernumerary roots
Paramolar tubercle or Bolk cusp
Enamel pearl or droplet or nodule
Globodontia
Mulberry molar
Moons molar
Hutchison incisor
Carabelli cusp
Shovel shaped incisor
Number of Teeth
Anodontia
Supernumerary teeth
Pre-deciduous dentition
Structure of Teeth
Amelogenesis imperfecta
Dentinogenesis imperfecta
Teeth Anomalies
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Dentin dysplasia
Regional odontodysplasia
Dentin hypocalcification
Disturbance of Eruption
Premature eruption
Delayed eruption
Impacted teeth
Embedded teeth
Ankylosis of teeth
Transposition
Eruption sequestration
Ectopic eruption
Premature exfoliation
Attrition
Abrasion
Erosion
Internal resorption
External resorption
Discoloration of Teeth
Extrinsic stain
Bacterial stain
Tobacco stain
Restorative material
Medication
Chlorhexidine stain
Intrinsic stain
Erythropoietic porphyria
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Alkaptonuria
Erythroblastosis fetalis
Hyperbilirubinemia
Trauma
Lepromatous leprosy
Tetracycline stain
Pulp Disease
Pulp calcification
Necrosis of pulp
Developmental Disturbances of
Teeth
Size of Teeth
Microdontia
It refers to teeth that are smaller than normal. Microdontia
is usually transmitted as an autosomal dominant with
incomplete penetrance.
Types
True generalizedall the teeth are smaller than normal.
It occurs in pituitary dwarfism, Downs syndrome and
congenital heart disease.
Relative generalizednormal or slightly smaller than
normal teeth; are present in jaws that are somewhat larger
than normal. It is hereditary. It often exhibits spacing
between the teeth.
Localizedit involves only single tooth. It occurs with
congenital heart diseases, Downs syndrome and
progeria.
Clinical features
Locationmost commonly affected teeth are maxillary
lateral incisors and 3rd molars. Supernumerary teeth
are frequently smaller than normal.
Peg shaped lateralit is one of the common form of
localized microdontia is peg shaped laterals in which
the mesial and distal sides converges or taper incisally,
forming peg shaped or cone shaped crown (Fig. 9-1).
Molarswhen molars are involved, they may also
undergo a change in shape from five to four cusps in
case of mandibular molar and from four to three cusps
in upper molars.
Radiographic features
Radiograph will permit evaluation of size of both, erupted
and non-erupted teeth.
Diagnosis
Clinical diagnosisby looking at the size of tooth clinical
diagnosis can be easily made.
Management
Crown and bridge workcrown and bridge work is
required for esthetic rehabilitation of teeth.
Macrodontia
It is also called as megadontia, megalodontia. These are the
teeth which are larger than normal.
Types
True generalizedall the teeth are larger than normal. It
is commonly associated with pituitary gigantism.
Relative generalizedteeth are normal or slightly larger
than normal, but present in a smaller jaw.
Localizedone or more large teeth exist in relation to an
otherwise normal dentition and body size.
Causes
Facial hemihypertrophyit is occasionally seen in facial
hemi-hypertrophy, in which half of the teeth in unilateral
distribution are affected.
Gigantismin this generalized overgrowth of the body
occurs.
Geneticgenetic component also responsible for
macrodontia.
Clinical features
Teeth sizeteeth are larger than normal (Fig. 9-2).
Malocclusionthere is crowding, which may result in
malocclusion.
Impactionas space is less, there is impaction of teeth.
Radiographic features
The increased size will be demonstrated on the radiograph.
Diagnosis
Clinical diagnosisby looking at the size of tooth clinical
diagnosis can be easily made.
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Management
Orthodontic treatmentif necessary orthodontic treatment is done.
Extractionif impacted, extraction is indicated.
Shape of Teeth
Differential Diagnosis
Fusiontooth structures with two separate root canals
and with either one root or two roots are result of fusion,
in contrast to the enlarged and possibly partially divided
pulp chamber in an enlarged tooth with bifid crown
which is a result of gemination. In gemination the full
complement of teeth is present while in the case of fusion,
tooth is missing.
Management
Reshaping of crownaffected tooth structure should be
removed and crown may be restored and reshaped.
Periodic diskingreduction of mesiodistal width with
periodic disking.
Crown preparationfinal jacket crown preparation.
Gemination
Twining
Clinical features
Sexmales and females are equally affected.
Sitescommonly affected teeth are deciduous mandibular incisors and permanent maxillary incisors.
Appearanceit appears clinically as bifid crown on single
root.
Number of teethit does not increase or decrease the
number of teeth present.
Crown featuresthere are common pulp canals and either
single or partially divided pulp chambers. Crown is wider
than normal with shallow groove extending from incisal
edge to cervical region. Enamel or dentin of crown of
geminated teeth may be hypoplastic or hypocalcified.
Complicationareas of hypoplasia and invagination
lines or areas of coronal separation represent caries
susceptible area, which may lead to pulpal infection.
It may also cause malocclusion and periodontal
pathosis.
Radiographic features
Cleft crowncleft in the crown and invagination are
usually outlined by the radiopaque enamel which
accentuates them.
Fusion
Etiology
Geneticit is transmitted as autosomal dominant trait
with reduced penetration.
Physicalphysical force or pressure generated during
development causes contact of tooth germs.
Clinical features
Sexmale to female ratio is 1:1.
Locationit is seen more commonly in anterior teeth. It
is more common in deciduous dentition than in
permanent dentition. It may occur between a normal
tooth and a supernumerary tooth such as mesiodens or
distomolar.
Size of toothtooth is almost twice in size than normal,
with or without bifid crown (Figs 9-3 and 9-4).
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Fig. 9-3: Fusion of central incisor with lateral
incisor in the maxillary region.
Differential Diagnosis
Geminationit is discussed in Differential Diagnosis of
gemination.
Management
Endodontic treatmentmorphology of teeth should be
determined radiographically for endodontic treatment.
Reshaping of toothafter endodontic treatment, tooth
may be reshaped with a restoration that will mimic
independent crown.
Fig. 9-4: Fusion of central and lateral incisor
showing large tooth.
Concrescence
It is a form of fusion that occurs after the root and other
major parts involved in teeth are formed or when the roots
of two or more teeth are united by cementum, below the
cementoenamel junction (Fig. 9-6). It is also called as false
gemination.
Etiology
Developmentalspace restriction during development
resulting in extends of cementum deposition between
closely approximated roots of teeth.
Inflammatoryin cases of inflammatory damage to the
roots of teeth are repaired by cementum.
Traumatic injurythis may also lead to concrescence of
teeth.
Overcrowdingovercrowding of the teeth with resorption
and interdental bone loss.
Distal inclinationdistal inclination of crown of molar
will results in contact between cementum resulting in
concrescence of the tooth.
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Fig. 9-7: Concrescence showing union of the tooth
with the help of cementum (Courtesy Dr Mody).
Pathogenesis
Focal proliferationa focal proliferation of tissue during
development.
Exuberant developmentexuberant development of the
fourth lobe (cingulum) may occur.
Radiographic features
Diagnosis is made by radiographs. It is not always possible
to distinguish between concrescence, teeth in close contact
and superimposed teeth (Fig. 9-7).
Diagnosis
Clinical diagnosisit is difficult to differentiate between
fusion and concrescence.
Radiological diagnosisradiograph will show union of
two teeth with the help of cementum.
Management
Dentist must be careful while doing extraction.
Talons Cusp
It projects lingually from cingulum area of maxillary and
mandibular teeth or it is an anomalous hyperplasia of
cingulum on the lingual surface of maxillary and mandibular incisors, resulting in the formation of supernumerary
cusp.
Clinical features
Sexit may be found in both sexes.
Locationit is common in both dentitions. Most
commonly seen on maxillary lateral or central incisor.
Appearanceit resembles like an eagles talon.
Signsit blends smoothly with the erupted tooth,
except that there is deep developmental groove where
the cusp blends with sloping lingual tooth surface.
Compositionit is composed of normal enamel, dentin
and contains a form of pulp tissue.
Shapecusp may or may not contain pulp horn and is
usually T shaped (Figs 9-8 and 9-9).
Significancepatients can face the problems with esthetic.
There is also high incidence of caries. Occlusal
interference may be there.
Syndromeit is associated with Rubinstein-Taybi
syndrome and Sturge Weber syndrome.
Radiographic features
Superimposed with incisors, on which it occurs.
Appearanceoutline is smooth and a layer of normal
appearing enamel is distinguishable (Figs 9-10A and B).
Diagnosis
Clinical diagnosisT shaped elevation on tooth will
easily diagnoses talon cusp.
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Fig. 9-8: T-shaped talon cusp seen in maxillary
lateral incisor (arrow).
Differential Diagnosis
Supernumerary teethclose association can be
determined by tube shift technique.
Management
Restorationprophylactic restoration of the groove
should be done to avoid early carious lesion.
Endodontic therapyremoval of cusp followed by
endodontic therapy.
Periodic grindingperiodic grinding should be done to
maintain vitality of teeth. After grinding, exposed dentin
should be coated with desensitizing agents like fluoride
varnish.
B
Figs 9-10A and B: Talon cusp is seen as
radiopacity with smooth outline
Cusp of Carabelli
It is accessory lingual cusp located on the mesiopalatal
cusp of maxillary second deciduous molars and 1st, 2nd
and 3rd permanent molars (Fig. 9-11).
It may be unilateral or bilateral, with marked deviation
in size. In some cases, accessory cusp is seen occasionally
on mandibular permanent or deciduous molar. This is
called as protostylid.
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Dilaceration
Radiographic features
Locationit will show angular distortion of unusual
relationship between coronal and radicular portion of
the tooth, on either side of defect (Fig. 9-13).
Root resorptionthere may be inappropriate resorption
of deciduous tooth which will delay the eruption of
permanent teeth.
Appearanceif the malformed teeth bend over the fold,
the defect will be obscured. If the root bends mesially or
distally condition will clearly appear on radiograph.
Buccal and lingual dilacerationwhen it is tilted buccally
or lingually, dilacerated portion will appear at apical
end as a rounded opaque area with dark shadow in
central region by apical foramen. Periodontal space about
this is evidenced as a radiolucent halo.
Fig. 9-13: Bending of root occur in the middle portion of the teeth.
Diagnosis
Clinical diagnosisnot possible.
Radiological diagnosisradiograph will show curved
root.
Differential Diagnosis
Fused rootin this case, you will be able to find two
different root canals.
Condensing osteitis- the tooth is non-vital in case of
condensing osteitis.
Management
Difficult extractiondifficulty at the time of extraction.
Restorationdilacerated crown has to be restored
improve esthetics and function and to preclude dental
caries and periodontal disease.
Dens in Dente
Fig. 9-12: Unusual bend in the root is seen in case
of dilaceration (Courtesy Dr Mody).
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Etiopathogenesis
Focal growth retardationaccording to Kronfeld, there is
relative retardation in growth of a portion of the enamel
organ. Due to this, part of the tooth remains stationary
and the remaining grows around it causing invagination.
Active proliferationaccording to Swanson and
McCarthy, it occurs due to proliferation of enamel organ
at the inner epithelium apically into dental papilla
during the stage of differentiation of developing tooth
germ. It grows into dental papilla, as a sort of adenoma.
Continuous differentiationRabinowitch said that, it may
be formed by continued differentiation of some cells of
the inner enamel epithelium.
Increased pressurestudy shows that there is presence of
extravascular fluid in the soft tissue that fills the
potential invagination cavity of the tooth, before it
erupts, suggesting that there is increased venous
pressure within the invagination. It could be due to
pressure on the blood vessels as they pass through the
entrance channel of the invagination cavity where
enamel is forming concentrically and centripetally, thus
tending to progressively narrow the entrance. Expansion
of the invagination could then result from the increased
venous pressure and transudation.
Local causesit can occur due to the infection of the
deciduous predecessor or trauma. Pressure on the
growing teeth can also cause invagination.
Classification
1st classification
Coronal dens invaginatusit is anomalous infolding of
enamel organ into dental papilla. It results in the fold of
hard tissue within the tooth, characterized by enamel
lining the fold and covering the dentin peripheral to it.
Radicular dens invaginatusit is a result of invagination
of Hertwigs epithelial root sheath resulting in accentuation of normal longitudinal root grooves. It is lined by
cementum. Root sheath may bud off sac like invagination
that results in a circumscribed cementum defect in root.
2nd classification depending upon site of invagination given by
Ohler
Type Iinvagination limited to the crown .
Type IIinvagination extending to cementoenamel
junction.
Type IIIinvagination extends beyond the cementoenamel junctions. It is commonly seen in 2nd premolar
either periapical tissue or in the periodontal ligament.
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Radiographic features
Coronal dens invaginatus
Radiodensityinfolding is recognized by its greater
radiodensity (Fig. 9-15).
Sizeit may vary in size from very small and superficial,
to large and deep.
Pulp chamberin addition to small but otherwise normal
pulp chamber, there is sometimes an additional cavity
of variable shape and size which may be separated from
real pulp chamber or may unite with it.
Diagnosis
Clinical diagnosisinfolding of tooth is seen clinically
Radiological diagnosisinverted umbrella appearance
seen radiographically.
Management
To prevent caries, pulp infection and premature loss of
tooth, dense in dente must be treated prophylactically.
Dens Evaginatus
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Clinical features
Siteit occurs on premolar and molar teeth and usually
occurs unilaterally or bilaterally.
Raceit develops in persons of Mongoloid ancestry.
Compositionit consists of all three dental tissues, i.e.
enamel, dentine and cementum.
Appearanceit appears as a tubercle of enamel on
occlusal surface of the affected tooth. Polyp-like
protuberance in central groove, on lingual ridge of buccal
cusp is seen.
Significancethere may be incomplete eruption.
Displacement of teeth with pulp exposure and
subsequent infection may present, following occlusal
wear or fracture.
Radiographic features
Dentin and enameldentin core is covered with opaque
enamel.
Pulpfine pulp horns may be apparent. Pulpal
extension is seen in the cusp of the tooth.
Tuberculated appearanceocclusal surface have
tuberculated appearance (Fig. 9-17).
Taurodontism
It is described in 1913 by Sir Arthur Keith. In this, body of
tooth is enlarged at the expense of root. It is characterized
by clinical and anatomical crown of normal shape and
size, an elongated body and short roots with longitudinally
enlarged pulp chambers. Taurodont teeth resembles that
of cud-chewing animal (tauro- bull and dont-tooth).
Etiology
Hereditaryit is caused by genetically determined trait.
Developmentalit occurs due to failure of Hertwigs epithelial root sheath to invaginate at proper horizontal level.
Mutationresulting from odontoblastic deficiency
during dentinogenesis of the root.
Diagnosis
Clinical diagnosistubercle on occlusal surface of enamel
is the key to diagnosis.
Radiological diagnosistuberculated appearance of
occlusal surface.
Management
Grinding of tubercleif tubercle is a cause of occlusal
interference, it should be removed and should be
followed by indirect pulp capping with calcium
hydroxide.
Composite reinforcementit should be done to protect a
cusp from the fracture.
Classification
Hypotaurodontit is mild form of Taurodont and
it represents slightly apical displacement of pulpal
floor.
Mesotaurodontit is moderate form and pulpal
floor displacement is about midline of the root of teeth
(Fig. 9-19).
Hypertaurodontit is severe form and apical
displacement of pulpal floor is present at the apex.
Clinical features
Sex and ageit is common in early aged men. It has got
no sex predilection.
Siteit may affect either deciduous or permanent
dentition and teeth involved are invariably molars. It
may be unilateral or bilateral, or may exhibit any
combination of quadrant involvement.
Shapeinvolved teeth tend to be of rectangular shape
rather than the normal tapering towards root.
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If the two apices are on the labial and lingual side, they
may get superimposed on each other appearing as a
bulbous root, which may mimic hypercementosis.
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Fig. 9-19: Moderate form of taurodontism seen in
molar teeth (Courtesy Dr Tapasya Karamore).
Radiographic features
Pulp and pulp chamberpulp chamber is extremely large
with much greater apicoocclusal height than normal.
Extensions of rectangular pulp chamber occur into
elongated body of the tooth. Pulp lacks the usual
constriction at the cervix of tooth.
Rootsthe root and root canals are exceedingly short.
Increased dimension between cementoenamel junction
and furcation.
Differential Diagnosis
Hypercementosisin a case when root appears bulbous
due to superimposition of root on the labial and lingual
surfaces, hypercementosis should be ruled out. In a tooth
with supernumerary roots, the pulp canal may appear
to end a short distance from the blunt square end apex.
Arising from blunt end to the canal, are two fine channels
which extend one into each root, these channels suggest
the presence of two apices, thus excluding hypercementosis.
Diagnosis
Clinical diagnosisrectangular shaped crown.
Radiological diagnosisextremely large pulp chamber.
Management
Assume significance only during exodontia as these roots
may be broken off during extraction.
Differential diagnosis
Developing mandibular molarit has got wide apical
foramina; the incomplete root and dental papilla will
rule out taurodontism.
Management
No specific treatment is necessary as it does not cause any
clinical problems.
Supernumerary Roots
Teeth that are normally single rooted exhibit two roots.
Clinical features
Sitesboth, maxillary and mandibular molars
particularly 3rd molars, exhibit supernumerary roots.
Appearancethey develop as slender outgrowths at the
center of furcation area of molar teeth.
Radiographic features
If the bifurcation produces two distinct apices and these
are arranged as one mesial to the other, then it will be
seen on the radiographs (Fig. 9-20).
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Diagnosis
Clinical diagnosisnot possible.
Radiological diagnosisrounded opacity in the furcation
area.
Differential Diagnosis
Calculusclinically detectable.
Pulp stonecan be diagnosed by changing angulation.
Management
Maintain oral hygieneoral hygiene should be
maintained. If it is causing periodontal problems, mass
can be removed.
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Diagnosis
Clinical diagnosisglobular portion of tooth can be
diagnosed clinically.
Management
Regular follow up, scheduled tooth extraction and
eventually orthodontic treatment should be done.
Mulberry Molar
It is a characteristic syphilitic lesion of posterior teeth in
which hyperplastic enamel develops with spherical
aggregates or globules on the surface of dentin.
Moons Molar
It is syphilitic lesion of posterior teeth. 1st molar is
commonly involved. Cusp of teeth show exaggerated
rounded or nodular shapes.
Appearancesit is often grossly distorted, usually
narrower mesiodistally with loss of angulation of occlusal
edge, which may give cusp a squarish appearance.
Hutchinsons Incisor
Commonly affected teeth are the anterior teeth. Center of
the incisal edge shows typical notching. An affected tooth
Hypercementosis
It is also called as cementum hyperplasia or exostosis of
root. It is characterized by deposition of excessive amount
of cementum on the root surface. New tissue formation is
in direct contact with the cementum of roots of teeth.
Types
Localizedhypercementosis of single tooth. It is usually
a reactive, inflammation dependent phenomenon
seen on single tooth and usually in relation to
periapical osteitis or due to loss of occluding antagonistic
tooth.
Generalizedgeneralized hypercementosis affecting
many (all) teeth, but which is seldom recognized as such,
occurs with increasing age, i.e. as an age dependent
factor. It is also seen as a sign accompanying specific
diseases, as for instance, Pagets disease of bone.
Etiology
Loss of antagonistthere is accelerated elongation of tooth
occurs due to loss of antagonist. It occurs due to inherent
tendency of the periodontium to maintain normal width
of the periodontal ligament.
Inflammation of the rootit does not occur at the apex of
the root directly adjacent to the area of inflammation, as
cementoblasts and their direct precursors in this area
are lost. Instead, it occurs at some distance above the
apex as the inflammatory reaction acts as stimulation
for the cementoblasts.
Trauma repairocclusal trauma results in mild root
resorption and it is then repaired by cementum formation.
Root fracture is also repaired on occasion by deposition
of cementum between the root fragments as well as in
their periphery.
Osteitis deformans or Pagets disease of boneit is
a generalized skeletal disease characterized by
excessive amount of cementum formation on roots of
teeth and by apparent disappearance of lamina dura of
teeth.
Othersother disease which can cause hypercementosis
are hyperpituitarism, calcinosis, thyroid goiter, vitamin
A deficiency, cleidocranial dysostosis and rheumatic
fever.
Clinical features
Ageit is predominately seen in adults.
Sitepremolar teeth are often bilaterally affected and
symmetrical in distribution. The permanent teeth are
affected more commonly than deciduous teeth. In
multirooted teeth, one or more roots are involved.
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Management
Treatment of the primary cause should be done.
Number of Teeth
Anodontia, Hypodontia and Oligodontia
Several terms are used to discuss number of missing teeth.
It is congenital absence of teeth.
Classification
Trueit is congenitally absence of teeth
Anodontiait is complete lack of tooth development.
Hypodontiait is lack of development of one or more
teeth (Fig. 9-25).
Oligodontiait is lack of development of six or more
teeth (Fig. 9-26).
Falseit occurs due to extraction of teeth.
Pseudoit occurs due to multiple unerupted teeth in the
jaw.
Radiographic features
Appearancethere is thickening and apparent blunting
of root with rounding of apex. If cementum is distributed
eccentrically there is a localized protuberance
Apexapex appears bulbous in some instances, after
symmetrical distribution of cementum.
Lamina duralamina dura will follow the outline of teeth
in normal periodontal ligament space.
Bone resorptionthere may be mildly irregular
accumulation of cementum that is accommodated by
related area of bone resorption.
Diagnosis
Clinical diagnosisnot significant.
Radiological diagnosisbulbous appearance of root of
tooth due to cementum deposition.
Differential Diagnosis
Multirooted teeth and dilacerated rootsuccessive
radiographs from different angle should be taken.
Fused rootrecognized by expanded region of root that does
not have lower radiodensity of hyperplastic cementum.
Fig. 9-26: Oligodontia showing missing teeth which is more than six
in number (Courtesy Dr Parate).
Etiology
Geneticmany hereditary syndromes have been
associated with less number of teeth. More commonly
they are hereditary ectodermal dysplasia, cleidocranial
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Clinical features
Sex and raceit is higher in women and most probably
in Mongoloid, than whites.
Locationabsence may be unilateral or bilateral.
Commonly missing are 3rd molar, maxillary lateral
incisor (Fig. 9-27), maxillary or mandibular 2nd premolar.
Associated featureassociated features include
microdontia, reduced alveolar development, increase
freeway space and retained primary teeth.
Management
Orthodontic treatmentit should be carried out as many
patients may develop malocclusion.
Prosthesistraditional fixed prosthesis and resin bonded
bridges should be given.
Supernumerary Teeth
It is also called as hyperdontia. It is defined as any tooth or
tooth substance in the excess of the usual configuration of
twenty deciduous or thirty two permanent teeth.
Pathogenesis and etiology
The various factors which are responsible for formation of
supernumerary teeth as follows:
Phylogenetic reversion theorythis theory is nowadays
discarded.
Dichotomy theorythis theory states that tooth bud is
split to form two different tooth,
Hyperactivity of dental laminaa supernumerary tooth
develops from 3rd tooth bud arising from dental lamina
near the permanent tooth bud.
According to form
Supplemental supernumerary teeththese teeth duplicate
the typical anatomy of posterior and anterior teeth.
Rudimentary supernumerary teeththese are dysmorphic
and can assume conical (Fig. 9-28) or tuberculated forms.
Odontome likein some cases odontome may be form in
place of supernumerary teeth.
According to location
Mesiodensit is located at or near the midline in the
incisal region of maxilla between central incisors (Fig.
9-29). It may occur singly or paired, erupted or impacted
or even inverted. It is a small tooth with cone shaped
crown and short root. It may cause retarded eruption,
displacement or resorption of adjacent root. It frequently
causes improper alignment.
Distomolarit is found in molar region frequently
located distal to 3rd molar (Fig. 9-30). Generally,
these teeth are smaller than normal 2nd and 3rd molar
(Fig. 9-31), crown morphology is highly abnormal.
Paramolarit is supernumerary molar, usually small
and rudimentary and is situated buccally or lingually
to one of the maxillary molars or interproximally
between 1st, 2nd and 3rd maxillary molars.
Peridenssupernumerary teeth that erupt ectopically,
either buccally or lingually to the normal arch are referred
as peridens (Fig. 9-32).
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Fig. 9-32: Peridens seen erupted lingually in mandibular premolar
region (Courtesy Dr Bhaskar).
Clinical features
Prevalencethe prevalence of supernumerary teeth is
about 0.1 to 3.6% of the population.
Sexmales are affected more than females. Male to
female ratio is 2:1.
Dentitionit may occur in both dentitions, but frequently
found in permanent dentition and more often in
mandible.
Siteit is more commonly seen in anterior maxilla
(Fig. 9-33A) followed by mandibular premolar region
(Fig. 9-33B).
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Radiographic features
When it is neededif abnormal clinical signs are present
you can go for OPG examination, IOPA, occlusal radiographic examination.
Significanceradiograph will aid in determining the
location and number of unerupted teeth. It can also used
to see if there is any cyst formation.
Appearancetheir radiographic picture is characteristic
of teeth.
Clinical features
Appearanceteeth may be conical or may be normal in
size and shape and opaque yellow-brownish in color.
Signsthey are hypermobile because of their limited
root development. Within relatively short time, premature
erupted tooth will become stabilized and other teeth of
the arch are erupted. Teeth appear to be attached to a
small mass of soft tissue.
Significancesome teeth are so much mobile that there
is danger of displacement and possible aspiration and
in this case, removal is indicated.
Riga fede ulcerthere is ulceration of the ventral surface
of the tongue caused by the sharp incisal edges (Figs
9-34 and 9-35). It leads to interference with proper
suckling and feeding and thus the neonate is at risk of
nutritional deficiency.
Associated syndromesit may associate with syndromes
like Ellis-van Creveld syndrome and cleft palate.
Management
Surgical extractionit depends on potential effect on
normal dentition, their position, number and
complications that may result from surgical removal. If
required, they should be extracted.
Pre-deciduous Dentition
It is also called as congenital teeth, fetal deciduous teeth,
dentition proceox and natal and neonatal teeth. There is
premature eruption of teeth or teeth like structures that are
present at birth.
Natal teeth are the teeth which are present at the time of
birth and neonatal teeth are the teeth which are present within
30 days after the birth.
Etiology
Hereditarysuperficial position of tooth germ.
Hormonal influenceeruption accelerated by febrile
incident or hormonal stimulation.
Classification
Maturethey are fully developed in shape and
comparable in morphology to the primary teeth.
Prognosis is relatively good.
Immaturetheir structure and development is
incomplete. Poor prognosis of teeth.
Radiographic feature
Radiographs fail to show any root substance and teeth
are very small to represent the normal teeth.
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Management
Extractionextraction of the teeth should be carried out
if it is causing inconvenience during suckling,
interference with breastfeeding and causing traumatic
injury. Extraction should be done after 10 days of life.
Rounding of sharp anglethe other option that may be
used is rounding of the sharp angle of incisal edges of
teeth.
Retaining the toothif not necessary, tooth should not be
removed.
Post-permanent Dentition
Persons who have all the permanent teeth extracted and
yet have subsequently erupted teeth, particularly after
insertion of complete denture come in this category. They
possibly develop from bud of dental lamina beyond the
permanent tooth germs.
Structure of Teeth
Amelogenesis Imperfecta
It is also called as hereditary enamel dysplasia, hereditary
brown enamel and hereditary brown opalescent teeth.
It represents group of hereditary defects of enamel
associated with any other generalized defect. It is an
ectodermal disease and mesodermal component is normal.
Classification
Classification depends upon the stage of at which the
disease occurs. According to it, there are mainly three types
of amelogenesis imperfecta
Hypoplastic typethere is defective formation of enamel
matrix.
Autosomal dominant
Generalized pitted
Localized pitted
Diffuse smooth
Diffuse rough
Autosomal recessive
Localized pitted
Enamel agenesis
X-linked dominant
Hypocalcification typethere is defective mineralization
of formed matrix.
Autosomal dominant
Autosomal recessive
Hypomaturation typein this, enamel crystal lattice
remains immature.
Autosomal dominant
Autosomal recessive
Snow-capped teeth.
Clinical features
Hypoplastic type
It includes localized portions of enamel that do not reach
normal thickness during development.
Autosomal dominant
Generalized pittedit appears as thin enamel on teeth
that do not contact with each other mesiodistally.
Pinpoint to pinhead pits are randomly distributed over
the surface. Enamel on newly erupted teeth is hard with
normal yellow-white color. Staining of teeth occurs after
exposure to oral environment, giving teeth a black
appearance.
Localized pittedhorizontal rows of depressions or one
large hypoplastic area with hypocalcification adjacent
to and below the hypoplastic area is found. Defects are
most prominent on buccal surfaces of the teeth, involving
middle 3rd of enamel. Incisal or occlusal surfaces of the
teeth are usually not involved.
Diffuse smoothin this enamel is thin, hard and glossy
with smooth surface (Fig. 9-36). Enamel is 1/4th to
1/8th of its normal thickness. On newly erupted teeth,
they have yellow color, but may vary from opaque white
to translucent brown. Some of the enamel may be missing
on newly erupted teeth, especially on the incisal and
occlusal surface and may be chalky in inter-proximal
areas. Delay in eruption occurs with resorption of teeth
in the alveolus.
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Hypomaturation type
In this there is defect in the maturation of enamel crystal
structure. The enamel can be pierced by an explorer point
under firm pressure and can be lost by chipping away from
the underlying, normal appearing dentin.
Autosomal dominant
Sexit is more commonly found in males.
Dentitionboth primary and permanent dentitions are
affected
Color of teethpermanent teeth are mottled yellow white
in color, but may be darkened with absorption of stains
(Fig. 9-38). Primary teeth of affected males have ground
glass opaque white appearance. Patient occasionally
shows slight yellow cast to enamel surface.
Intact contact pointteeth meet at contact points and have
normal contour.
Thickness of enamelenamel approaches normal
thickness, but it may be thinner. Point of explorer can be
forced into enamel.
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Dentinogenesis Imperfecta
There are various names for dentinogenesis imperfecta like
hereditary opalescent dentin and Capadeponts teeth. It
segregates as an autosomal dominant trait with variable
expressivity.
Classification
Shield type Identinogenesis imperfecta always occurs
with osteogenesis imperfecta. According to Witkop it is
called as dentinogenesis imperfecta
Shield type IIIt does not occur in association with
osteogenesis imperfecta. According to Witkop it is called
as hereditary opalescent dentin.
Shield type IIIIt has got shell teeth appearance and
multiple pulp exposure. According to Witkop it is also
called as Brandywine type.
Clinical features
Shield type I
General featuresfeatures of this condition are multiple
bone fractures, hyperextensible joints, blue sclera and
progressive deafness.
Dentitiondeciduous teeth are more severely affected
than permanent teeth.
Color of teethcolor of teeth may vary from blue to
brownish violet to yellowish brown. Amber translucency
of both primary and permanent dentition may be seen
(Fig. 9-40).
Rapid attritionenamel may be lost and dentin
undergoes rapid attrition (Fig. 9-41).
Diagnosis
Clinical diagnosischeesy consistency of enamel with
loss of enamel aid in diagnosis of amelogenesis
imperfecta.
Radiological diagnosismissing enamel cap with low or
absent cusp.
Differential Diagnosis
Dentinogenesis imperfectaShape and size of crown and
root with relatively normal density, obliteration of pulp
chamber and root canals in the absence of any marked
abrasion should identify dentinogenesis imperfecta.
Management
Cosmetic improvementit should be done with the help
of placement of crown or facial veneer on the teeth.
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Radiographic features
Appearanceconstriction of cervical portion of tooth that
imparts bullous appearance.
Attritionthere may be slight to marked attrition of teeth.
Pulp, root and root canalpartial or complete obliteration
of pulp chamber (Fig. 9-43). Pulp obliteration may take
place before or after eruption of teeth. Root canals may
be absent or thread like or may be blunted.
Periapical areaperiapical radiolucency without pulpal
involvement and periodontal ligament space widening.
Flame shaped pulp canalin some cases, the radicular
portion of pulp cavities is very narrow, while the pulp
chambers have a bulbous expansion terminating in a
point deep to the occlusal aspect which resembles flame.
Shell teethIn Brandywine type, enamel of tooth appears
normal, while the dentin is extremely thin and the pulp
chambers are enormous. Teeth appear as shell teeth. In
addition, root of tooth are extremely short, so it appears
as if enamel and dentin surrounded by extremely large
pulp chamber and root canals.
Diagnosis
Clinical diagnosisrapid loss of enamel with attrition of
tooth. Clinically multiple pulp exposure can be seen.
Radiological diagnosisobliteration of pulp chamber.
Presence of periapical radiolucency without pulpal
involvement.
Shield type II
Clinical features are same as that of shield type I, except
they are somewhat of severe form and it is not associated
with osteogenesis imperfecta.
Management
OverdentureOverdenture should be given and teeth
should be covered with fluoride releasing glass inomer
cement.
Crowncast metal crown in posteriors and jacket crown
in anterior can be given.
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Dentin Dysplasia
Radiographic features
1. Radicular
Pulp canalspulp chamber and canals are obliterated
before eruption and appear as half moon shaped.
Rootsthey have short roots with sharp conical and
apical constriction. These are abnormally shaped;
primary teeth are represented by spicule.
Periapical pathologymultiple periapical radiolucencies
are present.
Pulp chamberobliteration of pulp chamber produce
crescent or chevron shaped (V shaped line or strip) pulp
remnants.
Classification
According to Shield (clinical)
Shield type Identin dysplasia.
Shield type IIanomalous dysplasia.
According to Witkop (radiological)
Radicular dentin dysplasia
Coronal dentin dysplasia.
Clinical features
Shield type I
Synonymit is also called as rootless teeth, nonopalescent and opalescent dentin and radicular dentin
dysplasia.
Appearancepermanent and primary teeth are of normal
size, shape and consistency.
Coloraffected teeth are occasionally slightly amber and
translucent.
Mobilityas the root size is short patient notice mobility
of the teeth. There is also premature exfoliation of teeth
(Fig. 9-44).
Significancemalalignment and malpositioning due to
extreme mobility. Minor trauma may result in exfoliation.
Shield type II
Colorsignificant differences of color in both the
dentitions. Primary teeth with yellow, brown, bluish,
grey-amber translucent appearances. Permanent teeth
of normal color.
Rootroot size is normal in size.
2. Coronal
Thistle tube appearancepermanent teeth exhibit
abnormality, large chamber in coronal portion often
described as thistle tube in shape due to radiating
extension of pulp chamber.
Pulp stoneteeth show multiple pulp stones.
Diagnosis
Clinical diagnosisunusual mobility of tooth without
periodontal involvement may suspect dentin dysplasia.
Radiograph is necessary.
Radiological diagnosisvery short root of the teeth.
Laboratory diagnosisnormal dentinal tubule formation
appears to be blocked so that new dentin forms around
obstacle and takes the characteristic appearance
described as lava flowing around boulder.
Differential Diagnosis
Hereditary opalescent dentinpulp chamber never fills
before eruption in type II dentin dysplasia. Thistle
shaped pulp chamber occurs in dentin dysplasia. Teeth
in opalescent dentin have bell shaped crown with
constriction in cervical region while in dentin dysplasia
it is normal. If root is short and narrow it is opalescent
dentin, while normal appearing root or no root at all is
dentin dysplasia. Periapical rarefaction in association
with non-carious tooth is in dentin dysplasia.
Management
Oral hygienemeticulous oral hygiene should be
maintained to avoid early loss of teeth.
Retrograde endodontic treatmentit should be done in
patient who have periapical pathology and have a short
root.
Periapical curettageit should be done in cases when
there is periapical inflammatory conditions are present.
Regional Odontodysplasia
It is also called as odontogenic dysplasia or ghost teeth. It is
an unusual development anomaly in which ectodermal
and mesodermal tooth component are affected. It is a
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Radiographic features
Ghost teeththere is marked reduction in density, so that
the teeth assume ghost appearance. Ghost teeth that do
not erupt are so hypomineralized and hypoplastic that
they appear to be resorbing.
Shell teethsometimes only the shell of enamel remain
on the teeth, this appearance is called as shell teeth.
Pulp and rootpulp chamber is very large with wide
root canals. Poorly outlined roots are shortened. In some
cases, calcification in the pulp is present.
Diagnosis
Clinical diagnosisirregular shaped teeth with brown
discoloration.
Radiological diagnosisshell teeth appearance seen
radiologically.
Differential Diagnosis
Shell teeth of dentinogenesis imperfectaIn dentinogenesis
imperfecta, familial involvement in contrast to odontodysplasia. Enamel is not hypoplastic in shell teeth as
compared to ghost teeth. Only few teeth are affected in either
dentition.
Management
Prosthetic replacementmany suggest to extract involved
tooth at the earliest which is followed by prosthetic
replacement.
Restorative procedurein some cases, root canal treatment
should be carried out and tooth should be saved.
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Turner hypoplasia
Dental fluorosis
Tetracycline hypoplasia.
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Classification
Questionable changesit is characterized by occasional
white flecking or spotting of enamel.
Mild changesit is manifested by white opaque areas
involving more of the tooth surface.
Moderate and severe changesshowing pitting and
brownish staining of the surface and sometimes even
corroded appearance.
Clinical features
Dentitiondental fluorosis in primary dentition is less
severe as compared to permanent dentition.
Color of teethit frequently becomes stained as unsightly
yellow to brown color, which is caused by coloring
agents from food, medicine and by disintegration of
increase protein contain in the hypomineralized parts
of the enamel (Figs 9-47A and B).
Severe fluorosisteeth which are moderately or severely
affected may show tendency to wear or even fracture of
enamel (Fig. 9-48). Sometimes, white patches in enamel
may become striated, pitted and mottled.
Clinical classification for fluorosis (TF)
Score 0the normal translucency of the glossy creamywhite enamel remains after wiping and drying of the
surface.
Score 1thin white opaque lines are seen running across
the tooth surface. The lines correspond to the position of
perikymata. In some cases snow-capping of cusps may
also be seen.
Score 2the opaque white flecks are more pronounced
and frequently merge to form small cloudy areas
scattered over the whole surface.
Score 3merging of the white lines occurs and cloudy
areas of opacity occur to spread into many parts of the
surface. In between the cloudy area, white lines can also
be seen.
B
Figs 9-47A and B: Mild type fluorosis seen in anterior region.
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Disturbance in Eruption
Premature Eruption
The eruption of teeth may occur before their normal eruption
time. In some cases tooth may be present as natal teeth and
neonatal teeth.
Etiology
Familial patternthis can be occurred as familial
disease.
Endocrine disorderssecretion of several endocrine
organs like thyroid, adrenals and gonads may alter the
eruption rate of teeth. It can also be occurred in
adrenogenital syndrome.
Clinical features
Sitesusually only one or two teeth erupt early, mostly
deciduous and mandibular central incisors.
Symptomsthey are often well formed and normal in all
aspects, except they may be mobile.
Premature loss of deciduous teethpremature loss of
deciduous teeth may give rise to premature eruption of
permanent teeth.
Delayed Eruption
In some cases eruption may be delayed. It may occur due to
various conditions.
Etiology
Systemic conditionslike rickets, cretinism and
cleidocranial dysplasia.
Local factorslike fibromatosis gingiva in which dense
connective tissue does not permit the eruption of teeth.
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Management
Extraction of teeth and space maintainerextract the
primary teeth and use space maintainers until the
permanent tooth erupts.
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Fig. 9-52: Mesioangular impacted of mandibular right and left third
molar (Courtesy Dr Parate).
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Management
Surgical excisionkeep tooth under observation. If
required, surgical excision is carried out.
Transposition
Tooth may be found occupying an unusual position in
relation to other teeth, in the dental arch, i.e. two teeth
apparently exchanging their position.
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Clinical features
Locationpermanent canine is most oftenly involved,
with its position interchange with lateral incisor. Second
premolar is infrequently found between first and second
molar. Transposition of central and lateral incisor is rare.
Transposition does not occur in primary dentition (Figs
9-57A and B).
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Fig. 9-58: Transposition of canine with premolar in maxillary region.
Clinical features
Locationit is a tiny irregular spicule of nonviable bone
overlying the crown of an erupting permanent molar.
Spicule directly overlies the central occlusal fossa, but is
contained within the soft tissues.
Signsas the tooth continues to erupt, the cusps emerge
and the fragments of bone completely sequestrate
through mucosa and are then lost.
Symptomschild may complain of slight soreness
produced by compression of soft tissues over the spicule,
by the movement of the spicule in the soft tissue crypt
during mastication and following eruption through
mucosa.
Radiographic features
It appears as a tiny irregular opacity overlying the central
occlusal fossa, but separated from the tooth itself.
Management
Removal of spicule, if necessary.
Ectopic Eruption
B
Figs 9-57A and B: Transposition of canine occur with premolar
in maxillary left region.
Radiographic features
It can be recognized on radiograph by the unusual
sequence of teeth in dental arch (Fig. 9-58).
Management
These teeth can be prosthetically altered to improve function
and esthetics.
Eruption Sequestrum
As the molar teeth erupt through bone, they will
occasionally separate small osseous fragments of bone like
corkscrew. If bony spicule is large or eruption is fast,
complete resorption of bone cannot occur.
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Management
Brass looped wires in contact area should be given.
Premature Exfoliation
Etiology
Syndromeit is seen in Papillon-Lefvre syndrome.
Hereditaryit occurs in familial juvenile periodontitis
and familial fibrous dysplasia.
Nutritional disorderslike hypophosphatasia and cyclic
neutropenia.
Othershistiocytosis and acrodynia.
Clinical features
Bone lossthere is widespread loss of supporting
alveolar bone.
Teethloosening, migration and spontaneous loss of
teeth (Fig. 9-60).
Management
No treatment, except to correct the etiological factors.
Types
Physiological attritionattrition which occurs due to
normal aging process, due to mastication.
Pathological attritionit occurs due to certain abnormalities in occlusion, chewing pattern or due to some
structural defects in teeth.
Etiological factors for pathological attrition
Abnormal occlusion
Developmentmalocclusion and crowning of teeth,
may lead to traumatic contact during chewing, which
may lead to more tooth wear.
Acquireddue to extraction of teeth. Extraction causes
increased occlusal load on the remaining teeth, as
the chewing force for the individual remains constant.
Premature contactin case of edge-to-edge contact,
pathological attrition can also occur.
Abnormal chewing habitsparafunctional chewing habit
like bruxism and chronic persistent chewing of coarse
and abrasive food or other substances like tobacco.
Occupationin certain occupations, workers are exposed
to an atmosphere of abrasive dust and cannot avoid it
getting into mouth.
Structural defectin defects like amelogenesis imperfecta
and dentinogenesis imperfecta, hardness of enamel and
dentin is reduced and such teeth become more prone to
attrition.
Clinical features
Sexmen usually exhibit more severe attrition than
women due to greater masticatory forces.
Sitesit may be seen in deciduous as well as permanent
dentition. It occurs only on occlusal, incisal and proximal
surfaces of teeth. Severe attrition is seldomly seen in
primary teeth, as they are not retained for any great
period. Palabal cusps of maxillary teeth and buccal cusps
of mandibular posterior teeth show most wear.
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Physiological attrition
Onsetphysiological attrition begins with wearing
of the incisal edge of an incisor, which is followed by
the palatal cusp of maxillary molars and buccal cusp
of mandibular molars. It commences at the time of
contact or occlusion. Physiological tooth surface loss
results in a reduction, in both vertical tooth height
and horizontal tooth width (Fig. 9-61).
Radiographic features
Crownsmooth wearing of incisal and occlusal surfaces
of involved teeth is evident by shortened crown image
(Fig. 9-63).
Pulpsclerosis of pulp chamber and canals is seen due
to deposition of secondary dentin which narrows the
pulp canals.
Periodontal ligamentwidening of periodontal ligament
space and hypercementosis.
Alveolar bonesome loss of alveolar bone.
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Fig. 9-64: Wedge shaped ditch seen in the cervical area of
anterior teeth.
Abrasion
It is the pathological wearing away of tooth substance
through abnormal mechanical process caused by external
agents. In case of tooth wear which is accelerated by
chewing an abrasive substance between opposing teeth,
exhibits a features of attrition and abrasion. This is called
as demastication.
Etiology
Abrasive dentifricesuse of abrasive dentifrices can lead to
abrasion of the incisal surface.
HabitualHabitual pipe smoker may develop abrasion
on the incisal edges of lower and upper anterior teeth. In
some cases habitual opening of bobby pins may lead to
abrasion.
Horizontal tooth brushinghorizontal tooth brushing
may lead to abrasion of the cervical area of teeth.
Occupationalit occurs when objects and instrument are
habitually held between the teeth by people during
working. Holding nails or pins between teeth e.g. in
carpenters, shoemakers or tailors.
Dental floss or tooth picks injuryimproper use of dental
floss and tooth picks.
Ritual abrasionit is mainly seen in Africa.
Clinical features
Tooth brush injury
Sitesit usually occurs on exposed surfaces of roots of
teeth. It is more commonly seen on left side of right
handed persons and vice versa.
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Management
Modified teeth cleaning habitsmodification of teeth
cleaning habits will be indicated.
Removal of causeelimination of causative agent should
be carried out.
Restorationrestoration should be done for esthetics
purpose and to prevent further tooth wear.
Erosion
Fig. 9-66: Abrasion seen on the proximal surface of the patient due
to dental floss injury.
Radiographic features
Tooth brush injury
Locationradiolucent defect at the cervical level of teeth.
Shapewell defined semilunar shape, with borders of
increasing density (Fig. 9-67).
Pulppulp chamber may be partially or fully sclerosed
in severely affected teeth.
Dental floss injury
Appearancenarrow semilunar grooves in the
interproximal surfaces of teeth near cervical area.
Etiology
Local acidosisit is seen in periodontal tissue from
damage due to traumatogenic occlusion.
Chronic vomitingcomplete loss of enamel on lingual
surfaces of teeth through dissolution by gastric
hydrochloric acid. Vomiting can also occur in alcoholics,
peptic ulcer, gastritis, pregnancy and drug side effect.
Acidic foods and beveragesLarge quantities of highly
acidic carbonated beverages or lemon juice can produce
erosion. Most of the fruits and fruits juices have a low
pH and can cause erosion. Frequent consumption of
carbonated drinks, which are acidic in nature, may result
in the erosion of teeth.
Anorexia nervosait induces chronic vomiting often after
bouts of uncontrolled eating that is interspersed between
periods of starvation, because of inner rejection of food.
Occupationalworkers involving in manufacturing of
lead batteries, sanitary cleaners or soft drinks can
develop erosion.
Poorly monitored pH swimming poolin cases of poorly
monitored pH swimming can also cause erosion of the
teeth.
Medicationmedication like chewable vitamin C and
aspirin tablet may lead to erosion of teeth.
Clinical features
SitesIt occurs most frequently on labial and buccal
surfaces of teeth; some times, may occur on proximal
surfaces of teeth. Usually confined to gingival thirds of
labial surface of anterior teeth. Erosion may involve
several teeth of dentition. From extrinsic source, it causes
erosion on labial and buccal surface and from intrinsic
source, it causes erosion on lingual or palatal source.
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Abfraction
It is also called as stress lesion. It is the loss of tooth structure
that results from flexure which is caused by occlusal
stresses. The magnitude of tooth tissue loss depends on the
size, duration, direction, frequency and location of the
forces.
Causes and mechanism
Eccentric forcesit has been suggested that the stress
lesion or abfraction is a consequence of eccentric forces
on the natural dentition. In this case when occlusal force
is applied eccentrically on the tooth, it get concentrated
at the cervical margin of the tooth. This will cause flexure
which causes stress at the cervical fulcrum and results
in loss of the overlying tooth structure. Thus this theory
propounds tooth fatigue, flexure and deformation via
biomechanical loading of the tooth structure, primarily
at the cervical region.
Resorption of Teeth
It is a chronic progressive damage or loss of tooth structure
due to the action of cells called odontoclasts. It can be
physiological as in case of root resorption of deciduous teeth
or pathological, which occurs in permanent teeth.
Pathological resorption may be external or internal. In
external resorption odontoclasts are located in periodontal
ligament and in case of internal resorption cells are located
in the dental pulp.
External Resorption
It is lytic process occurring in the cementum or cementum
and dentin of the roots of teeth.
Types
External resorptionresorption occurring at the apex or
along the lateral surface of the roots.
External internal resorptionin this external resorption
is very severe and it leads to involvement of pulp.
Etiology
Periapical infectionperiapical granuloma (arising due
to pulpal infection or trauma), causes subsequent
resorption of root apex. On the radiograph, it appears as
slight raggedness or blunting of the root apex in the
early stages.
Reimplanted teethIt may result in severe resorption of
root. Tooth root is resorbed and replaced by bone which
produces ankylosis. Many implanted teeth exhibit
complex resorption of root and are gradually exfoliated.
Tumors and cystsresorption due to tumors and cysts
appears to be essentially by pressure phenomenon. In
most cases, tissue is present between the tumor and the
tooth and it is from this tissue, cells chiefly osteoclasts
arise and initiated root resorption. Cysts like apical
periodontal cyst may exert such pressure on the apex of
tooth the intervening connective tissue may in turn get
stimulated for osteoclasts formation and thus, resorption
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Clinical features
Sitesthe most frequent site for external resorption is
upper incisors, upper and lower bicuspids.
Symptomsthe affected tooth is usually asymptomatic.
SignsWhen the root is completely resorbed, the tooth
may become mobile. If root resorption is followed by
ankylosis then the tooth is immobile, in infraocclusion
and with high percussion sound.
Radiographic features
External resorption
Appearancewhen the lesion begins at the apex, it causes
smooth resorption of the root surface. The conical end is
removed and replaced by more or less blunt or usually
square apex (Fig. 9-68).
Bone and lamina durabone and lamina dura show
normal appearance. It appears as concave and ragged
area on the root surface.
Lateral external resorptionif it involves lateral aspect of
the tooth, the lesion will be irregular.
External-internal resorption
It appears as eccentrically shaped notch with areas of
resorption which are uneven and appears like
trabeculae. The resorptions extend apically into pulp or
coronally under the enamel. This is also called as
invasive cervical resorption.
Differential Diagnosis
Internal resorptionin external resorption, the radiograph
shows blunting of the apex, a ragged area, a scooped
out area on the side of the root. In internal resorption,
one can see root canal with well demarcated enlarged
ballooning area of resorption. It appears as expansion
of pulp chamber and canals. We can also use SLOB
technique for the diagnosis of external resorption. In
this, external resorption appear to be shift away from
the pulp if the angulation moves mesially.
Incomplete root formationin this, incomplete canal diverges; whereas in external resorption, they usually converge.
Short rootit has conical apex and the root canal is
usually not visible at the extreme apex nor is the foramen.
Apicectomyit revels evidence of root filling and the
history is available.
Foreshortening of rootdespite the short root, the canal
at the apical end cannot be seen and neither can be the
foramen.
Management
Removal of causethis is most important management of
external resorption.
Apicoectomyit should be carried out to save the
tooth.
Curettage and fillingif the area is broad and on lateral
surface, curettage and filling of resorbed area should be
carried out.
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B
Figs 9-69A and B: Pink tooth appearance seen in cases of internal
resorption of tooth in upper anterior region.
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Fig. 9-70: Internal resorption in the root showing widening of canal.
Differential Diagnosis
Dental cariescarious lesion show more diffused
margins than internal root resorption. In most cases of
internal resorption, enamel is not involved. So, there is
no evidence of external orifice.
External resorptiondescribed above
Management
Endodontic treatmentextirpation of pulp with routine
endodontic treatment or retrograde filling stops the
internal resorption process.
Extractionextraction of the tooth, if perforation occurs.
Discoloration of Teeth
The color of teeth ranges from yellowish to grayish-white
depending on enamel translucency. Discoloration defined
Classification
Changes that occur solely in structure and thickness of
dental hard tissues:
Disturbances of dental hard tissue
Dentinogenesis imperfecta
Dental fluorosis
Enamel opacities
Physiologic color changes due to age
Obliteration of pulp chamber
Internal resorption
Initial enamel caries
Discoloration caused by coloring agents taken up by
dental hard tissue:
During formation
Erythroblastic fetalis
Neonatal hepatitis
Congenital defect in the bile duct
Tetracycline administration
Congenital heart disease
After eruption
Endogenous
Necrosis of pulp
Hemorrhage of pulp
Exogenous
Amelogenesis imperfecta
Turner tooth
Dental caries
Denudation of dentin
Attrition, abrasion and erosion
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Fig. 9-72: Brown discoloration seen in patient of porphyria.
Porphyria
It is an autosomal recessive condition. It is an inborn error
in metabolism in which hepatoporphyrin circulating in
blood is seen in urine, teeth and bone.
The deciduous and permanent teeth may show red or
brown or pinkish discoloration (Fig. 9-72) which is called as
erythrodontia. Under ultraviolet light, the teeth always
exhibit red fluorescence. It occurs due to its physical affinity
of calcium phosphate.
Congenital defect in bile duct
In children with this disease, the primary teeth may become
discolored by bile pigment, generally green discoloration is
seen.
Fig. 9-73: Tetracycline stain.
Tetracycline Staining
Discoloration of either deciduous or permanent teeth may
occur as a result of prophylactic or therapeutic regimen
instituted for pregnant females or infants.
Mechanisms
It may cause discoloration during formation period,
tetracycline react with calcium to form calcium
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Fig. 9-74: Yellowish discoloration of teeth due to tetracycline staining.
Oxalosis
It is an autosomal recessive condition. In this disorder,
oxalate is deposited in kidney. The slate gray intrinsic stain
has been demonstrated with odontoblasts, dentinal tubules
and within dental pulp.
Discoloring Agents
Food and drinkstain with beverage results in staining
on the lingual side of teeth. Foods that contain more
chlorophyll produce green discoloration of enamel.
Tobaccotobacco chewing or smoking causes yellowish
brown to black discoloration of teeth (Fig. 9-75). Tar present
Black stain
It usually results due to contact with certain metallic
elements such as silver, iron and lead.
It may appear as thin line running approximately 1 mm
or so above the gingival margin, it may occur on both the
facial and lingual surfaces of teeth.
Stain is firmly attached to the surface but remains
extrinsic, thus it may be removed by brush and abrasives.
But, it recurs later on.
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Management
Extrinsic
Scaling and polishing with paste containing fine powdered
pumice.
Intrinsic
Fluoride stains are treated by applying bleaching solution.
It consist of
Anesthetic ether0.2 ml
HCl 30%1 ml etches the enamel surface.
H2O2 30%1 ml bleaches enamel.
Suggested Reading
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case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
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celiac patients. Oral Surg, Oral Med, Oral Pathol, Oral Radiol, Endod
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3. Aldred MJ, Crawford PJM. Amelogenesis imperfectatoward a
new classification. Oral Dis 1995;1:2-5.
4. Alling CC III, Catone GA. Management of impacted teeth. J Oral
Maxillofac Surg 1993;51(suppl):3-6.
5. Badger GR. Three rooted mandibular first primary molar. Oral Surg,
Oral Med, Oral Pathol 1982;53:547-8.
6. Bentley EM, Ellwood JM. Fluoride ingestion from tooth paste by
young children. Br Dent J 1999;186:460-2.
7. Bishop K, Kelleher M, et al. Wear now? An update on the etiology
of tooth wear. Quintessence Int 1997;28:305-13.
8. Bodin I, Julin P, Thomsson M. Hyperdontia: frequency and
distribution of supernumerary teeth among the 21,609 patients.
Dentomaxillofac Radiol 1978;7:15-7.
9. Brook AH, Winter GB. Double teeth: a retrospective study of
geminated and fused teeth in children. Br Dent J 1970;129:123-30.
10. Bull WH, et al. The abrasion and cleaning properties of dentifrices.
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11. Canger EM, elenk P, Sezgin S. Dens Invaginatus a Geminated
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1965;19:373-82.
13. Chen RJ, Chen HS, Lin LM, Lin CC, Jorgenson RJ. Otodental
dysplasia. Oral Surg, Oral Med, Oral Pathol 1988; 66:3538. doi:
10.1016/0030-4220(88)90245-9 .
14. Chen RJ, Sen H. Talon cusp in primary dentition. Oral Surg, Oral
Med, Oral Pathol 1986;62:67- 72.
15. Chlappinell JA, Waltron RE. Tooth discoloration resulting from
tetracycline therapy: a case report. Quintessence Int 1992;23:53941.
16. Ciola B, Bahn SL, Goviea GL. Radiographic manifestation of unusual
combination of Type I and type II dentin dysplasia: Oral Surg, Oral
Med, Oral Pathol 1978;45:317-22.
17. Crawford PJM, Aldred MJ, regional odontodysplasia: a bibliography. J Oral Pathol Med 1989;18:251-63.
18. Crawford PJM, Aldred MJ. X-linked amelogenesis imperfecta,
presentation of two kindreds and review of the literature. Oral Surg,
Oral Med, Oral Pathol 1992;73:449-55.
19. Dayan D, Heifferman A et al. Tooth discoloration-extrinsic and
intrinsic factors. Quintessence Int 1983;14:195-9.
20. Duncan WK, Helpin ML. Bilateral fusion and gemination: a literature
analysis and case report. Oral Surg Oral Med Oral Pathol 1987;
64:82-7.
21. Durr DP, Campos CA, Ayers CS. Clinical significance of taurodontism. JADA 1980;100:378-81.
22. Eccles JD. Tooth surface loss from abrasion, attrition and erosion.
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23. Eitan Dankner, Doran Harare and Ilan Rotstein. Dens evaginatus
of anterior teeth. Oral Surg, Oral Med, Oral Path, Oral Radio, Endod
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24. Ennis LM, Berry HM, Phillips JE. Dental roentgenology, Lea Febiger,
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26. Goldman HM. Spontaneous intermittent resorption of teeth. JADA
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27. Goldstein AR. Enamel peral a contributing factor in periodontal
breakdown. JADA 1979;99:210-11.
28. Goultschin J, Nitzan D, Azaz B. Root resorption, review and
discussion. Oral Surg Oral Med Oral Pathol 1982;54:586-90.
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58. Phillips JR. Apical root resorption under orthodontic therapy. Angle
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59. Rabinowitch BZ. Internal resorption. Oral Surg Oral Med Oral Pathol
1972;33:263-82.
60. Rao SR, Witkop CJ Jr, Yamane GM. Pulpal dysplasia. Oral Surg,
Oral Med, Oral Pathol 1970;30:682-9.
61. Sadeghi EM, Ashraffi MR. Regional odontodysplasia: clinical,
pathologic and therapeutic consideration. JADA 1981;102:336-9.
62. Saini TS, Kharat DU, Mokeem S. Prevalence of shovel shaped incisor
in Saudi Arabian dental patient. Oral Surg Oral Med Oral Pathol
1990;70:540-44.
63. Schwartz S, Tsipouras P. Oral finding in osteogenesis imperfecta
Oral Surg 1984;57:161.
64. Segura JJ, Jimenez-Rubio A. Talon cusp affecting permanent
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Med, Oral Path, Oral Radio Endod 1999; 88: 90-2.
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66. Smith DMH, Winter GB. Root dilaceration of maxillary incisor. Br
Dent J 1981;150:125-7.
67. Soames JV, Kyyebi TA. A radicular dens invaginatus. Br Dent J
1982;152;308.
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586.
70. Steidle NE, Radden BG, Reade PC. Dentin dysplasia: a
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72. Tannenbaum KA, Alling. Anomalous tooth development case
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73. Thorburn DN, Ferguson MM. Familial ogee roots, tooth mobility,
oligodontia and microdontia. Oral Surg Oral Med Oral Pathol
1992;74:576-81.
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year book medical publisher Chicago; 150-82.
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86. Younes SA, Al-Shammery AR, El-Angbawi MF. Three rooted
permanent mandibular first molar of Asian and black groups
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102-5.
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Oral Surg, Oral Med, Oral Pathol 1963;16:187-93.
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Developmental Defect of
Craniofacial Structure
Definitions
Congenital
Present at or before birth but not necessarily inherited, i.e.
transmitted through the genes.
Hereditary
They are apparent at birth but some may not become evident
for years.
The cell consists of cytoplasm and nucleus. Nucleus of
each somatic cell contains 23 pairs of chromosome out of
which one is the pair of sex chromosome; rest 22 pairs of
chromosomes are called as autosomes. Chromosome is a
nuclear structure composed of DNA, which contains units
of hereditary gene. Gene is a portion of DNA coded for the
synthesis of specific protein or polypeptide chain. Gene is
determinants of hereditary characteristics. Locus is the site
occupied by the gene on chromosome. An allele is number
of alternative form that gene may take.
If both the allele at a given locus is identical to pair, it is
called as homozygous and if the alleles are different it is
called as heterozygous. A gene showing trait in heterozygous
is considered as dominant. Genes are transmitted from one
generation to other in a generally predictive way.
X-linked Dominant
Since females have twice as many X chromosomes, they
exhibit a higher frequency of trait.
Affected female will transmit the gene to of her
offsprings.
X-linked Recessive
Incidence of the trait is much higher in males than in
females.
Affected man can transmit it to his daughters who are
carriers.
Trait cannot be transmitted from father to son.
Developmental anomalies of the head and neck are
originated during transformation of branchial system into
adults derivatives. They are also result from failure of
migration of neural crest cells.
Developmental Disturbances
of the Jaws
Agnathia
Clinical Features
Absence of mandibleif mandible is absent, the
upper part of the face may be normal and the skin of the
lower part will be continuous with the suprasternal
integument.
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Management
Surgical reconstructionsurgical reconstruction though
it is difficult it should be carried out.
Micrognathia
Micrognathia is severely deficient jaw, which most
commonly affects the mandible. It is common to see
individuals having a very small mandible.
Fig. 10-1: Acquired micrognathia occurs
due to ankylosis of jaw.
Types
Apparent micrognathia- this is not due to abnormality of
small jaw, in terms of size but rather to an abnormal
positioning or abnormal relation of one jaw to another,
which produces illusion of micrognathia.
True micrognathiaIt is due to small jaw. It is again
classified as
Congenital
Acquired
Etiology
Congenital
Congenital abnormalitiesin many instances it is
associated with other congenital abnormalities, particularly
congenital heart disease and Pierre Robin syndrome (cleft
palate, micrognathia, glossoptosis).
Forceps delivery traumaone of the main causes of this
condition is the use of forceps during birth where the
baby is pulled out by clamping a pair of forceps on either
side of the head. If the joint in this area, called the
temporomandibular joint is badly bruised, the mandible
does not develop. Sometimes this condition is also
associated with congenital heart disease.
Acquired
Ankylosisacquired type is post-natal type and result
from disturbances in the area of T.M joint (ankylosis)
(Fig. 10-1).
Mouth breathingmouth breathing can be a predisposing
factor for maxillary micrognathia.
Clinical Features
Micrognathia of maxillait is due to deficiency of
premaxillary area and patient with this deformity
appears to have the middle third of face retracted.
True mandibular micrognathiait is uncommon and
patient appears clinically to have severe retrusion of
chin, steep mandibular angle and deficient chin button.
Signsmicrognathia is one of the causes of abnormal
alignment of teeth. This can be seen by observing the
occlusion of teeth. Often, there will not be enough room
for the teeth to grow. If the upper jaw is short, then,
occlusion may be abnormal.
Symptomsin true micrognathia, the jaw is small enough
to interfere with feeding of the infant and may require
special nipples in order to feed adequately. There may
be difficulty in respiration. Due to the small size of the
arch, the jaw is not able to accommodate the tongue,
which is forced back into the oropharynx, blocking the
air passage.
Syndromes associated with micrognathiaPierre Robin
syndrome, Hallerman-Streiff syndrome, trisomy 13,
trisomy 18, Turners syndrome, Treacher-Collins
syndrome and Marfans syndrome.
Management
Orthognathic surgerythis is recommended treatment
modality for micrognathia. This surgery is followed by
orthodontic appliance to correct malocclusion.
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Macrognathia
It refers to the condition of abnormally large jaws. It is also
called as megagnathia. Macrognathia literally means a
large jaw. The mandible is most often affected in this case
giving rise to a condition where the bone protrudes.
Etiology
Pituitary gigantismthere is generalized increase in size
of entire skeleton.
Pagets disease of boneovergrowth of cranium and
maxilla occurs.
Acromegalyprogressive enlargement of mandible
owing to hyperpituitarism in adults.
Clinical Features
Prognathismmandibular protrusion or proganthism is
common occurrence, which is due to disparity in the
size of maxilla to mandible and posterior positioning of
maxilla in relation to the cranium.
Mandiblemandible is measurably larger than normal.
Increased mandibular body length.
Gummy smilein certain patients with congenital
abnormalities, there may be elongation of maxilla. There
is much show when the patient smiles, so that there is
a so-called gummy smile. This is due to the upper jaw
being too long.
Ramuslarge ramus which forms less steep angle with
body of mandible.
Chinthere is prominent chin button.
Etiology
Endocrine dysfunctionhormonal imbalance may lead
to hemihyperplasia of the face.
Geneticincomplete twinning, chromosomal abnormalities and localized alteration of intrauterine development also lead to facial hemihypertrophy.
Vascular abnormalitieslymphatic and vascular
abnormalities may act as causative factors.
Neurogenicsome neurogenic malformation may act as
causative factors for this disease.
Terminology
Complex hemihyperplasiain this, one whole side of the
body is affected.
Simple hemihyperplasiahyperplasia is limited only to
one limb.
Hemifacial hyperplasiaif the enlargement is confined to
one side of the face.
Clinical Features
Age and sex distributionit has vague onset, usually in
childhood, adolescence or early adult life. Females are
affected more than males.
Sitesit involves the eyelids, cheeks, lips, facial bones,
tongue, ears and tonsils. It is more common on right side
of body.
Symptomsoccasionally, poorly localized, vague,
painful sensation in muscles affected.
Appearanceenlargement of one half of the head present
since birth. Enlarged side grows at a rate proportional
to uninvolved side (Fig. 10-2).
Associated abnormalitiesit is associated with other
abnormalities like mental deficiency, skin abnormalities,
compensatory scoliosis, and hemi-megalencephaly
Management
Osteotomyresection of portion of mandible to decrease
the length, followed by orthodontic treatment.
Facial Hemihypertrophy
It is also called as Friedreichs disease, hemihyperplasia. It
may involve entire half of the body, one or both limbs, face,
head and associated structures. It represents the
hyperplasia of the tissue rather than hypertrophy of the
tissue.
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Oral Manifestations
Radiographic Features
Bone enlargementenlargement of bone on affected area.
The malar bone, zygomatic process and temporal bone
may be enlarged in all diameters, in some cases.
Alveolar processthe alveolar process is enlarged in some
cases on affected side (Fig. 10-3).
Mandibular canalit also increases on the affected side.
Teethcrown size of the tooth is enlarged.
Management
Cosmetic repaircosmetic surgery should be performed
which includes soft tissue debulking, face lifts ad
Orthognathic surgery.
Facial Hemiatrophy
It is also called as Parry-Romberg syndrome, Romberg
hemifacial atrophy, hemifacial microstomia and progressive
facial hemiatrophy. Parry-Romberg syndrome is a rare
disorder characterized by slowly progressive wasting
(atrophy) of the soft tissues of half of the face (hemifacial
atrophy). Wasting is associated with skin, cartilage,
connective tissue, muscle and bone. It is described by Parry
in 1825 and well documented by Romberg in 1846.
Etiopathogenesis
IdiopathicIn most cases, Parry-Romberg syndrome
appears to occur randomly for unknown reasons
(sporadically).
Familialcertain studies state that it has got familial
occurrence.
Localized sclerodermain scleroderma there is
constriction of tissue which may lead to progressive
hemifacial atrophy.
Malfunction of sympathetic nervous systematrophic
malfunction of cervical sympathetic nervous system can
lead to neurotrophic change which in turn leads to
hemiatrophy.
Trigeminal neuralgiaperipheral trigeminal neuralgia
is associated with hemiatrophy in some cases.
Loss of adipose tissuethis will lead to shrinkage of soft
tissue.
Clinical Features
Fig. 10-3: Enlargement of bone and teeth on the right side of patient
(Courtesy Dr Datarkar).
Diagnosis
Clinical diagnosisenlargement of one side of face can
be noticed clinically.
Radiological diagnosisit will also show enlargement of
bone and teeth on one side.
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Oral Manifestations
Lip and tonguemany individuals also experience
atrophy of half of the upper lip and tongue.
Teethdelayed eruption or wasting of the roots of certain
teeth on the affected side. This will lead to malocclusion
of teeth.
Deviation of jawswhile opening the mouth, jaw is
deviated on the affected side.
Jawsgrowth of jaws and teeth is affected. Ramus is
deficient vertically and there is delay in mandibular
angle development. The mandibular body can be shorter
than normal.
Posterior open bitedue to mandibular hypoplasia on
affected side there may be unilateral posterior open bite.
Diagnosis
Clinical diagnosiswhite line or furrow on one side and
patient is having coup de sabre.
Radiological diagnosisreduction of size of bone on
affected side.
Differential Diagnosis
Mandibulofacial dysostosishereditary pattern is present
and cleft palate is also seen.
Hemifacial microstomiathese are congenital and nonprogressive conditions.
Post-traumatic atrophyhistory is important.
Partial lipodystrophyit is usually bilateral.
Goldenhar syndromeit is congenital and nonprogressive.
Management
Surgical reconstructionit primarily involves augmentation of the affected areas. Surgery is deferred unless
diseased process is burned out.
Orthodontic treatmentit is given for the correction of
malocclusion.
Other treatment modalitiesit includes injection of
silicones and bovine collagen, inorganic implants and
autologous tissue transfer.
Hemi-maxillofacial Dysplasia
It is segmental odontomaxillary dysplasia. Etiology of this
condition is unknown and many times, it is mistaken as
craniofacial fibrous dysplasia or hemifacial hyperplasia.
This condition remains stable.
Radiographic Features
Clinical Features
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Radiological Features
Diagnosis
Clinical diagnosisunilateral enlargement of maxillary
bone with fibrous hyperplasia of gingiva will give clue
to diagnosis
Radiological diagnosissinus is smaller on radiograph.
Management
Orthodontic therapysome patients may require orthodontic therapy.
Orthognathic surgeryit is rarely recommended in patient
with segmental odontomaxillary dysplasia.
Cleidocranial Dysplasia
It is also called as cleidocranial dysostosis, Marie and Sainton
disease, craniocleido-dysostosis.
Etiology
Hereditaryit appears as a true dominant Mendelian
characteristic.
Geneticincomplete penetration of genetic trait. There
is defect in CBFA I gene chromosome.
Clinical Features
Sexthe disease affects men and women with equal
frequency.
Sitesit primarily affects skull, clavicle and dentition.
Shoulder meet in midlinethere may be complete absence
of clavicle and patients have unusual mobility. They
can bring their shoulders forward until they meet in
midline (Figs 10-5A and B).
Headthe head is brachycephalic (reduced anteriorposterior dimension but increased skull width) or wide
and short.
Skullin skull the fontanels often remain open or at
least exhibit delayed closing and for this reason, tend to
be rather large. Open skull suture and multiple wormian
bones are present and there is occasional stunting of
long bone.
Lacrimal and zygomatic bonelacrimal and zygomatic
bone are also underdeveloped.
Figs 10-5 A and B: Patient can bring his shoulders forward so that
they can meet in midline. Also note the depressed nasal bridge.
Oral Manifestations
Micrognathiamaxilla and paranasal sinus are underdeveloped, resulting in maxillary micrognathia.
Maxillamaxilla is underdeveloped and is smaller than
normal, in relation to mandible.
Prognathismmaxilla is small and mandible is usually
normal in size, which gives the appearance of
prognathism.
Teethprolonged retention of primary dentition and
delayed eruption of permanent dentition. Numerous
unerupted teeth are found which are most prevalent in
the mandibular, premolar and incisor area (Fig. 10-6).
Palatehigh narrow arched palate and cleft palate may
be common.
Hypoplasia of enamelthe crown may be pitted as a result
of enamel hypoplasia.
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Chest examinationexamination of chest reveals malformation and absence of clavicles (Fig. 10-8).
Diagnosis
Clinical diagnosismeeting shoulder in the midline is
typical feature of cleidocranial dysostosis.
Radiological diagnosissupernumerary teeth, open
sutures and absence of clavicle are present in cleidocranial dysostosis.
Management
Management of skull and clavicle anomaliesthere is no
treatment require for this anomalies. Patient can live its
normal life.
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Craniofacial Dysostosis
Oral Manifestations
Maxillary hypoplasiamaxillary hypoplasia with
shortened anteroposterior dimensions of maxillary arch.
Parrot beakin some cases, facial angle is exaggerated
and the patient nose is prominent and pointed,
resembling parrot beak (Fig. 10-12)
Clinical Features
AgeCrouzons syndrome is a rare genetic disorder that
may be evident at birth (congenital) or during infancy.
Craniosynostosisin most infants with Crouzon
syndrome, the fibrous joints between certain bones of
the skull (cranial sutures) close prematurely (craniosynostosis).
Proptosisin addition, facial abnormalities typically
include unusual bulging or protrusion of the eyeballs
(proptosis) due to shallow eye cavities (Fig. 10-11)
Strabismusoutward deviation of one of the eyes
(divergent strabismus or exotropia); widely spaced eyes
(ocular hypertelorism). This may lead to blindness of
the patient.
Cranial malformationthe premature closing of suture
may result in brachycephaly (short head), scaphocephaly (boat shaped head), or trigonocephaly (triangle
shaped head). In extreme cases patient may demonstrate
clover leaf skull (kleeblatt schadel deformity).
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Management
Midfacial advancementthis is done to correct midfacial
hypoplasia.
Craniectomyit is needed to alleviate the raise
intracranial pressure.
Fronto-orbital advancementthis is done to correct ocular
defect.
Mandibulofacial Dysostosis
It is also called as Treacher Collins syndrome and
Franceschetti syndrome. It is often inherited as autosomal
dominant trait. It is derived from first and second branchial
arch. It results from failure or incomplete migration of
neural crest cells to the facial region.
Fig. 10-14: Unilateral cross-bite on left side in Crouzons syndrome.
Radiographic Features
Absence of suturesdigital marking in skull as a result of
increased intracranial pressure from early synostosis of
cranial sutures.
Beaten silver appearancethe cranial walls are thin with
multiple radiolucencies appearing as depressions or
scalloped appearance of beaten silver (Fig. 10-15).
Othersmalformation of calvarium, flattened mandibular angle, conical teeth and partial anodontia.
Clinical Features
Zygomatic boneunderdevelopment of zygomatic bone,
resulting in midfacial deformities.
Eyesthere is downward inclination of palpebral
fissure. There is deficiency of eyelashes. In some cases,
eyes assume corresponding slant. A notching (coloboma)
from the outer third of lower eyelids, There is varying
degree of visual impairment in some cases.
Earsaffected infants may also have underdeveloped
(hypoplastic) and/or malformed (dysplastic) ears (Fig.
10-16) (pinnae) with blind ending or absent external ear
canals (microtia), resulting in hearing impairment
(conductive hearing loss). Absence of external auditory
canal resulting in partial or complete deafness is also
found.
Diagnosis
Clinical diagnosishigh arch palate, with midface
deformity, proptosis is a typical feature of Crouzon
syndrome.
Radiological diagnosisbeaten silver appearance seen
in Crouzon syndrome.
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Oral Manifestations
Appearanceunderdevelopment of mandible with steep
mandibular angle. Due to this, lower anterior teeth stand
away from upper teeth, when the mouth is closed.
Fish or bird appearancefacial appearance sometimes
resembles fish or bird (Fig. 10-17).
Micrognathiaan incompletely developed, abnormally
small lower jaw.
Macrostomiaan unusually large mouth.
Palatethere is presence of high arch palate with cleft
palate.
Malocclusionabnormal position and malocclusion of
teeth with anterior open bite.
Radiographic Features
Zygomatic bonereduction in size of zygomatic bone.
Maxillary sinusmaxillary sinus is underdeveloped or
completely absent (Fig. 10-18).
Articular eminencearticular eminence is either shallow
or absent.
Management
Cosmetic surgeryimprovement and surgical interventions should be done to improve osseous and ear defect.
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Diagnosis
Differential Diagnosis
Residual dental infectionsign of infection is present.
Central neoplasmmargins are not so corticated.
Management
There is no specific treatment for it.
Etiopathogenesis
Persistence of fetal marrowthey are derived from bone
marrow hyperplasia of persisting embryonic marrow
remnants.
After tooth extractionthere may be aberrant bone
regeneration after tooth extraction.
Increased demand for erythrocytemarrow hyperplasia can
occur in response of increased demand for erythrocyte.
Other factorsit can also occur in trauma and local
inflammation.
Chondroectodermal Dysplasia
It is also called as Ellis-van Creveld disease. The Ellis-van
Creveld (EvC) syndrome was first described by Dr. Richard
W.B. Ellis of Edinburgh and Simon van Creveld of
Amsterdam.
It is congenital and the patient present evidence of
chondrodysplasia, ectodermal dysplasia, polydactylism
and congenital morbus cordis.
Clinical Features
Clinical Features
Sexit is more common in females than males.
Common sitesmolar, premolar region in mandible.
Symptomsasymptomatic with history of pain in that
region.
Radiographic Features
Locationit is most common in edentulous areas.
Internal structureradiolucent area demonstrates
internal trabeculation. Occasionally, trabeculae with
spotty radiopaque flecks are seen within the radiolucency
(Fig. 10-20).
Oral Manifestations
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Radiographic Features
Diagnosis
Clinical diagnosispolydactyly with hairlip and partial
anodontia will favor the diagnosis of Ellis-van Creveld
syndrome.
Management
Surgicalmanagement of hairlip is done by surgical
method for cosmetic reason.
Phlebectasia
It is first used by Gerwig in 1928. It is an isolated,
abnormal, fusiform or saccular dilatation of veins. It is
also known as venous congenital cyst, venous aneurysm, venous
ectasia or essential venous dilatation.
Etiology
Mechanical compression of left innominate vein by a
high tortuous aorta in hypertension or of venous
structures between the sternum and the left innominate
artery in pectus excavatum.
Clinical Features
Appearanceit usually appears as isolated swelling.
Swelling is not visible before the compression but as
soon as patient clinch the jaws, swelling is visible (Figs
10-21A and B).
Arhinencephaly
It is a developmental abnormality of the skull and face in
which there is absence or deficiency of the olfactory portion
of brain.
Clinical Features
Hypotelorismabsence of the vertical and cribriform
plates of ethmoid and of crista galli result in the orbits
being more closely set, a condition known as hypotelorism.
Lack of nasal bonethere is depression of nose and
absence of the bridge because of lack of nasal bones and
nasal septum.
Prow of boat appearancein some cases, an associated
deformity of the frontal portion of skull presents an
angular appearance resembling the prow of a boat
presumably due to premature fusion of metopic sutures.
Oral Manifestation
Cleft lipthere is wide cleft in the central portion of the
lip, where the philtrum is absent and with failure of
development of any part of the premaxilla, the cleft is
continuous through the palate.
Diagnosis
Clinical diagnosisHypotelorism with cleft lip and
depressed nasal bridge will aid in diagnosis.
Management
Surgerysurgery of cleft lip is done for cosmetic reasons
and for functional reasons.
Fig. 10-21B: Note the swelling seen on left side of face below the ear
after the compression ( Courtesy Dr Abhishek Soni, Lecturer,
Periodontia, VSPM Dental College and Research Center, Nagpur, India).
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Radiological Features
Ultrasonographydilated blood vessels are usually seen
on ultrasonography (Fig. 10-22).
Treatment
It can be surgical, embolization or injection of sclerosing
agents.
Ectodermal Dysplasia
It represents a group of inherited diseases in which two or
more ectodermally derived structure does not develop. It
can be autosomal dominant, autosomal recessive and
Clinical Features
Sexmales are affected more frequently than females.
Appearanceit is characterized by hypotrichosis,
hypohydrosis and anhidrosis with saddle nose
appearance.
Hairsthe hair of scalp and eyebrows tend to be fine,
scanty and blond.
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Radiological Features
Oral Manifestations
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Management
Prosthetic replacementfrom dental point of view, partial
and complete dentures should be constructed for both
functional and cosmetic purpose.
Endogenous dental implantit can be considered by
selecting proper site in the patient older than 5 years of
age.
Radiological Features
Supernumerary teeththere is presence of unerupted
supernumerary teeth in the jaws (Fig. 10-30).
Osteomas of mandiblethese areas appears to be
increased in radiodensity. Size varies from small to large.
Gardners Syndrome
It is also called as familial multiple polyposis. It is hereditary
condition. The responsible gene for this syndrome is
chromosome 5.
Diagnosis
Clinical and radiological diagnosissupernumerary teeth
with osteoma in the jaw or other part of the body will
favor the diagnosis of Gardners syndrome.
Management
Prophylactic colectomyit should be done as there are
high degree of transformation into malignancy.
Removal of jaw osteomait can be removed for cosmetic
reason.
Turners Syndrome
It is also called as XO syndrome. Turner syndrome is a
chromosomal condition that alters development in females.
Turners syndrome is a chromosomal condition related to
the X chromosome.
Clinical Features
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Oral Manifestation
Palatepatient noticed high arch palate (Fig. 10-32)
Teetheruption of teeth occurs prematurely.
Corner of mouthcorners of mouth appears pulled down
(Fig. 10-33).
Diagnosis
Clinical diagnosiswebbed neck, a broad chest and short
stature. Orally high arch palate with corner of mouth
pull down is typical feature.
Management
Growth hormone injectiongrowth hormone injections are
beneficial in some individuals with Turner syndrome.
Estrogen replacement therapy is usually started at the
time of normal puberty.
Kallman Syndrome
Kallman syndrome is a rare X-linked recessive disease
characterized by anosmia, underdeveloped genitalia and
sterile gonads.
Clinical Features
Sex predilectionit affects primarily males.
Anosmiareduced or complete absence of the sense of
smell. Impaired or lack of sense of smell is caused by the
absence of the olfactory bulbs.
Underdeveloped genitalit is apparent when they fail to
begin puberty and to develop secondary sexual
characteristics (Fig. 10-34). Kallman syndrome also
affects the hypothalamus. The hypothalamus produces
reduced levels of GnRH, the hormone responsible for
the secretion of the hormone LH. LH is the hormone that
stimulates gonadal and genital development.
Osteoporosisit can occur in some cases.
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Suggested Reading
Oral Manifestation
Tooth agenesisit occurs more frequently.
Mandibular inclinationincreased mandibular inclination and mandibular angulation is also present.
Cleft lipcleft lip is also present in this syndrome. When
clefting occurred, extreme retrognathism of both maxilla
and mandible was seen, a deviation which worsened
during growth (Fig. 10-35).
Management
Hormonal therapyhormone, estrogen or testosterone,
replacement, and pulsatile GnRH injections should be
given.
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41. Pensler JM, Murphy GF, Muliken JB. Clinical and ultrastructural
studies of Romberg hemifacial atrophy. Plast Reconstructive Surg
1990;85:669-76.
42. Phlip M, Prasanth KS, Laxmikanth C. Progressive hemifacial
atrophy: a case report. JIAOMR 2006;18(4):239-42.
43. Ponnick JG. Treacher Collins syndrome: perspective in evaluation
and treatment. J Oral Maxillofac Surg 1997;55:1120.
44. Posnick JC. Treacher Collins syndrome: perspective in evaluation
and treatment. J Oral Maxillofac Surg 1997;55:1120-33.
45. Rabinowitch B. Dens in dente report of cases of bilateral dens in
dente. Oral Surg, Oral Med, Oral Patho 1949;2:1480-84.
46. Roddi R, Riggo E, et al. Clinical evaluation of progressive hemifacial
atrophy. J Craniomaxillofac Surg 1994;22:23-32.
47. Sadeghi E, Asharfi M. Regional odontodysplasia: clinical,
pathologic and therapeutic consideration. JADA 1975;91:105766.
48. Shah J, Mehata D. Odontodysplasia affecting maxillary segment
with localized gingival involvement. JIAOMR 2006;18(4):23438.
49. Singer SL, Walpole I, et al. Dentofacial features of family with
Crouzon syndrome. Aust Dent J 1997;42:11-17.
50. Sotiris N, Sykara, Greece, mesiodens in primary and permanent
dentition. Oral Surg, Oral Med, Oral Patho 1969;27:360-362
51. Spencer W, Redding, Ronald I, et al. Gardner syndrome: report of
case. J Oral Surg 1981;39:50-52.
52. Sujatha S, Ganapathy K. Cleidocranial dysostosis: A case report,
IIAOMR 2002;13(2):49-52.
53. Therese G, Barry H, Blake M. Supernumerary teeth-an overview
of classification, diagnosis and management. J Canadian Dental
Association 1999;65(11):612-16.
54. Whaites E. In essentials of dental radiography and radiology
(2nd edn), Churchill Livingstone, 1996;303-16.
55. White SC, Pharoah MJ. In oral radiology, principle and
interpretation (5th edn), Mosby. 2004;516-37.
56. Whyman RA, Doyle TCA, Ferguson MM. An unusual case of
hemifacial atrophy. Oral Surg, Oral Med, Oral Pathol 1992;73:64569.
57. Worth HM. In principle and practice of oral radiologic interpretation;year book medical publisher Chicago;111-49.
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11
Keratotic and
Non-keratotic Lesions
Introduction
White lesion of oral mucosa comprises of a group of conditions which can appear in variety of clinical forms. A white
lesion is described as abnormal area of the oral mucosa that
appear whiter than the surrounding tissue and are usually
slightly raised, roughened, or otherwise of a different texture
from adjacent normal tissue. The white lesion may be smooth,
folded, shaggy, elevated, lacy or annular. Each of these may
be in turn fissured, ulcerated, eroded or inflamed and occur
as solitary, multiple, focal or diffuse lesions.
Classification of lesion is described in Table 11-1.
Normal Variation
Leukoedema
It is an abnormality of the buccal mucosa, which clinically
resembles early leukoplakia.
Etiology
Racialas it is prevalent in black racial cause can be
present.
Tobaccoit is seen more commonly in smokers than nonsmokers.
Poor oral hygienethis can also predispose for the
occurrence of leukoedema.
Clinical Features
Age, race and sex distributionit is common in age group
of 15 to 35 year with prevalence in black. Male
predilection is in the ratio of 2:1.
Sitesthe most common sites of involvement are buccal
mucosa and lip. The lesion is bilateral in occurrence.
Velvet-like folded appearancebuccal mucosa retains the
normal softness and flexibility but exhibits grayish white,
Normal variation
Leukoedema
Fordyces granules
Linea alba
Non-keratotic white lesions
Habitual cheek biting
Burns
Uremic stomatitis
Radiation mucositis
Candidiasis
Thrush
Acute atrophic candidiasis
Chronic atrophic candidiasis
Id reaction
Extraoral candidiasis
Chronic mucocutaneous candidiasis
Systemic candidiasis
Keratotic white lesion
Traumatic keratosis
Keratosis associate with dental restoration
Intraoral skin graft
Focal epithelial hyperplasia
Psoriasis
Oral genodermatoses
White sponge nevus
Hereditary benign intra-epithelial dyskeratosis
Pachyonychia congenita
Porokeratosis
Keratosis follicularis
Warty dyskeratoma
Hyalinosis cutis et mucosa oris
Pseudoxanthoma elasticum
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Pathogenesis
It has been postulated that the occurrence of sebaceous
glands in the mouth may result from the inclusion in the
oral cavity of the ectoderm having some of the potentialities
of the skin in the course of development of the maxillary
and mandibular processes during embryonic life.
Clinical Features
3
Fig. 11-1: Leukoedema showing slightly
folded appearance.
Diagnosis
Clinical diagnosisfaint milky folded appearance which
is eliminated by stretching the mucosa.
Differential Diagnosis
Leukoplakialeukoedema has faint milky appearance,
folded and wrinkled pattern as compared to definite
whiteness of leukoplakia. Leukoplakia cannot be
eliminated by stretching.
Cheek biting lesionit is usually unilateral in appearance
as compared to bilateral occurrence of leukoedema.
Tissue tag is usually seen.
White sponge nevuswhite sponge nevus is thicker,
plaque-like. It is not eliminated on stretching.
Hereditary benign intraepithelial dyskeratosissame
as white sponge nevus. It has typical microscopic
features.
Management
No treatment is necessary as it has no pre-malignant
potential.
Fordyces Granules
Fordyces granule is a developmental anomaly characterized by heterotrophic collection of sebaceous glands at
various sites in oral cavity which is covered with intact
mucosa. These are usually submucosal.
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Diagnosis
Management
Management
Linea Alba
It is also called as while line. Linea alba refers to the line of
keratinization, found on the buccal mucosa parallel to the
line of occlusion expanding to a triangular area inside each
labial commissures.
Etiology
Dietary variationlinea alba may occur due to variation
in dietary practice. The person who is taking hard diet
has got more chances of having linea alba.
Frictional irritationit may occur due to contact of teeth
with buccal mucosa.
Increases overjetlinea alba is more prominent in people
with little overjet of molars and premolars.
Other factorssome other causative agents like smoking,
and environmental irritants can also lead to linea alba.
Clinical Features
Sitescommon sites are buccal mucosa at the line of
occlusion and where the mucosa overlies the bone as in
hard palate and gingiva.
Appearancepalate and gingiva appears whiter than the
adjacent mucosa of the soft palate and alveolar gingiva.
Extent of lineline extending horizontally from
commissure to most posterior teeth (Fig. 11-3).
Etiology
Neurologicalunconscious nervous habits, uncontrolled
tongue thrusting and neuromuscular disorders such as
tardive dyskinesia may lead to chronic biting of cheek
or lip mucosa.
Psychologicalstress and anxiety may lead to cheek
biting. Patient is aware of the habit but refuses to accept
it.
Dentalocclusal discrepancies, rough tooth surface
may lead to chronic trauma in cheek mucosa.
Clinical Features
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Management
Psychotherapysmall doses of diazepam 5 to 10 mg at
bed time for the management of neurological disorders.
But this does not give any long-term effect.
Acrylic guardthis should be given to cover the facial
surface of teeth and thereby restricting access to buccal
and labial mucosa.
Burns
Burns cause transient non-keratotic white appearance of
the mucosa which is attributed to superficial pseudomembrane composed of coagulated tissue with an
inflammatory exudate (saliva protects oral mucosa).
Types of Burns
Fig. 11-4: Habitual cheek biting showing patch of partly detached
epithelial surface in retromolar area.
Diagnosis
Clinical diagnosistypical clinical appearance with
typical location will lead to easy clinical diagnosis of
the lesion.
Differential Diagnosis
White sponge nevusin cheek biting if the cause is
removed the white lesion will disappear.
Chemical burnshistory will confirm the diagnosis of
chemical burns.
Reaction to locally applied medicinehistory will confirm
the diagnosis.
According to severity
Mild burnsmild burn causes keratotic white lesions.
Intermediate burnsintermediate burns cause localized
mucositis.
Severe burnssevere burns coagulate the surface of the
tissue and produces diffuse white lesions. If coagulation
is severe, tissue cannot be scraped off easily leaving raw
and bleeding painful surface.
According to cause
Thermal burnit is caused by hot food and beverages. It
may occur by snow or dry ice.
Electrical burnit is caused by electrical rods.
Contact burnit occurs when the patient is grounded
and the body act as conductor with current passing
through him along the path of least resistance. These
burns are fatal.
Arc burnit is sustained when arcs or sparks appear
in the gap between a live wire and tissue.
Chemical burnsit is caused by chemical agents.
Radiation burnthis occurs in patient under radiation
therapy for the management of malignancy in the oral
cavity.
Thermal Burns
Clinical features
Sitesanterior 1/3rd of tongue and palate.
Symptomsthere is pain which lasts for short duration.
Appearanceit may produce coagulation necrosis of
superficial tissue that appears whitish.
Signsin some cases, there may be frank ulceration and
stripping of mucosa. Red area is tender to painful, it
may blanch on pressure and there is bleeding on manipulation. Surface layer of epithelium is desquamated.
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Electrical Burns
More commonly type of burn occurs in oral cavity in
which saliva acts as conducting medium. This burn can
generate 3000 degree Celsius heat and causes lot of tissue
destruction.
Clinical features
Ageit is usually seen in children as they can
accidentally chew live wire or end of an extension cord.
Siteit occurs more frequently at the commissure region
of the lips.
Symptomsas there is destruction of neural tissue the
lesions are usually painless. There is also loss of sensory
and motor function of surrounding tissues.
Appearancethe clinical appearance of the burn is a gray
white tissue surrounded by narrow rim of erythema.
Chemical Burns
Burns due to caustic chemical agents will produce
coagulation necrosis of the epithelium with subsequent
inflammation. It can occur in children which hold drug in
oral cavity for extended period of time.
Causes
Aspirin and aspirincontaining compoundsit occurs when
it is kept in mucobuccal fold to relieve toothache.
Hydrogen peroxideconcentration greater than 3% can
cause epithelial necrosis.
Silver nitrateit is used in treatment of aphthous ulcer
for pain relief. This may cause severe mucosal damage.
Toothache drop burnssuch drops contain creosote,
guiacol and phenol derivatives. In this phenol can cause
extensive mucosal necrosis and underlying bone loss.
Ethyl alcohol burnstopical application of ethyl alcohol
solution which results in sloughing of the oral mucosa.
Some of the mouth wash contain 25% ethyl alcohol.
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Clinical features
Symptomsthe lesion is usually painful.
Appearanceirregularly shaped, white pseudomembrane covered lesion develops (Fig. 11-7).
Signsgentle lateral pressure causes the white material
to slide away exposing an exquisitely painful central
red ulceration and more adherent patches of white
material on the periphery. Diffuse border may present if
the burn is more extensive.
Cotton roll burns (cotton roll stomatitis)cotton roll is used
for control of moisture during dental treatment.
Sometimes dry mucosa can adhere to cotton roll. While
removing cotton roll from the oral cavity epithelium can
also be removed along with it. This type of lesion is called
as cotton roll burns or cotton roll stomatitis.
Radiation Mucositis
It is secondary to therapeutic radiation of head and neck
cancer develops towards the end of the 1st week of therapy.
It occurs if radiation given in excess of 3500 to 4000 rads.
Mucositis occurs when the rate of epithelial growth and
repair are affected by radiation, resulting in epithelial
thinning, erosion and ulceration.
Clinical Features
Age and sexmost commonly found in children and
elderly adults with male predilection.
Siteradiation has more marked effect on rapidly
proliferating epithelium and therefore, mucositis
involves the non-keratinized mucosa first.
Appearancethere is redness of oral mucosa followed
by pseudomembrane formation with large area of oral
mucosa covered with grayish, white slough alternating
with areas of more severe ulceration (Fig. 11-8).
Signsthe first sign of mucositis may be whitish
appearance of the mucosa due to hyperkeratinization
and intraepithelial edema or a red appearance due to
hyperemia.
Diagnosis
Clinical diagnosishistory is very important while
coming to clinical diagnosis. If patient gives history of
any medicament kept in oral cavity diagnosis of chemical
burn can be made.
Differential diagnosis
Candidiasisin chemical burns there is acute onset, pain
and focal area of involvement which is usually not a
feature of candidiasis.
Management
Preventionprevention is best treatment for the chemical
burn. Patient should be asked to not to keep tablet in
oral cavity for longer period of time.
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Diagnosis
Management
Mouth rinsea soothing mouth rinse such as an
antihistaminic with kaopectate will offer pain relief.
Good oral hygieneit is the most effective treatment for
complication of radiation therapy. Once radiation
therapy is initiated, all foci of infection from oral cavity
should be removed.
Betamethasone mouth washhigh dose of betamethasone
mouth wash is very effective treatment for radiation
mucositis.
Other therapyother therapy like topical allopurinol,
antimicrobial lozenges, benzydamine, capsaicin,
chamomile, dyclonine HCL, milk of magnesia are tried
but there is limited success for this therapy.
Uremic Stomatitis
Non-keratotic white lesions caused due to elevated
creatinine or blood urea nitrogen. It has been suggested to
be consequence of strongly alkaline saliva due to ammonia
formation from retained urea secreted in the saliva. Most of
the cases of uremic stomatitis occur in acute renal failure.
Types
Type Igeneralized or localized erythema with pseudomembrane formation. After removal of pseudomembrane
no ulceration is present.
Type IIthis is severe form and after removal of
pseudomembrane ulceration is present.
Diagnosis
Clinical diagnosispatient with uremic ulcer will
manifest the clinical signs of the uremic syndrome, an
ammonia odor of the breath, weight loss, anemia and
cardiac arrhythmias confirms the diagnosis of uremic
stomatitis.
Management
Palliative oral rinseulcer, if painful may be treated by
prescribing a palliative oral rinse such as an
antihistamine oral suspension with kaopectate.
Acidic mouth rinsemild acidic mouth rinse like diluted
hydrogen peroxide can clear oral lesion.
Clinical Features
Candidiasis
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Classification
There are many classifications for Candidiasis (Tables
11-2 to 11-4). Some of them are listed below. Classifications
are made on the basis of clinical presentation, location, etc.
Causative Organisms
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Category
Condition
Mechanism
Altered local
resistance to
infection
Compromised
immune system
function
Early infancy
Genetic immune deficiency
AIDS
Corticosteroids therapy
Pancytopenia
Generalized patient
debilitation
Pathogenesis
Overgrowth of yeastovergrowth of yeast on the oral
mucosa leads to desquamation of epithelial cells and
accumulation of bacteria, keratin, and necrotic tissue.
Formation of pseudomembranethis debris combines to
form a pseudomembrane, which may adhere closely to
the mucosa.
Clinical Features
In infants
Agein neonates, oral lesions start between the 6th and
10th day after birth.
Causeinfection is contracted from the maternal vaginal
canal where Candida albicans flourishes during the
pregnancy.
Appearancethe lesions in infants are described as soft
white or bluish white, adherent patches on oral mucosa
which may extent to circumoral tissue.
Symptomsthey are painless and noticed on careful
examinations. They may be removed with little difficulty.
In adult
Sitescommon sites are roof of the mouth, retromolar
area, and mucobuccal fold. But it is common on any
other mucosal surface.
Sexit is common in women as compared to male.
Prodormal symptomsprodormal symptom like rapid
onset of bad taste may be there. Spicy food will cause
discomfort.
Symptomspatient may complain of burning sensation.
White plaquespearly white or bluish white plaques are
present on oral mucosa. They resemble cottage cheese or
curdled milk (Figs 11-10 and 11-11). Patches are loosely
adherent to oral mucosa.
Composition of plaquesit is composed of tangled mass
of hyphae, yeast, desquamated epithelial cells and debris.
Adjacent mucosaMucosa adjacent to it appears red and
moderately swollen.
Wiping of patcheswhite patches are easily wiped out
with wet gauze which leaves either a normal or
erythematous area or atrophic area (Fig. 11-12). This area
may be painful. Deeper invasion by the organism leaves
an ulcerative lesion upon the removal of patch.
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3
Fig. 11-10: White plaque resembling as curdled milk present on lip
(Courtesy Dr Chole).
Diagnosis
Clinical diagnosispseudomembranous lesion which can
be scraped off will diagnose candidiasis.
Differential Diagnosis
Clinical Features
Fig. 11-12: Red atrophic mucosa seen in patient after
adherent patches are removed (Courtesy Dr Chole).
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Diagnosis
Clinical diagnosiserythematous area with condition
causing diminished host resistance will diagnose acute
atrophic candidiasis.
Clinical Features
Age and sexit predominantly occurs in men of middle
age or above. The majority of these patients are heavy
smokers.
Sitesit occurs on cheek, lip and tongue.
Appearancecandidal leucoplakia is extremely chronic
form of oral candidiasis in which firm, and white
leathery plaques are found (Fig. 11-15).
Symptomslesions may persist without any symptoms
for years.
Differential Diagnosis
Chemical burnfocal white area that rub off and
underlying condition of diminished host resistance
favors candidiasis. History of medicament is present.
Drug reactionidentification of condition causing
diminished host resistance is reliable differential
diagnostic feature of atrophic candidiasis.
Syphilitic mucus patchesdiscrete small white necrotic
lesions on tongue, palate or lip while candidiasis is
diffuse. Skin lesion of syphilis is also present.
Necrotic ulcer and gangrenous stomatitisulcer is deeper
than candidiasis.
Traumatic ulcerhistory of trauma is present.
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Diagnosis
Clinical diagnosisa firm white leathery appearance seen
which cannot rubbed off.
Differential Diagnosis
Id Reaction
A person with chronic candida infection may develop
secondary response characterized by localized or generalized sterile vesicopapular rash that is believed to be allergic
response to candida antigen (also called as monolids).
Management
Troches containing clotrimazole and Nystatin 4 to 5
times should be applied on the denture after meal and
bed time.
Denture Stomatitis
It is also called as chronic atrophic candidiasis. It is common
clinical manifestation of erythematous candidiasis. Candida
albicans is always found in this lesion but the typical white
patch of thrush does not usually develop in it. It occurs due
to tissue invasion but organism effect of fungal toxin
hypersensitivity to fungus.
Clinical features
Siteit is usually found under complete denture or
partial denture and found mostly in women and always
include palate.
Appearanceit exhibits patchy distribution often
associated with speckled curd-like white lesion.
Symptomssoreness and dryness of mouth.
Signspalatal tissue is bright red and somewhat
edematous and granular. Red patches may be
erythematous or speckled. The redness of mucosa is
rather sharply outlined and restricted to the tissue
actually in contact with the denture (Fig. 11-17). The
multiple pinpoint foci of hyperemia usually involving
the maxilla frequently occurs.
Diagnosis
Clinical diagnosisan erythematous area under the
complete denture will aid in diagnosis of candidiasis.
Differential diagnosis
Allergic reaction due to denture baseit is very rare
condition. If there is failure to respond to antifungal
therapy then one should suspect allergic reaction.
Angular Cheilitis
It is described in Chapter 23: Diseases of Lip.
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Types
Chronic familial mucocutaneous candidiasisit is an
inherited disorder, probably an autosomal recessive
disorder and affects both sexes.
Chronic localized mucocutaneous candidiasisthis form
occurs early in life with oral mucosal, skin and nail
involvement.
Endocrinopathy candidiasis syndromein this there is
subsequent appearance of hypoparathyroidism,
hypoadrenocortism and other endocrine abnormalities.
Chronic diffuse mucocutaneous candidiasislesions
involve pharyngeal mucosa and it is diffuse in nature.
Chronic mucocutaneous candidiasis in association with
thymomararely patient with thymoma manifest chronic
mucocutaneous candidiasis.
Clinical Features
Chronic familial mucocutaneous candidiasisit is
characterized by candidiasis of mouth, nails, and skin.
Children under the age of 10 years show superficial
candidal infection. Oral candidiasis is chronic
hyperplastic exhibiting firm white patches involving
either buccal or lingual mucosa.
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Management
Antifungal drugsfor resistance form of CMC and for
systemic candidiasis miconazole (250 mg 6 hourly),
5- flucytosine (200 mg daily) in addition to Amphotericin
B is available.
Transfusion of transfer factortransfusion of transfer
factor and transplantation of culture of thymic fragments
have been used to correct T. cell deficiency associated
with CMC.
Systemic Candidiasis
This term is used when there is presence of both necrotizing
inflammation and candida granuloma formation in one or
more visceral organ usually as a result of hematogenous
dissipation of organism.
Etiology
Immunosuppressive patientit occurs in immunosuppressive patient as a result of leukemia, lymphoma,
steroids, cytotoxic therapy and extensive therapy.
Contaminated instrumentcontaminated IV instruments
and indwelling catheter may lead to systemic candidiasis.
Drugsuse of contaminated drug, paraphernalia by
drug abuses.
Clinical Features
Candidal endocarditisit is characterized by fever,
dyspnea and edema of congestive cardiac failure.
Vascular vegetations of candidal growth often result in
embolization to major vessels. The disease is fatal in
majority of cases.
Candidal meningitisit is predominately disease of male
children characterized by variable features ranging from
stiffness of the neck, hemiplegia and other neurological
signs. The finding of Candida in spinal fluid is of
diagnostic importance. The condition is fatal in half of
the cases.
Candidal septicemiait occurs in those with severe oral
and esophageal thrush. Features include fever, chills,
shock and coma. Condition can be fatal if not treated in
time.
Management
Systemic candidiasis requires systemic administration
of high doses of Amphotericin-B 10 mg QID, miconazole
and 5-flucytosine. Mycostatin 50,000 unit 8 hourly. Daily
use of 200 mg ketoconazole for 2 weeks. Side effects are
increased liver enzyme, abdominal pain.
Gastrointestinal Candidiasis
An extension of oral infection may occasionally lead to
either pharyngeal or esophageal involvement.
Causes
Drugslong term broad-spectrum antibiotics,
corticosteroid therapy and immunosuppressive drugs.
Diseasesleukemia, diabetes and acquired immunodeficiency syndrome.
Clinical Features
Symptomsit presents acute enterocolitis, diarrhea, as
proctitis with anal pruritis of perineal eczemation.
Dysphagia, chest pain, and GIT bleeding may be
presenting symptoms.
Esophageal candidiasisesophageal candidiasis with or
without gastric ulceration are common forms of GIT
candidiasis.
Appearanceit is diagnosed by characteristic appearance
of edematous ulcerated mucosa on barium swallow.
Management
The use of topical and systemic antifungal agents.
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Interdigital Candidiasis
It is also called as erosion interdigitalis. It commonly involves
3rd and 4th fingers.
It is characterized by pruritic, inflamed, and scaling
lesions between fingers. Treatment includes topical
application of amphotericin B lotion or nystatin ointment.
Intertriginous Candidiasis
It is the candida infection of skin surface such as waist,
groin, armpit, elbows, submammary area, gluteal fold,
axilla, and scrotum. Intertriginous candidiasis causes
colonization in skin like axilla or submaxillary fold.
Opposing skin surface in these sites, particularly in obese
person prevent adequate ventilation and remain moist
favoring candidal growth.
Candida has characteristic way of causing dry pustulation with desiccation in lower level of stratum cornium
of skin. Lesions are very tender. Lesion spread from affected
skin as an area of glaze red skin or an easily detached
overlying epidermis i.e. often invaded leaving paper-like
fungal lesion along the margin. Satellite lesion may develop
around deeper denuded tissue.
Bronchial Candidiasis
It is a chronic infection of bronchial mucosa which may
last for years without producing severe discomfort. It mimics
chronic bacterial infection of the bronchus and chronic
cough with mucoid sputum is common symptoms
experienced by the patients.
Diagnosis is established by the demonstration of
candida in sputum and through culture studies.
Management includes systemic use of antifungal agents.
Etiology
Local irritantsill fitting denture, sharp clasp and rough
edges of restoration are responsible for traumatic
keratosis.
Cigarettes smokingheavy cigarettes smoking may also
lead to this type of lesion.
Clinical Features
Sitesmost common sites are lip and buccal mucosa.
Appearancethere is isolated thickened whitish area (Fig.
11-18).
Glassblowers white patchit is variant of traumatic
keratosis affecting the cheek and lips, which occur in
glass factory.
Diagnosis
Clinical diagnosisisolated white patch with identified
local irritant will diagnose the traumatic keratosis.
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Types (Clinical)
Stable plaque psoriasisit is most common type. The
lesions are red with dry, silvery-white scaling, which
may be obvious only after scraping the surface.
Guttate psoriasisit is seen in children adolescents and
may follow streptococcal sore throat. Individual lesions
are droplet-shaped, small and scaly.
Erythrodermic psoriasisthe skin becomes universally
red and scaly or more rarely just red with very little scale
present.
Pustular psoriasisit is a severe form of psoriasis with
eruption of minute pustule with shedding of nails is
common.
3
Fig. 11-18: Isolated white patch seen on buccal mucosa
due to sharp cusp.
Management
Removal of local irritantupon removal of the offending
agent, the lesion should resolve within 2 weeks.
Biopsy in cases of unhealed lesionbiopsies should be
performed on lesions that do not heal to rule out a
dysplastic lesion.
Psoriasis
It is a common dermatological disease characterized by
white, scaly papules and plaque on an erythematous base
that preferentially affects the extremities and scalp. It is
characterized by increased activity of keratinocytes.
Clinical Features
Ageit commonly affects adults and arises in 2nd and
3rd decades of life.
Sitesit commonly occurs on extremities, and scalp.
Progressit is usually chronic with acute generalized
exacerbations. It is more severe in winter and less severe
in the summer as a result of increase exposure to
ultraviolet light.
Symptomsin some cases, patient may complain of
itching.
Appearanceit is characterized by occurrence of small
sharply defined, dry papules each covered by delicate
silvery scale which appear as a thin layer of mica
(Fig. 11-19).
Margins and shapepapules are enlarged at periphery
and may form large plaques which are roughly
symmetrical (Fig. 11-20).
Signsafter removal of scale the surface of skin is red
and dusky in appearance.
Auspitzs signif the deep scales are removed one or
more bleeding points are seen.
Psoriatic arthritisthis is the complication of psoriasis
which can involve the temporomandibular joint.
Oral Manifestations
Sitesoral lesions are reported on lip, buccal mucosa,
palate, gingiva and floor of mouth.
Appearancethey appear as plaques, silvery, scaly
lesions with an erythematous base.
Signssometimes they are multiple papular eruptions
which may be ulcerated or as small, papillary elevated
lesions with scaly surface.
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Diagnosis
Clinical diagnosissilvery scale appearance with positive
Auspitzs signs will diagnose psoriasis.
Laboratory diagnosisintraepithelial micro-abscess
formation (Munro abscess) is seen. There is also test tube
rete pegs appearance.
Management
Topical agents
Emollientsit has modest effect in terms of reducing
scale.
Dithranolit is gold standard therapy with dithranol.
It inhibits proliferation when applied to psoriatic
plaques.
Tarcrude tar is used which is pro-inflammatory and
action same as dithranol.
Calcipotriolit is vitamin D agonist and it reduces
the thickness of plaque.
Retinoidit diminishes the induration, scaling and
redness of plaque.
Corticosteroidsuse of potent topical corticosteroid
on the face or hair margins should be under close
and expert medical supervision.
Ultraviolet lightit is mainstay of management of patient
with moderate to severe psoriasis. It is used 3-7 times in
a week.
PUVA (psoralens and ultraviolet A) therapypsoralens are
natural photosensitizes found in number of plants. It
includes clearance to greater degree than any other
therapy.
Systemic treatmentthree main systemic agents are used,
i.e. methotrexate, oral retinoid and cyclosporine.
Etiology
Papillomavirusit is possibly caused by papillomavirus
type 13 and 32.
HIV virussome lesions may be seen in HIV seropositive
patients.
Clinical Features
Age and sex predilectionit occurs predominately in
children between ages of 3 and 18 years. There is no sex
predilection.
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Sitecommon sites are lip, buccal mucosa, commissures, tongue and less commonly on the gingiva, and
anterior facial pillar.
Appearancesit appears as multiple nodular lesions with
sessile base. It can occur in cluster or in isolated crops.
Some time it is present as flat, slightly raised whitish
plaque on roughened surface.
Cobblestone appearancein some cases these lesions are
cluster so closely the entire area appear as cobblestone
or fissure appearance.
Signthey become less conspicuous when the mucosa
is stretched. It is non-tender. After drying, the lesion
reveals finely granular surface texture.
Sizethese lesions are soft having size of 1 to 5 mm in
diameter with same color as adjacent mucosa.
Colorthey are pale to normal in color.
Progressthey often appear to undergo spontaneous
regression after 4 to 6 months.
Diagnosis
Clinical diagnosissessile, pedunculated pale color
clustered multiple lesions may go in favor of focal
epithelial hyperplasia.
Laboratory diagnosisbiopsy will show acanthosis with
mild hyperparakeratosis usually present over the surface
of lesion.
Differential Diagnosis
Condyloma acuminatumit is the condition with greatest
similarity to focal epithelial hyperplasia. Condyloma
acuminatum has got cauliflower like appearance as
compared to focal epithelial hyperplasia which has got
finely granular surface texture.
Tuberous sclerosispresence of cutaneous lesion.
Dariers diseasethere is presence of cutaneous lesion.
Management
Regress spontaneouslyno treatment is necessary as
these are harmless lesion and it will regress spontaneously.
Surgical excisionconservative surgical excision may be
performed for esthetics purpose.
Oral Genodermatoses
These are also a type of keratotic lesion without increased
potential for malignant transformation. They are called
genodermatoses as they are genetically determined skin
disorders.
Clinical Features
Age and sexit has no definite sex predilection with
children most commonly affected and may be present at
birth and may become intense at puberty.
Sitethe most common sites are cheek, palate, gingiva,
floor of mouth, portion of tongue. It may be widespread
and may involve entire mucosa. It can also occur on the
mucous membranes of the nose, esophagus, genitalia,
and rectum.
Appearancemucosa appears as thickened and folded
or corrugated with soft or spongy texture and a peculiar
white opalescent line. It has got soaked through,
furrowed or wrinkled appearance.
Extentthe lesion varies in extent from a small patch to
involvement of a large area of mucosa.
Signfriction may strip superficial keratotic area leaving
zone of normal looking epithelium or raw area. Ragged
white area may be present which can be removed by
gentle rubbing without bleeding.
Diagnosis
Clinical diagnosisdiffuse thickened white folded
appearance in children on buccal mucosa which doesnt
disappear after stretching is typical feature of white
sponge nevus.
Laboratory diagnosisbiopsy shows thickened epithelium with hyperkeratosis, and acanthosis. In some cases
there is extensive keratosis showing basket-weave
appearance.
Differential Diagnosis
Leukoedemait is only opalescent and white sponge
nevus has rough granular and lethargic appearance.
Leukoplakiaunusual in patients under the age of 30
years.
Lichen planussame as above.
Pachyonychia congenitapresence of nail anomalies as
well as skin lesions.
Management
No treatmentthere is no specific treatment for this
disease but prognosis is very good.
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Clinical Features
Age and sexit is most commonly seen in children with
no sex predilection.
Sitesit is commonly seen in eyes. Superficial gelatinous
looking plaques occur on a hyperemic bulbar
conjunctiva.
Symptomsthere may be photophobia and blindness
cause a by involvement of cornea by plaque formation
and scarring.
Appearanceeye is characterized by superficial, foamy,
gelatinous white plaque overlying the cornea, sometimes
producing temporary blindness.
Seasonal variationeye lesion shows seasonal variation
tending to appear or increase in severity in the springs
and disappear.
Oral Manifestation
Sitesthey are most commonly seen in buccal mucosa,
floor of mouth, ventral and lateral surfaces of the tongue,
the gingiva, and palate.
Appearanceit appears generally as white, spongy,
macerated lesions of the buccal mucosa with or without
folds.
Signsthese lesions vary from delicate, opalescent white
membranous areas to a rough, shaggy mucosa.
Angle of mouthlesion frequently involves the corners
of the mouth and appears as soft plaques with pinpoint
elevation when the mucosa is stretched.
Candidial infectionin some oral lesions, candidial
infection may superimpose.
Diagnosis
Clinical diagnosiswhite spongy macerated lesion
which is accompanied by eye lesion will diagnosed
these conditions.
Laboratory diagnosisbuccal mucosa exhibits thickening
of the epithelium with pronounced hydropic degeneration.
Differential Diagnosis
White sponge nevuseye involvement is not present in
case of white sponge nevus.
Management
Ophthalmologist consultationfor eye lesion ophthalmologist consultation should be done.
Antifungal medicationit is given in the condition when
candidiasis superimposed on oral lesion.
Pachyonychia Congenita
It is also called as Jadassohn-Lewandowsky syndrome,
Jackson-Lawler type. It is extremely uncommon disease,
inherited as an autosomal dominant characteristic with
incomplete penetrance.
Clinical Features
Age and sexit usually occurs shortly after birth with no
sex predilection.
Sitesfingernails, toenails, palms, soles, knees, elbows,
hands, and feet.
Nailsthere is marked thickening, increasing toward
the free border with nailbed becoming filled with
yellowish keratotic debris, often causing the nail to
project upward at the free edge.
Hair and corneaassociated sparse hair and corneal
dyskeratosis producing corneal opacities have been
reported.
Feetbullae formation occurs on the feet, and secondary
infection of these may lead to crippling deformity.
Othersthickening of the laryngeal commissures,
tympanic membrane and nasal mucosa and mental
retardation are also reported.
Oral Manifestation
Sitesthe buccal mucosa, tongue and lips.
Appearancethey consist of focal or generalized white,
opaque thickening of the mucosa (Fig. 11-21).
Ulcersthere is frequent oral aphthous ulceration is seen.
Angular cheilitisin some cases inflammation of angle
of mouth is seen.
Teethnatal teeth are also present.
Diagnosis
Clinical diagnosisdystrophic nail changes with
thickened white appearance.
Laboratory diagnosisthe mucous membrane exhibits
an intracellular edema or vacuolization of the spinous
cell reminiscent of white sponge nevus.
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Diagnosis
Clinical diagnosisthickened and ridge nails with
opalescent palatal lesion.
Laboratory diagnosisthe elevated horny margin of the
lesion exhibits hyperkeratosis and acanthosis with a
deep groove filled with parakeratin.
Management
Fig. 11-21: Thickened white appearance seen on buccal mucosa in
pachyonychia congenita (Courtesy Dr Pincha).
Differential Diagnosis
White sponge nevusin pachyonychia congenita there is
fingernail changes in association with oral changes.
Lichen planusWickhams striae are seen.
Hereditary benign intraepithelial dyskeratosisin these
disorders there is combination of eye and oral lesion.
Management
No treatmentthere is no treatment for this disease.
Porokeratosis
It is also called as Mibellis disease and it is autosomal
dominant. It is characteristic by faulty keratinization of the
skin followed by atrophy.
Clinical Features
Age and sexthe majority of disease begins in early
childhood but progression of disease is extremely slow.
It appears to occur in males with greater frequency than
in females.
Sitesit occurs most commonly in extremities
particularly in hands and feet, as well as shoulder, face
and neck and the genitalia.
Appearanceit consists initially of crateriform keratotic
papules which gradually enlarged to form elevated
plaques. In some cases there is ring-like keratotic lesion
of the skin with atrophic center.
Sizeit ranges in size from a few millimeters to several
centimeters.
Marginsthe plaques are surrounded by a distinct
raised border of epidermal proliferation.
Nailsthe nails commonly become thickened and
ridged. The central portion of the lesions ultimately
becomes atrophic, leaving permanent scarring.
Keratosis Follicularis
It is called as Dariers disease, Darier-White disease. It is
autosomal dominant trait. A lack of cohesion among the
surface epithelial cells is characterized of this disease.
Clinical Features
Age and sexit is usually manifested during childhood
or adolescence and has equal sex distribution.
Sitesthey are generally distributed above the forehead,
scalp, neck, and over the shoulders.
Cutaneous lesionthe cutaneous lesion appear small,
firm papules (Fig. 11-22).
Colorthey are red when they first appear but characteristically become grayish brown or even purple later.
Signsit can ulcerate and crust over.
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Oral Manifestation
Siteskeratotic papule occur on oral mucosa particularly
on hard and soft palate, gingiva, tongue have whitish
appearance.
Signsthey are multiple whitish papules which feel
rough upon palpation. In some cases it has been
described as rough, pebbly areas with verrucous white
plaque or as having cobblestone appearance. Papules
become confluent as disorder progress.
Diagnosis
Clinical diagnosiserythematous papular lesion on skin
with white plaque lesion in oral cavity.
Laboratory diagnosisdyskeratosis is characterized by
typical cells called corps ronds and grains (cell within cells).
Oral Manifestation
Management
Diagnosis
Differential Diagnosis
Warty Dyskeratoma
It is also called as isolated Dariers disease which bears
histologic similarity to keratosis follicularis but it presents
as single isolated focus.
Clinical Features
Age and sexit usually occurs in older age group with
male predominance.
Sitethe skin lesion occurs on face, scalp, neck and
upper chest.
Appearancethey appear as elevated nodules,
umbilicated, with raised borders and varying in color
from yellow or brown to gray or black (Fig. 11-23).
Differential Diagnosis
Keratoacanthomait can attain dimension upto 1-2 cm
while warty dyskeratoma are usually small. Keratoacanthoma fails to exhibit a smooth round border.
Molluscum contagiosumbiopsy may require making the
diagnosis.
Management
Conservative surgical excisionit should be treated by
surgical excision.
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Pseudoxanthoma Elasticum
Clinical Features
Clinical Features
Age and sexalthough widely variable, the age of onset
averages 13 years with no predilection for sex.
Sitesraised yellowish papules develop on areas of
thickened, coarsely grained skin especially around the
mouth, neck, axilla, elbows.
Appearancebrownish gray streaks of the optic fundus
(angioid streaks), recurrent gastrointestinal hemorrhage,
weak pulse, and failing vision.
Cutaneous lesionsthe typical cutaneous lesions are
small yellowish papules or larger coalescent plaques
with an appearance similar to plucked chicken skin.
More severely affected skin results in hanging, redundant
folds.
Oral Manifestations
Sitesmucous membranes, mainly of the inner aspect
of the lower lip is affected.
Hound dog appearanceskin around mouth becomes
redundant, producing a hound dog appearance.
Liplower lip exhibits yellowish intramucosal nodule.
Diagnosis
Clinical diagnosisyellowish lesion seen on skin with
hound dog appearance.
Laboratory diagnosisbiopsy shows intramucosal
nodules showing large number of thickened and twisted
elastic and collagen fibers.
Management
No specific treatmentat present, no specific treatment
exists. The knowledge, however, of the potential
complications may lead physicians to take some
necessary precautions.
Oral Manifestation
Sitesmost commonly affected area is lower lip. It can
be seen on tongue, buccal mucosa.
Appearanceaffected tissue becomes infiltrated with
yellowish white elevated pea sized plaque which
gradually increased in size in puberty.
Symptomsrestriction of oral function such as saliva
flow, tooth eruption, and swallowing.
Angle of mouthradiating tissue may appear at angle of
mouth.
Tonguetongue become firm and large and bound to
floor of mouth. The dorsum of tongue may losses its
papilla and ulcer may develop.
Gingivadiffuse hyperplastic appearing gingival
infiltration is present.
Teeththere is hypodontia of maxillary lateral incisors
and premolars.
Diagnosis
Clinical diagnosisaceneform scar with hypodontia,
xerostomia, and delayed tooth eruption.
Laboratory diagnosisbiopsy shows diffuse hyalinization with prominent hyaline perivascular cuffing. These
deposits are PAS positive and show equivocal reaction
for amyloid.
Differential Diagnosis
Focal epithelial hyperplasia, Cowden syndrome and
amyloidosisit may show similar clinical features. A
dermatological examination should be performed.
Biopsy should be performed to confirm the diagnosis.
Management
Gingivectomyit is recommended when diffuse
hyperplastic appearing gingival infiltration is present.
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Suggested Reading
1. Allen CM. Diagnosing and managing oral candidiasis. JADA
1992; 123:77-82.
2. Baruchin AM, Lustig JP, et al. Burns of the oral mucosa: report of
6 cases. J Craniomaxillofac Surg 1991;19:94-96.
3. Bazopoulou-Kyrkanidou E, Tosios KI, et al, Hyalinosis cutis et
mucosae: case report and review of literature. J Oral Pathol Med
1998;27:233-7.
4. Bergendal T, Isacsson G. A combined clinical, mycological,
histological study of denture stomatitis. Acta Odontol Scand
1983; 41:33-44.
5. Carlos R, Sedano HO. Multifocal papilloma virus epithelial
hyperplasia. Oral Surg, Oral Med, Oral Pathol 1994;77:
631-5.
6. Chau MNY, Radden BG. Oral Warty dyskeratoma. J Oral Pathol
1984; 13:546-56.
7. Chaudhary SJ, Dayal PK. Hyalinosis cutis et mucosae: review
with a case report. Oral Surg, Oral Med, Oral Pathol, Oral Radiol
Endod 1995;80:168-71.
8. Fanibunda KB. Adverse response top endodontic material
containing paraformaldehyde. Br Dent J 1984;157:231-5.
9. Fotos PG, Vincent SD, Hellstein JW. Oral candidosis: clinical,
historical and therapeutic features of 100 cases. Oral Surg, Oral
Med, Oral Pathol, 1992;74:41-49.
10. Frost DE, Barkmeier WW, Abrams H. Aphthous ulcer-treatment
complication. Oral Surg, Oral Med, Oral Pathol 1978;45:863-69.
11. Gormley MD, Marshall J et al. Thermal trauma: review of 22
electrical burns. J Oral Surg 1972;30:531-33.
12. Halazonetis J, Harley A. Uremic stomatitis: a report of case. Oral
Surg, Oral Med, Oral Pathol 1967;23:573-77.
13. Hersh SP. Pachyonychia congenita: manifestation for the
otolaryngologist. Arch Otolaryngol Head Neck Surg 1990; 116:
732-4.
14. Holmstrup P, Axell T. Classification and clinical manifestation
of oral yeast infection. Acta Odontol Scand 1990;48:57-59.
15. Jorgenson RJ, Levin LS. White sponge nevus: Arch Dermatol
1981;117:73-76.
16. Lehner T. Oral thrush or acute pseudomembranous candidiasis:
clinico-pathological study of forty four cases. Oral Surg, Oral
Med, Oral Pathol 1964;18:27-37.
17. McCreary CE, Flint SR, et al. Uremic stomatitis mimicking oral
hairy leukoplakia: report of case. Oral Surg, Oral Med, Oral
Pathol, Oral Radiol Endod 1997;83:350-53.
18. Mecleod RI, Munro CS. The incidence and distribution of oral
lesions in patients with Dariers disease. Br Dent J 1991;171:
133-6.
19. Miles AEW. Sebaceous glands in the lip and cheek mucosa of
man. Br Dent J 1958;105:235-48.
20. Morris LF, Phillips CM, Binnie WH, et al. Oral lesions in patients
with psoriasis: a controlled study. Cutis 1992;49(5):339-44.
21. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology
(2nd edn), 2004: Saunders Elsevier.
22. Padayachee A, van Wyk CW. Human papilloma virus (HPV)
DNA in focal epithelial hyperplasia in situ hybridization. J Oral
Pathol Med 1991;20:210-14.
23. Plevova P. Prevention and treatment of chemotherapy and
radiotherapy induced oral mucositis: a review. Oral Oncology
1999;35:453-70.
24. Richardson LJ, Kratochvil FJ, Zieper MB. Unusual palatal
presentation of oral psoriasis. J Can Dent Assoc 2000; 66(2):
80-2.
25. Ross WF, Salisbury PL. Uremic stomatitis associated with
undiagnosed renal failure. Gen Dent 1994;42:410-12.
26. Sadeghi EM, Witkop CJ. The presence of Candida albicans in
hereditary benign epithelial dyskeratosis: an ultrastructural
observation. Oral Surg, Oral Med, Oral Pathol 1979;48:342-46.
27. Sewerin I, Praetorius F. Keratin filled pseudocyst of ducts of
sebaceous gland in the vermilion border of lip. J Oral Pathol
1974; 3:279-83.
28. Sewerin I. A clinical and epidemiologic study of morsicatio
buccarum/labiorum. Scand J Dent Res 1971;79:73-80.
29. Younai FSW, Phelan JA. Oral mucositis with features of psoriasis:
report of case and review of literature. Oral Surg, Oral Med, Oral
Pathol, Oral Radiol Endod 1997;84:61-7.
30. Zhu JF, Kaminski MJ, Pulitzer DR, et al. Psoriasis:
pathophysiology and oral manifestations. Oral Dis 1996; 2(2):
135-44.
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12
Oral Premalignant
Lesions and Conditions
Concept of Precancer
Precancerous Lesions
Leukoplakia
Classification
According to clinical description
Homogenousit is completely whitish lesion.
Flatit has smooth surface.
Corrugatedlike a beach at ebbing tide.
Pumice likewith a pattern of fine lines (cristae).
Wrinkledlike dry, cracked mud surface.
Non-homogenous
Nodular or speckledcharacterized by white specks
or nodules on erythematous base.
Verrucousslow growing, papillary proliferations
above the mucosal surface that may be heavily
keratinized. Extensive lesion of this type is called as
oral florid papillomatosis.
Ulceratedlesion exhibits red area at the periphery of
which white patches are present.
Erythroleukoplakialeukoplakia is present in association with erythroplakia.
According to etiology
Tobacco induced
Non-tobacco induced.
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According to histology
Dysplastic
Non-dysplastic
According to extent
Localized
Diffuse
According to Banoczy
Leukoplakia simplexa uniform raised plaque formation,
varying in size, with regular edges. It corresponds to
homogenous type of leukoplakia.
Leukoplakia erosivaa lesion with slightly raised,
rounded, red and/or whitish excrescence, that may be
described as granules or nodules.
Leukoplakia verrucosait is characterized by verrucous
proliferation raised above the mucosal surface.
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3
Fig. 12-5: Leukoplakia occurring on alveolar region in edentulous
patient.
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3
Fig. 12-7: In this leukoplakia, considerable portion of oral
mucosa is involved.
Clinical Types
Pre-leukoplakia or mild or thin leukoplakiaa different
entity termed as pre-leukoplakia has been distin-
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A
Fig. 12-12: Nodular leukoplakia showing pinhead size nodule in
retromolar area.
B
Figs 12-10A and B: Homogenous leukoplakia showing thick white
patches on buccal mucosa (Courtesy Dr Parate).
Staging of Leukoplakia
According to size, clinical aspect and pathological features
Sizeit is denoted by L
L1size is less than 2 cm.
L2size is in the range of 2-4 cm.
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3
Fig. 12-14: Proliferative verrucous leukoplakia showing multiple
keratotic clefts in anterior region.
Diagnosis
Clinical diagnosisclinically any white patch with
history of tobacco chewing which cannot be rub off is
the diagnostic indicator for leukoplakia.
Laboratory diagnosisin biopsy you can see hyperorthokeratosis, hyperparakeratosis, acanthosis of epithelium,
epithelial dysplasia, liquefaction degeneration basal cell
hyperplasia. Scanning electron microscopy will show
epithelial dysplastic changes.
Differential Diagnosis
Lichen planusdistinguished by the often occurrence of
multiple lesions and presence of Wickhams striae.
Chemical burnhistory is important in chemical burn.
Syphilitic mucus patchesother features like split papule
or condyloma latum may be present.
White sponge nevusoccurs soon after birth or at least by
puberty and is widely distributed over the oral mucus
membrane. Familial pattern is seen, in contrast to
leukoplakia which occurs over 40 years of age and not
so disseminated throughout the oral cavity.
Discoid lupus erythematosuscentral atrophic area with
small white dot and slightly elevated border zone or
radiating white striae.
PsoriasisAuspitzs sign is positive and skin lesions
are also present.
Leukoedemaclassically occurs on buccal mucosa
covering most of the oral surface of cheek and extending
onto labial mucosa. Faint milky appearance with folded
and wrinkled pattern as compared definite whiteness
of leukoplakia.
Hairy leukoplakiacorrugated leukoplakic lesion
occurring on lateral and ventral surface of tongue in
patients with AIDS or ARC (AIDS related complex).
Verruca vulgariscommonly occurs in the oral cavity as
small, raised white lesion, more than 0.5 cm in diameter
as compared to verrucous leukoplakia which is larger
and surrounded by inflamed mucosa.
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Management
Elimination of etiological factors
Prohibition of smokingpatient should be asked to cease
smoking immediately. Many cases of leukoplakia get
regress after smoking is ceased.
Removal of chronic irritantdentist should remove sharp,
broken teeth.
Elimination of other etiological factorsother etiological
factors like syphilis, alcohol, dissimilar metal restoration
etc. should be eliminated.
Conservative treatment
Vitamin therapyit has a protective effect on the
epithelium. Daily requirement is 4000 IU. It is given
orally, parentally or topically. Therapeutic dose75000300000 IU for 3 months. Vitamin A may be used topically
after painting the lesion with podophyllin solution (it
inhibit mitosis).
Vitamin A + vitamin Ethis therapy is given to inhibit
metabolic degradation.
13-cis-retinoic acidIt is a synthetic analogue of vitamin
A; usually given in high doses of 1.5 to 2 mg/kg body
weight for 3 months. If relapse occurs then low doses of
13-cis-retinoic acid 0.5 mg/kg body weight are given for
9 months. It may be given with carotene (this drug may
produce a variety of toxic effects which include facial
erythema, dryness, peeling of skin, conjunctivitis and
hypertriglyceridemia).
Antioxidant therapyconsiderable data shows that
-carotene supplementation can be beneficial for
treatment of oral leukoplakia.
Vitamin A palmitateShort-term treatment with vitamin
A palmitate along with aromatic retinoid of all trans -BA vitamin acid plus, B-cis-B-A vitamin acid may show
healing and improvement.
Nystatin therapyIt is given in candidial leukoplakia.
500,000 IU twice daily plus 20% borax glycerol or 1%
gentian violet or mouth rinses with chlorogen solution.
Vitamin B complexit is given as supplement in cases of
commissural and lingual lesion.
Antimycotic preparationthe antimycotic preparation can
hasten and pimafucin have also been effective.
Panthenolpanthenol lingual tablet and oral spray may
be used against glossitis and glossodynia, in case of
tongue lesion.
Estrogenin some cases, administration of estrogen can
be helpful.
Surgical management
To give proper treatment, microscopic examination is
necessary for which biopsy is taken. The most meaningful
sites for taking biopsy specimen are the areas that display
greater surface irregularities such as cracks and fissures
and those associated with erythematous areas.
Conventional surgeryyou should make an incision
around the lesion including safe margins. The incision
should be deep and wide. Affected area is then
undermined and dissected from the underlying tissue.
Sliding mucosal flap is prepared for covering the
wound. Fine iris scissors and skin hook should be used
to decrease trauma. Fairly extensive undermining of the
mucosal flap is necessary so that when it is advanced
into position, there will be minimum amount of tension.
Excessive tension will restrict circulation and can result
in necrosis. After proper mobilization of the mucosal
flap, it is advanced and multiple interrupted black silk
sutures are used. Approximate the free edges.
Postoperative application of ice bags to the site is advised
to minimize bleeding and swelling.
Cryosurgerytissue is exposed to extreme cold to
produce irreversible cell damage. Cell death occurs at
20 degree Celsius. Disc type probe (cryo probe)
refrigerated by liquid nitrogen or pressurized nitrogen
oxide is used. Incorporated in the probe is re-warming
device, thus tissue can be rapidly frozen and thawed as
required. The probe is applied to the surface lesion, which
is moistened by water-soluble jelly. It produces very low
temperature in tissue. First freeze for 1 minute, followed
by 5 minute thaw. 1 minute freeze and then administered.
Freezing produces white area of necrosis. The process is
repeated two to three times to achieve maximum
destruction. Freezing induces crystal formation within
the cell and intracellular spaces. When cooling rates are
rapid, intracellular ice crystal may rupture cell
membrane and cell death can occur. Slower cooling
produces large ice crystals in the space between cells.
As the crystals grow, water is removed from neighboring
cells, leading to an increased concentration of the
electrolytes. These soon reach toxic levels initiating cell
death by osmotic shock when thawing commences. Cell
is also killed by change in microvasculature of the part
being exposed to cryosurgery.
Fulguration (electrocautery and electrosurgery)It is a
technique in which there is destruction of tissues by
high voltage electric current and the action is controlled
by movable electrode. Advantages of this are its ability
to coagulate lesion and provide easy control of
hemorrhage. Disadvantages are tasteless (foul) odor,
hazards of explosion, need for profound local anesthesia
and sometimes general anesthesia, slow healing process,
pain and scarring.
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LASER
LASER stands for light amplification of stimulated
emission of radiation. CO2 lasers are most commonly used
in oral lesions due to their great affinity for any tissue with
high water content and their minimum penetration depth,
i.e. 0.2 to 0.3 mm in oral tissue. CO2 laser contain CO2,
nitrogen and helium gases
Biopsyin performing incisional or excisional biopsy
in cases of leukoplakia, CO2 laser is used as precise
cutting tool. Laser is placed in a cutting or focused mode
held perpendicular to the tissue. A predetermined
surgical outline is followed by means of a tissue pickup;
a border of the outline is raised and the lesion is then
undermined with traction and counter traction would
be done with scalpel.
Laser peelit is usually used to remove the lesion that
involves relatively large surface area. Beam is highly
defocussed and kept distant from the tissue. Initially, no
effect will be seen on the tissue plane Beam is gradually
brought closer into focus, but is still in defocussed mode
until tissue takes white appearance and begins to blister.
Blistering occurs at the basement membrane of the tissue.
This whitening technique is extended over the rest of
the lesion to be peeled. This white area is then grafted
with tissue forceps or hemostat and it is laser peeled
away to expose the underlying tissue or vitalization.
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Erythroplakia
It is also called as erythroplasia of Queyrat, erythroplasia.
Erythroplakia is a persistent velvety red patch. Reddish
color results from absence of surface keratin layer and due
to presence of connective tissue papillae containing
enlarged capillaries projected close to the surface.
Definition
It is applied to any area of reddened, velvety-textured
mucosa that cannot be identified on the basis of clinical
and histopathologic examination as being cause by
inflammation or any other disease process.
A chronic red mucosal macule which cannot be given
any other specific diagnostic name and cannot be
attributed to traumatic, vascular or inflammatory causes.
Classification
Homogenousthese commonly occur on buccal mucosa
with well demarcated margin.
Erythroleukoplakiaerythroplakia interspersed with
patches of leukoplakia.
Granular or speckledthese are elevated lesions.
Etiology
Idiopathicin most of the cases cause for erythroplakia
is not found.
Alcohol and smokingthese can act as predisposing
factors for erythroplakia.
Candida infectiona secondary infection or super
infection with candidiasis may be associated with
dysplastic oral mucosal cells. Candida albicans has often
been demonstrated in erythroleukoplakia lesions and
the red component of these lesions (often the white
component as well) diminishes or disappears after
antifungal therapy, in at least some cases.
Clinical Features
Age and sexmale predilection and most common in
6th and 7th decade of life.
Siteserythroplakia occurs on all mucosal surfaces of
the head and neck area. Half of all cases, however, are
found on the vermilion or intraoral surfaces, with the
rest being evenly divided between the larynx and the
pharynx. Vermilion lesions are relatively common and
are most often seen on the lower lip. Intraorally, the lateral
and ventral tongue, floor of mouth , buccal vestibule
and soft palate are most frequently involved.
Symptomserythroplakia, as the name obviously
implies, is asymptomatic.
Appearanceit is nonelevated, red macule or patch on
an epithelial surface. The exact cause of the red
appearance is unknown, but may be related to an increase
in the number of underlying blood vessels through
which the blood flows, which in turn may be secondary
to localized inflammatory or immunological responses
caused by the dysplastic, i.e. foreign, epithelial cells. In
some cases, the color may result from a lack of surface
keratin or extreme thinness of the epithelium.
Extentunlike leukoplakia, erythroplakia is seldom
multiple and seldom covers extensive areas of mouth.
Also unlike leukoplakia, erythroplakia seems seldom to
expand laterally after initial diagnosis, although this
may be an artifactual feature because most lesions are
completely removed or destroyed immediately after
formal diagnosis.
Homogenous formhomogenous form appears as a bright
red, soft, velvety lesion with straight or scalloped, welldemarcated margins (Fig. 12-16). It is often quite extensive
in size. Regardless of the cause of the color change, the
typical lesion is less than 1.5 cm in greatest diameter
and half are less than 1.0 cm, but lesions larger than
4 cm have also been seen. It usually quite sharply
demarcated from the surrounding pink mucosa and its
surface is typically smooth and regular in coloration.
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Differential Diagnosis
Candidiasislesion can be rubbed off and it is commonly
seen on the tongue.
Denture stomatitisunusually site is the palate or any
denture bearing area.
Tuberculosistuberculous ulcers are present which have
rolled margins.
Histoplasmosisit is more common in farmers and
present as a single ulcer.
Area of mechanical irritationcause can be identified.
Macular hemangiomalesions blanch on pressure.
Talangiectasiacharacteristic appearance seen on soft
palate.
Traumatic lesioncause can be identified.
Management
Removal of causeelimination of a suspected irritant
should be carried out.
Incisional biopsyit is always preferred method for
establishing a microscopic diagnosis of suspicious
intraoral lesions. Since erythroplakia is so closely
correlated with severe dysplasia, carcinoma in situ and
invasive carcinoma, incisional biopsy is especially
indicated. Excisional biopsy of a potential malignancy
may result in under treatment and violation of surgical
oncologic principles.
Surgical strippingthe definitive treatment of erythroplastic lesions remains controversial. A conservative
surgical procedure such as mucosal stripping is often
performed, with minimal damage to the deeper
connective tissues. This has the distinct advantage of
preserving tissues for microscopic evaluation of potential
regions of invasion.
Destructive techniquedestructive techniques such as
laser ablation, electrocoagulation and cryotherapy have
also proved to be effective.
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Carcinoma in situ
It is also called as intraepithelial carcinoma. Severe
dysplastic changes in a white lesion indicate considerable
risk of development of cancer (Fig. 12-18). The more severe
grade of dysplasia merges with the condition known as
carcinoma in situ. It is more common on skin but can also
occur on mucous membrane.
Management
Surgical removallesion may be surgically excised,
cauterized and even exposed to solid carbon dioxide.
Actinic Keratosis
Actinic keratosis is a cutaneous premalignant lesion.
Similarly actinic cheilitis which is associated with lower
lip is described in Chapter 23: Diseases of Lip.
Etiology
Ultraviolet radiationthis radiation can produce
mutation in p53 suppressor gene. This will cause
alteration in skin.
Clinical Features
Clinical Features
Diagnosis
Clinical diagnosisclinically one cannot diagnose
carcinoma in situ. It may appear like leukoplakia,
erythroplakia or both.
Laboratory diagnosisin biopsy, keratin may or may not
be present in/on the surface of lesion; but if present, is
more apt to be parakeratin, rather than orthokeratin. Loss
of orientation of cells and their polarity (Fig. 12-18). Sharp
line of division between normal and altered epithelium
extending from the surface, down to the connective tissue
rather than blending of the epithelium. An increase in
nuclear/cytoplasmic ratio and nuclear hyperchromatism are sometimes seen.
Management
Cryotherapyit is done with the help of liquid nitrogen.
Other therapyother therapy like topical application of
5-fluorouracil, curettage, electrodessication or surgical
excision.
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Fig. 12-19: Well defined redden area seen in palate of patient who
is having habit of reverse chutta smoking (Courtesy Dr Chole).
Types (Clinical)
Mildconsisting of red, dot like opening on blanched
area.
Moderatecharacterized by well defined elevation with
central umbilication.
Severemarked by papules of 5 mm or more with
umbilication of 2-3 mm.
Clinical Feature
Age and sex distributionit is usually seen in men who
are pipe smokers. It is common in middle age and elderly
adults.
Sitemost commonly affected site is palate. The lesion
is well developed and prominent on keratinized hard
palate. It is restricted to the area which is exposed to
heavy cigarette smoke.
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Diagnosis
Etiopathogenesis
Differential Diagnosis
Papillary hyperplasiathe lesion displays cobblestone
appearance and in stomatitis nicotina, there is red center
located on the palate of pipe or cigar smokers. The
papules of the papillary hyperplasia are focal.
Dariers diseasethey appear diffusely on palate in
cobblestone pattern.
Focal epithelial hyperplasiait is not common on palate
and they are not erythematous.
Cowden syndromethese are multiple papillary nodules
commonly seen on gingiva.
Clinical Features
Locationit occurs in mucosal surface, where snuff is
habitually held.
Gingiva and periodontal tissuethere is painless loss of
gingival and periodontal tissue in the area of tobacco
contact.
Teeththere is extrinsic stain present on the teeth. There
is also cervical erosion of teeth with more prevalence of
dental caries.
Smokeless tobacco keratosisit is white plaque present in
the mucosa where chewing tobacco is kept. It is thin,
gray or gray-white translucent lesion (Fig. 12-23). Margin
of the lesion blends gradually into surrounding mucosa.
Management
Stoppage of habitit is completely reversible, once the
habit is discontinued. The lesions usually resolve within
2 weeks of cessation of smoking.
Biopsybiopsy of nicotine stomatitis is rarely indicated.
But biopsy should be performed on any white lesion of
the palatal mucosa that persists after 1 month of
discontinuation of smoking habit.
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Management
Stoppage of habitmaximum lesion is regress following
the caseation of habit.
Biopsyany lesion which remains after 6 months
quitting the habit should be send for biopsy.
Pre-malignant Conditions
Lichen Planus
Erasmus Wilson described it in 1869. The term lichen planus
is derived as lesion they look like lichen on the rock and
planus is for flat. Various mucosal surfaces may be involved,
either independently or concurrently, with cutaneous
involvement or serially. Oral mucosa is frequently involved.
It is a probable pre-cancerous condition. Lichen planus is a
common inflammatory disease of the skin presenting with
characteristic violaceous, polygonal, pruritic papules. The
disease may also affect the mucosa, hair and nails.
It is relatively common dermatological disorder
occurring on skin and oral mucous membrane and refers
to lace-like pattern produced by symbolic algae and fungal
colonies on the surface of rocks in nature (lichens).
Prevalence of lichen planus in general population is
about 0.9% to 1.2% and prevalence of oral lichen planus is
reported between 0.1% and 2.2%.
Etiology
Cell mediated immune responseit is a cell mediated
immune response associated with lymphocyteepidermal interactions, resulting in degeneration of
basal cell layer. This occurs due to alternation of
B
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Types
Reticular
Papular
Plaque
Atrophic
Classical
Erythematous
Ulcerative
Hypertrophic
Erosive
Bullous
Hypertrophied
Annular
Actinic
Follicular
Linear
Clinical Features
Age and sexit occurs in adulthood with age range for
males as 35-44 years and for females 45-54 years. It has
more predilections for females.
Siteit may involve skin, oral and other mucous
membranes. About 50% of the patients with skin lesions
have oral lesions whereas 25% of all lichen planus have
only oral lesions. Other mucosal surfaces including
larynx, glans penis, esophagus, stomach, nasal and
vulva may get involved.
Symptomsthe chief complaint is usually of intense
pruritus. The itching associated with LP usually
provokes rubbing of the lesions, rather than scratching.
Signsthe lesions have a characteristic violet hue. They
are flat-topped, shiny, polygonal papules and plaques.
The surface is dry with thin, adherent scales (Fig. 12-25).
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Fig. 12-28A
Fig. 12-28B
Fig. 12-28C
Figs 12-28A to C: Reticular type of Lichen Planus seen
on buccal mucosa.
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Fig. 12-32: Bullous form of Lichen Planus showing
ulceration in posterior area.
Variations in morphology
Hypertrophic lichen planusthis may occur as a sole
manifestation or as a part of a more generalized subacute
disease. The lesions are elevated, warty, pigmented
plaques typically occurring on the shin or around the
ankle. These lesions tend to be persistent.
Atrophic lichen planusthe lesions are few in number.
There are depressed, pigmented lesions.
Follicular lichen planusit is also known as lichen
planopilaris, this may accompany typical lesions or may
be the sole morphologic type. There are small lesions
centered on hair follicles. Lesions on scalp may result in
alopecia. The combination of follicular LP with scarring
alopecia of scalp and non-scarring alopecia of axilla
and pubis or other areas is known as Graham-Little
syndrome.
Actinic lichen planusdescribed mainly from the Middle
East and India, these lesions are common on the face
and present as hyperpigmented patches with a
surrounding zone of hypopigmentation.
Bullous lichen planusvesicles and bullae may occur on
typical lesions of LP in this variant, due to severe basal
cell degeneration induced by the inflammatory process.
Ulcerative lichen planuschronic ulcers occur on the feet.
It may accompany oral ulcer and loss of nails.
Lichen planus pigmentosusdescribed mainly from India
and Middle East, these lesions present with deeply
pigmented macules on the face and extremities.
Variations in shape:
Linear lichen planusthis may follow marks of injury by
koebnerization, or may occur spontaneously in long
linear arrays or rarely in a dermatome in a zoster-like
fashion.
Annular lichen planusthese lesions have central
depressed areas with raised margins. Typically occurs
on penis.
Guttate lichen planuslarge number of drop-shaped
lesions.
Variation by site
Oraloral lesions frequently occur in lichen planus.
Genitalannular plaques often occur on glans penis,
vulval or vaginal lesions, often presenting with chronic
ulcers, may rarely occur.
Nailsnail dystrophies may occur in lichen planus. The
various changes that may occur are: thinning of nail
plate, longitudinal ridging, onycholysis, subungual
hyperkeratosis and pterygium formation (fusion of
proximal nail fold with the nail plate).
Palms and soleslichen planus of these locations lack
the typical color; they are yellowish rather that
violaceous papules and plaques.
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Diagnosis
Clinical diagnosisthe interlacing white striae appearing
bilaterally. Presence of Wickham striae and Koebner
phenomenon is also diagnostic.
Laboratory diagnosisthere is hyperorthokeratosis,
hyperparakeratosis, acanthosis with intercellular edema
of spinous cells. Biopsy also shows civatte bodies in
spinous and basal cell layers and lamina propria. Saw
tooth appearance of the rete pegs is seen.
Immunofluorescent studypositive for direct immunofluorescence reaction with IgA, IgM, IgG antisera. Most
constant feature is presence of sub-epithelial deposits of
fibrinogen and antigenically related substance, which
can be stain by anti-fibrinogen antisera.
Differential Diagnosis
Leukoplakiamen are more commonly affected as
compared to lichen planus. Also in lichen planus,
Wickhams striae are present.
Candidiasispseudomembrane can be rubbed off in case
of candidiasis.
Pemphiguscharacteristic clinical white striation of
lichen planus are usually evident in cases. Diagnosis of
pemphigus can be made by microscopic finding of
acantholysis.
Lupus erythematosusNot in fine reticular pattern, but
have much broader dimension. Flaky and feathery
appearance of lupus lesion.
Management
Removal of causethe causative factor is removed and
this may lead to resolution of lesion subsequently. This
can be particularly applicable to lichenoid drug
eruption.
Steroidsin most patients with erosive and ulcerative
lesion steroids are commonly used. The rationale behind
their use is their ability to modulate inflammation and
immune response. Topical and intralesional routes are
used when systemic steroids are contraindicated. These
routes are useful when the patient refuses needle
injection or when treating painful gingival sites, where
injection delivery is impossible. The topical, injectable
and systemic routes are used when there is no systemic
contraindication and a full steroid dose is required.
Steroid spraysmall and moderately sized painful
lesions can be treated with beclomethasone dipropionate
spray, triamcinolone acetonide in gel or cream base.
Steroid coating in soft custom trayin case of some
painful gingival lesions topical steroids may be
applied using soft custom trays by coating steroids
on the undersurface of the tray. This tray anchors to
the dental arch while covering the painful gingival
lesion.
Topical delivery regimenthis earlier regime called
topical delivery QID, for 3 or more weeks, once a week
intralesional injection, for 3 weeks (usually -0.5 ml
1.5 ml) and systemic steroid (prednisolone 5 mg tab)
in tapering doses of 30 mg/day for the first of 3 weeks,
15 mg/ day for second week and 5 mg/day for third
and final week. Intralesional injections which are
used are methylprednisolone 40 mg/ml and
triamcinolone acetonide 10 mg/ml.
Topical applicationtopical application of fluocinolone
acetonide for 4 weeks is also effective in curing the
disease (Fig. 12-34).
Combination of prednisolone and levamisoleanother
regime consisting of prednisolone and levamisole has
also been tried successfully recently. This systemic
regime calls for prednisolone 5 mg and levamisole
50 mg tablets for first three days of rest and this
schedule to be followed for two to three more weeks.
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Fig. 12-34: Post-treatment photograph of Lichen
Planus (Courtesy Dr Tapasya Karamore).
Group
Treatment
No treatment is required
Regular follow-up
Diazepam for anxiety
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Immediate biopsy
Local control of pain
Intralesional steroid
If infected, antibiotic
Etiology
Drug therapy like NSAIDs, hydrochlorothiazide,
penicillamine, angiotensin converting enzyme
inhibitors.
Chronic hepatitisunderlying medical disorders like
chronic hepatitis.
Dental restorationreaction to dental restorations.
Graft versus host diseasegraft versus host disease due to
bone marrow transplantation.
Stressemotional stress can lead to erosive lichen
planus.
3
Fig. 12-36: Irregular shaped ulcerated lesion with lacy white pattern
at the periphery is seen in erosive Lichen Planus.
Clinical Features
Age and sexfemale to male ratio is 2:1. Average age is
50 years. It is primarily a disease of whites, but may be
seen in blacks.
Sitescommon site is buccal mucosa and lingual mucosa.
Symptomspatient complains of burning sensation and
pain.
Appearanceafter rupture of vesicles, eroded or frankly
ulcerated lesion are seen which appears as a raw painful
areas (Fig. 12-35). Lacy white pattern may be present.
Size and shapeeroded and frankly ulcerated lesions are
irregular in size and shape and appear as raw and
painful areas (Fig. 12-36).
Surfacethe surface is generally granular and brightly
erythematous and may bleed upon slight provocation
or manipulation.
Signsa fibrinous plaque or pseudomembrane may be
seen over erosion, while later is significant.
Malignant potentialmalignant potential is 1 to 25%.
Diagnosis
Clinical diagnosisulcerative lesion with white lacy
pattern is diagnostic indicator of erosive lichen planus.
Laboratory diagnosisIn the erosive form, the epithelium
is completely missing or only remnants of epithelial
tissues are seen. It shows classical feature of lichen
planus, i.e. hydropic degeneration of basal cell layer with
juxtaepithelial inflammatory cell infiltrate.
Differential Diagnosis
Speckled leukoplakiasurface is speckled, as compared
to erosive lichen planus where it is granular.
Squamous cell carcinomaborders of the lesion are ill
defined and surface is irregular.
Lichenoid drug reactionhistory of drug administration.
Electrogalvanic mucosal lesiondissimilar restorations
present in the oral cavity.
PsoriasisAuspitzs sign is positive.
Atrophic candidiasis with keratotic borderscan be confused
with an erosive lichen planus especially when the
candidial focus is circumscribed by a keratotic border;
proof of cause is searched for typical lichen planus.
Cicatricial pemphigoideye lesions are present in cases
of cicatricial pemphigoid.
Erythema multiformeonset less acute, whitish lichen
design on the borders of erosion and skin changes occur
in case of lichen planus.
Desquamative gingivitisthe gingival surface is smooth
and shiny and there is patchy distribution of red and
gray areas.
Bullous skin lesionlichen planus lesion yields a negative
blister induction test.
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Management
It is same which is given for other type of lichen planus.
Diagnosis
Clinical diagnosislichen planus type of lesion with
history of allogenic bone marrow transplantation will
diagnose this condition.
Laboratory diagnosisthere is abnormal deposition of
collagen. Other features are similar to lichen planus.
Clinical Features
Acute GVHDit is seen after one or two weeks of
allogenic bone marrow transplantation. The skin lesion
ranges from mild rash to diffuse severe sloughing. It is
also associated with diarrhea, nausea, vomiting,
abdominal pain, liver dysfunction.
Chronic GVHDit may develop after 3 months of
duration. Skin lesion resembles as lichen planus.
Some patients may notice features similar to lupus
erythematous, Sjgren syndrome.
Oral Manifestation
Sitetongue, labial mucosa, and buccal mucosa are most
commonly involved site.
Symptomsburning sensation and mucosal discomfort
is present. Patient also complains of xerostomia.
Lichen planus like lesionoral lesion of graft versus host
resistance resembles lichen planus (Fig. 12-37).
Fig. 12-37: Lichen Planus type lesion seen in patient with allogenic
bone marrow transplantation.
Management
Topical steroidstopical steroids will facilitate healing
of oral ulceration.
Topical anesthetics gelit is also used to control burning
sensation of oral cavity.
Thalidomidethis is useful drug in cases of chronic
GVHD which are resistant to standard therapy.
Preventionprophylactic therapy with immunomodulator and immunosuppressive drugs such as
cyclosporine and prednisone should be given to prevent
GVHD. Doses the above drugs should be increased if
GVHD occurs.
Lichenoid Reaction
The unifying feature of lichenoid reaction and lichen
planus is the similar clinical and light microscopic
appearance of the skin and mucous membrane lesions.
Lichenoid reactions were differentiated from lichen planus
on the basis of association of lichenoid reaction with
administration of a drug or a systemic disease and their
resolution, when the drug was discontinued.
Etiopathogenesis
Disorderslichen planus, lupus erythematous, erythema
multiforme, fixed drug eruptions, secondary syphilis
and graft-versus-host reaction.
Drugs and chemicalthe tissues of a person with
diathesis react in a special way to certain extrinsic
stimuli, making it more susceptible to certain diseases.
Drugs act to increase temporarily the specific antigenic
stimulus and hence increase the reaction. If the drug is
withdrawn at a later time, the antigenic stimulus is
reduced, followed by reduction in clinical severity. It is
suggested that drugs that are known to induce lichenoid
response, act as agents who amplify the disorder, rather
than induce it. To implicate a drug responsible for a
lichenoid reaction can be difficult as there is no specific
test for it. Association between dental filling material
and lichen planus has also been suggested. Following
drugs can cause lichenoid reaction.
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Clinical Features
Lichenoid mucositisthis is a term used for lesion of
mucosa similar to lichen planus due to drugs.
Lichenoid dermatitiswhen lesion presents on the skin it
is called as lichenoid dermatitis (Figs 12-38A and B).
Lichenoid foreign body gingivitisthis occurs due to foreign
material embedded in gingiva causing host response.
Diagnosis
Clinical diagnosislichen planus type lesion with drug
history will diagnose lichenoid reaction
Laboratory diagnosislichenoid drug reaction may show
deep as well as superficial dermal lymphocyte infiltrates
rather than the classical band-like infiltrate of the lichen
planus.
Management
Majority of it are resolved after discontinuation of drug.
Definition
An insidious, chronic disease affecting any part of the
oral cavity and sometimes pharynx. Although
occasionally preceded by and/or associated with vesicle
formation, it is always associated with juxtaepithelial
inflammatory reaction followed by fibroelastic changes
of lamina propria, with epithelial atrophy leading to
stiffness of oral mucosa and causing trismus and
inability to eat.
Epidemiology
Etiopathogenesis
B
Figs 12-38A and B: Lichenoid dermatitis seen on hand of the
patient (Courtesy Dr Pincha).
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Clinical Features
Age and sex distributionit affects both sexes. The age
group varies, although majority of patients are between
20 and 40 years of age.
Site distributionthe most frequent location of oral
submucus fibrosis is the buccal mucosa and the retromolar areas. It also commonly involves soft palate,
palatal fauces, uvula, tongue and labial mucosa. Sometimes, it involves the floor of mouth and gingiva.
Prodromal symptomsthe onset of the condition is
insidious and is often of 2 to 5 years of duration. The
most common initial symptom is burning sensation of
oral mucosa, aggravated by spicy food, followed by either
hypersalivation or dryness of mouth. Vesiculation,
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Fig. 12-45: Hockey stick appearance of uvula seen in oral
submucus fibrosis (OSMF) (Courtesy Dr Parate).
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Table 12-2: Clinically grading of oral submucus fibrosis according to its severity
Features
Grade I incipient
(Very early stage)
Grade II
(Mild)
Grade III
(Moderate)
Grade IV (a)
(Advanced stage)
Grade V (b)
(Advanced
pre-malignant and
malignant change)
Symptoms
Burning sensation,
dryness of mouth,
vesicle or ulceration
Burning sensation,
dryness of mouth
Burning sensation,
dryness of mouth
Burning sensation,
dryness of mouth
Spicy food
Irritation with
spicy food
Irritation with
spicy food
Irritation with
spicy food
Irritation with
spicy food
Mucosal color
No changes in
mucosal color
Mucosa is blanched
and loses its elasticity
Blanched opaque
leather-like mucosa
Blanched opaque
leather-like mucosa
Fibrosis
No fibrosis, bands
palpable
No clear-cut
fibrotic bands
Vertical fibrotic
bands on buccal
mucosa making it stiff
Mouth opening
Mouth opening
normal (44 mm)
Slight restriction
of mouth opening
(26-35 mm)
Considerable
restriction of
mouth opening
(15-25 mm)
Tongue
Tongue protrusion
normal
Tongue protrusion
normal
Tongue protrusion
not much affected
Restricted tongue
protrusion
Difficulty in eating
and speaking
Oral hygiene
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Diagnosis
Clinical diagnosisclinically reduced mouth opening
with palpable fibrous band is enough to make diagnosis.
Laboratory diagnosisoral epithelium is markedly
atrophic which exhibits intercellular edema, signet cells,
and epithelial atypia. The inflammatory cells are mostly
mononuclear; eosinophils and occasional plasma cell
may be seen.
Malignant Potential
Atrophic epithelium first becomes hyperkeratotic and later,
intracellular edema and basal cell hyperplasia develop
eventually, following epithelial atypia with moderate
epithelial hyperplasia and then, carcinoma can develop at
any time (Fig. 12-48).
The WHO Collaborating Centre for Oral Precancerous
Lesions has concluded that although oral submucus
fibrosis predisposes to cancer, it is not absolutely
conclusive. It is highly probable that such relationship does
exist. Following facts support this hypothesis:
The frequency of oral leukoplakia in oral submucus
fibrosis patient is 6-8 times higher than in control group.
Carcinoma patients exhibiting oral submucus fibrosis
have a frequency which exceed the 1.2% of submucus
fibrosis in general population.
Immunological alternations observed in oral submucus
fibrosis are almost similar to that observed in oral
cancer.
Management
Restriction of habit/behavioral therapy
The preventive measure should be in the form of stoppage
of habit, which can be encouraged through public
education. Affected patients should be explained about the
disease and its possible malignant potential. Improvement
in clinical features like gradual increase in inter-incisal
opening has been observed in most of the patients who
discontinue the habit.
Medicinal therapy
Supportive treatment
Vitamin rich dieta vitamin rich diet along with iron
preparation is helpful to some extent but has little
therapeutic value in relieving trismus.
Iodine B complex preparationiodine-B-complex
preparation (Injection Ranodine) is a combination of
iodine preparation with synthetic vitamin B complex.
The combination of iodine compound with vitamin B
complex is responsible for the stimulation of metabolic
process and enzymatic process within the body (oxygen
reduction, transamination). Intramuscular injection
starts with small doses and continuing with larger doses
(2 ml ampule daily). The course of 5 injections is repeated
after 7 days. Each 2 ml consists of:
Methyltrioxyethyl iodomineprogressive increasing
doses equivalent to 0, 25, 50, 75 and 125 mg of active
iodine
Vitamin B11.0 mg
Vitamin B6- 0.3 mg
Vitamin B20.6 mg
Nicotinamide15.0 mg
Calcium pantothenate1.0 mg
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Oral Physiotherapy
Oral exercises are advised in early and moderately
advanced cases. This includes mouth opening and
ballooning of mouth. This is thought to put pressure on
fibrous bands. Forceful mouth opening have been tried with
mouth gag and acrylic surgical screw.
Diathermy
Microwave diathermy is useful in some early or moderately
advanced stages. Low current is used (20 watts 2450
cycles). It acts by physiofibrinolysis of bands. Its value is
increased if it is combined with other treatment modalities.
Dyskeratosis Congenita
It is also called as Zinssner-Engman-Cole syndrome. It is a
well recognized but rare genokeratosis, which is probably
inherited as a recessive characteristic. Mutation in DKC 1
gene will cause disruption in maintenance of telomerase
which is critical in determining the normal cellular
longevity. Disease manifested has three typical signs: oral
leukoplakia, dystrophy of nails and pigmentation of skin.
Clinical Features
Age and sex distributionit is evident during first 10 years
of life. It is almost exclusively seen in males.
Nail changesnail changes are the first manifestation,
becoming dystrophic and shedding some time after the
age of 5 years (Fig. 12-49).
Pigmentationgrayish brown pigmentations appear in
some time which is seen usually on trunk, neck and
thigh.
Skinthe skin may become atrophic, telangiectatic and
face appears red.
Laser
Mechanismthe use of laser for treatment of submucus
fibrosis is useful. CO2 laser surgery offers advantage in
alleviating the functional restriction, when compared to
traditional surgical technique and subsequent grafting.
Techniqueunder general anesthesia a CO2 laser is used
to incise the buccal mucosa and vaporize the submucosal connective tissue to the level of the buccinator
muscle. Hemostasis is provided by lased surface itself
and the mouth opening increases immediately.
Cryosurgery
Mechanismit is the method of local destruction of tissue
by freezing it in situ. Open liquid sprays are better suited
for mucosal lesion that are extensive and superficial and
do not involve the basement membrane.
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Oral Manifestations
Sitesmost common sites are tongue and buccal mucosa.
Appearanceit appears as diffusely distributed vesicles
and ulcerations, followed by accumulation of white
patches of necrotic epithelium and sometimes,
superimposed monolial infection. There is also atrophy
of tongue (Fig. 12-50).
Recurrent ulcerationafter some time, in the age group of
14 to 20 years, there are repeated recurrent ulceration
and development of erythroplasia or red mucosal lesion.
Erosive leukoplakiafinally between the age of 20 and 30
years, there is development of erosive leukoplakia and
carcinoma.
Lupus Erythematosus
It is characterized by presence of abnormal antibodies and
immune complex.
Types
Discoid or cutaneous lupus erythematosusif it is confined
to skin and mucosa.
Systemic lupus erythematosusif multiorgan involvement
occurs.
Etiology
Genetic predispositionrelative of patients have higher
incidences of auto-antibodies, immune deficiency and
connective tissue disease. This tendency is greatest
among identical twins.
Immunological abnormality possibly mediated by viral
infectionimmune complex consisting chiefly of nucleic
acid and antibody account for majority of the tissue
changes.
Autoimmune diseaseas these patients develop
antibodies to many of their own cells.
Endocrinethere is high incidence in females in pregnancy. This finding suggestive of increased estrogen level.
Biochemical increase in excretion of metabolic products,
particularly tyrosine and phenylalanine, in certain SLE
patient.
Management
Oral Manifestations
Radiographic Feature
There may be severe periodontal bone loss.
Diagnosis
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Oral Manifestation
Sitethe most common sites are buccal mucosa, lip and
palate.
Symptomscomplain of burning sensation, xerostomia
or soreness of mouth.
Signslesions similar to DLE, except that hyperemia,
edema and extension of lesion is more pronounced.
Diagnosis
Clinical diagnosisskin lesion with lesion present on
oral mucosa which is atrophic and erythematous will
suspect lupus erythematous. Oral and nasopharyngeal
ulceration is major diagnostic criteria for SLE.
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Dental Consideration
Thrombocytopeniait may be sometimes severe. The
result of a recent platelet count should be studied before
undertaking oral surgery.
Bacterial endocarditisLibman-Sacks vegetation under
the mitral valve may occur in patients with SLE, it can
lead to bacterial endocarditis. So patients with SLE
should have antibiotic prophylaxis before dental
treatment that is likely to cause bacteremia.
Exacerbation by drug therapydrugs that have been
related to exacerbation include penicillin, sulfonamide
and NSAIDs with photosensitizing potential.
Exacerbation by surgeryall elective surgeries including
dental procedure to be avoided.
Susceptibility to shock and infectionpatients with SLE
may be taking adrenal suppressive dose of
corticosteroids or cytotoxic drugs and hence, they may
be susceptible to shock and infection.
Differential Diagnosis
Lichen planushomogenous picture, no dark erythema
and no telangiectasia. Mucosal changes are usually
extensive and symmetrical.
Lichenoid reactionhistory of drug is always there.
Ectopic geographic tonguesystemic manifestation
present is lupus erythematous, which is absent in ectopic
geographic tongue.
PsoriasisAuspitzs sign is positive.
Electrogalvanic lesiondissimilar restorations are seen
in oral cavity.
Leukoplakia and erythroplakialesions tend to maintain
same appearance and there are no skin changes.
Geographic stomatitisno skin changes, mucosal lesions
change location rapidly.
Benign mucous membrane pemphigoidno systemic
complain and serology test to be done.
Management
Corticosteroidsystemic lupus erythematous should be
treated by systemic corticosteroids therapy and should
be managed by physician. Discoid lupus erythematous
should be treated with topical steroid.
Anti-malarial drugsanti-malarial drug like hydroxychloroquine combined with nonsteroidal anti-inflammatory agents is also effective treatment modality.
Suggested Reading
1. Albert BE, et al. Fluocinonide in an adhesive for treatment of
OLP. Oral Surg, Oral Med, Oral Pathol 1993;75:181-5.
2. Amagasa T, Yokoo E, et al. A study of the clinical characteristic
and treatment of oral carcinoma in situ. Oral Surg, Oral Med,
Oral Path 1985;60:50-5.
3. Andresen JO. Oral lichen planus: A clinical evaluation of 115
cases. Oral Surg, Oral Med, Oral Path 1968;25(1):31-42.
4. Axell T, Holmstrup P, et al. International seminar on leukoplakia
and associated lesions related to tobacco habits-Lund Uni, Malmo,
Sweden June 27-30.Commu. Dent and Oral Epi 1984;12:145-54.
5. Axell T, Mornsad H, Sundstrom B. The relation of the clinical
picture to the histopathology of snuff dipper lesion in a Swedish
population. J Oral Pathol 1976;5:229-36.
6. Axell T, Pindborg JJ, et al. Oral white lesion with special reference
to precancerous and tobacco related lesion: conclusion of
International symposium help in Uppsala, Sweden, May 18-21
1994. international collaborative group of white oral lesion.
J Oral Pathol ME 1996;25:49-54.
7. Banoczy J. Follows up studies in oral leukoplakia. J Maxillofac
Surg 1977;5:69-75.
8. Banoczy J. Text Book of Oral Leukoplakia, 1982.
9. Besly W. Laser in treatment of OSMF. Br J of Oral Surg 1996;
34:225-69.
10. Boisnic S, Frances C, Marie-Christine Branchet. Immunohistochemical study of oral lesions of lichen planus: Diagnostic
and Pathophysiology aspects. Oral Surg, Oral Med, Oral path
1990;70: 462-5.
11. Borghelli RF, Pettinari IL, et al. Oral lichen planus in patients
with diabetes: an epidemiologic study. Oral Surg, Oral Med,
Oral Pathol 1993;75:498-500.
12. Borle RM, Borle SR. Management of oral submucous fibrosis: A
conservative approach. J Oral Maxillofac Surg 1991;49:788-91.
13. Caniff JP. OSMF: Its Pathogenesis and Management. Br Dent J
1986; 160(12):429-34.
14. Chaiyarit P, Kafrawy AH, Miles DA. Oral lichen planus: An
Immunohistochemical study of heat shock proteins and
cytokeratins and a unifying hypothesis of Pathogenesis. J Oral
Path Med 1999;28:210-5.
15. Chaturvedi VN. Salivary coagulopathy and humoral response in
OSMF. JIDA 1991;62(3):51-3.
16. Coleman GC, Nelson JF. Principles of Oral Diagnosis, 1993.
17. Cox SC, Walker DM. Oral submucus fibrosis: A review. Aust
Dent J 1996;41:294-9.
18. De Rossi SS, Glick M. Lupus erythematous: consideration for
dentistry. JADA 1998;129:330-9.
19. Dudani IC. Oral submucous Fibrosis. J Indian Med Asso 1971;
57:347-8.
20. Eisenberg E. Oral lichen planus: a benign lesion. J Oral Maxillofac
Surg 2000;58:1278-85.
21. Eversole LR, Eversole Gm, Kopcik J. Sanguinaria associated oral
leukoplakia: comparison with other benign and dysplastic
leukoplakic lesion. Oral Surg, Oral Med, Oral Pathol, Oral Radiol
Endod 2000;89:455-64.
22. Eversole LR, Mont Ringer. The role of dental restorative metals in
the Pathogenesis of oral lichen planus. Oral Surg, Oral Med, Oral
Patho 1984;57:383-7.
23. Eversole LR. Clinical outline of oral pathology, diagnosis and
Treatment (3rd edn), 1992.
24. Fettig A, Pogrel MA, et al. Proliferative verrucous leukoplakia of
the gingiva. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod
2000;90:723-30.
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90. Van der Wall I, Shepman KP, et al. Oral leukoplakia a clinicopathologic review. Oral Oncol 1998;33:291-301.
91. Voute ABE, Schulten EAJM, et al. Fluocinonide in an adhesive
base for treatment of oral lichen planus: a double blind placebo
controlled study. Oral Surg, Oral Med, Oral Pathol 1993;75:
181-5.
92. Walsh LJ, Savage NW, et al. Immunopathogenesis of oral lichen
planus. J of Oral Path Med 1990;19:389-96.
93. Walsh PM, Epstein JB. The oral effect of smokeless tobacco.
J Can Dent Assoc 2000;66:22-5.
94. Waun Ki Hong. 13-cis-retionic acid in the treatment of oral
leukoplakia. The New England J of Med 1986; 315(24):1501-05.
95. Zegarelli DJ. The Treatment of oral lichen planus. Annals of
Dentistry 1993;52(2):3-8.
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13
Cysts of Jaw
Introduction
Cyst has been known to arise in man (ever since he has
teeth) and in certain animals. It takes some odontogenic
epithelium plus some unknown initiating factor which
stimulates it to proliferate to cause this destructive lesion,
which can be found from the mildest form to a greatly
disfiguring form.
Cysts of jaws are of great clinical importance, not only
because they often attain a large size but also produce facial
asymmetry, disturbance of dentition, neurological symptoms and predispose the jaws to fracture but particularly
because they have a very high frequency of occurrence.
Definitions
By Killey and Key 1966this entity constituted an
epithelium-lined sac filled with fluid or semifluid
material.
By some unknown author 1966a cyst is an abnormal
cavity in hard and soft tissue which contains fluid,
semifluid, or gas and is often encapsulated and lined by
epithelium.
By Kramer in 1974pathologic cavity having fluid,
semifluid, or gaseous content but not always is lined by
epithelium.
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Symptoms
Pain and swellingoften the first symptom that patient
experience is pain and swelling, if the cyst becomes
infected. Sometimes the patient notices lump in the
sulcus.
Anesthesia or paresthesiaalthough large mandibular
cysts invariably involve the neurovascular bundle and
deflect structure into an abnormal position, still it is
unusual to find anesthesia of the mental distribution.
Since an uninfected cyst grows slowly and exerts a very
slight pressure on the neurovascular bundle. However,
in cases of acute infection there is a sudden increase in
pressure due to pus accumulation in the sac and this
can cause neuropraxia of the nerve and the immediate
onset of labial paresthesia or anesthesia. After surgical
drainage of infected cyst, sensation returns back to
normal.
Salty tastewhen the cyst becomes secondarily infected
and discharges into the mouth and when a sinus tract is
present, then patient may complain of salty taste or a
sinus tract is present.
Displacement of dentureedentulous patients may seek
treatment because of displacement of denture.
Tooth discolorationdiscoloration or loosening of tooth
may prompt patients to visit the dentist.
Radiographic Features
View takenin the radiographic diagnosis of cysts of
jaws, periapical and occlusal views are helpful. In
addition, in case of large cysts, extraoral views provide
an essential supplement to conventional intra-oral
radiographs, which include lateral oblique, PA view for
mandible, Waters view and panoramic view (OPG).
Well defined radiolucencyclassically, radiographic
appearance of a cyst is that of a well-defined round or
oval areas of radiolucency circumscribed by a sharp
radiopaque margin. Nevertheless, there is much
variation to this standard pattern, which depends not
only on the type of cyst but also on its location and the
degree of bone destruction and expansion.
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Mural Growth
Peripheral cell division
Cell division of lining epitheliumperipheral enlargement
of cyst occurs due to active cell division of the lining
epithelium. This is in response to an irritant stimulus.
Cyst regression occurs following the removal of such
stimulus.
Cons of theorythe theory has been criticized on the basis
that such regression would lead to an irregularly
thickened inner surface because of the resistance of the
surrounding bone. However, this ignores the possibility
that the cyst wall is not only well supported by its fluid
content but can also actively resorb bone sufficiently
and rapidly to accommodate the expanding perimeter.
Accumulation of cellular content
Accumulation of mural squamesKramer has suggested
that keratocyst enlarges by the increasing accumulation
of mural squames which is the result of casting off the
living epithelium. The characteristic finger-like
projections of growth represents local areas of increased
cell division. An alternative explanation for this
elongation is that keratocyst although persistent in their
growth are poor bone resorbers and simply extend
preferentially along the less dense cancellous bone with
little resorption and expansion of dense cortex.
Fig. 13-1: Theories of cyst enlargementdiagrammatic representation
Hydrostatic Enlargement
Growth of cyst occurs due to distension of the cystic wall
by fluid that has accumulated by secretion, transudation
and dialysis.
Secretionit occurs from goblet cells. Apart from the
occasional goblet cells usually found in follicular cyst,
there is little morphological evidence of intracystic
secretion.
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Classification
It is described in Tables 13-1 to 13-4.
Table 13-1: Classification of cysts by Robinson (1945)
From odontogenic tissues
Periodontal cyst
Radicular or dental root apex type
Lateral type
Residual type
Dentigerous cyst
Primordial cyst
From non-dental tissues
Median cyst
Incisive canal cyst
Globulomaxillary cyst
Epithelial
Odontogenic
Developmental
Dentigerous cyst (follicular)
Eruption cyst
Primordial cyst
Gingival cyst of adults
Lateral periodontal cyst
Calcifying odontogenic cyst
Inflammatory cyst
Radicular cyst
Residual cyst
Inflammatory collateral cyst
Paradental cyst
Non-odontogenic
Nasopalatine duct (incisive canal) cyst
Median palatine, median alveolar and median mandibular cysts
Globulomaxillary cyst
Nasolabial cyst
Non-epithelial
Simple bone cyst (traumatic solitary hemorrhagic bone cyst)
Aneurysmal bone cyst
Cysts associated with maxillary antrum
Benign mucosal cyst of the maxillary antrum
Surgical ciliated cyst of maxilla
Cysts of the soft tissue of the mouth, face and neck
Dermoid and epidermoid
Branchial cleft cyst (lymphoepithelial)
Thyroglossal duct cyst
Anterior medial lingual cyst
Oral cyst with gastric or intestinal epithelium
Cystic hygroma
Cysts of salivary glands
Parasitic cyst, hydatid cyst, cysticercosis cellulosae
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Epithelial Developmental
Odontogenic Cyst
Dentigerous Cyst
Origin
Fluid accumulationit is formed due to fluid accumulation in the layer of reduced enamel epithelium or
between it and the crown of unerupted teeth.
Proliferation of epithelium in dental follicleit may
originate initially by proliferation and cystic
transformation of islands of epithelium in the connective
tissue wall of the dental follicle or even outside the follicle
and this transformed epithelium then unite with the
lining of follicle epithelium forming a solitary cystic
cavity around tooth crown.
Clinical Features
Age and sexas it arises from the follicle of an unerupted
tooth, it is usually found in children and adolescents
with a higher incidence in 2nd and 3rd decades. It is
slightly more common in males.
Siteit is most commonly associated with mandibular
3rd molars and maxillary canines (Fig. 13-2) which are
most commonly impacted. It may also be found enclosing
a complex compound odontome or involving a
supernumerary tooth.
Symptomsgenerally, it is painless but may be painful
if it gets infected. When dentigerous cyst expands rapidly
to compress sensory nerve, it produces pain which may
be referred to other sites and described as headache.
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Fig. 13-4: Expansion in patient of dentigerous cyst
(Courtesy Dr Bhaskar Patle).
Radiographic Features
Radiodensitywell defined radiolucency usually
associated with hyperostotic borders unless they are
secondarily infected and are usually seen around an
unerupted tooth (Fig. 13-5).
Internal structureusually, it is unilocular but sometimes
it may appear multilocular, this image is caused by ridges
in the bony wall and not by the presence of bony septa.
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Fig. 13-8: CT scan of dentigerous cyst showing cyst
associated with tooth.
Radiographic Types
According to Thoma
Central varietyin it, crown is enveloped symmetrically.
In this instance, pressure is applied to the crown of the
tooth and may push it away from its direction of
eruption. In this way, the mandibular third molar may
be found at the lower border of the mandible and in the
ascending ramus and a maxillary canine in the sinus or
as far as the floor of the orbit (Fig. 13-10). The maxillary
incisors may be found below the floor of the nose.
Lateral typein it, dentigerous cyst is a radiographic
appearance which results from dilation of the follicle on
one aspect of the crown. This type is commonly seen
when an impacted mandibular molar is partially
erupted so that its superior aspect is exposed.
Circumferential typein it, the entire tooth appears to be
enveloped by the cyst (Fig. 13-11). The entire enamel
organ around the neck of the tooth becomes cystic often
allowing the tooth to erupt through the cyst.
According to Mourshed
Class Identigerous cyst associated with completely
unerupted teeth
Dentigerous cyst associated with unerupted teeth,
who failure to erupt is due to lack of space in the
dental arch.
Dentigerous cyst associated with unerupted teeth,
who failure to erupt is due to mal-positioning of the
tooth germ.
Dentigerous cyst associated with unerupted
supernumerary teeth.
Class IIdentigerous cyst associated with partially
erupted teeth.
Diagnosis
Clinical diagnosisexpansive swelling in the posterior
region of mandible will give clue to the diagnosis.
Radiological diagnosiswell defined radiolucency
associated with impacted teeth with hyperostotic border
and well defined margin will diagnose the dentigerous
cyst.
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Differential Diagnosis
Ameloblastoma and ameloblastic fibromathey are
multilocular and not associated with crown of an
unerupted tooth. They will grow laterally away from
the tooth in comparison to dentigerous cyst, which
envelopes the tooth symmetrically and it is more
common in premolar and molar area. There is internal
structure present in ameloblastoma and in case of
dentigerous cyst, it is most unlikely.
Adenomatoid odontogenic tumorthey are rare and occur
in the maxillary anterior region.
Calcifying odontogenic cystit may occur as pericoronal
radiolucency and may contain evidences of calcification.
Developmental primordial and follicular primordial cyst
it can also be considered in the differential diagnosis. It
occurs in close proximity to the crown of unerupted teeth
and superimposition of its image causing cyst like
radiolucency can appear as dentigerous cyst on the
radiograph. However, in cases of follicular primordial
cyst, the cystic lining surrounds the crown, whereas in
dentigerous cyst, it is attached to the neck of tooth. The
diagnosis of primordial cyst can be confirmed by taking
a radiograph with different angulations.
Hyperplastic folliclethe size of the normal follicle is 2 to
3 mm. If the follicular space exceeds 5 mm a dentigerous
cyst is more likely the diagnosis. Region should be
reexamined after 6 months to see any increase in size
and effect on surrounding teeth.
Odontogenic keratocystit does not expand the bone as
severely as dentigerous cyst and also is less likely resorbs
the tooth. It is usually attached more apically than the
dentigerous cyst.
Management
Surgicalsmaller lesions can be surgically removed
with little difficulty. The larger cyst involves surgical
drainage and marsupialization. This procedure results
in relief of pressure and gradual shrinking of the cystic
lesion by peripheral opposition of new bone.
Decompressionsmall acrylic button or short section of
rubber is placed in preformed surgical opening in cyst
which keeps the opening open and permits drainage.
Recurrence is relatively uncommon unless there has been
fragmentation of the cystic lining with remnants allowed
to remain.
Orthodontic treatmentin cases when you want to retain
the tooth, orthodontic movement of teeth should be
carried out.
Eruption Cyst
A specific type of cyst, which must be classified as a form of
dentigerous cyst, is frequently associated with the erupting
deciduous or permanent teeth in children.
An eruption cyst is in fact a dentigerous cyst occurring
when a tooth is impeded in its eruption within the soft
tissues overlying the bone, whereas the dentigerous cyst
develops around the crown of an unerupted tooth which is
lying in the bone. This cyst has often been termed as
eruption hematoma.
Pathogenesis
Dilation of tooth follicleit is essentially a dilation of the
normal tooth follicle caused by accumulation of tissue
fluid or blood. In 11% of cases, it occurs during the
eruption of incisors and in 30% of cases, it occurs during
eruption of canines and molars.
Clinical Features
Appearanceclinically the lesion appears as a
circumscribed, fluctuant, often translucent swelling of
the alveolar ridge over the site of eruption of the tooth.
Ageit is most commonly seen in children younger than
10 years of age.
Siteit is most commonly seen first permanent molar
and maxillary incisors.
Eruption hematomawhen the circumscribed cystic
cavity contains blood, the swelling appears purple or
deep blue, hence it is termed as eruption hematoma.
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Radiological Features
Expansion of follicular spaceexpansion of the normal
follicular space of erupting tooth crown is seen.
Saucer shape excavationin some cases, there is saucer
shaped excavation of bone projecting (Fig. 13-13) very
slightly into the cavity.
Marginmargin is well defined.
Origin of Cyst
Fig. 13-13: Saucer shaped excavation of bone seen in
eruption cyst (Courtesy Dr Ashok L).
Diagnosis
Clinical diagnosiscircumscribed soft fluctuant
translucent swelling around first permanent molar or
maxillary incisor may give clue to the diagnosis.
Radiological diagnosissaucer shaped excavation of bone
with well defined margin.
Laboratory diagnosislamina propria shows variable
inflammatory cell infiltrated.
Management
Excision of roof of cystthis is simple procedure to permit
tooth to erupt. In some cases, cyst rupture spontaneously
to facilitate tooth eruption.
Odontogenic Keratocyst
The keratocyst was probably first described by Mikulicz in
1876. According to Pindborg and Hansen, the designation
keratocyst was used to described any jaw cyst exhibiting
keratinization in their lining which may occur in follicular,
residual and very rarely in a radicular cyst.
11% of all jaw cysts are OKC. OKC is not a clinical
diagnosis but a designation for a group of cysts of possibly
diverse origins which have a number of highly characteristic microscopic and clinical features in common with
highest recurrence rate of any of the odontogenic cyst.
Clinical Features
Ageodontogenic keratocyst occurs over a wide age
range and cases have been recorded as early as the first
decade and as late as the ninth with age group 4 to 84
years. Initiated early in life, during the period of tooth
development with a peak incidence in 2nd and 3rd
decades.
Sexit is found more frequently in males than in females
and this sex predilection is more pronounced in blacks
than in whites.
Siteit is more common in mandible with a greater
incidence at the angle and extending for varying
distance into the ascending ramus and forward into the
body (Fig. 13-14).
Symptomsasymptomatic unless they become
secondarily infected, in which case patient complains
of pain, soft tissue swelling and drainage. Occasionally,
they experience paresthesia of the lower lip or teeth.
Paresthesia can also occur, if there is a pathological
fracture.
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Fig. 13-18: Radiolucency extending in anteroposterior
direction in OKC (Courtesy Dr Ariji).
Fig. 13-20: CT scan of OKC showing dimension of
radiolucency ( Courtesy Dr Iswar).
Diagnosis
Fig. 13-19: Extensive involvement of ramus and body of
mandible in OKC.
Differential Diagnosis
It can be given in two ways:
Most likely
AmeloblastomaThis usually occurs in older age. It is
generally multilocular though a unilocular lesion may
also occur. Mostly, it appears with paresthesia. As it is
benign, it may show resorption of root with displacement.
In cases of cyst, it shows amber colored fluid on aspiration.
Primordial cystit is also common in third molar area.
Absence of a tooth without a history of extraction favors
primordial cyst. It also shows amber colored fluid on
aspiration.
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Management
Enucleationenucleation of entire cyst with vigorous
curettage of the cystic wall. Periodic post-treatment
examination should be done.
Peripheral osteotomyperipheral osteotomy of bony
cavity can be done to reduce chances of recurrence.
Chemical cauterizationchemical cauterization of bony
cavity with intraluminal injection of Carnoys solution
allow freeing the cyst from bony wall which in turn allow
easier removal of cyst.
Decompressionthis is achieved with the help of
polyethylene drainage tube kept in the bony cavity.
Recurrence
Rate of recurrence of odontogenic keratocyst is very high.
There are number of reasons for it.
Satellite cystoccurrence of satellite cyst, which is a budlike projection of basal cell layer into the connective
tissue. Cystic lining may be retained during the
enucleation procedure.
New cyst formationsome instances of recurrence are
likely because of new cyst formation rather than true
recurrence.
Clinical Features
Locationit is seen in anterior region of the maxilla.
Age and sex distributionit is common in young age group
with predilection for women.
Symptomsit is usually asymptomatic. In some cases,
expansion of jaw occur which is also associated with
pain.
Sizesome of the lesion may enlarge up to size of 10 cm.
Signsexpansion can be palpated and facial
asymmetry can be present due to swelling.
Radiological Features
Appearanceit appears as well demarcated unilocular
radiolucency associated with impacted tooth (Fig. 13-21).
Calcificationcalcification can be seen. In some cases,
this calcification will appear as small pebbles
appearance.
Effect on surrounding structureseparation of roots or
displacement of an adjacent tooth occurs frequently.
There is also cortical expansion and root resorption. The
lesion may inhibit the eruption of involved tooth.
Differential Diagnosis
Dentigerous cystit is seen in 2nd to 4th decade as
compared to adenomatoid odontogenic cyst which is
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Fig. 13-21: Cystic radiolucency seen in anterior maxillary region
suggestive of adenomatoid odontogenic cyst (Courtesy Dr Parate).
Management
Exploration and enucleationAOC is treated by direct
exploration and enucleation.
Marsupializationin some cases when lesion is
associated with impacted tooth, marsupialization is
done for eruption of tooth.
Types
Inflammatoryit occurs near alveolar crest. Pocket
content may irritate and stimulate rest of Malassez.
Developmentalit is associated with developing tooth
germ.
Clinical Features
Age and sex distributionthe lateral periodontal cyst
occurs chiefly in adults with an age range from 22 to 85
years with a mean age of 50 years. It shows a male
predilection for occurrence.
Sitethe most frequent location of lateral periodontal
cyst reported on lateral surface of the roots of vital teeth
in mandibular canine and premolar region (Fig. 13-22)
and is followed by the anterior region of the maxilla.
Symptomsgingival swelling may occur on the facial
aspect and in such cases, it must be differentiated from
the gingival cyst. In gingival cyst, the overlying mucosa
is blue but in lateral periodontal cyst the overlying
mucosa appears normal. When the cyst is located on the
labial surface of the root, it appears as a slight obvious
mass, overlying the mucosa.
Tooththe associated tooth is vital.
Infected cystif the cyst becomes infected, it may resemble
a lateral periodontal abscess.
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Radiographic Features
Shapethe intra-bony lateral periodontal cyst is seen as
a round or ovoid well defined radiolucency with
hyperostotic borders.
Siteit is usually found between the cervical margins
and the apex of adjacent root surfaces and may or may
not be in contact with root surfaces.
Sizemost of them are less than 1 cm in diameter except
the botryoid variety which may larger and multilocular.
Management
The lateral periodontal cyst must be surgically removed
if possible without extracting the associated tooth. If this
cannot be accomplished, the tooth must be sacrificed.
There is a tendency for recurrence for this type of cysts
following its surgical excision.
Diagnosis
Clinical diagnosisnormal color swelling seen in canine
region.
Radiological featuresovoid shaped radiolucency seen
between roots of teeth with hyperostotic borders.
Laboratory diagnosisit is lined by a layer of stratified
squamous epithelium with connective tissue wall.
Cuboidal and columnar cells may be found compassing
the lining. The lumen of the cyst shows focal thickened
plaque of proliferating lining cell. These are especially
prominent in botryoid cyst.
Clinical Features
Agethe gingival cyst may occur at any age, but it is
most common in adults in the 5th and 6th decade of life.
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Radiographic Features
Superficial bone erosionthere may be no radiological
changes or only a faint round shadow indicative of
superficial bone erosion (Fig. 13-24).
Diagnosis
Clinical diagnosisbluish color swelling of gingiva
which is dome shaped will suspect gingival cyst of
adults.
Radiological featuresbone erosion can be present.
Laboratory diagnosisbiopsy has similar feature as that
of lateral periodontal cyst.
Management
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Pathogenesis
Entrapment of epitheliumduring the formation of
secondary palate, small island of epithelium is entrapped
below the surface along the median palatal raphe.
Epithelium may be derived from minor salivary gland
of palate.
Epsteins pearlsthese are cystic keratin filled nodules
found along the midpalatine raphe probably derived
from entrapped epithelial remnants along the line of
fusion.
Bohns nodulesthese are keratin filled cyst scattered over
the palate most numerous along the junction of hard
and soft palate and apparently derived from palatal
salivary gland structure. The nodules are considered as
remnants of mucus gland and are histologically different
from Epsteins pearls.
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Fig. 13-25: Dental lamina cyst showing elevation on alveolar ridge
(Courtesy Dr Bhaskar Patle).
Clinical Features
Appearanceit is white or yellowish papule seen along
the midline of palate.
Locationit is present at junction of hard and soft palate.
Sizeit is usually 1 to 3 mm in diameter. Sometimes it
may form clusters.
Management
No treatment is required and cyst ruptures onto mucosal
surface and eliminate their keratin content.
Diagnosis
Dental Lamina Cyst
The cyst is apparently originated from remnants of dental
lamina. They are multiple, occasionally solitary nodule on
the alveolar ridge of newborn originating from remnants of
the dental lamina (Fig. 13-25).
Management
Clinical Features
Agethese cysts are rarely seen after 3 months of age.
Siteit is found on the crest of the maxillary and
mandibular dental ridges.
Appearanceclinically it appears as small whitish
projection on the alveolar ridge of the jaws of infants
giving mistaken appearance of a tooth (Fig. 13-26) at
times appearing blanched due to internal pressure.
Sizeit is raised nodules, usually multiple, measuring
a fraction of a millimeter to 2-3 mm in diameter.
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Types
Clinical
Central or intraosseous varietyit is also called as intraosseous odontogenic cyst. Cyst occurs centrally within
the bone.
Peripheral or extraosseous varietyit may occur
peripherally in the soft tissue overlying the tooth bearing
area.
Associated with odontogenic tumorthis variety associated
with odontogenic tumor.
Diagnosis
Clinical diagnosisnot specific.
Radiological featurescystic lesion with calcification seen
inside the bony cavity (Fig. 13-27) may give clue to the
diagnosis.
Laboratory diagnosisfocal areas of stellate reticulum and
ghost cell may be present as well as sparse amount of
dentinoids may be seen. Ghost cells are pale eosinophilic
swollen epithelial cells that have lost its nucleus and
nuclear membrane.
Praetorius
He divided this variety into three types:
Simple unicystic type.
Unicystic odontome producing type.
Unicystic ameloblastomatous proliferating type.
Clinical Features
Age and sex distributionmost of the cases are diagnosed
in 2nd and 3rd decade of life. It is slightly more prevalent
in women.
Site3/4th of the lesions occur centrally, with about
equal in both jaws and 75% occurring anterior to the
first molar.
Symptomsit is slow growing, painless, non-tender
swelling of the jaws. Occasionally, some patients may
complain of pain.
Signsin some cases, cortical plate over the expanding
lesion may be destroyed and cystic mass may be palpable
with patients reporting of discharge. Aspiration yields
viscous, granular, yellow fluid.
Teethadjacent teeth may be displaced.
Radiographic Features
Radiodensitythe central lesion may appear as a cyst
like radiolucency.
Marginsit presents with variable margins which may
be quite smooth with a well defined outline or irregular
in shape with poorly defined borders.
Teethit is not unusual to find these associated with
unerupted teeth and in some cases as pericoronal radiolucency. Roots of adjacent teeth may show resorption.
Internal structureit may contain small foci of calcified
material that are only microscopically apparent. In some
cases, it is completely radiolucent while in other cases
an increasing amount of calcified material may be seen
as white flecks. It may be unilocular or multilocular. In
some cases, calcified material may occupy most of the
lesions.
Differential Diagnosis
Fibrous dysplasia (initial stage)it appears as mottled or
smoky defined border on radiographs. It has poorly
defined borders. It is more common in the maxilla.
Partially calcified odontomait appears within the capsule.
Adenomatoid odontogenic tumor (AOT)in intermediate
stage of development of AOT, radiographically it
appears like CEOC.
Ossifying fibroma (initial stage)the fibro osseous lesions
are likely to be situated in more inferior position in the
mandible. It may show root resorption. Histologically, it
shows Chinese letter shaped islands of bone or calcification distributed throughout the connective tissue.
Odontogenic fibromahistologically, it shows odontogenic tissue like cementum.
Cementoblastomathe radiographic image is well defined
and attached to the root of tooth.
Management
Surgeryenucleation and curettage should be done.
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Clinical Features
Ageit is more commonly occur in middle aged adults.
Siteit is more commonly seen in mandible with slight
predilection for anterior region.
Sizesize is usually less than 1 cm in diameter.
Symptomssmall lesions are asymptomatic but large
lesions may associate with pain and paresthesia.
Signexpansion may be present in large lesion.
Radiological Features
Appearanceit is a unilocular or multilocular radiolucency with either smooth or scalloped margins (Fig.
13-28).
Marginmargin of the lesion is well defined with
sclerotic margin.
Diagnosis
Clinical diagnosisnot specific.
Radiological featuresmultilocular appearance with
scalloped margin may suspect this cyst.
Laboratory diagnosishistologically, it shows cystic
space lined by non-keratinized epithelium. The mucus
and cylindrical cells form an integral part of the
epithelial component with mucinous material within
the cystic space.
Management
Surgeryenucleation or curettage should be performed
in this case. Recurrence is common in this type of cyst.
Inflammatory Cysts
Radicular Cyst
It is also called as apical periodontal cyst, periapical cyst, or
dental root end cyst. It is a common sequelae in progressive
Clinical Features
Agepeak frequency occurs in the 3rd decade and there
are large numbers of cases in the 4th and 5th decades
after which there is a gradual decline. Although dental
caries is more common in deciduous teeth in the first
decade but radicular cysts are not often found in
deciduous teeth may be because teeth tend to drain more
readily than the permanent teeth and the antigenic
stimuli which evoke the changes leading to the formation
of radicular cyst may be different.
Sexmale predominance, as females are less likely to
neglect their maxillary anterior teeth and males are more
likely to sustain trauma to their maxillary teeth. It shows
a higher frequency of occurrence in whites.
Sitemaxillary anterior are more commonly affected.
Also in addition to caries, maxillary teeth are more prone
to traumatic injuries which lead to pulp death.
Symptomsit represents an asymptomatic phase in
periapical inflammatory process following death of the
dental pulp. It is associated with non-vital tooth (Fig.
13-30).
Signsit rarely causes non-tender expansion of the
overlying cortical bone. Intraoral and extraoral swelling
may be visible in some cases (Fig. 13-29).
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Fig. 13-31: Radicular cyst, occlusal view seen as pear shaped
radiolucency.
Radiographic Features
Shapeit appears as a rounded or pear shaped
radiolucency at the apex of non- sensitive tooth or with
non-vital tooth (Fig. 13-31).
Siteit appears on the mesial or distal surface of a tooth
root, at the opening of an accessory canal or infrequently
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Diagnosis
Differential Diagnosis
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Management
Root canal treatmentit is the treatment of choice as in
many cases, radicular cyst resolve after root canal
treatment. The reason behind it is that as drainage is
established, the inflammatory process subsides and the
fibroblast start producing collagen. The pressure of
proliferating- collagen reduces the blood supply to the
epithelium lining and causes it to degenerate.
Macrophages remove the degenerating epithelial tissue.
Extractionif the lesion fails to resolve, extraction of
associated tooth is carried out.
Enucleation and marsupializationenucleation or
marsupialization of a larger lesion is done.
Residual Cyst
It is a cyst that either remained as such in the jaw when its
associated tooth was removed or was formed in residual
epithelium of cell rests from a periodontal ligament of the
lost tooth. Low grade inflammation of parent cyst might
predispose formation of residual cyst.
Clinical Features
Age and sexcyst is common in patients older than 20
years with an average age of about 52 years. It is twice
more common in male than female.
Sitehigher incidence in the maxilla. Mostly found on
alveolar process (Fig. 13-36) or body of the tooth bearing
area with some cysts described in the lower ramus of the
mandible.
Symptomsit is asymptomatic with a previous history
of pain in the tooth.
Sizeit is seldom more than 5 to 10 mm in diameter.
Radiographic Appearance
Pre-extraction radiographpre-extraction radiographs
show tooth with an evidence of deep caries or fractured
tooth adequate for pulp involvement and/or an
associated cyst.
Differential Diagnosis
Primordial cystin it, tooth is missing without a history
of extraction. It is more common in mandibular posterior
teeth and at a younger age. On aspiration, it shows straw
colored fluid.
Keratocystit is more common in mandibular posterior
area and at an early age. It may appear multilocular.
The size of the cyst is larger when compared to residual
cyst.
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Diagnosis
Clinical Features
Age and sexit occurs between 10 to 39 years of age. It is
most common in the third decade of life. It shows
predilection for males.
Siteusually associated with the third molar on the
buccal surface (Fig. 13-38) and covers the bifurcation. It
may occur bilaterally.
Signsthe involved tooth is vital.
Management
EnucleationIf the cyst is not large and patients age
and health will tolerate the insult, the cyst wall should
be completely enucleated. The extent of repair of the
defect will depend on the size of the cyst and health of
the patient.
Marsupializationin cases where the surgical procedure
must be as atraumatic as possible, marsupialization or
decompression may be used.
Excisioncomplete excision and replacement with
autogenously bone graft or single segment of bone fixed
in it.
Radiographic Features
Paradental Cyst
Diagnosis
Origin
Cell rests of Malassezit can be the origin, but argument
is that if rests of Malassez were responsible then the
lesion should be equally distributed around the root
surface.
Reduced enamel epitheliumsecond theory is that it
originates from the reduced enamel epithelium as the
presence of reduced enamel epithelium over the enamel
projection might be the source and could explain the
common location of the cyst.
Management
Enucleationthe lesion is treated by surgical enucleation.
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Clinical Features
Diagnosis
Clinical diagnosisthe diagnostic features are the young
age of the patient, the mandibular molar sites, buccal
periostitis, usually vital pulp.
Radiological featuresintact lamina dura with buccal
expansion visible on radiograph.
Laboratory diagnosisnot so specific.
Management
Enucleationit is generally agreed that enucleation of
the cyst without removal of the associated tooth is the
treatment of choice.
Suppurating Cyst
When pyogenic organisms are present in sufficient number
to produce changes, suppuration results. The thin white
line which represents the cortex of the cyst becomes less
dense and thinner and may be entirely lost (Fig. 13-40). In
rare cases there is slight irregularity of the walls of the cyst,
with some decalcification extending into the bone to a short
distance. In the place of thin white cortex, there is sometimes
a broad band of sclerosed bone which is less dense but
wider than a normal cortex and presents a granular
appearance.
Fig. 13-40: Loss of thin line of cyst due to suppuration on left side of
radicular cyst in molar area (Courtesy Dr Tapasya Karamore),
Healing Cyst
Radiographic Features
Periosteumwith involvement of the periosteum, new
bone may be laid down either as a single linear band or
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Non-odontogenic Cysts
Nasopalatine Cyst
It is also called as nasopalatine duct cyst, incisive canal cyst,
median anterior maxillary cyst or vestigial cyst. It is the
most common non-odontogenic cyst in the oral cavity. It is
generally agreed that the nasopalatine duct cyst is an entity.
It may occur within the nasopalatine canal or in the soft
tissue at the opening of the canal where it is called as cyst of
the palatine papilla. They are found to form in the canal or at
the oral terminus of the canal.
Etiopathogenesis
Developmentit is developmental in origin and arises
in the incisive canal when embryonic epithelial
remnants of the nasopalatine duct undergo proliferation
and cystic transformation. Some workers believe that it
is derived from the epithelium included in the lines of
fusion of embryonic facial processes.
Traumain the form of direct blow to the incisive canal
or indirectly from mastication, particularly when illfitting dentures are involved, have been suggested. But
if this is true, the cyst would likely to be found more
often and there would not be a male predilection.
Bacterial infectioneither from the nasal cavity or from
the oral cavity, stimulates to the epithelial remnants to
proliferate has been suggested as a cause. However, since
Clinical Features
Age and sex distributionmost cases discovered in the
4th and 6th decades and it is also frequently found in
edentulous patients. It is three times higher in males
than in females and found equally in blacks and whites.
Onsetthere is a small well defined swelling just
posterior to the palatine papilla.
Painsometime it may become infected, producing pain.
Burning sensation and numbness may be experienced
due to pressure on the nasopalatine nerve.
Salty tastepatients complain of salty taste in mouth
produced by small sinus or remnant of nasopalatine
duct that permits cystic fluid to drain into oral cavity.
Fluctuantswelling is fluctuant and bluish if it is near
the surface.
Palpationit is opened by a tiny fistula on or near the
palatine papilla. In such cases, a tiny drop of watery
fluid or pus may be elicited by pressure in this area.
Surfacedeeper cysts are covered by normal mucosa,
unless it is ulcerated.
Expansionif cyst expands, it may penetrate the labial
plate and produce a swelling below the maxillary labial
frenum (Fig. 13-42).
Teethroots of central incisors diverge. It may bulge into
the nasal cavity and distort nasal septum.
Cyst of palatine papillaeSometimes, cyst formed in
palatine papilla will be evident as an elevation or a soft
round swelling of palatine papilla which extends
posteriorly along the midline of the palate. It occurs
anterior to the incisive foramen below the periosteum
and do not enter invades the underlying bone.
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Radiological Features
Diagnosis
Clinical diagnosisswelling posterior to palatine papilla
may give clue to the diagnosis
Radiological diagnosisheart shaped radiolucency in
maxillary anterior region is typical of nasopalatine duct
cyst.
Management
Surgical enucleationits removal is not indicated unless
there are clinical symptoms. Removal is indicated in
edentulous patients before dentures are introduced.
Intraoral approach should be taken for the surgical
enucleation.
Nasolabial Cyst
It is also called as nasoalveolar cyst or Klestadts cyst. It is
a soft tissue cyst, which involves the bone secondarily.
Pathogenesis
Differential Diagnosis
Clinical Features
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Radiographic Features
Nonepithelial Cysts
Pathogenesis
Differential Diagnosis
Acute dentoalveolar abscessin this case, tooth is tender
on percussion. Radiographically, cystic radiolucencies
are seen in case of nasoalveolar cyst.
Nasal furuncleno radiographic evidence of the lesion.
Mucus extravasation cystno radiographic sign are seen.
Cystic salivary adenomasame as above.
Diagnosis
Clinical diagnosisdifficulty in breathing from nose,
flaring of ala of nose and distortion of nostril will
diagnose nasolabial cyst.
Radiological diagnosisnot specific.
Management
Intraoral surgical approachit should be excised using
an intraoral approach. Some portion of nasal mucosa
should also be removed for complete removal of cyst.
There is no tendency to recur.
Endoscopic marsupializationin this case, transnasal
approach is taken.
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Clinical Features
Age and sexthe traumatic bone cyst occurs most
frequently in young persons at an age of 6 to 20 years
with a male predominance as they are exposed to
traumatic injury most frequently than females with the
ratio being 3:2.
Siteit is usually found in mandible anywhere from the
symphysis to the ramus, but about one-third are found
in the maxilla, usually in the anterior region.
Symptomsit is asymptomatic in most cases but occasionally, there may be evidence of pain and tenderness.
Signscortical swelling or slight tooth movement are
not the usual finding and the teeth are vital.
Aspirationneedle aspiration is actually unproductive
and if it is productive, it contains either a small amount
of straw colored fluid shed off necrotic blood clot and
fragment of fibrous connective tissue.
Radiographic Features
Sitethey may be found in dentulous as well as
edentulous arch.
Appearanceit appears as a radiolucent lesion with a
spectrum of well defined to moderately defined borders.
Marginsmost cases are unilocular with a fairly regular
border. There is evidence of hyperostotic borders around
the entire lesion but occasionally, such border is lacking.
Most characteristic radiographic feature of this cyst is
scalloped superior or occlusal margins where it extends
between the roots of the teeth.
Sizesome cysts may be only a centimeter in diameter
while others may be so large that they involve most of
the molar area of the body of the mandible as well as
part of the ramus.
Teeththey may be superimposed with the root or
scallop superiorly between the roots. Occasionally,
lamina dura of the tooth may be absent and even less
frequently the root may show resorption.
Alveolar boneit rarely causes cortical expansion but if
it occurs, it is mostly buccal (Fig. 13-44). Surface is
smooth, the cortical plates are not disrupted and
pathological fracture does not result. The cavity occupies
the position in the body of the jaw, but it may extend to
involve the alveolar process.
Diagnosis
Clinical diagnosisit is very difficult to make clinical
diagnosis.
Radiological diagnosiswell defined radiolucency with
vital tooth with history of trauma will give clue to
diagnosis.
Laboratory diagnosisaspiration is non-productive.
Biopsy shows fragments of fibrin with enmeshed red
cells may be seen. Hemorrhage and hemosiderin
fragments are usually present and scattered small cells
are often found.
Differential Diagnosis
Radicular cystin radicular cyst, tooth is usually nonvital. Further, all the true cysts tend to have a more
rounded appearance.
Central giant cell granulomait usually shows evidence
of internal bony septa where traumatic bone generally
lacks. It is more common in mandibular anterior region.
Ameloblastoma and odontogenic myxomaare usually
multilocular.
Lesions of eosinophilic granulomathese lesions are not
well corticated as that of traumatic bone cyst.
Fibrous dysplasianot so corticated.
Management
Surgical explorationsimple surgical exploration to
establish the diagnosis. When the correct diagnosis is
determined, enucleation and curettage are carried out.
Intralesional steroid injectionthis can yield limited
success in some cases of traumatic bone cyst.
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Diagnosis
Epidermoid Cyst
Management
Pathogenesis
Traumaimplantation keratinizing epidermoid cyst may
occur in other parts of the mouth as a result of trauma.
This type of cyst is also called as epidermal inclusion cyst.
Infundibular epitheliumthere is non-neoplastic
proliferation of infundibular epithelium from healing
process of localized inflammation of hair follicle.
Clinical Features
Age and sex distributionit is more common in 2nd and
3rd decade of life. Males are more commonly affected as
compared to female.
Locationthese are most common on head, neck, face
and back of the patient.
Appearanceit is nodular lesion (Fig. 13-45) which may
be associated with inflammation.
Dermoid Cyst
It may occur as developmental anomalies and about 1 to
2% occurs in oral cavity. It contains sebaceous material as
well as keratin. If lumen contains elements such as bone,
muscles or teeth from various germinal layer is called as
teratoma. Dermoid cyst is benign cystic form of teratoma.
Dermoid cyst is lined by epidermis and skin appendages
are present in the fibrous wall.
Types
Median variety
Supramylohyoid variety
Inframylohyoid variety
Lateral variety
Supramylohyoid variety
Inframylohyoid variety
Clinical Features
Age and sexit occurs at any time from birth to
adolescence and it is small in infancy and large in
adolescence. Mainly, it is apparent between 12 to 25
years of age and occurrence is equal in both sexes.
Sitemidline of the floor of mouth is the commonest
location of these cysts which may cause a swelling in
the midline of the neck or sometimes, it may be lateral.
On the face, it can be seen on the forehead (Fig. 13-46).
Symptomsswelling is slow and painless. In the case of
supramylohyoid variety, swelling may displace the
tongue and it may interfere with breathing, speaking,
closing the mouth and eating.
Sizethe size may vary up to several centimeters in
diameter.
Palpationswelling is soft to firm, rubbery or cheesy
consistency and sharply delineated.
Aspirationit contains straw colored fluid.
Transillumination testit is usually negative.
Fluctuation testit is generally positive.
Color and surfaceif superficial, it is yellow to white and
surface is smooth and non-ulcerated until traumatized.
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Lymphoepithelial Cyst
Its location in the neck, parotid gland and other intraoral
areas will be dealt separately. Lymphoepithelial cyst of
neck is called as branchial cleft cyst.
Pathogenesis
Fig. 13-46: Dermoid cyst presenting as well defined swelling
on the forehead of patient.
Radiographic Appearance
CT scanCT scan may be useful for the detection of
dermoid cyst.
Contrast studyin some cases, if you want to see
the extent of the cyst, then we have to remove some
content of the cyst to enable introduction of an opaque
substance such as lipiodol, which is chemical
combination of iodine and poppy seed oil. After this,
radiograph is made from every position necessary to
enable opaque material find its way by gravity to each
portion of the cyst.
Differential Diagnosis
Ranulait is not in midline and appears bluish.
Transillumination test is positive.
Unilateral or bilateral blockage of Whartons ductin this
case patient experience pain during meals.
Thyroglossal duct cystit lifts when the patient swallows
or protrudes the tongue.
Cellulitisthe swelling is diffuse and widespread.
Submandibular lymph nodes swellingit is solid.
Diagnosis
Clinical diagnosismidline location is typical feature of
this disease.
Radiological diagnosiscontrast study will diagnose this
lesion.
Clinical Features
Lymphoepithelial cyst of the neck
Ageoccurs at all ages with a fairly equal distribution
from first to sixth decade.
Sitelocation is superficially in the neck, close to the
angle of the mandible, anterior to the sternocleidomastoid muscle.
Sizethe neck lesions vary in size from small to very
large (about 10 cm in diameter).
Symptomsthere is swelling, which may be progressive
or intermittent and pain may also be a feature.
Signit is soft, fluctuant swelling. Some of the cyst may
form mucoid discharge on to the skin through the
opening.
Lymphoepithelial cyst of parotid gland
Agethe age ranges from 16 to 69 years with a male to
female ratio of 3:1.
Symptomsthere is a nodule in the parotid gland.
Signsit is most commonly associated with HIV infection.
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Differential Diagnosis
Management
Management
Pathogenesis
Originit develops from remnant of thyroglossal duct.
Stimulationit is stimulated by inflammatory conditions
which lead to reactive hyperplasia of the lymphoid tissue
near remnant of thyroglossal duct.
Accumulationthis reactive hyperplasia block the
thyroglossal duct, resulting in accumulation of secretion
and formation of cyst.
Clinical Features
Age and sex distributionit is slightly more common in
women and occurs commonly in the first, second and
third decades of life.
Sitemost commonly located in midline in the area of
hyoid bone and when they occur in the mouth, they are
either in the floor or at the foramen caecum.
Symptomsit is painless and movable swelling. Pain
may occur if the cyst is infected. If they are located high
in the tract, they may cause dyspnea.
Pathogenesis
Location of primitive stomachGorlin pointed out that in
the 3-4 mm embryo, the undifferentiated primitive
stomach lies in the mid-neck region, not far from
analogue of the tongue. Gastric mucosa has been shown
to occur in the esophagus of 7.8% of infant and in 51% of
these, heterotrophic tissues were located in the upper
third.
Fusion of endodermal and ectodermal epitheliait is
suggested that in the sublingual region of the oral cavity
and in the region of apex and dorsum of tongue, the
ectodermal and endodermal epithelia fuse and this will
explain presence of heterotrophic gastric or intestinal
mucosa.
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Clinical Features
Diagnosis
Clinical diagnosisnot specific.
Laboratory diagnosisthe cyst may be lined partly by
stratified squamous epithelium and partly by gastric or
intestinal mucosa.
Management
Surgical excisionsurgical excision should be carried
out. Recurrence is rare but has been reported.
Thymic Cysts
They are rare clinical entities, which arise in persistent
thymic tissue, which may occur in any location between
the angle of the mandible and midline of the upper neck to
the sternal notch.
Histologically, the cyst is lined by squamous and cuboidal epithelium and thymic tissues are present in the wall.
Cystic Hygroma
Clinical Features
Diagnosis
Clinical diagnosispainless swelling present from birth
with transillumination test positive will give clue to the
diagnosis.
Laboratory diagnosishistologically, the cystic hygroma
consists of dilated cystic spaces lined by endothelial
cells.
Management
Surgical excisioncomplete surgical removal of the mass.
Nasopharyngeal Cyst
They are rare clinical entities. They may be classified as
congenital or acquired and in midline or lateral. They are
Pathogenesis
Ingestion of tapeworm ovathis tapeworm lives in the
intestinal tract of the dog. Its ova are excreted in the
faeces of the dog and may be ingested by the intermediate
host like cattle sheep and pigs. Man is also susceptible
as an intermediate host as dogs are common household
pets, so may accidentally ingest the ova.
Hatching of ovathe ingested ova hatch in the upper
gastrointestinal tract, from where the small embryo
permeate the intestinal mucosa and are distributed
through the blood vessels and lymphatics to all parts of
the body.
Clinical Features
Siteit is more common in liver, but others are found in
lung, bones and brain.
Symptomsusually they are asymptomatic but they
enlarge progressively to cause pressure symptoms.
Signsliver involvement causes hepatomegaly and
jaundice. Pulmonary hydatid cyst may cause shortness
of breath and hemoptysis.
Complicationsrare complication of hydatid cyst includes
rupture, suppuration and calcification of the cyst.
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Cysticercosis Cellulosae
Radiographic Features
There are four stages in the radiographic evolution of
the disease. They are as follows:
First stagethere is cystic bone destruction involving
medullary portion of the bone. The cysts are rounded
and are described as grape like. The medulla is
expanded and disease is sharply demarcated.
Second stageit is of secondary infection. In this stage,
osteitis is the main change and new bone is formed
beneath the periosteum. Septa between the cysts
become coarser and the margins become less distinct.
Pathologic fracture may occur.
Third stagethe third stage is characterized by
confluent abscesses which break into the soft tissue.
Fourth stagein fourth and final stage, bone is
destroyed. The whole affected portion of the bone is
represented by a meaningless jumble of calcareous
bubbles. The patient is likely to be crippled and
bedridden.
Diagnosis
Clinical diagnosispainless, elastic and well
circumscribed swelling in tongue may give clue to
diagnosis.
Radiological featuresappearance of meaningless jumble
of calcareous bubbles. In initial stage, it appears like
grapes.
Laboratory diagnosisthe outer layer is derived from
fibrous tissue and is infiltrated by chronic inflammatory
cells, eosinophils, lymphocytes and giant cells. The
intermediate layer is white, non-nucleated and consists
numerous delicate laminations. Innermost layer is a
nucleated germinal layer. The cystic fluid is usually
clear, albumin free and contains so called hydatid sand
consisting of brood capsule and scolices.
Management
Surgicalthe ideal treatment for hydatid cyst is surgical.
Preventionlimiting contact between dogs and humans
and deworming dogs at regular intervals are useful
steps towards prevention.
Pathogenesis
Ingestion of wormthe adult worm may be ingested from
inadequately heated or frozen pork. Alternatively, man
may ingest the cysticerci themselves from infested pork
and these develop into adult worms.
Attachment to wall of intestinethese lives attach to the
wall of the small intestine where they fully grow and at
times, reach a length of 7 mm. Gravid proglottids or eggs
begin to drop off and are passed in the faeces.
Penetration into intestinal mucosain this way, man
through contaminated food or from their own dirty
hands may ingest them or they may be regurgitated into
the stomach. In the stomach, their covering is digested
off and the larval forms are hatched. It penetrate the
intestinal mucosa and are then distributed through the
blood vessels and lymphatics to all the parts of the body
where they develop into cysticerci.
Clinical Features
Signs and symptomsit depends upon the site and the
number of the cysticerci in the body. During the stage of
invasion, there are no symptoms or slight muscular pain
and mild fever may be present. CNS involvement
produces serious effects.
Oral Manifestations
Sitethere is very little report about cysticercosis of oral
region. In oral cavity, most common site involved is the
tongue. Other sites involved are cheek and lips.
Signsthere is a firm mass and contains watery fluid
and coiled white structure apparently attached to the
inner aspect of cyst.
Symptomsit is a painless, well circumscribed, elastic
and fluctuant swelling.
Radiological Features
Appearancewhen the larvae die in the soft tissue,
calcification takes place and it appears on the
radiograph. The shadow of calcific density is rod shaped
or resembles a drop. Some of these appear more of less
rounded when the projection of the rays happen to strike
the larvae in its long axis.
Sizethe size of the shadow is 1 mm or more in width
and 1.5 cm in length.
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Diagnosis
Management
Surgicalcutaneous cyst should be surgically removed.
MebendazoleMebendazole has some value in the
treatment.
Preventionpork should be properly cooked as
preventive measures.
Oral Manifestations
Odontogenic keratocystjaw lesions appear as multiple
odontogenic keratocysts usually appearing in multiple
quadrants.
Mandibular prognathismmild mandibular prognathism
is also present in this syndrome.
Radiographic Features
Odontogenic keratocystjaw cysts appear as a multiple
cysts like radiolucency of variable size varying from few
millimeters to several centimeters (Fig. 13-47). They occur
most frequently in premolar-molar region.
Calcified falx cerebriradiopaque lines of calcified falx
cerebri are prominent on PA projection.
Clinical Features
Ageit appears early in life after 5 years and before 30
years.
Basal cell carcinomaNevoid basal cell carcinoma is
brownish colored papules predominant on skin, neck
and trunk. Basal cell carcinoma is less aggressive in this
syndrome than in solitary basal cell carcinoma.
Cutaneous abnormalitiesdermal cyst and tumors,
palmar pitting, palmar and plantar keratosis and dermal
calcinosis. Skin lesions are small, flattened, flesh colored
or brownish papules occurring anywhere in the body,
but are prominent on the face and trunk.
Skeletal abnormalitiesrib anomalies and brachymetacarpalism, bifid rib, agenesis, deformity and synostosis
of rib; kyphoscoliosis, vertebral fusion, polydactyly and
shortening of metacarpals.
Skull featuresthere is frontal and temporoparietal
bossing, resulting in an increased cranial circumference.
Ophthalmologic abnormalitieshypertelorism with wide
nasal bridge, dystopia canthorum, congenital blindness
and internal strabismus.
Differential Diagnosis
Multiple myelomaBence Jones protein in the urine.
Metastatic carcinomahistory of primary tumor.
Histiocytosis Xdoes not have characteristic borders as
seen in cyst.
Cherubismjaw expansion is common in it.
Management
Enucleationcomplete enucleation of the lesion should
be done. Periodic examination should be done to check
for recurrence.
Treatment of Cysts
Regression of Cysts without Surgical Treatment
There is good evidence that some small radicular cyst will
regress if the necrotic pulp remnant and bacteria are
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Indication
Agein a young child, with developing tooth germs.
Proximity to vital structurewhen proximity of the cyst
to vital structure can create an oronasal or oroantral
fistula or injure the neurovascular structure, this
treatment modality should be considered.
Eruption of teethin a young patient with a dentigerous
cyst, marsupialization will permit the eruption of the
unerupted tooth or any other developing tooth which
has been displaced.
Vitality of teethwhen the apices of many adjacent
erupted teeth are involved within a large cyst,
enucleation can prejudice the vitality of these teeth.
Fracture in cystic regionit is the simplest way to treat a
fracture complicating a large cyst of the mandible.
Disadvantages
Regular postoperative carethe need for regular
postoperative care, possibly over a substantial period
of time. It is necessary to supervise healing so that
opening remains large in proportion to the underlying
cavity. Prolonged follow-up visits and periodic
irrigation.
Problems of openinga rapid reduction in the size of the
opening may be difficult to prevent. Indeed an opening
into a large cyst in the ramus may present significant
problems.
Uneven reductionuneven reduction in size of the cavity
may result in slit-like cavity, difficult to keep clean.
New cyst formationthere is risk of invagination and new
cyst formation.
Adjustment of plugregular adjustments of plug.
Enucleation
Enucleation allows for the cystic cavity to be covered by a
mucoperiosteal flap and the space fills with blood clot
which will eventually organized and form normal bone.
Indications
Odontogenic keratocystit is indicated in treatment of
odontogenic keratocyst.
Recurrent lesionrecurrence of cystic lesion of any cyst
type.
Advantages
Simple procedurethis procedure at least for large cysts,
is technically simple.
No general anesthesia requiredeven quite large cysts can
be dealt with under local anesthesia. As anesthesia of
deeper recesses is not essential and this is particularly
an advantage in the maxilla.
Preservation of adjacent mucosabecause the deeper part
of the lining is not disturbed, adjacent important
structures are not put at the risk, i.e. the blood vessels to
the apices of adjacent vital teeth, the inferior dental
neurovascular bundle and the integrity of lining of the
antrum or nose are well preserved.
Conservation of toothmarsupialization may be the best
way to conserve the tooth of origin of a dentigerous cyst
and to permit its eruption.
Prevention of fistulait prevents oronasal and oroantral
fistula.
Reduce operating time and blood lossit reduces operating
time and blood loss and helps in the shrinkage of cystic
lining.
Preservation of alveolar ridgealveolar ridge is preserved.
Advantages
Primary closureas the complete cyst is removed,
primary closure of the wound is possible.
Rapid healinghealing is rapid due to primary closure.
Less postoperative carepostoperative care is reduced.
Thorough examinationthorough examination of the
entire cystic cavity can be done.
Disadvantages
Healing cannot be observedafter primary closure, it is
not possible directly to observe the healing of the cavity
as with marsupialization.
Removal of unerupted teethin young persons, the
unerupted teeth in a dentigerous cyst will be removed
with the lesion in this mode of treatment.
Mandibular weakeningremoval of large cysts will
weaken the mandible making it prone to jaw fracture.
Damage of adjacent structureit will damage to adjacent
vital structures.
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Suggested Reading
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75. Shear M. Cyst of oral region. Bristol J Wright and son ltd (2nd
edn).
76. Shear M. Developmental odontogenic cyst: an update. J Oral
Pathol Med 1994;23:1-11.
77. Skoteric CA, Patterson GT, Sotereanos GC. Benign cervical
lymphoepithelial cyst: report of cases. J Oral Maxillofac Surg
1989; 47:1106-12.
78. Smith I, Shear M. Radiological features of mandibular primordial
cyst (keratocyst). J Oral maxillofacial Surg 1978;6:147-54.
79. Soskolne WA, Shteyer A. Median mandibular cyst. Oral Surg,
Oral Med, Oral Pathol 1977;44:84-8.
80. Spinelli HM, Isenberg JS, OBrian M. Nasopalatine duct cyst and
role of magnetic resonance imaging. J Craniofac Surg 1994;5:5760.
81. Stoneman DW, Worth HM. The mandibular infected buccal cystmolar area. Dental Radiography and Photography 1983;56:1-14.
82. Syrjuanen S, et al. Radiological interpretation of the periapical
cyst and granulomas. Dentomaxillofac Radiol 1982;11:89.
83. Takagi R, Ohashis Y, Suzuki. Squamous cell carcinoma in the
maxilla probable originating from nasopalatine duct cyst: report
of case. J Oral Maxillofac Surg 1996;54:112-5.
84. Toida M. So called calcifying odontogenic cyst: a review and
discussion on the terminology and classification. J Oral Pathol
Med 1998;27:49-52.
85. Tuffin JR, Theaker E. True lateral dermoid cyst of the neck. Int J
Oral Maxillofac Surg 1991;20:275-6.
86. Vedtofte P, Holmstrup P. Inflammatory Paradental cyst in the
globulomaxillary region. J Oral Pathol Med 1989;18:125-7.
87. Whaites E, Differential Diagnosis of radiolucent lesion the jaws,
in essentials of dental radiography and radiology (2nd edn).
Churchill Livingstone, 1996;279-302.
88. White SC, Pharaoh MJ. Oral radiology-principle and interpretation
(5th edn), Mosby Imprint of Elsevier, 2004.
89. White SW, Pharaoh MJ. In oral radiology; principle and
interpretation (5th edn), Mosby, St Louis, 384-409.
90. Woolgar JA, Rippin JW, Browne RM. The odontogenic keratocyst
and its occurrence in nevoid basal cell carcinoma syndrome. Oral
Surg, Oral Med, Oral Pathol 1987;64:727-30.
91. Worth HM. Odontome and cysts of the jaws: in principle and
practice of oral radiologic interpretation; year book medical
publisher Chicago 420-74.
92. Wysocki GP, Goldblatt LI. The so called globulomaxillary cyst
an extinct. Oral Surg, Oral Med, Oral Pathol 1993;76:185-6.
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14
Odontogenic Tumor
of Jaw
Classification
First Classification
Benign
Benign
Epithelial
With inductive changes in the connective tissue
Ameloblastofibroma
Dentinoma
Calcifying odontogenic tumor
Odontoameloblastoma
Odontoma
Without inductive changes in the connective tissue
Ameloblastoma
CEOT
Epithelial atypia
Ameloblastic changes in odontogenic cyst
Mesenchymal
Odontogenic myxoma
Odontogenic fibroma
Cementoma
Periapical cemental dysplasia
Cementifying fibroma
Benign cementoblastoma
Malignant tumor
Malignant
Epithelial
With inductive changes in the connective tissue
Ameloblastic fibrosarcoma
Ameloblastic odontosarcoma
Without inductive changes in the connective tissue
Malignant ameloblastoma
Primary intraosseous carcinoma
Malignant changes in odontogenic cyst
Odontogenic carcinoma
Malignant ameloblastoma
Primary intraosseous carcinoma
Malignant variant of other odontogenic epithelial
tumors
Malignant changes in odontogenic cyst
Odontogenic sarcoma
Ameloblastic fibrosarcoma
Ameloblastic fibrodentinosarcoma
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Benign Tumors
Ameloblastic Fibroma
It is also called as fibrous adamantinoma, soft odontoma,
soft mixed odontoma, and fibroadamanblastoma. It is
characterized by simultaneous proliferation of both
epithelial and mesenchymal tissue without formation of
enamel and dentin. If this tumor is left undisturbed, it will
ultimately differentiate into a lesion known as ameloblastofibroodontoma. It may mature into a complex odontoma. It
is characterized by neoplastic proliferation of maturing and
early functional ameloblasts as well as the primitive
mesenchymal components of the dental papilla.
Mesenchymal
Dentinoma
Cementoma
Cementoblastoma
Odontogenic fibroma
Mixed
Ameloblastic fibroma
Ameloblastic fibroodontoma
Ameloblastic odontoma
Odontogenic myxoma
Compound composite odontoma
Complex composite odontoma
Odontogenic fibroma
Origin
Dental follicleit develops from the dental follicle usually
after the onset of calcification of the tooth.
Tooth budin some instances, it may develop from tooth
bud before onset of calcification and abort the formation
of normal tooth.
Developmental
Dense invaginatus or dilated odontome
Dense evaginatus
Clinical Features
Fourth Classification
Lesions consisting of odontogenic epithelium
Ameloblastoma
Adenomatoid odontogenic tumor
Calcifying epithelial odontogenic tumor
Calcifying odontogenic cyst
Lesions consisting of odontogenic epithelium and
mesenchyme
Ameloblastic fibroma
Ameloblastic sarcoma
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Radiographic Features
Differential Diagnosis
Central giant cell granulomait has a honeycomb pattern
and is usually seen in anterior location.
Odontogenic myxomafiner trabeculation resembling a
string of tennis racket pattern.
Central hemangiomahoneycomb pattern and local
gingival bleeding and pumping action of tooth or teeth.
Primordial cystthick yellowish granular fluid.
Ameloblastomaassociated with much older group.
Management
Curettageit can be done which has successful results
in many cases. But there are chances of recurrence in
this tumor.
Surgical excisionaggressive surgical excision should
be done for recurrent lesion.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisnot so specific. Sometimes, CT
scan may be helpful to diagnose the tumor (Fig. 14-3).
Laboratory diagnosisbiopsy shows scattered islands of
epithelial cell in a rosette, long finger-like strands, nests
and cords-like pattern. Cells resemble the primitive
odontogenic epithelium. The mesenchymal component
is made up of a primitive connective tissue.
Clinical Features
Age and sexit is more common in men with an age
range of 8 to 92 years with a mean age of 42 years.
Sitemandible is more commonly affected than the
maxilla in the ratio of 2:1 and developed in premolarmolar area (Fig. 14-4).
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Fig. 14-4: Swelling seen in mandibular region due to calcifying
epithelial odontogenic tumor (Courtesy Dr Bhaskar Patle).
Radiographic Features
Radiodensityit may be totally radiolucent to mostly
radiopaque area around the crown of unerupted teeth.
The radiopacity is produced by mineralization of
amorphous proteinaceous material generated by the
tumor cells rather than the disorganized formation of
dental tissue (Fig. 14-6).
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosistypical driven snow appearance
is seen.
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Differential Diagnosis
Management
Conservative surgical excisionit has limited invasive
potential therefore local excision with limited margins
is indicated. Simple enucleation can be done.
Odontoma
It is a hamartoma of odontogenic origin in which both
epithelial and mesenchymal cells exhibit complete
differentiation with enamel, dentin and cementum that are
laid down in abnormal position. Odontome may arise from
any of three dental tissues, i.e. enamel, dentin and
cementum.
Origin
There is growth of epithelial and mesenchymal
component exhibiting complete differentiation with a
result that functional ameloblasts and odontoblasts laid
down in abnormal fashion.
Mixed
Complex composite odontomanon-discrete masses of
dental tissue.
Compound composite odontomamultiple well formed
teeth.
Compound-complex odontomasome tumors contain not
only multiple teeth like structures, but also calcified
masses of dental tissue in a haphazard manner, such
lesion are called as compound-complex odontoma.
Geminated odontoma.
Dilated odontoma with dens in dente.
Enameloma
It is also called as enamel nodule, enamel drop or enamel
pearl. It is a small focal excessive mass of enamel on the
surface of the tooth. It is formed by small group of misplaced
ameloblasts. This enamel may contain a small core of
dentin and rarely, small strands of pulp tissue extending
from pulp chamber or root canal of the tooth.
Clinical Features
Siteenamel pearls are most commonly found in the
bifurcation or trifurcation of roots or on the surface near
the cementoenamel junction. The most common site is
upper molar.
Appearanceit appears as a tiny globule of enamel firmly
adherent to the tooth.
Significancein some cases, it occupies such a position
on cementoenamel junction that leads to pocket
formation which may predispose to periodontal
diseases.
Radiographic Features
Classification
Ectodermal origin
Enameloma (enamel pearl, enamel nodule).
Diagnosis
Mesodermal origin
Dentinoma
Cementoma.
Etiology
Genetic transmissionit may occur due to mutant gene or
interference with genetic control of tooth development.
Local trauma or infectionin some cases of trauma or
infection to tooth in developing stage may cause some
alteration in ectomesenchymal interaction causing
odontoma formation.
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Management
Management
Removal of massmass has to be removed if it is causing
periodontal diseases.
Etiology
Traumalocal trauma or infection may lead to
production of such a lesion.
Geneticthey are either inherited or are due to a mutant
gene or interference, possibly postnatal, with genetic
control of tooth development.
Mechanism
Dentinoma
It is a rare tumor of odontogenic origin composed of
immature connective tissue, odontogenic epithelium and
irregular or dysplastic dentin.
Clinical Features
Age and sexit is seen in patients younger than 36 years
with an average age of 26 years with no sex predilection
for occurrences.
Siteit is predominately seen in the mandibular molar
area and is frequently associated with an impacted tooth.
Symptomspatient notices a swelling over a variable
period of time with pain.
Signperforation of mucosa and subsequent infection
may be present. There may be redness of overlying
mucosa with discharge.
Radiographic Features
Radiodensityradiopaque mass associated with the
crown of unerupted tooth.
Internal structureit contains either a large, solitary,
opaque mass or numerous smaller, irregular radiopaque
masses of calcified materials which may vary
considerably in size.
Boneit may cause local destruction of bone.
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosisradiopaque mass with crown of
tooth.
Laboratory diagnosisbiopsy shows irregular dentin,
which has been termed as dentinoid or osteodentin.
There is also presence of undifferentiated odontogenic
epithelium.
Clinical Features
Age and sexit is more commonly seen in first and
second decade of life. Most begin to form while normal
dentition is developing. Slight predilection for occurrence
in males.
Sitecompound odontome occurs in incisor, canine area
of maxilla and complex odontome occurs in mandibular
1st and 2nd molar area. Unusual situation includes the
maxillary sinus, inferior border of the mandible, ramus
and condylar region.
Frequencycompound odontome is twice as common
as complex odontome.
Sizecompound odontoma is between 1 to 3 cm in
diameter. It usually remains small and diameter of the
mass only occasionally increases than that of the tooth.
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Fig. 14-8: Odontoma causing swelling on right side of face
causing facial asymmetry (Courtesy Dr Parate).
Radiographic Features
General
Siteit is situated between the roots of teeth.
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Fig. 14-11: Complex odontome showing well defined
radiopacity (Courtesy Dr Parate).
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosiscompound shows shapeless
mass of tooth structure while complex show
disorganized mass of tooth structure.
Laboratory diagnosisbiopsy shows multiple tooth
structures contain in loose fibrous matrix (compound)
and mature tubular dentin (complex).
Management
Local excisionsimple local surgical excision is the
treatment of choice.
Differential Diagnosis
Difference between compound and complex typecompound
odontome has more than one fragment while in complex,
it is one solid mass. Compound is seen most commonly
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Classification
Ameloblastoma
First detailed description of ameloblastoma was given by
Falkson in 1879. It is an aggressive tumor that appears to
be arising from remnants of dental lamina or dental organs.
It represents 1% of all oral tumors and 11% of odontogenic
tumors. It is the most common epithelial tumor producing
minimal inductive changes.
There are different names given to this tumor. Term
adamantine epithelioma was given by Malassez in 1885. It
was replaced by ameloblastoma in 1934 by Churchill. It is
also called as adamantinoma, adamantinoblastoma,
epithelial odontome and multilocular cyst.
Definition
It is a benign but locally invasive polymorphic neoplasm
consisting of proliferating odontogenic epithelium which
is usually in a follicular or plexiform pattern, lying in fibrous
stroma.
Etiology
Irritationit might be considered as one of the etiological
factors as it often occurs in the posterior region of the
mandible which is most susceptible to irritation.
InfectionRobinson found that 1/3rd of the cases have
history of oral infection, extraction of teeth and injuries
to teeth.
On pathological basis
Conventional ameloblastoma
Unicystic ameloblastoma
Peripheral ameloblastoma
Pituitary ameloblastoma
Adamantinoma of long bones
On histological type
Follicular ameloblastoma
Plexiform ameloblastoma
Acanthomatous ameloblastoma
Basal cell ameloblastoma
Unicystic ameloblastoma
Plexiform unicystic ameloblastoma
Granular cell ameloblastoma
Papilliferous ameloblastoma
Hemangioameloblastoma
Desmoplastic ameloblastoma
Clear cell ameloblastoma
Dentinoameloblastoma
Melanoameloblastoma
Keratoameloblastoma.
Pathogenesis
The resemblance of the tumor epithelium to the normal
enamel organ indicates that ameloblastoma arises from
dental epithelium. The possibilities for its development are
as follows.
Enamel organdue to histological similarities such as
its origin, it has been thought that the tumor growth
starts at an early age; i.e. during the period of existence
of enamel organ but most of the patients are middle aged
i.e. in a period which is long after regression of the enamel
organ. However, the occasional occurrence of the tumor
as a unilocular cystic lesion surrounding the crown of
an unerupted tooth also suggests that in some cases, the
enamel organ may give rise to it.
Cell restscell rests of enamel organ either remnants of
dental lamina or remnants of Hertwigs sheath i.e.
epithelial cell rests of Malassez have the potential of
transforming into ameloblastoma.
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Clinical Features
Incidenceameloblastoma accounts for approximately
1% of all oral tumors and 11% of all odontogenic tumors.
Sex and raceit has slight predilection for males and
often seen in blacks.
Agemost patients are between 20 to 50 years of age
with mean age of discovery being 40 years. The tumor
can occur in young children. Unicystic type of
ameloblastoma is more common in the 2nd and 3rd
decade and the extraosseous form is more common in
the older age group.
Siteit develops in the molar ramus area (approximately
th of cases) in the mandible and also occurs in maxilla
in third molar area, followed by the maxillary sinus and
floor of the nose. The right side of the mandible is affected
slightly more as compared to the left side.
Preceding factorsneoplasm is frequently preceded by
extraction of teeth, cystectomy and some other traumatic
episodes.
Onsetit begins as a central lesion of the bone which is
slowly destructive but tends to expand bone rather than
perforating it.
Symptomspatient notices a gradually increasing facial
asymmetry (Fig. 14-15). Teeth in involved region are
displaced and become mobile (Fig. 14-17). Pain and
paresthesia may occur, if the lesion is pressing upon a
nerve or is secondarily infected.
Signsin later stages, the lesion may show ovoid and
fusiform enlargement that is hard but non-tender. If it is
left untreated for many years the expansion may be
extremely disfiguring (Fig. 14-16), fungating and
ulcerative type of growth characteristic of carcinoma can
be seen.
Eggshell crackingas tumor enlarges, palpation may
elicit a hard sensation or crepitus. Surrounding bone
may become thin so that fluctuation and eggshell
cracking may be elicited.
Maxillary ameloblastomamaxillary lesions are more
dangerous than mandibular lesions due to tendency for
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Radiographic Features
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Fig. 14-21: Unicystic ameloblastoma (Courtesy Dr Mody).
B
Diagnosis
Clinical diagnosisswelling in posterior mandible with
expansion and eggshell cracking will give clue to
diagnosis.
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Peripheral Ameloblastoma
It is also called as extraosseous ameloblastoma. It is a tumor
which occurs in the soft tissue outside and overlying the
alveolar bone. It originates from either the surface epithelium
or the remnants of dental lamina.
Clinical Features
Types of Ameloblastoma
Radiological Features
Bone erosionsometimes underlying bone may exhibit
evidence of pressure resorption in the form of saucershaped depression beneath the tumor.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosissaucer shaped bone depression
beneath the tumor mass may suspect the lesion.
Laboratory diagnosisbiopsy shows same pattern as seen
in intraosseous ameloblastoma.
Management
Surgerysimple surgical excision of the lesion is
treatment of choice. Prognosis of this tumor is very good.
Pituitary Ameloblastoma
It is also called as craniopharyngioma or Rathkes pouch
tumor.
Originit occurs in anterior lobe, which is of ectodermal
origin. The lobe is derived from Rathkes pouch, an
outgrowth of oral ectoderm. The pouch gives rise to
craniopharyngeal duct, which in due course degenerates
itself leaving residues of squamous epithelial cells. From
these squamous epithelial cells, ameloblastoma-like
tumor develops.
Ageit is most common in childhood and adolescents
before the age of 25 years.
Management
Curettageit is least efficient as it makes recurrence
inevitable. Curettage may leave bone that is invaded by
tumor cells.
Intraoral block excisionexcision of a block of bone may
be recommended if the ameloblastoma is small. The
segment in which the tumor is contained is removed
with a safe margin of normal bone.
Extraoral En-block resectionif the lesion is large and
horizontal ramus is involved then this is carried out.
Peripheral osteotomyit is a procedure which allows
complete excision of the tumor but at the same time a
part of bone is retained which preserves the continuity
of the jaw. The procedure is based on the observation
that cortical inferior border of the horizontal body, the
posterior border of the ascending ramus and condyle
are generally not involved by tumor process. These areas
are resistant and strong because of the dense cortical
bone. Bone regeneration will proceed from such areas
with considerable restoration of the jaw architecture.
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Clinical Features
Age and sexthere is a wide age distribution in the range
of 11 to 67 years with mean age 40 years and females are
more commonly affected than the males.
Siteit occurs with equal frequency in maxilla and
mandible. In maxilla, it occurs in incisor-cuspid area
and in the mandible; it has got a predilection for the
bicuspid-molar area.
Onsetit is slowly growing tumor.
Symptomsit is usually asymptomatic but there may be
mobility of the involved teeth, pain, tenderness to
percussion and occasionally abnormal sensation.
Radiological Features
Siteit occurs usually in association with the cervical
portion of the tooth.
Radiodensityit is well circumscribed radiolucent area.
Shapeit presents as a semicircular or roughly
triangular area (Fig. 14-24).
Marginborder may or may not be sclerotic.
Differential Diagnosis
It is a rare lesion so, it should not be high on the differential
diagnostic list when considering radiolucent jaw lesions.
If at exploration one discovers a solid fleshy lesion which
is associated with a vital tooth root on cervical portion
then squamous odontogenic tumor is the most likely
diagnosis.
Management
Surgeryconservative enucleation and curettage is
usually curative with a low recurrence rate.
Odontogenic Myxoma
It is also called as odontogenic fibromyxoma, myxofibroma.
It is a rare non-invasive neoplasm that arises from the
dental papilla, follicular mesenchyme and periodontal
ligament.
Origin
Overgrowth of dental papillathe myxomatous tissue
arises as a direct outgrowth of dental papilla of tooth or
as an indirect effect of odontogenic epithelium on
mesenchymal tissue.
Changes in fibrous tissueas a direct myxomatous change
in fibrous tissue.
Clinical Features
Diagnosis
Clinical diagnosisnot so specific.
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Radiographic Features
Differential Diagnosis
Central giant cell granulomaanterior location in
mandible.
Ameloblastomausually occurs in older patients.
Cherubismyounger age group and bilateral involvement.
Giant cell lesions of hyperthyroidismhistory of kidney
disease and abnormal serum chemistry.
Metastatic carcinomaolder age group and presence of
primary tumor.
Aneurysmal bone cystit is tender and painful.
Central hemangiomait is not associated with missing
tooth. Pumping tooth syndrome is seen in hemangioma
with aspiration being useful.
Management
Surgical excisiontumors may be difficult to enucleate
due to their loose consistency, therefore surgical excision
is indicated.
Resectionresection with generous amount of
surrounding bone.
Etiology
Irritationit is associated with irritation (overextended
margin of faulty restoration and deposits of calculus).
Clinical Features
Fig. 14-25: Tennis racket pattern seen in odontogenic myxoma.
Diagnosis
Clinical diagnosismissing teeth with hard swelling may
suspect this disease.
Radiological diagnosistennis racket pattern seen in
odontogenic myxoma.
Laboratory diagnosisbiopsy shows loosely arranged,
spindle shaped and stellate cells, many of which have
long fibrillar processes that tend to be intermeshed.
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Clinical Features
Age and sex distributionit occurs more frequently in
older individual with mean age of 40 years. There is
marked female predilection.
Siteit is more common in maxilla and in anterior region.
Symptomsit is generally asymptomatic except for the
swelling of the jaws.
Signsit may cause localized bony expansion and
loosening of teeth.
Radiological Features
Radiographic Features
Bone erosionon rare occasion, there may be superficial
erosion of bone.
Calcificationthere may be presence of some radiopaque
foci within the tumor mass which occur due to
calcifications within the tumor.
Diagnosis
Clinical diagnosissessile mass attached to gingiva may
suspect peripheral odontogenic fibroma.
Radiological diagnosisnot specific.
Laboratory diagnosisbiopsy shows cellular fibrous
connective tissue parenchyma with non-neoplastic
islands, strands and cords of columnar or cuboidal cells.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosismultilocular radiolucency in
anterior maxilla may suspect central odontogenic
fibroma (Fig. 14-27).
Laboratory diagnosisbiopsy shows tumor mass made
up of mature collagen fibers interspersed usually by
many plumps of fibroblasts that are very uniform in
their placement and tend to be equidistant from each
other.
Differential Diagnosis
Chondrosarcoma and osteogenic sarcomaless frequent
gingival lesion, severe bony changes, asymptomatic with
widening of PDL.
Inflammatory hyperplasiano separation of teeth occurs.
Management
Surgical excisionsimple surgical excision and submitted for microscopic examination for confirmation of
diagnosis.
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Management
Curettage and enucleationcentral odontogenic fibroma
is treated with enucleation and curettage. It does not
recur.
Clinical Features
Age and sex distributionit occurs more frequently in
older person (more than 40 years of age). There is slightly
female predilection.
Siteit is common in premolar and molar area of
mandible.
Symptoms and signlesion is painless with expansion
of the jaw is noted.
Radiological Features
Appearanceit appears as well demarcated radiolucency. It is unilocular or multilocular.
Calcificationsmall degree of calcification is noted in
the lesion.
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosiscalcification in unilocular
radiolucency may suspect the lesion.
Laboratory diagnosisbiopsy shows large eosinophilic
granular cells. Narrow cords or small islands of
odontogenic epithelium are scattered in granular cells
area. Small cementum-like calcification is also seen.
Management
Curettagesimple curettage of the lesion should be
carried out. No recurrence is reported.
Etiology
Local factorsit occurs as a result of trauma, chronic
irritation.
Pathogenesis
Bone at the apex of the affected tooth may be replaced by
fibrous tissue which may be small in amount or occupy an
area of a square inch or more the fibrous tissue may
remain unchanged for months to years but in most
instances, there is a tendency for a change to occur the
affected area may become partially reduced in size by
peripheral ossification bone or cementum forms either
as a single mass which enlarges by aggregation at its
margin or as several masses this mass either enlarges
individually or they fuse the fibrous tissue may be
replaced entirely by bone of greater density than that of
normal bone once cementum is formed it remains
unchanged without any reduction.
Clinical Features
Age and sex distributionit occurs during the middle age
with a mean age of 39 years. Male to female ratio is 1:9
and is three times more common in blacks than in whites.
Sitemandibular anterior region is commonly affected.
Single area of one jaw may be involved or the greater
part or both the jaws is affected.
Symptomsinvolved teeth are vital with no history of
pain or sensitivity. Occasional lesions localize near the
mental foramen and impinge on the mental nerve and
produce pain, paresthesia or even anesthesia.
Signshypercementosis is usually associated with it. It
rarely enlarges.
Radiographic Features
Siteit usually lies at the apex of the tooth. In rare cases,
epicenter is high and over the apical thirds of the root. In
most cases, lesion is multiple and bilateral.
Marginsmargins are well defined. A radiolucent
border of varying width, surrounded by band of sclerotic
bone is seen. Sclerotic bone represents immediate
reaction of surrounding bone.
Stage IRadiolucent (fibrous)
Radiodensitysince there is loss of bony substance
and replacement by connective tissue, the lesions
appear radiolucent.
Shapethere is formation of a circumscribed area of
periapical fibrosis accompanied by localized bone
destruction (Fig. 14-28).
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Fig. 14-29: Mixed stage of PCD showing
radiopacity in the radiolucency.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisradiolucency at the apex of vital
teeth with no loss of lamina dura in early stage. In the
mature stage radiopaque lesion is seen.
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Differential Diagnosis
Management
Continuous observationit requires continuous
observation and subsequent verification through
periodic radiographic examination.
Surgical enucleationsurgical enucleation is indicated
for larger lesions which have caused expansion of the
cortical plates or when the clinician is unsure of the
working diagnosis.
Benign Cementoblastoma
The benign cementoblastoma is also called as true
cementoma. It is rare odontogenic tumor representing less
than 1% of all odontogenic tumors.
Norberg initially described it in 1930 and defined as a
true neoplasm of cementum or cementum-like tissue that
formed on a tooth root by cementoblasts.
The WHO defines the benign cementoblastoma as a
neoplasm characterized by the formation of sheds of
cementum-like tissue which may contain a very large
number of reversal line and may be unmineralized at the
periphery of the mass or in the more active growth areas.
The accepted theory of its origin is that it is a
mesenchymal odontogenic tumor. The cementoblastomas
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Clinical Features
Age and sex distributionthe benign cementoblastoma
occurs most frequently under the age of 25 years and
there appears to be a slight predilection for males.
Sitecementoblastoma can occur in both maxilla and
the mandible. The mandible, however, is involved three
times more frequently than maxilla. The mandibular first
permanent molar is the most frequently affected tooth.
Symptomspain is frequently present and it is the most
common symptom.
Signthe associated tooth is vital unless coincidentally
involved. The lesion is slow growing and produces
cortical expansion. Extraoral (Fig. 14-31) and intraoral
swelling can also be present (Fig. 14-32).
Radiographic Features
Marginswell defined radiopacities usually attached
to the roots of premolars and molars surrounded at the
border by a radiolucent halo are seen.
Appearancethe radiological appearance of the cementoblastoma is highly characteristic, seen as circular
radiopaque mass attached to the root of the one or more
teeth. A narrow radiolucent zone surrounds the lesion
and delineates from adjacent bone (Fig. 14-33).
Root outlinethe outline of the affected root is generally
obliterated because of resorption of the root and fusion
of the mass to the tooth.
Internal structurethey are mixed radiolucentradiopaque lesion that may be amorphous or may have
wheel-like spoke pattern. Density of cementum obscures
the outline of the enveloped root.
Effect on surrounding structuresthe outline of the tooth
is obliterated because of resorption of the root and fusion
of the mass to the tooth.
Expansionocclusal radiograph will demonstrate its
expansive nature.
Diagnosis
Clinical diagnosisnot so specific
Radiological diagnosisradiopaque lesion surrounded
by radiolucent capsule attached to root surface is typical
of cementoblastoma.
Laboratory diagnosisbiopsy shows cementum-like
tissue, deposited in globular pattern resembling giant
cementicles.
Differential Diagnosis
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Management
Ameloblastic Fibro-odontoma
The name is applied to an odontogenic lesion that exhibits
features of ameloblastic fibroma as well as dentin and
enamel. It is mixed epithelial-mesenchymal proliferation
and both mature and immature areas.
Clinical Features
Age and sexit is usually seen in a young age group
with mean age of occurrence of 12 years. Males are more
commonly affected than females.
Sitemaxilla and mandible are equally affected. In
mandible, it occurs in the molar area and in the maxilla
it usually involves the maxillary sinus.
Symptomsthe most common presenting complaint is
swelling and failure of tooth eruption. The maxillary
tumor if large interferes with nasal respiration, eating
and speech.
Signsameloblastic fibro-odontoma consists of elements
of ameloblastic odontoma and is more aggressive than
the common odontoma.
Radiological Features
Radiodensitya well-circumscribed lesion presenting as
an expansile radiolucency generally containing either a
solitary radiopaque mass or multiple small opacities
representing the odontoma portion of the lesion (Fig.
14-34).
Sizesome of the lesions are relatively small, not over 1
to 2 cm in diameter; while others may be exceedingly
large involving a considerable portion of the body of
mandible and extending in the ramus.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisradiopaque calcified mass in the
radiolucent defect.
Laboratory diagnosisbiopsy shows epithelial component with dysplastic dentin. There are cords, fingers,
strands and rosettes of primitive odontogenic columnar
or cuboidal epithelial cells often resembling dental
lamina. The mesenchymal component is an embryonic
fibrous connective tissue with delicate fibrils interspersed by large primitive fibroblast all resembling dental
papilla.
Management
Curettageit is treated by curettage since it does not
appear to locally invade the bone.
Ameloblastic Odontoma
It is also called as odontoameloblastoma. It is characterized
by the simultaneous occurrence of an ameloblastoma and
a composite odontome. It is extremely rare odontogenic
tumor.
Clinical Features
Ageit occurs in children early in the second decade of
life.
Sitegreater incidence in mandible as compared to
maxilla.
Symptomsit produces considerable facial deformity or
asymmetry if left untreated. Mild pain may be present as
well as delayed eruption of teeth also occurs.
Signit causes bony expansion and destruction of the
cortex and displacement of teeth.
Radiological Features
Radiodensityradiographic density of ameloblastic
odontoma may be radiopaque and similar to the complex
odontoma or may be mixed.
Internal structurethere is presence of numerous small
radiopaque masses (Fig. 14-35) which may or may not
bear resemblance to the formed albeit miniature teeth. In
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Radiological Features
Fig. 14-35: Large masses of calcified structure seen in
ameloblastic odontoma (Courtesy Dr Parate).
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisradiopaque calcified mass with
cortical destruction.
Laboratory diagnosisbiopsy shows undifferentiated
epithelial cells with ameloblasts, enamel and enamel
matrix, dentin, osteodentin, dentinoid and osteoid
material. There is presence of sheets of typical
ameloblastoma of one or the other of the recognized types
usually basal cells, follicular or plexiform cells.
Diagnosis
Management
Malignant Tumor
Ameloblastic Fibrosarcoma
Management
Radical resectionhemimandibulectomy or hemimaxillectomy can be done in patient of ameloblastic fibrosarcoma. Recurrence is common and prognosis is poor.
Clinical Features
Ameloblastic Odontosarcoma
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Terminology
Clinical Features
Age and sexmales are affected more commonly than
females. It occurs in 1st to 6th decade with mean age of
diagnosis 28-32 years.
Siteit is almost exclusively seen in the mandible.
Symptomsswelling followed by pain and/or rapid
growth.
Signteeth may be displaced and loosened. Tenderness
of overlying soft tissue is present.
Sites for metastasislungs, spleen, kidney, lymph nodes
and ileum.
Local extensionit may occur in adjacent bone, connective
tissue or salivary gland.
Radiological Features
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisloss of cortical boundary with
features suggestive of ameloblastoma.
Laboratory diagnosisthere may be cytological features
of malignancy.
Differential Diagnosis
Benign ameloblastomain it, there is no evidence of
metastasis in benign ameloblastoma.
Central giant cell granulomaif the lesion is anterior to
the premolar, central giant cell granuloma should be
suspected.
Management
En block resectionit is treated with en bloc resection.
Prognosis is poor in this case.
Pulmonary metastasisradiation therapy and chemotherapy for pulmonary metastasis.
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Radiological Features
Origin
Malignant transformationprimary intraosseous
carcinoma may occur from malignant transformation of
epithelial lining of odontogenic or non-odontogenic cyst,
or ameloblastoma by metastases from different sites.
Primary tumor of maxillary sinusin case of maxilla, it
may arise from primary tumor of the maxillary sinus.
Cell rests of odontogenic epitheliumthe tumor arises from
the cell rests of the odontogenic epithelium or from the
epithelial remnants at the site of fusion between two
embryonic processes.
Cells of dental laminain normal situation for some of
the original cells of the dental lamina or enamel organ to
remain in the jaw long after the function of these cells
are completed. Malignant tumor may develop from these
cells.
Types
Those arising from odontogenic cysts.
Those arising from ameloblastoma either well
differentiated (malignant ameloblastoma) or poorly
differentiated (ameloblastic carcinoma).
Those arising de novo from odontogenic epithelium
residues, either keratinizing or non-keratinizing.
Fig. 14-38: Irregular radiolucency seen in mandible of intraosseous
carcinoma.
Clinical Features
Age and sex distributionthere is a wide range of age
distribution with majority of cases occurring in 6th and
7th decade of life. It is more common in males than in
females with a ratio of 2:1 and more common in
mandible than in maxilla.
Symptomsthe early symptom is swelling of the jaw
with pain and mobility of the teeth before ulceration has
occurred. Pathological fracture and lip paresthesia also
occurs.
Signsthere is rapid expansion and destruction of jaw
bones. Tumor invades the periodontal ligament and the
alveolar bone, destroying it. There may be lymphadenopathy. Surface epithelium is normal. Occasionally, the
pulp of the teeth may be invaded by neoplasm. Perforation
of cortical plate may occur.
Non-healing socketextraction of teeth result in nonhealing socket and sometimes tumor may protrude from
the non-healed socket.
Diagnosis
Clinical diagnosisrapid expansion, lymphadenopathy,
and pathological fracture may suspect this disease.
Radiological diagnosisit is purely lytic lesion with
expansion and destruction of cortical plate.
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Differential Diagnosis
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosissmoothness of cyst is lost and
margin becoming ill defined may give clue to the
diagnosis.
Laboratory diagnosisthey are same as that of squamous
cell carcinoma.
Management
Surgical resectionit is treatment of choice in primary
intraosseous carcinoma.
Differential Diagnosis
It is also called as carcinoma ex odontogenic cyst. It is uncommon lesion seen in oral cavity. There are carcinomatous
changes found in odontogenic cyst. In some cases adjacent
carcinoma may involve otherwise unrelated cyst. It occurs
due to epithelial dysplasia occurring in the cyst lining.
Clinical Features
Management
Radiological Features
Siteit is most commonly found in tooth bearing area of
the jaw. Most commonly in the mandible.
Marginif it is small lesion in the cyst wall, the periphery
may be well defined and corticated. As the malignant
lesion progressively replaces cyst lining, the smooth
border is lost or becomes ill defined. Advanced lesion
Odontogenic Fibrosarcoma
It is the malignant counterpart of odontogenic fibroma. It
originates from same mesenchymal tissue, as same in
central fibroma.
Clinical Features
It is a destructive lesion which produces a fleshy, bulky
growth. It as such is asymptomatic but pain may be present
in many cases.
Diagnosis
Biopsy shows cellular element that may or may not be
prominent than the fibrillar component. The cells often
exhibit considerable mitotic activity. They resemble imma-
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Management
Radical surgical removal with resection of the jaw.
Prognosis is poor.
Clinical Features
Age and sexmost cases reported in women over 60 years
of age.
Siteboth maxilla and mandible have been involved.
Symptomsit may present as asymptomatic or painful
bony swelling.
Radiological Features
Appearanceunilocular or multilocular radiolucency
with ill defined margins.
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosisnot specific.
Laboratory diagnosisbiopsy shows nests of epithelial
cells with clear or faintly eosinophilic cytoplasm which
is separated by thin strands of hyalinized material.
Management
Extensive resectiontumors demonstrate aggressive local
behavior and potential lymphatic and pulmonary
metastases and therefore should be treated with extensive
resection.
Suggested Reading
1. Ackerman GL, Altini M, Shear M. The unicystic ameloblastoma:
a clinicopathologic study of 57 cases. J Oral Pathol 1988;17:
541-6.
2. Albert M, John K, Raymond J. Cementoblastoma: a clinicalpathological study of seven new cases. J Oral Surgery 1974;38
(3):394-403.
3. Allen CM, Hammond HL, Stimson PG. Central odontogenic
fibroma, WHO type: a report of 3 cases with an unusual
associated giant cell reaction. Oral Surg, Oral Med, Oral Pathol
1992;73:62-6.
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Benign Tumor
of Jaw
Introduction
It is a new growth representing the tissue of origin. The
study of the tumors of the oral cavity and adjacent tissues
constitute an important phase of dentistry because of the
role of a dentist in the diagnosis of the lesion.
Terminology
Hamartomasit is an abnormal proliferation of normal
tissue at its usual location. For e.g. Hemangioma.
Neoplasmtumors that continue to grow indefinitely are
called as neoplasm.
Hypertrophyenlargement caused by an increase in the
size of cells.
Hyperplasiaenlargement caused by an increase in the
number of the cells.
Classification
Epithelial tissue
Papilloma
Keratoacanthoma
Squamous acanthoma
Nevus
Fibrous connective tissue
Fibroma
Fibrous hyperplasia
Fibrous epulis
Giant cell fibroma
Fibrous histiocytomas
Desmoplastic fibroma
Myxoma
Myxofibroma
Cartilage tissue
Chondroma
Chondroblastoma
Chondromyxoid fibroma
Adipose tissue
Lipoma
Angiolipoma
Bone
Osteoma
Osteoid osteoma
Osteoblastoma
Exostosis-tori-torus palatinus-torus mandibularis
Osteomatosis
Vascular tissue
Hemangioma
Hereditary hemorrhagic telangiectasia
Lymphangioma
Arteriovenous fistula
Glomus tumor
Neural tissue
Neurofibroma
Neurolemmoma
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Schwanoma
Ganglioneuroma
Traumatic neuroma
Melanotic neuroectodermal tumor of infancy
Muscles
Leiomyoma
Rhabdomyoma
Granular cell myoblastoma
Teratoma
Types
Squamous cell papillomait may arise in the tongue, cheek,
lip and esophagus
Congenitalit is usually present since birth.
Infectiveit arises from viral infection.
Soft papillomait is often seen in eyelids of elderly
people.
Keratin hornsit is due to excess keratin formation
and seen in older people.
Basal cell papillomait is also called as seborrhoeic or senile
wart. It occurs on the trunk, face, arms and armpits.
Clinical Features
Ageaverage age of occurrence is in the 3rd and 4th
decade of life, only 20% of cases are found below 20
years of age.
Common sitesit is most commonly seen on tongue,
palate, buccal mucosa, gingiva, lip, mandibular ridge
and floor of mouth.
Cauliflower appearanceit is typically an exophytic lesion
with a cauliflower-like surface or with finger-like
projection (Fig. 15-1). Projections are pointed or blunt.
This appearance is caused by presence of deep clefts
that extend well into lesion from the surface.
Baseit generally arises from a pedunculated base. Some
time, base may be broad rather than pedunculated.
Shapesmall mass on mucosa with a papillomatous
shape.
Diagnosis
Clinical diagnosiswhite cauliflower-like projection in
oral cavity favors the diagnosis of papillomas.
Laboratory diagnosishistopathologically it consists of
many long, thin, finger-like projections extending from
the epithelium.
Differential Diagnosis
Verruca vulgariscommon in skin and always has a
sessile base.
Papillary squamous cell carcinomabase is not
pedunculated. It grows rapidly and exceeds 0.5 to 2 cm
in size.
Verrucous carcinomaseen at the age of 60 and 70 years
and is associated with smoking and chewing tobacco or
snuff, the mass is wider than the surface area with the
base almost as wide as the lesion. It does not achieve
much vertical length.
Condyloma latum and acuminatumthey are less common
and patient has a history of oral sex.
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Management
Etiology
Surgical excisionelliptic incision on the tissue underlying the lesion should be given. Incision should be from
the base of mucosa, into which the pedicle or stalk is
inserted. If the tumor is properly excised, recurrence is rare.
Other modalitiesapplication of formaldehyde at night
on the wart may cure the condition. Sometimes, silver
nitrate application also cures the condition.
Verruciform Xanthoma
It is also called as Histiocytosis Y. It is a papillomatous
lesion of oral cavity in which accumulation of lipid laden
histiocytes occur below the epithelium. The lesion occurs
as an unusual reaction to localized epithelial trauma or
damage.
Clinical Features
Age and sexthere is strong female predilection and is
usually seen in middle age.
Siteit can occur at any site and is most frequently found
on the gingiva or alveolar ridge, followed by the buccal
mucosa, palate, floor of the mouth, lip and lower
mucobuccal fold.
Verruciform appearancethe lesion appears as soft, well
demarcated slightly elevated mass with white, yellowish
white or red in color. It has got papillary or roughened
appearance which is called as verruciform appearance.
Crateriform surfacein some cases, crateriform surface
have also been reported.
Baseit is either sessile or has a pedunculated base.
Sizeit may be as small as 2 mm to as large as 1.5 cm.
Diagnosis
Clinical diagnosisthe lesion has got verruciform surface
and it is usually solitary.
Laboratory diagnosisbiopsy will show large swollen
foam cells or xanthoma cells, which are presumably
histiocytes.
Management
Surgical excisionit is treated with conservative surgical
excision.
Keratoacanthoma
It is also called as self healing carcinoma, molluscum
sebaceum, and pseudocarcinoma. It, clinically and
Types
Ferguson Smith typethere are large number of
keratoacanthoma which is hereditary in nature.
Eruptive Grazybowski typein this, there are hundreds
of small papules on skin and upper digestive tract.
Clinical Features
Age and sexmale to female ratio is 2:1 and majority of
cases occur between the ages of 50 to 70 years.
Common siteexposed skin including cheeks, nose and
dorsum of the hands. Intraoral lesion is uncommon; if
found, is more common on lips.
Symptomsthe lesion is often painful and regional
lymphadenopathy may be present.
Appearancethe lesion appears as an elevated
umbilicated or crateriform with depressed central core
which represent a plug of keratin. Lesion appear to be
fixed to surrounding tissue.
Shapeit appears as dome shaped.
Color of keratin plugkeratin pit is frequently discolored,
being yellowish brown in color.
Lipon the lower lip, the lesion shows smooth, raised,
rolled borders with a central plug of hard keratin.
Marginsmargins are sharply delineated. There may
be elevation of the rolled margins.
Sizeit grows to maximum size of 1 to 2 cm in diameter.
Progressit begins as small, firm nodules that develop
to full size over a period of four to eight weeks and persist
as static lesions for another 4 to 8 weeks. After that, it
undergoes spontaneous regression over the next six to
eight weeks period by expulsion of the keratin core with
resorption of the mass. There may be unsightly scar
formation.
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Diagnosis
Differential Diagnosis
Keratinizing squamous cell carcinomacancerous lesion
usually fails to exhibit a smooth round regularity, which
is present in keratoacanthoma.
Warty dyskeratomais usually small, i.e. less than
0.5 cm, as compared to keratoacanthoma which can
attain a dimension of 1-2 cm.
Management
Clinical Features
Congenital melanocytic nevus
Siteit is more commonly seen in head and neck region.
Intraoral involvement is rare congenital form.
Small congenital nevithey are greater than 1 cm in
diameter and less than 20 cm in diameter.
Large nevithey are greater than 20 cm in diameter and
can cover larger areas of the skin.
Appearancelesion appear as brown to black plaque
with rough surface (Fig. 15-2). Early lesion is flat and
dark tan which later on becomes elevated, nodular and
rougher.
Hypertrichosisthere is presence of excess hair within
the lesion. These hairs become prominent with the age
giving the appearance of giant hairy nevus.
Bathing trunk nevus or garment nevusa very large
congenital nevus is termed as bathing trunk nevus or
garment nevus as patient gives appearance of wearing
an article of clothing.
Types
Congenital melanocytic nevusThese are nevus which are
present at birth. Around 15% of congenital nevi is found
in head and neck region.
Acquired melanocytic nevus (common mole)it is present
later in life
Intradermal nevus
Junctional nevus
Compound nevus
Halo nevusit results from nevus cell destruction by
immune system.
Blue nevus (Jadassohn-Tieche nevus, dermal melanocytoma)
benign proliferation of dermal melanocytes deep in
subepithelial connective tissue.
Spitz nevus (benign juvenile melanoma, spindle and
epithelioid cell nevus)it shares histological features
with melanoma. This lesion was described by Spitz in
1948.
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Diagnosis
Clinical diagnosisclinically, nevi can be diagnosed
easily by their features.
Laboratory diagnosisnevus contain granules of melanin
pigment in their cytoplasm. Epithelium is thin and irregular and shows abtropfung or dropping off effect.
Management
Surgical removalit has been customary to recommend
the removal of pigmented mole if it occurs in areas where
they are irritated by clothing, such as belt of collar line
or if they suddenly begin to increase in size, deepen in
color or become ulcerated.
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Clinical Features
Diagnosis
Clinical diagnosissessile, firm on palpation with pink
color and smooth surface will go in favor of fibroma.
Laboratory diagnosisbiopsy shows bundles of interlacing collagenous fibers interspersed with varying
number of fibroblasts or fibrocytes and small blood
vessels.
Differential Diagnosis
Lipofibromafeels softer on palpation.
Myxofibromafeels softer on palpation.
Management
Surgical excisionsit is treated by conservative surgical
excision.
Fibrous Hyperplasia
It is also called as inflammatory fibrous hyperplasia, denture
injury tumor and epulis fissuratum.
Etiology
Clinical Features
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Management
Elimination of irritationelimination of irritation should
be done.
Excisional biopsyit should be treated with excisional
biopsy.
Fibrous Epulis
It is the term used when fibrous growth occurs in the
gingiva. The possible cause of it is irritation from subgingival calculus or adjacent carious tooth.
Clinical Features
Diagnosis
Clinical diagnosisfibrous growth in relation with
denture flanges.
Laboratory diagnosisbiopsy shows hyperplastic mass
of tissue which is composed of an excessive bulk of
fibrous connective tissue covered by a layer of stratified
squamous epithelium, may be of normal thickness or
show acanthosis.
Differential Diagnosis
Hemangiomait is present at birth.
Management
Surgical excisionlesions are excised with small amount
of adjacent normal tissue.
Fibrous Histiocytoma
It is also called as fibroxanthoma dermatofibroma, sclerosing
hemangioma, and nodular subepithelial fibrosis. It may occur
in dermis and rare in oral cavity.
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Clinical Features
Radiological Features
Sitethe most common site is ramus and posterior area
of mandible.
Radiodensityit appears as well defined radiolucency,
either unilocular or multilocular. The larger lesions
appear to be multilocular with very course and thick
septa. Smaller lesions are completely radiolucent.
Marginmargin can be well defined or ill defined.
Extentit may perforate the cortex and infiltrate the
adjacent tissues.
Teethdivergence of contiguous tooth roots is a common
finding. In some cases, there may be root resorption.
Diagnosis
Fig. 15-10: Fibrous histiocytoma showing extraoral swelling.
Diagnosis
Clinical diagnosisdermal tumor with intraoral soft
fibrous growth will go in favor of fibrous histiocytoma.
Laboratory diagnosisbiopsy shows rich vascular
growth, made up of histiocytes and collagen producing
fibroblast-like cells, which are arranged in a whorl or
cartwheel pattern.
Differential Diagnosis
Management
Surgical excisionit can be done and recurrence is
uncommon.
Management
Desmoplastic Fibroma
It arises from the mesenchyme of bone. It is also called as
aggressive fibromatosis. It produces an abundant number
of collagen fibers. It is thought to be counterpart of soft
tissue fibromatosis.
Clinical Features
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Diagnosis
Diagnosis
Management
Surgical excisionit is the treatment of choice.
Clinical Features
Age and sex distributionit is common in young adults
with slight female predilection.
Sitegingiva is the most common site followed by hard
palate.
Appearancelesion is sessile, painless and nodular mass
of same color of surrounding tissue (Fig. 15-12).
Surfaceit is smooth and non-ulcerated.
Sizesize can vary from few mm to 2 cm in diameter.
Management
Surgical excisionsurgical excision is done and
recurrence is rare.
Myofibroma
Diagnosis
Clinical Features
Ageit can occur at any age, but more commonly found
in fourth decade of life.
Siteit is more common in head and neck region.
Common oral site are lips, cheeks, and tongue.
Appearanceit is painless mass and it exhibits rapid
enlargement.
Management
Surgical excisionit is the treatment of choice in oral focal
mucinosis.
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Myxofibroma
Some areas of fibroma undergo myxomatous degeneration.
Clinical Features
Siteit occurs anywhere in the oral cavity, most
commonly on palate, lip and gingiva.
Signsit feels softer than fibroma and is less pale.
Diagnosis
Clinical diagnosisnot so specific.
Laboratory diagnosisthere are regions of dense
fibroblastic tissue which are interspersed with pale
myxomatous appearing tissue.
Differential Diagnosis
Plexiform neurofibromait is spongy and fluctuant.
Management
Complete excisioncomplete excision of the lesion should
be carried out.
Myxoma
Myxoma appears to be true neoplasm which consists of
tissue that resembles mesenchymal tissue. Soft tissue
myxoma is very rare in the oral cavity.
Clinical Features
Age and sexit can occur at any age and there is no
definite sex predilection.
Siteit occurs on skin of the subcutaneous tissues,
genitourinary tract and gastrointestinal tract, or liver,
spleen, or even in parotid gland. Intraorally, it occurs on
the tongue, buccal mucosa and retromolar area.
Appearanceit is present as soft tissue growth in oral
cavity.
Nerve sheath myxomait arises from perineural cells of
peripheral nerves and contain prominent mucoid matrix.
It may be present on tongue, buccal mucosa and
retromolar area.
Diagnosis
Clinical diagnosisit is not specific.
Laboratory diagnosisbiopsy shows loose textured tissue
which contains delicate reticulin fibers and mucoid
material, probably hyaluronic acid.
Management
Surgicalit is essentially surgical and recurrence is
common.
Types
Enchondroma or centralit develops deep into the bone.
It is most commonly seen.
Ecchondromait develops on the surface.
Origin
Meckels cartilageit is present in the mandibular arch,
prior to the appearance of the bone. It usually disappears
with the occurrence of ossification in the mandibular
arch, but it is possible that the remnants still persist.
Fibrocartilagein some cases, secondary cartilage like
fibrocartilage of mandibular symphysis may persist in
the jaw bone and thus can give rise to chondroma.
Chondrocraniumthe maxilla develops in close
association with chondrocranium. The maxillary sinus
develops as an outgrowth from the lateral walls of the
nasal capsule. As it grows into the maxilla, it may take
remnants of the cartilage from the capsule.
Remnants of paraseptal cartilagein some cases, remnants
of the paraseptal cartilage might persist within the
maxilla.
Clinical Features
Age and sexit occurs in the 5th and 6th decades and
males are slightly favored.
Siteit usually occurs in the phalanges and metacarpals.
Intraorally, maxilla is slightly favored and it occurs in
the anterior region, while in mandible it occurs in
premolar-molar region and at symphysis; it may be
found in condyle and coronoid process.
Symptomsit is painless, slowly growing and is locally
invasive. Teeth become loose and may be exfoliated.
Signsthe overlying mucosa is seldom ulcerated.
Syndrome associatedit is associated with Olliers
syndrome, in which there are multiple enchondromatosis. It is also seen in Maffucci syndrome in which there
are soft tissue angiomas.
Radiographic features
Radiodensityirregular radiolucent areas.
Marginsborders may be well defined or ragged or
poorly defined.
Mottled or blurry appearanceit may develop radiopacities
in osteolytic areas, which produce mottled (Fig. 15-13) or
blurry appearance.
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Chondroblastoma
It is also called as Codmans tumor. It usually involves
long bone. In some cases, it may be found in cranial bones.
Clinical Features
Age and sexit occurs in young persons, under the age
of 25 years, with male predominance over the female,
usually in the ratio of 2:1.
Siteit occurs usually in epiphyseal region of long
bones. The usual site is femur and tibia. In some cases, it
can occur in condyle of mandible.
Symptomsit is slow growing, painless mass.
Diagnosis
Clinical diagnosisnot so specific.
Laboratory diagnosisit consists of uniform, closely
packed, polyhedral cells, with occasional foci of
chondroid matrix. Multinucleated giant cells are also
present.
Management
Surgical excisionconservative surgical excision is
carried out. Recurrence is possible after excision.
Chondromyxoid Fibroma
Fig. 15-13: Mottled appearance seen in chondroma in
mandibular posterior region (Courtesy Dr Parate).
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosismottled appearance in jaw.
Laboratory diagnosisbiopsy shows hyaline cartilage
with calcification or necrosis. Cartilage cells are small.
Differential Diagnosis
Chondrosarcomapain is present in case of chondrosarcoma.
Osteogenic sarcomatypical sun ray appearance is seen.
Osteoblastic metastatic carcinomapresence of primary
tumor.
Ossifying sub-periosteal hemangiomaaspiration should
be done to rule out hemangioma.
Fibrous dysplasiaground glass appearance and
histological features.
Clinical Features
Age and sexit occurs in young persons under the age of
25 years, with no definite sex predilection.
Siteit is extremely rare in jaws, but there are some cases
reported in mandible. It is more commonly seen in
metaphyseal region of lone bone.
Symptomspain is the outstanding feature of this
disease and sometimes, swelling can be seen.
Radiological Features
Marginmargin is sclerotic and scalloped.
Appearanceit is circumscribed radiolucent defect.
Central radiopacity is present within the radiolucent
defect.
Sizesize of lesion varies from 1 to 6 cm.
Management
Diagnosis
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Management
Types
Encapsulated lipomait is the commonest tumor.
Diffuse lipomait does not possess typical features of
lipoma. It is also called as pseudolipoma.
Lipomatosisit has multiple lipomas. It refers to the
symmetrical masses of fat, which sometimes occur
around the neck in middle aged man and occurs as
painful deposits of fat in women in Dercums disease.
Clinical Features
Age and sex distributionoccurs age after 40 years with
peak at 50 years, male to female ratio is 1:1.
Common sitesit usually occurs in upper parts of the
trunk, neck (Fig. 15-14) and arms. In oral cavity, it occurs
on buccal mucosa and mucobuccal fold followed by
tongue, floor of mouth and lip.
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Diagnosis
Clinical diagnosispositive slip sign, soft well defined
swelling will go in favor of lipoma.
Laboratory diagnosisbiopsy shows mature fat cells,
collagen strands coursing through the lesion.
Management
Local excisionsurgical excision is done. Recurrence is
uncommon.
Bone Tumors
Osteoma
It is a benign neoplasm characterized by proliferation of
either compact or cancellous bone, usually in an endosteal
or periosteal location.
Origin
Periostealit arises on the surface of bone as a
pedunculated mass.
Endostealit is located in the medullary bone.
Cancellous osteoma
Age and sexit more commonly occurs in females with
age same as for ivory osteoma.
Sitethere is predilection to occur in the alveolar process.
Baseit is usually pedunculated, although it might have
a broad base.
Surfacethe surface may be smooth or slightly irregular.
Clinical Features
Radiographic Features
Ivory osteoma
Age and sex distributionit occurs in individuals older
than 40 years. It is more common in males, as compared
to females.
Siteit occurs exclusively on skull and facial bone. It
may occur in more than one bone. Mandible is more
affected on the lingual side of ramus and inferior border,
below the molars.
Ivory osteoma
Sitethere is small mass of dense bone situated below
the level of the root of lower molar. It may be located
within paranasal sinus.
Sizethe size of mass is usually few centimeters in
diameter.
Appearanceit appears as a uniform radiopaque mass
(Fig. 15-18). There may be granular appearance in some
Types
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Differential Diagnosis
3
Fig. 15-18: Well defined completely radiopaque lesion present due to
osteoma.
Cancellous osteoma
Internal structureit shows evidence of internal
trabecular structure. Due to these trabeculations,
individual spaces appear to be small. There may or may
not be superficial layer of cortical bone.
Bone structurebone structures, within the tumor, are
continuous with that of the parent bone.
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis.
Radiological diagnosiswell defined complete
radiopaque lesion will give clue to diagnosis. CT scan
may be useful in some cases (Fig. 15-19).
Management
Resection of osteoma is generally successful.
Osteoblastoma
It is also called as giant osteoid osteoma. It is a benign
uncommon tumor of osteoblasts, with area of osteoids and
calcified tissues.
Clinical Features
Age and sex distributionmale to female ratio is 2:1. Most
lesions occur in 2nd and 3rd decades of life.
Siteit more commonly occurs in vertebral column and
sacrum. It is rare in jaws and if it occurs, found more
commonly in tooth bearing areas of mandible.
Symptomsit is characterized by pain and swelling of
the affected region, which may be of few weeks to a year
duration. Pain is not relieved by aspirin as compared to
osteoid osteoma.
Signsthere is local expansion of the bone.
Aggressive osteoblastomait is characterized by locally
aggressive behavior. It is seen in older patient. Pain is
present and severe.
Radiographic Features
Fig. 15-19: CT scan showing osteoma on
right side in condylar region.
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Osteoid Osteoma
It is a variant of osteoblastoma. It is a true neoplasm of
osteoblastic derivative. It is small oval or rounded tumorlike nidus which is composed of osteoid and trabeculae
of newly formed bone deposited within the substratum
of highly vascularized osteogenic connective tissue tumor.
It has usually intracortical lumen. It contains concentration of peripheral nerves which is not seen in other bony
lesion.
Clinical Features
Radiographic Features
Diagnosis
Clinical diagnosisbony pain which is not relieved by
aspirin with swelling in jaw may suspect osteoblastoma.
Radiological diagnosiswell defined lesion with patchy
distribution of mineralization.
Laboratory diagnosisbiopsy shows dilated capillaries,
multinucleated giant cells and proliferating osteoblasts.
Differential Diagnosis
Osteoid osteomamore eccentric radiolucency with
sclerotic borders. Histologically, osteoid trabeculae in
osteoblastoma are larger, broader and longer, with wider
trabecular space than those in osteoid osteoma. An
osteoblastoma is more vascular and less painful. Size of
osteoblastoma is more than 2 cm and size of osteoid
osteoma is less than 2 cm.
Osteogenic sarcomabenign radiographic appearance of
osteoblastoma, as compared to osteogenic sarcoma.
Management
Curettage and conservative surgical excision.
Recurrence may occur.
Diagnosis
Clinical diagnosisbony pain which is relieved by aspirin
with swelling in jaw may suspect osteoid osteoma.
Radiological diagnosiswell defined lesion with size less
than 2 cm with target-like appearance will give clue to
diagnosis.
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Differential Diagnosis
Management
Salicylatessevere pain may be relieved by mild
obtundants such as aspirin.
Excisioncomplete excision of tumor is carried out.
Osteochondroma
It is most likely to represent a choristoma, rather than a
neoplasm. It is developmental in origin. There is
intermingling of two lesions resulting in the term
osteochondroma.
Radiological Features
Appearancethe radiolucent area in the bone tends to be
spherical or oval in shape.
Margins- margins of the tumor tend to be more sharply
localized and corticated.
Internal structureit shows the presence of bone in the
lesion, unlike chondroma which does not show any bone
in the lesion. The bone within the tumor is either
trabecular or as irregularly shaped amorphous mass.
Coronoid processin some cases, coronoid process is
enlarged, resembling a drumstick appearance.
Effect on surrounding structuresthe malar bone may show
destruction of bone on its deep and inferior surface, while
superficial surface of the adjacent maxilla is indented to
receive the additional size of the coronoid.
Diagnosis
Clinical diagnosisif deviation of mandible during
mouth opening, facial asymmetry in the condylar lesion
is present, this disease should be suspected.
Radiological diagnosisdrumstick appearance of
coronoid process and radiolucent lesion seen in condyle
will give clue to diagnosis.
Laboratory diagnosisbiopsy shows a well circumscribed
lesion of mature lamellar bone, cartilage or a mixture of
those tissues. Haversian canals may be present in the
bone and rarely, blood forming elements may be present.
Management
Surgical excisionsurgical excision of the lesion should
be carried out.
Torus Palatinus
Clinical Features
Age and sexit occurs most often in women, between the
ages of 20 and 39 years.
Siteit is commonly seen in lower end of femur, upper
end of tibia. It is rare in jaw and if found, it is seen in
coronoid process of mandible and mandibular condyle.
In some cases, tongue may be involved.
Symptomsdysphagia may be the only symptom in
this patient. If there is involvement of the condyle, there
is difficulty in movements of mandible. Pain is
experienced, either in opening and closing the mouth or
in deviating the mandible to one side.
Appearanceon the tongue, it appears as a pedunculated
swelling of about 1 to 2 cm in the posterior part of the
dorsum of tongue, near the foramen cecum.
Signthere is facial asymmetry and lesion has got broad
base.
Etiopathogenesis
Geneticit is inherited as autosomal dominant trait.
Functional stressenvironmental factors such as
functional stress can also lead to torus palatinus.
Types
They are classified according to their morphology
Flat torusit has broad base and smooth surface. Extent
of this tori is even on both side of midline of palate.
Spindle torusit has midline ridge along the palatal
raphe.
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Clinical Features
Age and sexfemales are affected twice more commonly
than males. Development is initiated in young adults,
before 30 years.
Siteit occurs in the midline of the palate and may
extend to involve the palatal process of the palatine bone.
Progressthe growth may be slow or there may be a
period of rather rapid growth which ceases altogether
before the patient has advanced into adult life.
Sizethey are usually less than 2 cm in diameter. In
some cases, lesion may progress to such an extent that it
can fill whole palatal surface.
Signsit is covered with normal mucosa, which appears
pale and occasionally ulcerated, when traumatized.
Management
Surgeryas it is benign it is usually not treated, except
in some cases where patient requires a complete denture
and tori is causing more undercuts and problems for
fitting of complete denture. In these cases surgical
removal of tori can be done.
Torus Mandibularis
It is also called as mandibular torus. It is an exostosis or
outgrowth of bone found on the lingual surface of the
mandible. They consist primarily of compact bone. it occurs
in 8% of the population.
Causes
Geneticit occurs as an autosomal dominant trait.
Masticatory stressmasticatory stress is reported as an
essential factor underlying the formation. The reason
behind is that torus mandibularis is seen in patient who
is having bruxism.
Radiographic Features
Clinical Features
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Radiographic Features
Management
Surgeryremoval may be necessary, if a mandibular
denture is planned.
Exostosis
It is also called as hyperostoses. They are small regions of
osseous hyperplasia of cortical bone and occasionally,
cancellous bone, on the surface of the alveolar process. They
are less common than mandibular and palatal tori.
Clinical Features
Age and sex distributionit is more commonly seen in
adults as compared young.
Siteit may develop on the palatal surface of maxillary
alveolar process, at the border between the attached
gingiva and vestibular mucosa, in canine or molar area.
Sizethey seldom attain large size and may be solitary
or multiple.
Shapetheir shape may be nodular, pedunculated or
flat protuberance on the surface of bone.
Consistencythey are bony hard on palpation.
Buccal exostosesit usually occurs as bilateral row of
bony hard nodule on buccal aspect of an alveolar ridge.
Ulceration of overlying mucosa may occur if trauma
occurs.
Palatal exostoses (palatal tubercle)it is also bilateral and
seen in maxillary tuberosity area.
Solitary exostosesit occurs as reaction of local irritation.
Mostly occur below the free gingival graft (Fig. 15-23).
Reactive subpontine exostosis (subpontic osseous proliferation,
subpontic osseous hyperplasia)it occurs from alveolar
crestal bone beneath the pontic of posterior bridge.
Radiographic Feature
Radiodensitythe internal aspect of an exostosis usually
is homogenous and radiopaque.
Management
Surgicalsurgical removal is required if exostosis is
exposed to frequent trauma and if you want to place
prosthesis in that area. Reactive subpontine exostoses
need to be remove as they interfere with oral hygiene.
Enostosis
It is also called as dense bone island. They are internal
counterparts of exostosis. They are localized growth of
compact bone that extends from the inner surface of cortical
bone into the cancellous bone. It is also called as whorl. A
rare condition in which there are thousand of dense islands
of bone scattered through the skeleton is known as
osteopoikile or osteopoikilosis.
Clinical Features
Ageit is more commonly seen in 2nd and 3rd decade.
Siteit is more common in mandible than maxilla and
commonly found in premolar molar area.
Symptomsit is asymptomatic.
Radiographic Features
Marginssingle isolated radiopacities that may be either
well defined (Fig. 15-24) or diffuse, so that the trabeculae
blend with trabacular pattern of adjacent normal bone
of jaw.
Sizeit is more or less rounded, with size varying from
a few millimeters upto a centimeter or more.
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Clinical Features
Fig. 15-24: Single isolated radiopacity seen at the apex of first molar
suggestive of enostosis (Courtesy Dr Parate).
Diagnosis
Clinical diagnosisnot possible to make clinical diagnosis.
Radiological diagnosisrounded opacity with lack of
expansion will give clue to diagnosis.
Differential Diagnosis
Periapical idiopathic osteosclerosisdifficult to distinguish,
but these periapical lesions may be associated with
periodontal ligament widening, which is absent in case
of enostosis.
Periapical cemental dysplasiaradiolucent margins.
Hypercementosisassociated with roots of teeth.
Cementoblastomait is also associated with roots of teeth.
Osteosarcomaradiolucent component is present.
Metastatic osteoblastic carcinomaradiolucent component
is present.
Chondrosarcomaradiolucent component is present.
Central
Age and sex distributionmost of cases are found at birth
or arise at early age. Female to male ratio is 2:1.
Originthe lesion can originate either from the
periosteum and resorbs the underlying bone or it occurs
within the bone as an anomaly of blood vessels in the
marrow spaces.
Sitemandible to maxilla ratio is 2:1. 50% cases are
found in mandible, mostly in the body and ramus area.
Symptomspain is present in many cases of central
hemangioma. The nature of the pain is throbbing. Patient
also complaint of swelling in the jaw (Fig. 15-25). In
some cases, there is paresthesia of skin supplied by
mental nerve.
Management
No treatmentmost cases are unrecognized and are not
clinically important.
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Capillary Hemangioma
Strawberry angioma
Agetypical history of red mark is noticed after 1-3
weeks of birth. After 1st birthday, it regresses in size and
involution is completed by 7 to 8 years.
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Fig. 15-29: Strawberry hemangioma presented as typical
strawberry type lesion in the floor of mouth.
Port-wine stain
Ageit generally starts at birth and darkens as the child
grows, but it does not really grow.
Siteit is common on the face (Fig. 15-31) and at the
shoulders, neck and buttock.
Appearancereddish macular hemangiomas are called
as port-wine stain. The port wine stain is generally
smooth, but could be slightly raised (Fig. 15-32).
Sizeit is seldom more than 5 mm in diameter.
Colorit is deep purple-red in color, which may become
paler later. Color blanches readily on pressure.
Salmon patch
Ageit is present since birth and usually disappears
before the first birthday.
Radiographic Features
Siteit is more commonly found in mandible. In
mandible they are often located within the inferior
alveolar canal. It can also occur in the body and ramus
of the mandible.
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3
Fig. 15-35: Honeycomb appearance of hemangioma
seen in mandibular posterior region.
Fig. 15-33: Hemangioma of lip presented as increased radiopacity
seen on the lower lip (Courtesy Dr Tapasya).
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Management
It usually regresses by itself during adolescent period.
Sclerosing techniqueintralesional injections of sclerosing
chemicals, such as 1 ml of 5% sodium morrhuate are
effective. These agents will produce localized inflammatory reaction with resultant thrombosis, subsequent
fibrosis of the endothelial spaces and regression of the
lesion. After first injection second injection should be
repeated after two weeks. Another agent which is used
is 95% ethanol.
Surgeryen bloc resection with ligation of external
carotid artery. Sometimes, rash surgical excision of such
central lesion of bone results in severe loss of blood,
which occasionally leads to exsanguinations of the
patient to the point of death. Laser surgery, cryosurgery
by dry ice can also be effective.
Other injectionsinjection of boiling water or hypertonic
saline may also be given.
Radiation therapy in the form of external radiation or
radium can be used to successfully sclerose the lesion.
But risk of inducing neoplastic changes later in life is
very high and its use is contraindicated particularly in
children.
Corticosteroidsintralesional injections of corticosteroid
can be given. This may reduce the size of tumor.
Flash lamp pulsed dye laserthis is useful in case of port
wine stain.
Embolizationintroduction of inert material into the
lesion by vascular route can cause embolization and
subsequent regression of the lesion.
Classification
1st
Complete trisymptomaticin this, all three organ systems
(eye, skin and CNS) are involved.
Incomplete bisymptomaticin this, involvement is either
oculocutaneous or neurocutaneous.
Incomplete monosymptomaticin this, there is only neural
or cutaneous involvement.
2ndthe Roach scale classification
Type Iboth facial and leptomeningeal angioma with
glaucoma.
Type IIfacial angioma alone without CNS involvement.
Some cases having glaucoma.
Type IIIisolated leptomeningeal angioma without
glaucoma.
Etiology
Dysplasia of embryonal vascular system (Royle)this will
result in hemangiomatosis. It occurs in sixth week of
intrauterine life.
Developmental insult (Del)Sturge-Weber syndrome
affects the precursor of tissue which originated in
promesencephalic and mesencephalic neural crest.
These developmental insults give rise to vascular
malformation.
Aberrant migration (Crinzi)it may arise from aberrant
migration of mesodermal and ectodermal elements in
the brain and meniges in the fetal growth.
Clinical Features
Port-wine stain or nevus flammeusit is present at birth. It
presents at the distribution of trigeminal nerve. The color
varies from light pink to deep purple due to overabundance of capillaries beneath the surface of the
involved skin (Fig. 15-36).
Sturge-Weber Syndrome
It is also called as encephalotrigeminal angiomatosis. It is
congenital disorder belongs to grouped anomalies
collectively known as phakomatoses (mother spot disease).
Fig. 15-36: Port-wine stain seen on left side of face in the patient
with Sturge-Weber syndrome (Courtesy Dr Amit Parate).
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Lymphangioma
Fig. 15-37: Intraoral purplish discoloration of oral mucosa on left side
in the palate is seen (Courtesy Dr Amit Parate).
Radiological Features
Conventional radiographyit may show classical
tramlines or tram-track or trolley-tract calcification
in the skull.
Computed tomographyit may show calcification
(Fig. 15-38). It can also demonstrate brain atrophy,
ipsilateral choroids plexus enlargement and abnormal
draining veins.
Angiographyit demonstrates lack of superficial cortical
veins, nonfilling of dural sinues and abnormal tortus
vessels.
Other modalitiesother imaging modalities like MRI,
SPECT, PET can also be useful.
Types
Superficial or lymphangioma simplex (capillary
lymphangioma)it presents a circumscribed lesion,
which appears as small blisters and slightly elevated
skin patches. It involves capillary size vessels.
Cavernous lymphangiomait is composed of larger
dilated lymphatic vessels.
Cystic or deep lymphangiomathey are large, cystic, and
translucent and may be seen in the neck, mediastinum
or axilla. These are called as cystic hygroma.
Management
Clinical Features
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Fig. 15-40: CT scan of lymphangioma of eye showing destructive
lesion of left eye (Courtesy Dr Bhaskar Patle).
Diagnosis
Clinical featuresirregular nodular lesion of tongue can
give clue to diagnose lymphangioma.
Laboratory diagnosiscapillary types are composed of
proliferation of thin walled endothelium-lined channels,
primarily devoid of erythrocytes. Cavernous type is
characterized by presence of dilated sinusoidal
endothelium-lined vascular channels, devoid of
erythrocytes.
Fig. 15-39: Lymphangioma affecting left eye of the patient
(Courtesy Dr Bhaskar Patle).
Management
Surgical removalit is done to remove bulk of the lesion.
Partial or complete spontaneous involution is
occasionally noted.
Sclerosing agent therapyas such it does not respond to
sclerosing agents. But some success has been reported
by using OK-432 a lyophilized incubation mixture of
low virulent strain of Streptococcus pyogens with
penicillin G potassium which has lost streptolysin S
producing ability.
Arteriovenous Fistula
It is also called as arteriovenous shunt or arteriovenous
malformation. It is a direct communication between an artery
and vein that bypasses the intervening capillary bed. It
may be congenital or acquired.
Radiological Features
Classification
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Clinical Features
Radiographic Features
Siteit develops in the ramus and retromolar areas of
the mandible and may also involve the mandibular
canal.
Radiodensityit causes a resorptive radiolucent lesion.
Marginsthey are well defined and corticated.
Appearanceit is multilocular. Walls of shunt may
contain apparent calcified material.
Angiographyit is seen as abnormal collection of vessels
located in the suspected area, with many vessels feeding
and draining the lesion.
Diagnosis
Clinical diagnosisa lesion with a thrill or bruit, or with
an obviously warmer surface, is most likely a special
vascular malformation, called arteriovenous malformation
Radiological diagnosisirregular alveolar canal will give
clue to the diagnosis. Angiography (Fig. 15-41) and
contrast study CT scanning will be helpful in conforming
the diagnosis.
Glomus Tumor
It is also called as glomangioma. It is a rare neoplasm derived
from glomus cells. They are thought to be closely related to
hemangiopericytoma. The glomus is arteriovenous anastamosis that controls the blood supply and temperature of
the skin and certain deeper tissues. These functions appear
to be mediated in some way by the rich nerve supply and
by certain epithelioid cells that ensheath the arteriole of the
glomus. The epithelial cells are though to be comparable to
pericytes.
Clinical Features
Management
Diagnosis
Differential Diagnosis
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Management
Surgical excisionit is a benign tumor and removal of
this surgically effects the cure.
Hemangiopericytoma
Clinical Features
Age and sexit is more common in younger age group
within the range of 10 to 18 years. It is exclusively found
in males.
Sitemore commonly affected sphenoid sinus followed
by maxillary and ethmoid sinuses.
Symptomsnasal obstruction, epistaxis, facial deformity
(Fig. 15-42), proptosis, nasal voice, sinusitis, nasal
discharge, serous otitis media, headache and anosmia.
Signsit is slow growing angiofibroma and growth is
asymmetric.
Clinical Features
Age and sexthere is no sex predilection with age
ranging from birth to old age.
Siteit can occur at any site in the oral cavity.
Symptomsit is usually painless.
Appearancethe lesions are firm, apparently
circumscribed and often nodular. It may or may not
exhibit redness indicative of vascular nature.
Progressmajority of tumors grow rapidly and are
therefore of short duration.
Fig. 15-42: Facial deformity seen in angiofibroma
(Courtesy Dr Ashok L).
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisbiopsy shows proliferation of
occult capillaries. Each vessel in turn is surrounded by
a connective tissue sheath, outside of which are found
mass of tumor cells. The tumor cells may appear large or
small, round or spindle shaped and show tendency for
concentric layering about the capillaries.
Management
Surgical excisionlocal excision of the tumors is
treatment of choice.
Radiographic Features
Plain radiography featuresthere is soft tissue nasopharyngeal mass. There is also widening of the
pterygopalatine fossa with anterior bowing of the
ipsilateral posterior antral wall. A polypoid nasal mass
may cloud the ipsilateral ethmoid and maxillary sinuses.
Contrast-enhanced CTenhancing mass with appearance
same as plain film radiography. Intraorbital and
intracranial extension are much better visualized.
MRIit shows intermediate signal intensity on T1
weighted and T2 weighted sequences.
Diagnosis
Nasopharyngeal Angiofibroma
It is also called as juvenile nasopharyngeal angiofibroma as
its presence in younger age group. Nasopharyngeal
angiofibroma is an uncommon, highly vascular, nonencapsulated polypoid mass that is histologically benign
but locally aggressive. Hormonal influence is also present
in this tumor.
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Management
Surgical excisionsurgical excision is the treatment of
choice depending upon extent of lesion. Preoperative
embolization will help to prevent blood clot.
Radiotherapyit is advised for recurrent lesion.
Olfactory Neuroblastoma
Clinical Features
Ageit has got bimodal age distribution with first
incidence in 2nd decade and 2nd incidence in 6th
decade.
Symptomsthe most common symptoms are nasal
obstruction, epistaxis and pain.
Appearanceit appears as solitary mass, sessile or
pedunculated, which bleeds profusely.
Radiological Features
CTit appears as homogenous, enhancing mass
that primary remodel the bone. It commonly extends
into ethmoid and maxillary sinus and rarely into
sphenoid sinus. Gross calcifications occur within the
tumor mass.
MRIOn MRI, there will be intermediate signal intensity
and high T2 weighted signal intensity are found.
Origin
Schwann cells and axonit arises from the connective
tissue sheath of Schwann cells and axons.
Sites of originthere are three sites of origin: within the
inferior dental canal, in the substance of the bone and
beneath the periosteum.
Clinical Features
Age and sex distributionit occurs at any age but is found
more in younger group with no sex predilection.
Sitemost commonly affected sites are trunk, face and
extremities.
Appearanceit may appear as numerous sessile (Fig. 1544) or pedunculated, elevated smooth surfaced nodules
of variable size, which are scattered over the skin surface.
In some cases, loose overgrowth of thickened, pigmented
skin may hang in folds (Fig. 15-43).
Elephantiasis neuromatosain other forms, there are
deeper, more diffuse lesions which are often of greater
proportion than superficial nodules and are sometimes
referred to as elephantiasis neuromatosa.
Diagnosis
Clinical diagnosisnot specific.
Radiological diagnosison computed tomography
homogenous mass in sinus may suspect this tumor.
Laboratory diagnosisbiopsy shows small, round to
ovoid basophilic cells which are arranged in sheets and
lobules.
Management
Surgical excisionit is the treatment of choice. This
surgical excision is also combined with adjunct radiation
therapy.
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Fig. 15-45: Discrete non-ulcerated nodules seen in oral
cavity due to neurofibromatosis.
Radiographic Features
Fig. 15-44: Numerous sessile nodules seen on patient body
suggestive of neurofibroma (Courtesy Dr Milind Chandurkar).
Oral Manifestations
Common sitesit may occur in mandibular canal, buccal
mucosa, and alveolar ridge and below the periosteum.
Central lesionthe central lesion may have multiple
lesions, occurring in both jaws simultaneously,
expanding and filling the maxillary sinus. Solitary
central lesion may infrequently be associated with brown
spots on skin.
Symptomsit may produce pain or paresthesia, if
associated with mandibular nerve.
Appearancethere are discrete, non-ulcerated nodules,
which tend to be of the same color as the normal mucosa
(Fig. 15-45).
Signsit may expand and perforate the cortex,
producing a swelling that is either hard or firm on
palpation.
Extraperiosteal neurofibroma
Appearancethere is an area of bone destruction
which presents a radiolucent shadow of varying
density, depending on the amount of bone that has
been replaced by tumor.
Sizethe size of the lesion is variable from less than
one centimeter up to a very large lesion.
Marginsmargins of radiolucency are well defined,
curved and may be hyperostotic.
Subperiosteal neurofibromain some cases the periosteum lays down a layer of bone on the superficial aspect
of the tumor. Tumor that causes relatively little
indentation of the surface of the bone appears as
radiolucent areas, the darkness depending on the depth
of bone loss; deeper lesion causing greater darkness in
the radiograph than the superficial ones. There is
tendency for the shadow to be more or less circular and
there may be well defined margins, with or without a
bony cortex.
Neurofibroma of inferior dental nerveit shows fusiform
or more or less circular enlargement of mandibular canal.
In some cases there may be an elongated lesion with an
undulating border.
Diagnosis
Clinical diagnosispigmented swelling with caf au lait
spots.
Radiological featuresradiolucent lesion with corticated
border (Fig. 15-46).
Laboratory diagnosisit is composed of proliferation of
delicate spindle cells with thin wavy nuclei intermingled
with neurites in an irregular pattern as well as delicate
intertwining connective tissue fibrils.
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Fig. 15-46: CT scan of neurofibroma showing circular
radiolucency with corticated border.
Differential Diagnosis
Vascular lesionchanges in the canal from neural lesion
are more localized and have a fusiform enlargement,
while the vascular lesion enlarges the whole canal and
alters its path.
Management
Radiographic Features
Schwannoma
It is also called as neurilemmoma, perineural fibroblastoma,
neurinoma and lemmoma. But nowadays all above terms
are not used and Schwannoma is the only term used. It is of
neuroectodermal origin, arising from Schwann cells that
makes the inner layer covering the peripheral nerves.
Clinical Features
Age and sexoccurs at any age, from very young to very
old, with equal frequency in both the sexes.
Sitethe tumor usually occurs in the subcutaneous
tissue, but internal organs such as stomach may be
affected. Intraorally, mandible and tongue is the most
commonly affected site for central lesion. Other sites
which can be involved in these tumors are palate, floor
of mouth and buccal mucosa.
Progressit is a slow growing lesion and is usually of
long duration at the time of presentation.
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Differential Diagnosis
Cystsin neurilemmoma there is an expansion of the
inferior alveolar nerve canal.
Ameloblastomait usually occurs above the canal.
Vascular lesionthe expansion of the canal caused by
neural neoplasm is more concentric, creating a fusiform
shape; whereas vascular lesion increases the girth of
the canal down the entire length and often alters the
shape into a serpiginous form.
Radiographic Features
Sitein mandible it is associated with the mandibular
canal. In maxilla, it is seen in anterior maxilla.
Radiodensityit is seen as a destructive lesion. It appears
as a radiolucent area.
Marginsit has got well defined and corticated borders
(Fig. 15-49).
Inferior alveolar nerve canal some expansion of the canal
is seen.
Management
Surgical excisionit is the treatment of choice.
Neuroma
It is also called as amputation neuroma or traumatic neuroma.
It is not a true neoplasm, but an exuberant attempt at repair
of a damaged nerve trunk.
Etiopathogenesis
Causesnerve damage may result from fracture,
dissection, removal of cyst, nerve avulsion for neuralgia
or even extraction of teeth.
Overgrowth of nerveit is an overgrowth of severed nerve,
attempting to regenerate when the scar tissue or
malalignment of a fractured nutrient canal blocks the
distal end.
Unorganized collection of nerve fibersproliferating nerve
forms unorganized collection of nerve fibers, composed
of varying proportion of axons, perineural connective
tissue and Schwann cells.
Clinical Features
Age and sex distributionit can occur at any age and it is
more common in females.
Siteit typically occurs near the mental foramen, on the
alveolar ridge in edentulous areas or on the lips and
tongue.
Appearanceit appears as a small nodule or swelling of
the mucosa.
Symptomsdue to the pressure applied by enlargement
of the tangled mass in its bony cavity, severe pain may
be experience. It may have reflex neuralgia with pain
referred to the eye, face and head.
Diagnosis
Clinical diagnosissevere pain, nodule in mental
foramina area with history of extraction will aid in
diagnosis of traumatic neuroma.
Radiological diagnosisradiolucent lesion in the mandibular region with corticated border.
Laboratory diagnosisbiopsy shows mass of irregular
and interlacing neurofibrils and Schwann cells, situated
in connective tissue stroma of either scanty or plentiful
proportion.
Management
Surgical excisionsimple excision of nodule along with
proximal portion of the involved nerve.
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Radiological Features
Clinical Features
Diagnosis
Clinical diagnosisnot so specific.
Laboratory diagnosisbiopsy shows interlacing fascicles
of spindle that consist of Schwann cells. Nuclei are wavy
and pointed. Palisading and Verocay bodies of Antoni
A cells are present.
Diagnosis
Clinical featuresblue black mass in anterior maxilla in
infant will give clue to diagnosis.
Laboratory diagnosishigh urinary level of vanillylmandelic acid (VMA). Biopsy shows both pigmented
and non-pigmented cells.
Management
Surgical removalconservative surgical excision should
be carried out. Recurrence is extremely low.
Management
Muscle Tumors
Leiomyoma
Ganglioneuroma
It is same like neuroblastoma, but in it, differentiated cells
are numerous. It grows less rapidly than the neuroblastoma
and when fully differentiated, it depicts benign
characteristic. The fully differentiated ganglioneuroma is
composed of cells that are very much like the normal cells.
Numerous nerve fibers and well differentiated nerve
bundles are present.
Clinical Features
Age and sexit occurs in infants under the age of six
months, with equal sex distribution.
Sitemaxilla is more commonly affected than mandible.
It is more common in anterior region.
Symptomsit is symptomless tumor.
Appearanceit is rapidly growing, non-ulcerated, darkly
pigmented lesion. It is blue black in color.
Clinical Features
Age and sexit occurs in middle decades of life. Males
are affected more commonly than females.
Siteit usually occurs in uterus. It is uncommon in oral
cavity due to general absence of smooth muscles except
in blood vessel walls and circumvallate papillae of
tongue. The smooth muscle of the arrectores pilorum
may be a source of cheek tumor.
Symptomsthe patient may complain of sore throat or
tumor in the throat. In some cases, there may be pain.
Appearanceit is a slow growing, painless lesion, which
is superficial and often pedunculated.
Sizein most of the cases, the lesion is small.
Colorit does not ulcerate and resembles the normal
mucosa in color and texture. In case of vascular
leiomyomas it can exhibits bluish hue.
Diagnosis
Clinical diagnosisit has got no typical clinical features.
Laboratory diagnosisbiopsy shows interlacing bundles
of smooth muscle fibers, interspersed by varying
amounts of fibrous connective tissue.
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Management
Surgical excisionit is treated by conservative surgical
excision of the tumor.
Origin
Striated muscleit may be derived from striated muscles.
But, these tumors may be found in areas like breast and
skin, where the striated muscles are absent.
Neural theoryin neural theory it is proposed that these
tumors are derived from the connective tissue of nerves
and hence was called as granular cell neural fibroma.
Stem cellssome authors state that it is derived from
stem cells with a leiomyofibrillogenic capacity, which
may be some type of specialized smooth muscle cells
peculiar to certain tissue, that are found in characteristic
sites of the tumor.
Rhabdomyoma
Clinical Features
Age and sexit can occur at any age and females are
affected more commonly than males.
Sitemost common site of occurrence is dorsum of tongue
followed by skin, lips, breast, subcutaneous tissue, vocal
cord and floor of mouth.
Appearancelesion which is found on tongue is usually
single firm, submucosal nodule within the substance of
the tongue itself.
Sizethe size of the tumor varies from a few millimeters
to few centimeters.
Colorcolor is usually pink but some tumor may appear
yellow in color.
Signslesion is not ulcerated and may have normal
covering or may exhibit some clinical leukoplakia.
Clinical Features
Agemost commonly occurs in 5th decade of life with
male to female ratio of 2:1.
Siteit mostly occurs in head and neck region. The most
common sites of occurrence, intraorally, are the floor of
the mouth, tongue, soft palate, buccal mucosa and lower
lip.
Symptomsit is painless and slow growing. Laryngeal
and pharyngeal lesion may lead to airway obstruction.
Appearanceit presents a well circumscribed tumor mass
which may have a known duration of months or even
several years.
Diagnosis
Clinical diagnosisit has got no typical clinical features.
Laboratory diagnosisthe nucleus is vesicular and cells
with several nuclei are sometimes seen.
Adults typein adult type, the tumor is composed of
large, round cells that have granular, eosinophilic
cytoplasm and show irregular cross striations. The
cytoplasm is rich in glycogen and glycoprotein.
Fetalfetal type is characterized by immature skeletal
muscles in varying stages of development and
undifferentiated mesenchymal cells.
Diagnosis
Clinical diagnosissubmucosal swelling on the dorsum
of tongue may give clue to diagnosis (Fig. 15-50).
Laboratory diagnosisthe lesion is composed of two types
of cells: granular cells and satellite cells. The large
granular cells are called as Abrikossoff myocytes.
Management
Surgical excisionit is excised conservatively usually
enucleating with ease.
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Management
Surgical excisionit is best treated by conservative local
excision of the tumor.
Fig. 15-51: Bluish color of central giant cell tumor shows its vascular
nature (Courtesy Dr Tapasya Karamore).
Radiological Features
Origin of Giant Cells
Different theories are given to describe the origin of giant
cells in these lesions:
Resorption of deciduous rootsGiant cells might be derived
from the proliferating giant cells associated with the
resorption of deciduous tooth roots. But for this,
association of the lesion in transition period i.e. from of
deciduous to permanent tooth should be there: but such
association is found only in few cases.
Endothelial cells of capillariesanother theory states that
it originates from the endothelial cells of capillaries. To
support this theory: there is a common occurrence of
giant cells in vascular channels, suggesting that they
arise from endothelial cells.
Modified form of cellsSapp found that giant cells,
ultrastructurally, contain a sufficient number of features
in common with osteoclasts. This concludes that they
represent a slightly modified form of the cells.
Clinical Features
Age and sex distributionit is most frequently seen in
3rd and 4th decades, it is unusual in patients less
than 20 years. Women are more affected as compared to
males.
Sitethe commonest sites for giant cell tumor are the
lower end of the femur, upper end of the tibia and lower
end of the radius. In the oral cavity it is rare and if found
it is in jaw.
Symptomsthe principal symptoms are swelling of the
bone accompanied in some cases by pain. The color of
lesion is blue due to its cortical and mucosal thinning
and internal vascularity (Fig. 15-51).
Signsthe swelling may be tender and egg shell
crackling can be elicited in large tumors. There is also
expansion of jaw which is painless.
Diagnosis
Clinical diagnosisbluish color vascular lesion may
suspect central giant cell tumor.
Radiological diagnosismultilocular lesion with thin
cortex will give clue to diagnosis.
Laboratory diagnosisthe tumor forms a maroon or
reddish brown fleshy mass that replaces the spongiosa
of the bone. It consists of numerous giant cells lying in
cellular matrix composed of spindle shaped cells and
scanty collagen.
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Etiology
Injuryit is an unusual response of tissue to injury. The
trauma may be caused by tooth extraction and dental
irritation.
Chronic infectionit can occur in chronic infections.
Hormonalit may appear under the stimulus of
increased circulating parathormone i.e. primary and
secondary hyperparathyroidism.
Clinical Features
Age and sex distributionmost oftenly seen over 20 years
of age, with an average of 45 years. Females are affected
twice as common as males. Predominant in white
persons.
Common siteit occurs on gingiva and alveolar mucosa,
most frequently anterior to molars. It is common in
mandible than maxilla.
Early lesionit appears as discoloration and slight
swelling of the buccal aspect of the gingiva.
Later lesionthe lesion increases in size and becomes
rounded and very often pedunculated (Fig. 15-53).
Hourglass appearancesometimes, it grows in an
hourglass manner, with the waist of the lesion between
two teeth and the globular extremities presenting
buccally and lingually (Fig. 15-54).
Colorthe color of the lesion is usually dark red (Fig.
15-55) or maroon color. If sufficient amount of
hemosiderin exists near the periphery, the lesion is
bluish, otherwise it is red and/or pink. Lesions with
much fibrous tissue are paler.
Consistencyit may feel soft to hard.
Sizethe lesions vary in size from 0.5 cm to 1.5 cm in
diameter.
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Radiological Features
Edentulous areain edentulous areas, the peripheral
giant cell granuloma characteristically exhibits
superficial erosion of the bone with peripheral cupping
of the bone.
Dentulous areain dentulous areas, there may be
superficial destruction of the alveolar margins or crest
of the interdental bone.
tissue, hair and skin are seen in this tumor. The lesion that
arises in the base of the skull often extends into the cranial
and oral cavity; newborn infants with such lesions rarely
survive.
Clinical Features
Ageit is known to be present at birth or is discovered
shortly thereafter.
Siteit can occur in ovaries, testes, anterior mediastinum, retroperitoneal area, presacral and coccygeal
regions, pineal region, head, neck and abdominal
viscera. In oral cavity it can be seen on hard palate and
soft palate area.
Symptomsthey are benign lesions and grow slowly.
Signsthey often contain recognizable hair, sebaceous
material and teeth.
Diagnosis
Clinical diagnosisdark red color lesion with hourglass
appearance soft in consistency will favor the diagnosis
of peripheral giant cell granuloma.
Laboratory diagnosismultinucleated giant cells and
young connective tissue spindle shaped cells are
scattered throughout the granulation tissue in delicate
reticular and fibrillar connective tissue stroma.
Differential Diagnosis
Hemangiomapresent at birth, seldom occurs on gingiva.
Lymphangiomait is rare on gingiva and color is same
as the tissue.
Metastatic carcinomahistory of primary tumor.
Oral nevi and nodular melanomafirm on palpation and
darker in color.
Management
Surgical excisionexcision with borders of normal tissue
with entire base of the lesion, so that recurrence is
avoided.
Removal of causeelimination of chronic irritant.
Teratoma
It is also called as teratoblastoma or teratoid tumor. It is a
neoplasm of different types of tissue which are not native
to the area in which the tumor occurs. True teratoma is
developmental tumor which is composed of all the three
germ layers ectoderm, mesoderm and endoderm. Out of
these three layers, one of the layers exhibits neoplastic
proliferation.
It is congenitally acquired and usually found in the
ovary. The finding of various organs like structure i.e. teeth,
B
Figs 15-56A and B: (A) Child patient with appearance of
double palate. (B) Same patient after 2 years showing
double arch and double palate ( Courtesy Dr Debta).
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Pyogenic Granuloma
Diagnosis
Clinical diagnosisit is not difficult to make clinical
diagnosis as tissue present in teratoma is not of that
particular site.
Laboratory diagnosisbiopsy shows epithelium and
epithelial appendages such as hair, sweat gland,
sebaceous glands, salivary glands and teeth as well as
discrete epithelial organs such as thyroid gland and
pancreas.
Management
Surgicalsurgical removal of the tumor should be
carried out.
Inflammatory Hyperplasia
Chronic injury produces inflammation, which in turn
stimulates the formation of granulation tissue that
consists of proliferative endothelial tissue with rich patent
Etiology
Microorganismsit is usually due to botryomycotic
infection, staphylococci and streptococci.
Traumait may occur as a result of minor trauma to the
tissue, which provides a pathway for the invasion of
tissues by non-specific of microorganisms.
Local irritantit is an inflammatory response to local
irritation such as calculus.
Hormonal imbalanceit is a contributing factor for the
development of some pyogenic granulomas.
Clinical Features
Age and sexfemales are affected more than males with
common age of occurrence are 11 to 40 years.
Sitescommon sites are gingiva, lip, tongue, buccal
mucosa, palate, vestibule and alveolar mucosa.
Symptomsit is an asymptomatic papular, nodular
polypoid mass.
Appearancelesions are elevated, pedunculated or
sessile masses with smooth, lobulated or even warty
surface.
Surfacesurface can commonly ulcerate and shows
tendency to hemorrhage upon slightest pressure or
trauma.
Pussometimes, there is exudation of purulent material.
Colorit is deep red to reddish purple depending on
the vascularity (Fig. 15-58); it is painless and rather soft
in consistency, with some lesions having brown cast, if
hemorrhage has occurred into the tissues. If lesion is of
mixed variety it appears red with pink areas and if it is
completely fibrous it is slightly pink and firm on
palpation.
Consistencyit feels moderately soft and bleeds readily.
Sizeit may develop rapidly, reaching full size and
remain static for an indefinite period with size ranging
from few millimeters to centimeters. Average size of
lesion being 0.9 to 1.2 cm.
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Fig. 15-58: Pyogenic granuloma presenting as reddish
purple mass on gingiva (Courtesy Dr Chole).
Diagnosis
Clinical diagnosisreddish purple lesion, soft in
consistency can be pyogenic granuloma.
Laboratory diagnosisbiopsy shows granulation tissue
which is exuberant and is usually localized. Overlying
epithelium, if present, is generally thin and atrophic,
but may be hyperplastic.
Etiology
Differential Diagnosis
Clinical Features
Management
Surgical excisionsurgical excision is done and care is
taken to remove the calculus of adjacent teeth as it may
act as a local irritant and cause recurrence.
Removal of irritantelimination of the causative agent
should be done.
Pregnancy Tumor
Pregnancy tumor usually develops in first trimester of
pregnancy. The size usually increases in 7 months of
pregnancy (Fig. 15-59).
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Diagnosis
Clinical diagnosiswell defined tumor-like lesion in
pregnancy will diagnose this condition.
Radiological diagnosisnot so specific.
Laboratory diagnosisbiopsy shows similar feature as
that of pyogenic granuloma.
Management
No treatmentno treatment should be given to patient as
maximum cases regress by its own after pregnancy.
Surgical excisionif pregnancy tumor does not resolve
after pregnancy, it should be surgical excised.
Parulis
It is a small inflammatory hyperplastic type of lesion that
develops on the alveolar mucosa at the oral terminal of
draining sinus (Fig. 15-61). Maxillary labial and buccal
mucosa are commonly affected. Slight digital pressure on
periphery of parulis may force a drop of pus from the sinus
opening. It usually regresses after the infection is eliminated.
Clinical Features
Age and sexIt can arise at any age in adults and has no
definite sex predilection.
Siteit occurs exclusively on palate beneath the
complete or partial denture. It occurs predominately in
edentulous patients and the site of lesion corresponds to the denture base. In rare cases, cheek may be
involved.
Appearancewhole palatal mucosa under the denture
may be covered with numerous small polypoid masses.
Warty appearancethe lesion presents as numerous
closely arranged, red, edematous papillary projections
(Fig. 15-62) often involving nearly all of the hard palate
and imparting it to a warty appearance.
Etiology
Frictional irritationit is produced by loose fitting
dentures on palatal tissues. It occurs in patients who
sleep with their dentures. It is much common in acrylic
dentures than in those with metallic dentures.
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Epulis Granulomatosum
It is reactive hyperplasia that develops within a tooth socket
after the extraction or exfoliation of tooth. It is caused by
sharp spicules of bone in socket.
Clinical Features
Diagnosis
Clinical diagnosispapillary projection beneath the
palatal denture will diagnose this lesion.
Laboratory diagnosisbiopsy shows numerous small
vertical projections, each composed of parakeratotic or
sometimes orthokeratotic stratified squamous epithelium
and a central core of connective tissue.
Differential Diagnosis
Nicotina stomatitisOccurs almost exclusively in pipe
smokers who are not wearing maxillary complete
dentures. Lesions are more nodular and broader but less
elevated. Red dot is seen in center.
Verrucous carcinomapapillary hyperplasia may mimic
verrucous carcinoma. But here the papillary hyperplasia
is not associated with denture. Biopsy should be done
to rule out verrucous carcinoma.
Management
Removal of dentureremove the denture at night to
provide rest to the tissue. In many cases tissue will
resume normal appearance after denture is removed.
Conditioning linerconditioning liner should be applied
under the denture. This will act as palatal dressing and
promotes greater comfort.
Topical antifungal treatmentin case with superimposed
candidal infection, topical application of antifungal
agents should be used. Most commonly used is nystatin
ointment.
B
Figs 15-64A and B: Epulis granulomatosum showing
growth in the extraction socket.
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Suggested Reading
Diagnosis
Clinical diagnosishyperplasia in extraction socket will
be diagnosed this condition.
Differential Diagnosis
Antral polypsinus wall defect is usually demonstrated
either radiographically or by requesting the patient to
blow air through the nose while nostrils are occluded.
Pulp polypextensive destruction of tooth can be seen.
Malignancyradiological changes are present.
Management
Curettageit is done to remove the granulation tissue
and smoothing of the socket borders is indicated.
Excisional biopsyit should be done.
Nodular Fasciitis
It is also called as pseudosarcomatous fasciitis. It is nonneoplastic connective tissue proliferation. It histologically
mimics malignant mesenchymal neoplasm but its clinical
behavior is benign. It appears to be an inflammatory reactive
phenomenon.
Clinical Features
Age and sex distributionit is more commonly seen in
4th and 5th decade of life. There is no sex predilection.
Siteit is more common on the trunk and extremities.
Intraorally, it is seen on buccal mucosa followed by
subcutaneous tissues overlying the mandible, zygoma,
parotid sheath and oral mucosa.
Symptomsit appears as a small lump, which may be
painful.
Signit has got exophytic presentation.
Sizethe lesion often enlarges rapidly, but only to
maximum size of 4 cm, where it remains stationary or
regresses.
Diagnosis
Clinical diagnosisit is not specific.
Laboratory diagnosisbiopsy shows proliferation of
fibroblast in haphazard manner in a vascular myxoid
matrix which is rich in acid mucopolysaccharide. It
results in a loose textured feathery appearance. There is
frequent patchy chronic inflammatory infiltration,
consisting of lymphocytes and occasional plasma cells
and macrophages.
Management
Surgical excisionlocal excision will yield excellent
result.
1. Abbey LM, Page DG, Sawyer DR. The clinical and histopathological features of series of 464 squamous cell papillomas.
Oral Surg, Oral Med, Oral Pathol 1980;49:419-28.
2. Al-Dewachi HS, AL-Naib N, Sangal BC. Benign Chondroblastoma
of the maxilla: a cases report and review Chondroblastoma in
cranial bones. Br J Oral Surg 1980;18:150-2.
3. Allen CM, Kapoor N. Verruciform Xanthoma in bone marrow
transplant patient. Oral Surg, Oral Med, Oral Pathol 1993;75:5914.
4. Antoniades DZ, Belazi M, Papanayiotue P. Concurrence of torus
palatinus with palatal and buccal exostoses: case report and
review of literature. Oral Surg, Oral Med, Oral Pathol Endod
1998; 85:552-7.
5. Auclair PL, et al. A clinical and histomorphologic comparison of
the central giant cell granuloma and the giant cell tumor. Oral
Surg, Oral Med, Oral Pathol 1988;66:197-208.
6. Barker DS, Lucus RB. Localized overgrowth of the oral mucosa.
Br J Oral Surg 1967;5:86-92.
7. Bataineh AB, Mansour MJ, Abalkhail A. Oral infiltrating lipoma.
Br J oral Maxillofac Surg 1996;34:520-3.
8. Bhaskar SN, Beasley JD III, Cutright DE. Inflammatory papillary
hyperplasia of the oral mucosa: report of 341 cases. JADA
1970;81:949-52.
9. Bhaskar SN, Jacoway JR. Pyogenic granuloma: clinical features,
incidence, histology and results of treatment: report of 242 cases.
J Oral Surg 1966;24:391-8.
10. Bodner L, Peist M, Gatot A, Fliss DM. Growth potential of
peripheral giant cell granuloma. Ora1 Surg, Oral Med, Oral Pathol,
Oral Radiol Endod 1997;83:548-51.
11. Bouckaert MMR, Raubenheimer EJ. Gigantiform melanotic neuroectodermal tumor of infancy. Oral Surg, Oral Med, Oral Pathol,
Oral Radiol Endod 1998;86:569-72.
12. Brener MD, Harrison BD. Intraoral blue nevus: a report of case.
Oral Surg, Oral Med, Oral Pathol 1969;28:326-30.
13. Brennan TD, Millar AS, Chen SY. Lymphangioma of the oral
cavity: a clinicopathologic, immunohistochemical and electron
microscopic study. J Oral Maxillofac Surg 1997;55:932-5.
14. Buchner A, Hansen LS. Pigmented nevi of the oral mucosa: a
clinicopathologic study of 36 new cases and review of 155 cases
from literature: Part I: a clinicopathologic study of 36 new cases.
Oral Surg, Oral Med, Oral Pathol 1987;63:566:72.
15. Buchner A, Hansen LS. Pigmented nevi of the oral mucosa: a
clinicopathologic study of 36 new cases and review of 155 cases
from literature: Part II: analysis of 191 cases. Oral Surg, Oral
Med, Oral Pathol 1987;63:676-82.
16. Budtz-Jorgensen E. Oral Mucosal lesion associated with the
wearing of removable dentures. J Oral Pathol 1981;10:65-80.
17. Bunel K, Sindet-Pederson S. Central hemangioma of the mandible.
Oral Surg, Oral Med, Oral Pathol 1993;75:565-70.
18. Carew JF, Singh B, Kraus DH. Hemangiopericytoma of head and
neck. Laryngoscope 1999;109:1409-11.
19. Chauvin PJ, Wysocki GP, et al. Palisaded encapsulated neuroma
of oral mucosa. Oral Surg, Oral Med, Oral Pathol 1992;73:71-4.
20. Chin DC. Ttreatment of maxillary hemangioma with sclerosing
agents. Oral Surg, Oral Med, Oral Pathol 1983;55:247-9.
21. Collins BM, Jones AC. Multiple granular cell tumor of the oral
cavity: a report of cases ad review of literature. J Oral Maxillofac
Surg 1995;53:707-11.
22. Corio RL, Lewis DM. Intraoral rhabdomyoma. Oral Surg, Oral
Med, Oral Pathol 1979;48:525-31.
23. Crinzi RA, Palm NV, et al. Management of dental infection in a
patient with Sturge Weber syndrome. JADA 1980;101:798-800.
24. Cutright DE. Osseous and chondromatous metaplasia caused
by dentures. Oral Surg, Oral Med, Oral Pathol 1972;34:625-33.
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16
Malignant Tumor
of Jaw
Oral Carcinoma
Oral carcinoma is one of the most prevalent cancers and is
one of the 10 major causes of death. Most common oral carcinoma is squamous cell carcinoma. It is a disease of increasing
age with 95% cases in people older than 40 years of age.
Cancer is a commonly used term for all malignant
tumors. In Latin language, cancer means crab which has
a fat meant body and mass extension which springs and
invades the surrounding tissues.
Cancer may be defined as an uncontrolled tissue growth
in susceptible patient, which result from imbalance
between cell division and programmed cell death.
Tumor is an autonomous new growth of tissue or it is an
abnormal mass of tissue, the growth of which exceeds and
is uncoordinated with that of normal tissue and persists in
Neural tissue
Neurosarcoma
Neurofibrosarcoma
Neuroblastoma
Ganglioneuroma
Muscle
Leiomyosarcoma
Rhabdomyosarcoma
Malignant granular cell myoblastoma
Lymphoid tissue
Hodgkins lymphoma
Non-Hodgkins lymphoma
Primary reticular cell sarcoma
Burkitts lymphoma
Leukemia
Myeloma
Multiple myeloma
Plasmacytoma
Tumor of salivary gland
Mucoepidermoid carcinoma
Adenocystic carcinoma
Adenocarcinoma
Acinic cell carcinoma
Malignant changes in pleomorphic adenoma
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Alcohol
Forms of alcoholall forms of alcohol; including hard
liquor, wine and beer has been implicated in the etiology
of oral caner.
Mechanismthe mechanism by which alcohol affects
includes the dehydrating effect of alcohol on the mucosa
which increases mucosal permeability and the effects of
carcinogens on the mucosa. Beverage congeners
include nitrosamines and impurities which can act as
carcinogens.
Associated habitmost of the heavy alcohol consumers
use tobacco, so it is very difficult to separate the ill effects
individually.
Actinic Radiation
It is a minor etiologic factor in case of lip cancer. Lip cancer
occurs more commonly in fair skinned people who are
generally engaged in outdoor occupation, such as farming
and fishing.
Atmospheric Pollution
Parts of the urban/rural difference in incidence of head
and neck cancers have been related to atmospheric
pollution.
Sulphur dioxide and smoke concentration in the
atmosphere are positively correlated with squamous cancer
of larynx and pharynx. The impact on cancer of the mouth
is likely to be less, but merits careful study.
Blue collar workers exposed to dust or inhalation of
organic and inorganic agents are at increased risk of cancers
of mouth.
Orodental Factors
It is more prevalent in patients with poor oral hygiene,
faulty restorations, sharp teeth, ill fitting dentures and those
with syphilitic glossitis.
Vitamin A Deficiency
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Immunity
The increasing incidence of oral cancers is clearly age
related, which may reflect declining immune surveillance
with age.
It may occur in immunosuppressed patients following
organ and bone marrow transplantation. HIV/AIDS
patients are at increased risk of oral cancer.
Syphilis
It is traditionally associated with oral cancer. Oral
malignancy is commonly found in tertiary stage of syphilis.
Another aspect why syphilis can lead to malignancy is
that in the management of syphilis previously we use
arsenic and heavy metal which has potential carcinogen.
Epithelial Tumors
Ionizing Radiation
Carcinoma of buccal mucosa may occur as a complication
of long-term radiotherapy.
Trauma
Trauma in combination with other factors like chronic
cheek biting, denture use and irregular teeth may act as a
co-carcinogen and may promote transformation of epithelial
cells.
Virus
The possibility of type I herpes simplex virus being
associated with oral cancer has been suggested.
Other viruses which can lead to oral cancer are human
papillomavirus and human immunodeficiency virus.
Intraoral Lesions
Chronic ulceration and fissureit can cause oral cancer
particularly of lip.
Lichen planusreports of carcinoma supervening on
lichen planus have been made in some cases.
Candidiasisit is possible precursor of carcinoma.
Candidal infection is often associated with acanthosis
and parakeratosis.
Leukoplakiait is common pre-malignant condition seen
in oral cavity. Nodular leukoplakia show higher rates
of epithelial dysplasia.
Median rhomboid glossitisin some cases, it has followed
by cancer.
Clinical Features
General features
Age and sexpredominately, it occurs in males with
ratio of 2:1, older than 50 years with an average age of
approximately 60 years.
Sitemost commonly involved are the posterior and
lateral borders of the tongue and lower lip and less
frequently the floor of mouth, alveolar mucosa, palate
and buccal mucosa. It may be solitary and multifocal.
Symptomspatient may present with awareness of a
mass in the mouth and neck. Small lesion is asymptomatic. Large lesions may cause some pain or paresthesia and swelling. Patients complain of persistent ulcer
in the oral cavity. Function of organ in which malignancy
occur is impaired.
Appearancethe clinical appearance of a carcinomatous
ulcer is that one of irregular shape (Fig. 16-2), indurated
and raised everted edges.
Baseusually have broad base and are dome-like or
nodular. Base is firm on palpation.
Exophytic lesionit has irregular, fungating, papillary
and verruciform surface. The surface is ulcerated and
base is hard on palpation (Fig. 16-3).
Endophytic lesionthis is depressed irregularly shaped
ulcerated central area with surrounding rolled border.
The rolled border results from invasion of tumor in the
tissue (Fig. 16-4).
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B
Figs 16-7A and B: Carcinoma of buccal vestibule which also
involve buccal mucosa (Courtesy Dr Suwas Darvekar).
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B
Figs 16-11A and B: Carcinoma of palate showing extensive lesion
and ulceration (Courtesy Dr Suwas Darvekar).
Carcinoma of palate
Causeit is common in area where reverse smoking is
practiced.
Sexit is seen more commonly in females as compared
to men, in case of reverse smoking.
Appearancepalatal cancer usually manifests as a poorly
defined ulcerated painful lesion on one side of the
midline (Figs 16-11A and B).
Base and surfacemost of the lesions are exophytic and
with broad base and nodular surface.
Carcinoma of oropharynx
Sitecarcinoma of soft palate and oropharyngeal
mucosa can occur.
Symptomsdysphagia, i.e. difficulty in swallowing is
the most common complaint. Patient may complain of
pain which is dull and sharp and is referred to ear.
Appearanceit is same as that of other carcinoma.
Sizesize of the tumor is always greater than other
carcinoma of the oral cavity.
Other specific carcinomas of gingiva, tongue, lip
and maxillary sinus are described in their respective
chapters.
Radiographic Features
Siteit may be found along the entire border of the tumor
or may be restricted to a relative small area. Irregular
spicule of bone may be left behind.
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3
Fig. 16-12: Saucer shaped erosion of mandible in
lower left posterior region.
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Differential Diagnosis
Clinical
Ulcerated benign tumorulcer should heal in one to two
weeks after removal of mechanical noxious agent.
Basal cell carcinomaa history of slower development
and more common due to exposure to sunlight.
Ulceration due to systemic diseasesusually multiple,
generalized poor condition and is usually painful.
Primary syphilitic lesioncausative agent is known, no
pain, indurated ulcer usually reddish brown with
copper color halo.
Necrotizing sialometaplasiarare inflammatory lesion of
smaller salivary glands, particularly in the posterior hard
palate, ulcers are usually painful with no raised borders,
no hardening and characteristic histology.
Peripheral metastatic tumorlow frequency.
Malignant salivary gland tumorcommon on posterior
hard palate, common in women and maintain their
dome-shape appearance.
Verrucous carcinomaslow growing and is associated
with prolonged use of tobacco, surface is papillomatous
and white due to retention of keratin.
Pyogenic granulomamoderately soft to palpation and
bleed easily.
Radiological
Osteomyelitisit usually produces some periosteal
reaction whereas squamous cell carcinoma does not.
Osteoradionecrosishistory of radiation therapy and
prior malignancy.
Periodontitisthe margins of periodontitis are smooth
and well defined as compared to carcinoma.
Periodontitis is usually generalized and if it is localized,
there is specific cause for it.
Papillon Lfevre syndromeit produces symptoms of
infection and shows areas of sequestration.
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Management
Management is discussed in detail at the end of this chapter:
Removal of causeremoval of any local irritants i.e. the
(5-S) smoking, spices, spirit, sepsis and syphilis.
Excisional biopsyexcisional biopsy, if lesions are small.
Surgerycryosurgery, laser surgery and radical surgery.
Radiationradiation can be given in squamous cell
carcinoma.
Chemotherapychemotherapy is usually given in
patient who cannot undergo surgical or radiation
therapy.
Metastatic Carcinoma
It is also called as secondary carcinoma. It is the most common
malignant tumor in the skeleton. This tumor is transported
to an area distant from its origin and establishes a new foot
holds and are said to have metastasized. Although the
metastatic carcinoma of jaw is uncommon, its recognization
is important because the jaw tumors may be the first
indication that the patient has a malignant disease. Oral
diagnostician can make an invaluable contribution of
pathologic process of bone. Most common sites of origin
are breast, lung, kidney, thyroid, prostate and colon.
Clinical Features
Ageit is found in patients between 40 and 60 years of
age and there may be history of primary tumor.
Sitemandible is involved much more frequently than
maxilla (Fig. 16-19), especially in the region near
premolars and molars as tumor metastasizes to those
bones which are rich in hemopoietic marrow. It is
said that blood flow rate is decreased in areas of
Radiographic Features
Osteolytic type
Radiodensityill-defined radiolucent destructive lesion
may be single or multiple and vary in size.
Siteit is seen in mandible (Fig. 16-20) and are bilateral
in occurrence. The lesion may be located in the
periodontal ligament space.
Appearancean appearance that is highly suggestive of
metastatic carcinoma is the combination of an area of
bone destruction having very irregular margins with
islands of bone within radiolucent areas.
Moth eaten appearancethe other appearance of the lytic
type of metastasis in the jaw is one that has considerable
Fig. 16-20: Osteolytic variety of metastatic carcinoma showing radiolucency in mandibular right posterior region (Courtesy Dr Ashok L).
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Diagnosis
Clinical diagnosisunexplained mobility of teeth,
unhealed socket with numb chin syndrome may suspect
metastatic carcinoma.
Radiological diagnosissalt and pepper appearance are
seen in osteoblastic variety and ill defined radiolucency
are seen in osteolytic variety.
Laboratory diagnosisbiopsy features are similar to
squamous cell carcinoma.
Differential Diagnosis
Exophytic squamous cell carcinomathere is history of
primary tumor. Clinically squamous cell carcinoma is
well distinguishable.
Multiple myelomathe borders of multiple myeloma are
better circumscribed than metastatic tumor.
Periapical inflammatory lesionif the metastatic tumor is
situated in the periodontal ligament space then it may
be confused with metastatic tumor. But in case of
inflammatory lesion, periodontal ligament space
widening is more centered around the apex of the teeth
and in metastatic tumor there is irregular widening.
Malignant salivary gland tumorit is not so common in
mandible.
Management
Combination therapyIt can be treated by chemotherapy,
radiation therapy, surgery, immunotherapy and
hormone therapy. Prognosis is poor and death occurs
within a short time.
Etiology
Prolonged exposure to sunlightthe specific factor in
sunlight responsible for skin carcinogenesis appears to
be an ultraviolet radiation.
Others factorsother factors are also responsible like
burn scars and ionizing radiation. General atrophy
associated with aging process; at least, predispose to
develop the skin cancer.
Clinical Types
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Histological Types
Clinical Features
Age and sex distributionit is seen in middle aged or
elderly person usually in 4th decade of life. It is much
more common in men than women because men are
exposed to the environmental elements more than
women.
Siteit develops most frequently on exposed surface of
skin, middle-thirds of face and the scalp. There is also
involvement of lip. The upper lip is involved more
commonly than the lower lip.
Raceblond people with fair complexion who have spent
much of their lives outdoors are often victim of these
lesions.
Appearanceit begins as a small, slightly elevated papule
which ulcerates, heals over and then breaks down again
to form crusted ulcer.
Marginsit develops a smooth, rolled border representing tumor cells spreading laterally beneath the skin
(Fig. 16-22).
Diagnosis
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Diagnosis
Management
RadiationX-ray radiation is the most commonly
accepted treatment.
Malignant Melanoma
It is also called as melanosarcoma. It is a neoplasm of
epidermal melanocytes. It is one of the biologically
unpredictable and deadly of all human neoplasms.
Etiology
Clinical Features
Age and sex distributionmean age of occurrence is 44
years.
Symptomsthere may be sore throat, nasal obstruction,
defective hearing or ear pain, headache, dysphagia,
epistaxis and ocular symptoms.
Primary lesionthe primary lesions are very small
often completely hidden, usually slightly elevated (Fig.
16-24). In some cases, primary lesion is ulcerated with
granular eroded surface.
Advanced lesionas the tumor is advanced, its size is
increased rapidly and base of tumor appear indurated.
In some instances, it appears as an exophytic or
fungating growth.
Lymph nodesswelling of regional lymph node is the
most common occurrence.
Types
Superficial spreading melanomaIt is the most common
cutaneous melanoma.
Nodular melanomait is a form of cutaneous melanoma
and occurs in head and neck area.
Lentigo maligna melanomait develops from precursor
lesion called lentigo maligna.
Acral lentiginous melanomait is the most common form
of melanoma in black. It is most common in oral cavity.
Growth Pattern
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Clinical Features
Oral Manifestations
Appearanceit begins as pigmented macule in superficial radial growth pattern, restricted mostly to
epithelium and junction. In advanced cases, melanoma
present as an ulcerated, fungating growth which is
associated with bleeding.
Amelanotic melanomaSome lesions are devoid of
pigmentation which is called as amelanotic melanoma.
Nodular melanoma
Sitethey have a predilection for occurrence on head
and neck of men.
Colorcolor varies from mucosal pink through brown
and blue to black.
Consistencyit is firm on palpation.
Marginsit has got erythematous borders which
surround the tumor.
Extentthere is rapid infiltration in nodular type of
melanoma. It may be focal or diffuse.
Signsmany times, it may ulcerate and hemorrhage may
be seen. In later stages, it becomes more diffuse, nodular
and tumefactive with foci of hypo- and hyperpigmentation. It presents as a sharply delineated nodule with
some degree of pigmentation.
Lentigo maligna melanoma
Sexit occurs more often in women than in men.
Siteit has got predilection for exposed parts.
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Radiographic Features
Radiodensitysome melanomas in the jaws may present
radiographic picture which is indistinguishable from
osteomyelitis. Sometimes, small radiolucency with
irregular border may be seen (Fig. 16-27).
Management
Surgical excisionit is treated by surgical excision.
Surgical removal of regional lymph nodes should also
be carried out.
Other therapyother therapy like irradiation, immunotherapy and chemotherapy or, by combination of these
methods can also be tried. Survival rate is very poor and
is worse with metastasis.
Verrucous Carcinoma
It is a slow growing low-grade carcinoma. It is also called
as Snuff dipper cancer, Ackermans tumor. It is reported by
Ackerman in 1948 as spit tobacco associated malignancy.
Etiology
Tobaccotobacco chewers have high percentage of these
cases. It occurs usually in a person habitual to hold the
quid in the buccal sulcus (Fig. 16-28).
Diagnosis
Clinical diagnosisdarkly pigmented lesion with
ulceration will give clue to the diagnosis.
Radiological diagnosisnot specific.
Laboratory diagnosisin superficial spreading melanoma
melanocytes are arranged in pagetoid manner. In case
of nodular melanoma, there are large, epithelioid
melanocytes within the connective tissue. Small ovoid
and spindle shaped cells may be present. Lentigo
melanoma is characterized by increased number of
atypical melanocytes with the basal epithelial layer.
Clinical Features
Age and sexit is generally seen in elder population
with mean age of occurrences of 60 to 70 years. Men are
affected more as compared to women.
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Diagnosis
Fig. 16-29: Pebbly surface of verrucous carcinoma surrounded by
leukoplakic film (Courtesy Dr Parate).
Differential Diagnosis
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Clinical Features
Sex and age distributionit is more common in male with
mean age of occurrence of 57 years.
Common sitelower lip, tongue and alveolar ridge or
gingiva with remainder scattered at other site.
Symptomsthere is swelling, pain and presence of a
non-healing ulcer.
Appearancethe initial lesions appear either with a
polypoid, exophytic or endophytic configuration. The
lesion is fleshy.
Progressit grows rapidly and diagnose at later stage.
Diagnosis
Clinical diagnosisrapidly growing polypoid exophytic
mass can yield in the clinical diagnosis of the lesion.
Laboratory diagnosisbiopsy will show proliferation and
dropping off of basal cell to spindle cell.
Diagnosis
Clinical diagnosislesion on lower lip with nodular
surface and scaling will yield in diagnosis.
Laboratory diagnosisin biopsy, epithelium show the
characteristic solid and tubular ductal structures which
are lined by a layer of cuboidal cells and often contain or
enclose acantholytic or dyskeratotic cells.
Management
Surgical excisionit is treated by surgical excision.
Management
Radical surgerysurgical removal of tumor with or
without radical neck dissection is usually recommended.
Radiotherapyradiation therapy is also used in some
cases.
Clinical Features
Sex and age distributionfemales are affected more with
age ranging from 20 to 50 years and older.
Common siteit more commonly occurs on lip and also
in head and neck region. The lower lip is affected more
commonly than upper lip and common on the vermilion
border of lip.
Nasopharyngeal Carcinoma
It is tumor which arises from lining epithelium of lymphoid
tissue rich nasopharynx. It can be caused by environmental
factors, infection with Epstein-Barr virus, vitamin C
deficient diet, and consumption of salt fish which contains
carcinogen N-nitrosamines.
Clinical Features
Age and sex distributionit is common in older age group
and more common in men as compare to women.
Onsetthe initial lesion is small and difficult to detect.
Symptomspatient may notice serous otitis media,
otalgia and hearing loss from obstruction of eustachian
tube. Other symptoms noticed are nasal obstruction and
pharyngeal pain. If the tumor involves brain, it may
cause neurological symptoms.
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Diagnosis
Management
Radiotherapyas the tumor is inaccessible, it is more
frequently treated with radiotherapy.
B
Figs 16-33A and B: Extraoral and intraoral view of fibrosarcoma
showing extensive ulcerative growth.
Clinical Features
Age and sexonset at any age with mean age of
occurrence of 50 years with male predominance.
Common sitesit is commonly associated with cheek,
maxillary sinus, pharynx, palate, lip and periosteum of
maxilla and mandible. Mandible is more commonly
affected than maxilla.
SymptomsIt produces fleshy bulky mass of tissue. There
may be pain and loosening of the teeth. Involvement of
TMJ and para-mandibular musculature are producing
trismus. Sensory neural abnormalities may occur if it
involves peripheral nerves.
Signsinitially they resemble benign fibrous outgrowth,
but they grow rapidly to produce large tumor. Large
tumors are prone to ulceration and hemorrhage (Figs
Radiographic Features
Radiodensitydestructive lesion may stimulate the
osteolytic form of osteosarcoma.
Marginsthey are poorly demarcated, non-corticated
and lack of any resemblance of capsule.
Extentthey tend to elongate through marrow space.
Appearanceif soft tissue lesions occur adjacent to bone,
they cause a saucer-like depression (Fig. 16-34) in the
underlying bone or invade it as seen in a squamous cell
carcinoma.
Teethteeth are displaced and loose their supporting
bone so that they appear to be floating in space. Lamina
dura and follicular cortices are obliterated. In some cases,
periodontal space widening may occur.
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Types (Histological)
Giant cell
Inflammatory
Myxoid
Storiform
Pleomorphic
Angiomatoid
Clinical Features
Age and sexthere is slight male predilection and
malignant variety is common in adults.
Sitein the head and neck area, more commonly
encountered in the paranasal sinuses or centrally, within
the jaw.
Appearanceoccasionally, it arises in the oral cavity and
in the lateral neck, it appears as indurated swelling.
Metastasisin nearly 1/4th of cases have been reported.
Radiological Features
Diagnosis
Diagnosis
Clinical diagnosisfleshy mass with ulceration in the
soft tissue area will suspect fibrosarcoma.
Radiological diagnosissaucer shaped erosion of bone
is present.
Laboratory diagnosisproliferation of fibroblasts and
formation of collagen and reticular fibers. Mitotic figures
are prominent in small group of poorly differentiated
tumors.
Differential Diagnosis
Management
Management
Radical surgical excisionit is most commonly used
treatment modality.
Synovial Sarcoma
It usually arises from articular or para-articular sites, bursae
or tendon sheath. Synovial sarcoma of head and neck are
rare.
Clinical Features
Age and sex distributionit is predominately seen in
young adults mean age being 19 years. It has got slight
male predilection.
Sitesintraoral sites are cheek, tongue, floor of mouth
and soft palate.
Symptomsthere is painless deep seated swelling which
may produce difficulties in breathing or swallowing.
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Diagnosis
Clinical diagnosisit is not specific.
Laboratory diagnosisit is characterized by biphasic
cellular pattern of cleft-like or slit-like spaces lined by
cuboidal epithelial-like cells. The space may contain PAS
positive mucoid material. There may be fibrosarcoma
like proliferation of cells, with associated collagen or
reticulum.
Cartilage Tumors
Chondrosarcoma
It is also called as chondrogenic sarcoma. It develop from
natural cartilage or a benign cartilaginous tumor. Most of
them develop from cartilage located in bone either centrally
in bone (medullary cavity) or peripherally, from the
cartilage cup of an osteochondroma.
Types
Management
Radical resectionearly radical resection is the best
method of treatment.
Adjunct radiotherapyit can also be given after radical
resection.
Prognosisit has got poor prognosis as tumor often
metastasized.
Clinical Features
Age and sexit most frequently occurs in adults over the
age of 40 years with predilection in males in ratio of 2:1.
Sitethe most common site is thigh, retroperitoneum
and inguinal region. The most frequent oral region
affected is cheek which is followed by tongue.
Symptomspain and tenderness may be present in
advanced cases of liposarcoma.
Appearanceit has a slow, silent growth, submucosal or
deep in location, producing firm, resilient lesions,
sometimes lobulated.
Colorcolor of lesion is normal or yellow in color.
Diagnosis
Clinical diagnosissoft, yellow color growth on the cheek
may suspect liposarcoma.
Laboratory diagnosishistologically, it is classified into
myxoid, round cell, adult and pleomorphic types. In
general, it consists of fat cells and lipoblast in varying
degrees of differentiation and anaplasia with variable
stromal component.
Management
Surgical excisionit is treated by surgical excision with
or without radiation therapy.
Clinical Features
Age and sexdevelop during 3rd to 6th decades and
male to female ratio is 2:1. Secondary chondrosarcoma
occur at early age than the primary type of chondrosarcoma.
Siteit is rare in jaws and may occur in maxilla or
mandible. Often found in anterior alveolar process of
maxilla and in mandible, it is found at angle and alveolar
ridge of premolar-molar region.
Progressit is slow growing and less malignant.
Symptomspainless in early stages with facial
asymmetry as first complain but as it enlarges, swelling
becomes bony hard and painful. There may be headache.
Signsteeth adjacent to the lesion are resorbed, loosened
and get exfoliated. In some cases, there may be
hemorrhage from the neck of teeth. There may be sensory
nerve deficit, proptosis and visual disturbances. If
swelling erodes through the cortical plate, it tends to be
tender, smoothly contoured firm mass due to presence
of cartilage.
Surface of lesionmucosal covering appears normal in
early stage (Fig. 16-35) but later, it ulcerates and develops
necrotic surface, if chronically traumatized.
Temporomandibular joint involvementif it occurs in/or
near the temporomandibular joint region (Fig. 16-36),
trismus and abnormal joint function may result.
Metastasismetastatic spread by vascular channel.
Malignant cells may erode through wall or venules and
extend along inside the venules without adhering to
vessels wall but still altered at their site of entry. Lung is
common region of metastasis.
Radiographic Features
Radiodensityit may be sclerotic or mixed, if there is
calcification of neoplastic tissue.
Marginslytic lesions with poorly defined borders.
Shapethe lesion is round, ovoid or lobulated.
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Diagnosis
Management
Surgerysurgical excision with wide margin is the
treatment of choice. The prognosis is poor and most
patients may die due to metastasis.
Differential Diagnosis
Osteosarcomathe typical calcification of chondrosarcoma is not present in osteosarcoma.
Fibrous dysplasiathe periphery of fibrous dysplasia is
better defined. In fibrous dysplasia there is thinning of
periodontal ligament space and in chondrosarcoma,
there is usually a widening of periodontal ligament
space.
Bone Tumors
Osteosarcoma
It is also called as osteogenic sarcoma. It is the most common
malignant tumor originated within the bone. It is derived
from osteoblasts in which tumor cells contain high level of
alkaline phosphatase.
Management
Surgeryit is the only treatment of choice and there is
5 years survival rate. Complete resection should always
be done to avoid recurrence.
Mesenchymal Chondrosarcoma
This is aggressive form of chondrosarcoma showing
biphasic histopathological pattern. It contains mesenchymal cells. It tends to metastasize to unusual locations
and that too after long period of time. Most of the tumors
arise in bone but an appreciable number occur in soft
tissues.
Clinical Features
Ageit is seen in younger age group than usual type of
chondrosarcoma. It is usually seen between the ages of
10 and 30 years.
Siteit is most commonly seen in maxilla, skull bone,
mandible and ribs. It also occurs in tubular bones and
pelvis.
Symptomsthere may be pain due to compression of
nerve. In some cases, there may be swelling.
Signpathological fracture may also occur.
Radiological Features
They are same as chondrosarcoma
Diagnosis
Clinical diagnosisyounger age group with complaints
of pain and swelling in maxillary area.
Etiology
After radiation therapythere are increased incidences
of osteosarcoma in bone that has been irradiated.
Traumatic irritationit may be causative factor for
osteosarcoma.
Fibro-osseous diseasesosteogenic sarcoma may be seen
in fibrous dysplasia and Pagets disease.
Othersother causes which can cause osteosarcoma are
genetic mutation and some viral causes.
Clinical Features
Age and sexmean age of occurrence in the jaws is 33
years and it is more common in males.
Siteit is more common in long bones like femur and
tibia and in jaw bone.
Progressit grows rapidly with a doubling time of 32
days and shows recurrence and early metastasis via
bloodstream to lungs (Fig. 16-39).
Signsthere is exophthalmos, blindness, nasal
obstruction and epistaxis.
Oral Manifestations
Incidenceit is rare and accounts for 7% of all
osteosarcomas.
Siteit is equal in maxilla and mandible. In the
mandible, lesion is seen in body and in maxilla it occurs
in antrum or alveolar ridge.
Symptomsswelling of a short history and is
accompanied by pain. Affected tooth may become
displaced or loose. Numbness of lip and chin may be
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Frankly osteolytic
Marginslesions are unicentric and borders of the
lesion are ill defined.
Appearancethere is moth eaten appearance.
Cortical plateperforation and expansion of cortical
margins by extension into sub-periosteal bone.
Neurovascular canalmandibular lesion may destroy
the cortex of neurovascular bundles. Alternatively,
neurovascular canal may be symmetrically widened
or enlarged.
Lamina duraadjacent lamina dura may be destroyed.
Pathological fracturepathologic fracture occurs more
readily as in sarcoma extending more deeply into the
bone.
Maxillary sinussarcomas which develop near the
floor of maxillary antrum or nasal fossa result in
destruction of bone with no demarcation on tumor
from the air cavity.
Spiking resorption of rootthere is resorption of root
which results in tapered narrowing of the root.
Mixed (Fig. 16-41)
The presence of new bone laid down deep to the
periosteum may be slight or it may be gross and
without any structures.
Marginssarcomas with small amount of new bone
formation usually present margins which are not well
defined.
Appearancethere is evidence of bone formation as
well as destruction. In some cases, there is a well
defined area of bone destruction, with partially
corticated borders and some bone within the tumor
itself.
Honeycomb appearancethe bone within the radiolucent area of destruction may take the form of strands,
which may be few and intersecting, or may produce a
more or less honeycomb appearance.
Radiographic Features
Periodontal ligament space wideningthere is symmetrical
widening of periodontal ligament space in early stage
of the disease.
Typesit may develop into a frankly osteolytic stage,
mixed stage, i.e. those which produce some bone and
thirdly those which are almost entirely bone forming.
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3
Fig. 16-43: Typical sunray appearance seen in osteogenic sarcoma.
Variant of Osteosarcoma
Peripheral (Juxtacortical)
Parosteal osteosarcomait is attached to the cortex by
short stalk. In this, there is no elevation of periosteum
and no peripheral reaction. It is uncommon, extremely
rare in the jaws and is characterized by slow growth.
It has good prognosis due to low tendency of tumor
for metastasis. It is treated by radical excision which
results in low risk of recurrence.
Periosteal osteosarcomait arises within the cortex and
elevate the overlying periosteum. It is an aggressive
variant of parosteal type of osteosarcoma. There is
occurrence of periosteal new bone formation. This
may perforate the surface of periosteum and lesion
may extend into surrounding soft tissue. In this,
radical surgical excision with wide margin is the
treatment of choice.
Extra-osseousosteosarcoma of soft tissue in absence of
primary skeletal tumor and occur in breast, liver and
kidney. It is highly malignant type of tumor.
Post-irradiation bone sarcomait can develop after 3 years
of radiation. It is dose related. If higher dose is given,
there are more chances of sarcoma.
Diagnosis
Clinical diagnosisrapidly growing swelling of bone
which is accompanied by pain and discomfort will give
clue to diagnosis.
Radiological diagnosisperiodontal ligament space
widening, sunray appearance, Codmans triangles are
typical radiological features of the osteosarcoma.
Laboratory diagnosisserum alkaline phosphatase level
is increased in osteosarcoma. Biopsy shows atypical
osteoblasts. Neoplastic osteoblasts are spindle shaped
or polyhedral. Pleomorphism in size and shape of cells.
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Management
Surgeryradical resection with amputation of bone can
be carried out.
Adjuvant chemotherapysometimes, adjuvant chemotherapy can be instituted.
Ewings Sarcoma
It was first described in 1921 by James Ewing. It is also
called as round cell sarcoma or endothelial myeloma. It is
derived from mesenchymal connective tissue of bone
marrow.
Origin
Endothelial elementit may arise from endothelial
elements in the marrow.
Neuroblastomait may be a secondary deposit of
neuroblastoma.
Marrow spacesit may arise from reticulum cell lining of
the marrow spaces.
Metastatic tumorsome considered it to be a metastatic
tumor, the primary of which is located in different sites,
including bronchus.
Clinical Features
Age and sexit occurs between the ages of 5 and 25 years
with a male to female ratio of 2:1.
Radiographic Features
Radiodensityit is ill-defined destructive radiolucent,
lesion which may be unilocular or multilocular (Fig.
16-45).
Sitemost commonly seen in mandibular posterior area.
Marginsit has ill-defined margins and is never
corticated. In advanced cases, bone is destroyed in
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Vascular Tumors
Malignant Hemangioendothelioma
It is a neoplasm of mesenchymal origin which is
angiomatous in origin and derived from the endothelial
cells.
Clinical Features
Age and sexit has slight predilection for females. It can
arise at any age and has been found at birth also.
Siteit may occur anywhere in the body but most
commonly found in skin and subcutaneous tissues. In
oral cavity, it can occur on lips, palate, gingiva, tongue
and centrally within the maxilla and mandible.
Symptomslocalized swelling with pain may be the
feature of lesion.
Appearanceit appears as flat or slightly raised lesion of
varying size, dark red or bluish red in color.
Signlesion can be ulcerated and show a tendency to
bleed even after slight trauma.
Bone destructionbone may be involved by tumor
producing a destructive process.
Diagnosis
Fig. 16-45: Radiolucent lesion seen in ramus area in Ewing sarcoma.
Diagnosis
Clinical diagnosisintermittent pain in the bone with
rapidly growing swelling may suspect this lesion.
Radiological diagnosisonion skin appearance is
seen.
Laboratory diagnosisbiopsy shows cellular neoplasm
which is composed of solid sheets or masses of small
round cells with very little stroma, although few
connective tissue septa can be seen.
Management
Surgerysurgical excision of the lesion should be carried
out.
Radiationsurgery and X-ray radiation can be given.
Differential Diagnosis
Osteomyelitisin osteomyelitis, there is presence of
sequestra within the confines of lesion.
Eosinophilic granulomait is associated with laminar
periosteal bone reaction whereas Ewings sarcoma does
not produce laminar bone reaction.
Osteosarcoma, chondrosarcomathese are difficult to
differentiate radiologically from Ewings sarcoma. In it,
histopathological investigation is conclusive.
Management
Combination therapysurgery combined with multidrug
chemotherapy gives more survival rate nowadays.
Angiosarcoma
Angiosarcomas are malignant vascular tumors that
comprise only 2% of soft tissue sarcoma. It is very rare in all
sites including oral cavity.
Clinical Features
Siteon the head it affect scalp. In the oral cavity, it
appears in lip, palate, tongue, floor of mouth, cheek and
gingivae. Mandible is more commonly affected than
maxilla.
Appearanceit appears as rapidly growing lesion that
tends to ulcerate.
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Radiological Features
Conventional filmill-defined ragged destruction of the
bone occurs.
CT scanit reveals extension of soft tissue.
Diagnosis
Diagnosis
Management
It is done by combination of surgery and radiation therapy.
Management
Neuroblastoma
It is a rare malignant tumor of the adrenal gland. It
sometimes arises in the nerves or ganglia of the sympathetic
system in the neck, thorax or abdomen. After leukemia, it is
the commonest malignancy of children.
Clinical Features
Ageit usually occurs in children under the age of
5 years.
Siteoral cavity and nasal sinuses are involved. Oral
involvement is usually due to metastasis and it occurs
in mandible and maxilla.
Symptomsthere is swelling, displacement of teeth and
neurological symptoms.
Metastasisskull is one of the commonest sites for
metastases. Metastases in bone tend to be multiple.
Neurofibrosarcoma
It is also called as malignant Schwannoma, malignant
peripheral nerve sheath tumor, neurogenic sarcoma. It arises
from nerve tissue, especially from nerve sheath cells. It is
rare in oral cavity.
Peripheral nerves are nerves that receive messages
from the central nervous system (brain and spinal cord)
leading them to stimulate voluntary movement. Neurofibrosarcoma, also known as peripheral nerve sheath tumor, is
a malignant tumor that develops in the cells surrounding
these peripheral nerves. It can sometimes arise in patients
with neurofibromatosis.
Clinical Features
Radiological Features
Radiodensitysome cases reveal areas of bone
destruction with evidence of new bone formation within
them and beneath the periosteum.
Sunburst appearancein some cases, there are spicules of
bone within the soft tissue mass associated with bone
destruction, these are roughly perpendicular to the
surface of the bone and may resemble the sunburst
appearance.
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Radiological Features
Management
Rhabdomyosarcoma
It is a malignant neoplasm of skeletal muscle origin and it
is uncommon in oral cavity.
Diagnosis
Clinical and radiological diagnosisit is difficult to make
clinical and radiological diagnosis.
Laboratory diagnosisbiopsy shows plumps of spindle
shaped cells arranged in streams and cords with random
nuclei. It exhibits variation in degree of malignancy, i.e.
tumors that are relatively acellular, show little cellular
pleomorphism. Tumors that are highly cellular shows
pleomorphism and bizarre mitotic activity.
Management
Radical surgical resectionthis is the treatment of choice
in neurofibrosarcoma.
Adjuvant radiotherapy and chemotherapythis can be
given in combination with surgical resection.
Muscle Tumors
Leiomyosarcoma
It is a malignant tumor of smooth muscle origin.
Clinical Features
Age and sexit can occur at any age with no sex
predilection.
Sitethe most common site is uterine wall and gastrointestinal tract. It is very rare in oral cavity and if present,
it is seen commonly on cheeks and floor of mouth.
Symptomsthe lesion appears as painful swelling.
Appearancethe mass is nonspecific in appearance.
Secondary ulceration of mucosal surface can be present.
Metastasisthey tend to metastasize through hematogenous route.
Diagnosis
Clinical and radiological diagnosisnonspecific
appearance.
Laboratory diagnosisthere is presence of mitosis, nuclear
pleomorphism, hyperchromatism and bizarre cell forms.
Proliferating smooth muscles cells are arranged as
interlacing bands or cords.
Types (Histological)
Pleomorphicit occurs most commonly in extremities and
in older individuals.
Alveolarit is found in head and neck region and in
extremities, with early age of occurrence.
Embryonalit is found in the genitourinary tract and in
nasopharynx, with cases reported in oral cavity in the
upper and lower labial folds.
Botryoidis a malignant tumor of vagina, prostate and
base of bladder in young children.
Clinical Features
Ageit is most common soft tissue sarcoma in children
and adolescents. It is exclusively found in males.
Siteit is a mass occurring in any region of the head
and neck where striated muscle or its mesenchymal
progenitor cells exist. Intraorally, the tonsils and soft
palate are most frequently involved.
Symptomsdepending upon of the size of lesion, there
may be divergence of eyes, abnormal phonation, dysphagia, cough, aural discharge or deviation of the jaw.
Appearancetypically, it is a rapidly growing soft tissue
mass. It forms polypoid fleshy growth beneath the mucous
membrane, with club-like extensions at periphery.
Signsthe overlying skin is usually erythematous or
telangiectatic.
Spreadit may spread by either lymphatic or hematogenous routes.
Metastasisthe lesions are occasionally ulcerated and
may invade the underlying bone and develop distant
metastasis.
Diagnosis
Clinicalrapidly growing soft tissue mass with polypoid
fleshy growth.
Laboratory diagnosisin pleomorphic rhabdomyosarcoma, spindle cells are arranged in haphazard
manner. The nuclei are situated often in an expanded
end of cells. The racquet cell, Strap-like and ribbon
cells typically show process of long streaming
cytoplasm. In alveolar rhabdomyosarcoma, epithelium cells
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Management
Local surgical excisionsurgical excision of the tumor
should be carried out.
Multiagent chemotherapyit consists of vincristine,
actinomycin D and cyclophosphamide.
Postoperative radiation therapyradiation therapy should
be given postoperatively.
Prognosisinitially, it has poor prognosis. But nowadays
due to advent of multimodal therapy, prognosis is
improved dramatically.
Clinical Features
Age and sexit is predominantly a tumor of females,
occurring usually in teens or early twenties. Occasional
cases also occur in older patients.
Sitehead and neck region are common site. The orbit
and tongue are most common in head neck location.
Appearancethey are usually slow growing, well
circumscribed masses.
Diagnosis
Clinicalnot possible to diagnose or suspect clinically.
Laboratory diagnosisbiopsy shows group of large
polygonal cells which are arranged around alveolar
spaces. Cells have abundant granular eosinophils
cytoplasm.
Management
Radical surgical excisiondue to the high recurrence rate,
radical surgical excision is the treatment of choice.
Types (Histological)
Lymphocyte predominantabundant lymphocytes, few
plasma cells, occasional Reed-Sternberg cell, localized
involvement of one side of diaphragm and most
favorable prognosis.
Mixed cellularitylymphocytes, plasma cells, eosinophils, easily identified Reed-Sternberg cell.
Nodular sclerosissparse lymphocytes, stromal cells,
fibrosis and numerous but bizarre Reed-Sternberg cells.
It has poor prognosis.
Lymphocyte depletionlymphocytes, plasma cells,
eosinophils with localized involvement.
Clinical Features
Age and sexit is characterized by a bimodal age
incidence, peak one in young adults and the second in
the 5th decade of life with equal distribution between
sexes.
Onsetthe onset is insidious, usually with enlargement
of one group of superficial nodes. The cervical lymph
nodes are usually the first to be involved but the disease
may start in the mediastinal, axillary, abdominal, pelvic
or inguinal lymph nodes.
Symptomsthe involved nodes are painless. Generalized
weakness, loss of weight, cough, dyspnea and anorexia
are seen. Pain in back and abdomen owing to splenic
enlargement, due to pressure of enlarged nodes or
involvement of vertebrae.
Signsthe lymph nodes are discrete and rubbery in
consistency with overlying skin being freely mobile (Fig.
16-46). Splenomegaly is usually seen in later stage. Some
patients may manifest pruritis.
Pel Ebstein fevercharacteristic features of this disease
are Pel-Ebstein fever, a cyclic spiking of high fever and
generalized severe pruritis of unknown etiology.
Effect on surrounding structurespressure of enlarged
lymph nodes on adjacent structures may cause dyspnea,
dysphagia, venous obstruction, jaundice and paraplegia.
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Oral Manifestations
Incidenceprimary jaw lesions are uncommon.
Secondary effectsecondary effect can be seen in oral
cavity in the form of infection due to reduced host
immune response.
Appearanceit may appear in the oral cavity as an ulcer
or a swelling or as an intra-bony lesion which presents
as a hard swelling.
Radiographic Features
Siteit is rarely seen in jaws. The common regions are
the posterior maxilla and mandible.
Appearancemalignant lymphoma arising in the oral
cavity spreads to bone and cause irregular bone loss to
the area of the lesion. There are radiolucent areas separated from each other by normal appearing bone which
later become confluent, unless treatment is carried out.
Marginstypically, the radiolucent lesions have diffuse
ill defined margins which suggest infiltration of bone.
Osteoblastic typeosteoblastic type is uncommon in jaws,
but it is seen in the vertebrae and pelvis. In it, there is
frank sclerosis with filling of the marrow spaces by bone.
It presents as grayness or whiteness which is abnormal.
The margins may be well defined and sharp or irregular
and trailing off gradually into the normal bone.
Differential Diagnosis
Non-Hodgkins lymphomaHodgkins lymphoma is
differentiated from non-Hodgkins lymphoma by the
presence of cells known as Reed-Sternberg cells which
have paired as mirror nuclei and prominent nuclei.
Management
Radiotherapyirradiation treatment 3500-4000 rads/
week over the involved region plus all adjacent sites
been given in stage I and II. It is also given after chemotherapy, to sites where there was originally bulk disease.
Chemotherapyit is given in stage III and IV. Usually
combination is given. First combination is MOPP, i.e.
mechlorethamine (6 mg/m2 IV on day 1 and day 8),
oncovin which is also called as vincristine (1.4 mg/m2
IV on day 1 and 8), procarbazine (100 mg/m2) orally
from day 1 to 14) and prednisone (40 mg/m2 orally from
day 1 to 14). MOPP combination given in six courses
with no drugs is given from day 15 to 28. Second
combination is ABVD regimen, i.e. adriamycin (25 mg/
m2 IV bolus on day 1,8 and 14), bleomycin (10 mg/m2
bolus on day 1,14), vinblastine (6 mg/m2 IV bolus on
day 1,14) and decarbazine (375 mg/m2 IV bolus on day
1,14). The cycle should be repeated on 20th day.
Combinationa combination of radiotherapy and
chemotherapy may increase the overall response and
long term survival but, it is associated with delayed
complications like leukemia, gonadal atrophy and
avascular necrosis of bone.
Splenectomysplenectomy is advocated in many
patients, except with stage IV disease.
Non-Hodgkins Lymphoma
It is also called as lymphosarcoma. In this group, there is
neoplastic proliferation of lymphoid cells, usually affecting
the B-lymphocytes. Unlike Hodgkins lymphoma, the
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Radiographic Features
Types (Histological)
Nodularneoplastic cells tend to aggregate in such a
way that large clusters of cells are seen.
Diffusethere is monotonous distribution of cells with
no evidence of nodularity or germinal center pattern.
Etiology
Viralthe etiology is unclear but herpes virus and
Epstein barr etiology has been suggested.
Immunologicalthere may be induced immunologic
effect permitting a malignant clone to proliferate.
Clinical Features
Age and sexit affects persons of all ages from infants to
the elderly. But is commonest in middle age group. Males
are affected more commonly than the females.
Onsetthe onset of symptoms may be insidious.
Painless lymph node enlargement of abdominal and
mediastinal region are the most common finding. Very
often the first group of lymph nodes affected may be
cervical, axillary or inguinal.
Symptomsthe patient complains of tiredness, loss of
weight, fever and sweating. Pain is the main symptom
of bone involvement which may present as a pathological fracture. Patient may complain of abdominal
pain, nausea, vomiting, diarrhea or intestinal obstruction which may occur due to involvement of gastrointestinal tract. Pressure effect of lymphoma may cause
dysphagia, breathlessness, vomiting, intestinal
obstruction or ascites and paraplegia.
Signsif liver and spleen are involved, hepatosplenomegaly is present. The growth is fleshy and is
prone to ulceration.
Diagnosis
Clinical diagnosisbluish color mass of the palate with
multiple lymph node involvement may suspect the
diagnosis of non-Hodgkins lymphoma.
Radiological featuresexpansion of bone with radiolucency is present.
Laboratory diagnosisblood count usually shows
hypersplenism or hemolytic anemia. The reduced WBC
and RBC counts are seen along with reduced hemoglobin levels and reticulocytosis. In some cases, there
may be slight increase in lymphocytes and thrombocytopenia. Moderate degree of anemia will also present
when there is considerable bone marrow involvement.
Some very aggressive high grade non-Hodgkins
lymphomas are associated with very high urate levels
which can precipitate renal failure.
Oral Manifestations
Differential Diagnosis
Management
Chemotherapywhen diagnosed in late stages,
chemotherapy is the treatment of choice. In most cases
single agent chemotherapy (chlorambucil) is usually
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Clinical Features
Age and sexit can occur in any age group but it is
common amongst young adults under the age of 40 years.
It is common in male as compared to females.
Sitesit most commonly seen in femur, tibia and humerus.
Symptomsmost common complaint is pain. There is
also presence of localized swelling of the involved bone.
Patient may also complaint of weight loss, fever, and
night sweats.
Signregional lymphadenopathy is usually present.
Oral Manifestations
Siteit is not common, but it usually occurs more in
mandible than maxilla.
Symptomspain is common complaint and usually
present for years and more. There is also presence of
expansile mass.
Signthe oral mucosa over the involved bone seldom
gets ulcerated but at times, appears diffusely inflamed.
Teeththe teeth usually become exceedingly loose,
owing to destruction of bone.
Maxillary lesionwhen the lesion involves maxilla, there
may be evidence of expansion of the bone as well as
symptoms of nasal obstruction due to superior growth
of tumor into the floor of nasal cavity.
Radiographic Features
Moth eaten appearancethere is diffuse radiolucency
involving the alveolar bone which may present
destruction of the supporting bone of the teeth. It may
present a moth eaten appearance.
Marginsin the jaw, the tumor usually gives rise to an
area of bone destruction with margins suggestive of
infiltration.
Diagnosis
Clinical diagnosisa primary focus is single bone.
Systemic symptoms with local pain with regional
lymphadenopathy will give clue to the diagnosis.
Radiological diagnosismoth eaten appearance with
periosteal reaction is present.
Laboratory diagnosisprimary cells of tumor are identical
with that of the soft tissue tumors. There may be inflammatory cell infiltration which can lead to confusion in
the diagnosis of the lesion. The individual cells are
mixed with both mature appearing lymphocytes and
large histiocytoid lymphoblast. Many patients have
increased level lactate dehydrogenase.
Management
Surgical ablationsurgical ablation is done.
RadiationX-ray radiation is the treatment of choice.
The 5 year survival rate is between 50 to 60%.
Mycosis Fungoides
It is derived from T lymphocytes. It is also called as T cell
lymphoma. This tumor has got propensity to invade the
epidermis of skin (epidermotrophism).
Clinical Features
Age and sex distributionit usually affects middle aged
adult with male predilection.
Sizeit varies in size from few millimeters to centimeters
in diameter.
Siteit involves lymph nodes, spleen and liver.
Eczematous stagethese are well demarcated scaly
erythematous patches. Patient complains of pruritus.
Plaque stagethese appear after eczematous stage in
which erythematous patches become elevated red lesion.
Tumor stageplaque grows and become papules and
nodules. In this stage visceral involvement is seen.
Sezary syndromeit is dermatopathic T cell leukemia.
Patient is suffering from exfoliative erythroderma, lymphadenopathy, and hepatomegaly and splenomegaly.
Oral Manifestation
Sitetongue, palate, buccal mucosa, lip, gingiva and
tonsils.
Appearanceoral lesions can be the first manifestation
and sometimes, appear after the skin lesions have been
treated and remitted. The lesions appear as indurated
areas, nodules or erythematous ulceration (Fig. 16-47).
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Etiology
Epstein-Barr virus (EBV) which also causes nasopharyngeal carcinoma and infectious mononucleosis is
considered to be the etiological factor. There are higher
EBV antibody levels in patients of Burkitts lymphoma.
Fig. 16-47: Indurated area in the maxillary tuberosity region which
later on histologically diagnosed as mycosis fungoides.
Diagnosis
Clinical diagnosiseczematous or plaque lesion on the
skin.
Laboratory diagnosisbiopsy shows dense infiltration
of lymphoid cells with irregularly shaped nuclei. In some
cases, nuclei are so convoluted that they are described
as cribriform.
Management
Early stagetopical nitrogen mustard, electron beam
therapy and photochemotherapy (PUVA) are used in
early stage.
Extracorporeal photopheresisextracorporeal photopheresis is used in this stage. This involves ingestion of
photoactive drug 8-methoxypsoralen followed by
removal of patients blood and separating red and white
blood cells. The white blood cells are irradiated outside
the body with ultraviolet radiation and then infused
back to patient. This will generate immunological
response to patient abnormal lymphocytes.
Clinical Features
Age and sexpeak incidence is in children between 6 to
9 years. Males are affected more commonly than the
females, with a ratio of 2:1.
Site distributionmore are found in maxilla than in
mandible, where it may spread rapidly to the floor of the
orbit. Almost always occurs in molar area. In the African
form, more than one quadrant is involved while in the
American form, only one quadrant is involved.
Onset and progressthe most important hallmark of this
tumor is the fast growth with a tumor doubling time of
less than 24 hours.
Symptomsthe most common presenting features are
swelling of the jaws, abdomen and paraplegia. It is
painless.
Signperipheral lymphadenopathy is common.
Prognosisit is rapidly fatal in the absence of treatment,
with death occurring within 6 months.
Oral Manifestations
Onset and extentit begins generally as a rapidly
growing tumor mass of the jaws, destroying the bone
Table 16-2: Difference between endemic (African) and non-endemic (non-African) form
Features
Endemic form
Non-endemic form
Age
Young children
Nodal tissue
Sex
No sex predilection
Jaw
Jaw uncommon
Visceral involvement
Nerve involvement
Not common
Antibody titre
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Radiographic Features
Moth eaten appearancesmall radiolucent foci scattered
throughout the affected area. These small foci coalesce
and form a multilocular moth eaten appearance. Focal
areas of radiolucency are darker and sharper than the
shadow of the marrow space lined by normal bony
trabeculae.
Sunray appearanceif periosteum is elevated, it will
produce sunray appearance.
Marginsmargins are ill defined and non-corticated.
Shapethey expand rapidly and are ballooned shaped.
TeethLesions are osteolytic with loss of lamina dura
about the erupted teeth and crypts of developing teeth
are enlarged. Erupted teeth in the area are grossly
displaced, as are the developing tooth crypts.
Effect on surrounding structuresthey expand very rapidly
and breach its outer cortical limits, causing gross
balloon-like expansion with thinning of adjacent
structures and production of soft tissue mass adjacent
to the osseous lesion. Inferior border of mandible is
thinned and later destroyed. Erosion and perforation of
the cortex is seen. In some cases, orbit is involved and
there is displacement of orbital content.
Maxillary sinusin the maxilla, there is blurring of
shadow of antrum.
Diagnosis
Clinical diagnosisswelling of the jaw and abdomen
with peripheral lymphadenopathy can give clue to the
diagnosis.
Differential Diagnosis
Non-Hodgkins lymphomait occurs in older age groups.
Cherubismit does not breach the bony borders.
Osteosarcomait is distinguishable from clinical features.
On radiograph, osteoblastic activity is visible.
Management
Cytotoxic drugscytotoxic drugs like cyclophosphamide
40 mg/kg in single IV administration and repeated
about 2 weeks later. Vincristine and methotrexate have
been successful in some cases.
Multiagent chemotherapycombination of drugs such as
cyclophosphamide, vincristine and methotrexate give
better results than any single drug. Majority of patients
show dramatic response to the therapy. The swelling
regresses and the displaced teeth return to their normal
position within 1 to 2 weeks.
Leukemia
It is also called as leucosis. It is defined as a neoplastic
proliferation of WBC in bone marrow, usually in circulating
blood and sometimes in other organs such as liver, spleen
and lymph nodes. Presence of leukemic cells in bone
marrow results in impairment of normal hemopoiesis with
resultant anemia, granulocytopenia and thrombocytopenia. Leukemia is a progressive and fatal condition
causing death from hemorrhage and infection. There is
presence of excessive number of abnormal cells in the
peripheral blood but leukemia is considered a primary
disorder of bone marrow.
Types
Stem or blast cell leukemiawhen the leukemic cells
are too immature to be classified as to cell type, the
leukemia is termed as stem or blast cell leukemia.
Subleukemiawhen the total WBC is normal and
leukemic cells are seen in the peripheral blood is termed
as subleukemia.
Aleukemiawhen no abnormal leukocytes are found in
the peripheral blood (i.e. they can be found only in the
bone marrow), the term aleukemia is used.
Leukemoid reactionwhen the peripheral blood picture
in non-leukemic patient resembles that of leukemia, it is
called a leukemoid reaction. In this, absolute neutrophil
count remains above 30,000/mm3.
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Acute Leukemia
Acute leukemia is a disorder in which there is a failure of
maturation of leukocytes. As a result, there is an accumulation of immature cells within the bone marrow and later
in the blood. It is the most common type of leukemia, except
in children (in whom acute lymphoblastic leukemia is more
common).
Etiopathogenesis
Leukemic blastthere is a block in differentiation of
leukemic and stem cells. Thus, accumulation of leukemic
blast in acute leukemia results primarily from failure of
maturation into functional stage.
Suppression of stem cellsas leukemic blast accumulates
in the marrow, they suppress the normal hematopoietic
stem cells. The mechanism is not fully understood.
Suppression part is related to physical replacement of
normal precursor cells by expanded clones of leukemic
cells.
Clinical manifestationclinical manifestations result
from paucity of normal red cells, white cells and platelets.
Etiology
Clinical Features
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Oral Manifestations
Lymph nodesthe submental, cervical and pre- and postauricular lymph nodes may be enlarged and tender.
Symptomsparesthesia of lower lip and chin may be
present. There may be toothache due to leukemic cell
infiltration of dental pulp.
Signsthe oral mucous membrane shows pallor,
ulceration with necrosis (Fig. 16-48), petechiae,
ecchymosis and bleeding tendency. There may be
massive necrosis of lingual mucosa with sloughing.
Gingivagingiva shows hypertrophy (Fig. 16-49) and
cyanotic discoloration. The hypertrophy may be due to
leukemic cell infiltration within gingiva or due to local
irritants. The gingiva appears boggy, edematous and
deep red bleed easily due to ulceration of sulcus
epithelium and necrosis of underlying tissue.
Diagnosis
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Phase
Lymphoblastic
Myeloid
Induction
Vincristine (IV)
Prednisone (oral)
A-asparaginase (IV)
Daunorubicin (IV)
Methotrexate (intrathecal)
Daunorubicin (IV)
Cytosine arabinoside (IV)
Etopiside (IV)
Thioguanine (oral)
Maintenance
Prednisone (oral)
Vincristine (IV)
Mercaptopurine (oral)
Methotrexate (oral)
Clinical Features
Agethe disease occurs chiefly between the age of 35
and 60 years.
Onsetthe disease may be discovered during routine
examination, when splenomegaly or an elevated count
is noted.
Symptomsthere may be slowly advancing anemia with
loss of weight, prominence of abdomen and discomfort
in the left upper quadrant due to splenomegaly. Attacks
of acute left upper abdominal pain may develop due to
infarction of spleen. Anemia causes weakness, fatigue
and dyspnea on exertion.
Signas the disease progress, thrombocytopenia can
cause petechiae, ecchymosis as well as hemorrhage from
the skin and mucous membrane. Liver may be enlarged
but lymph nodes are normal.
Diagnosis
Clinical diagnosisnot so specific
Laboratory diagnosisexamination of blood shows a
normocytic and normochromic anemia. WBC count is
considerably increased and may be between 50 106 to
500 106 cells per cu mm. Peripheral smear shows
mature leucocytes (Fig. 16-51) but, few immature forms
may also be present. The platelet count is often high
initially but with treatment, it comes down.
Management
Chemotherapythe treatment of choice is chemotherapy
using the drug busulphan given orally in a dose of 4 mg
daily or in large doses of 50-100 mg spaced 2 to 3 weeks
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Oral Manifestations
Clinical Features
Age and sexit occurs more frequently in males and
majority of the patients are over 45 years.
Onsetthe onset is very insidious.
Symptomstiredness and ill health are common,
although some patients are symptom free and the
disorder is found incidentally. Bone marrow infiltration
causes anemia and thrombocytopenia and results in
pallor, weakness, dyspnea and purpura.
Signsthere is a moderate enlargement of lymph nodes
which are firm, rubbery and discrete. Liver and spleen
are usually enlarged and palpable. There is an increased
susceptibility to infection as the leukemic B cells are nonfunctional. Leukemic infiltration results in skin nodules,
intestinal malabsorption, pulmonary obstruction or
compression of the central or peripheral nervous system.
Lymph nodesthe most common groups of lymph nodes
involved are cervical, axillary and inguinal group.
Clinical Staging
Stage ALymphocytosis is less than three areas of
lymphoid enlargement, no anemia or thrombocytopenia.
Management
Supportive treatmentgeneral measure to maintain good
health; adequate rest, good food and exercise should be
advised.
Chemotherapychlorambucil 6-10 mg/day for 14 days
with break of 14 days and cyclophosphamide 2-3 mg/
kg IV for 6 days.
Combination therapycyclophosphamide doxorubicin,
vincristine and prednisone have been recommended.
Radiotherapyit is useful for large granular masses, if
they cause symptoms. Radiotherapy with very small
doses, of only 150 rads over a period of five weeks, is
very effective and may induce satisfactory remission.
Steroidsif the bone marrow is severely involved, initial
treatment with prednisone 40 mg daily and 25-50 mg
daily later should be given.
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Differential Diagnosis
Metabolic disorderssome of the metabolic disorders can
cause generalized rarefaction of the jaw. But these can
be excluded on the basis of blood picture.
Lymphomaclinical picture and blood testing should
be done to rule out leukemia.
Variant of Leukemia
Hairy leukemiait is a variant of chronic lymphatic
leukemia in which there is splenomegaly, severe
neutropenia, monocytopenia and the characteristic
appearance of hairy cells in blood and bone marrow.
These hairy cells appear to be a cross between the
lymphocytes and monocytes. It occurs mainly in adults
and show male predilection. Manifestations result from
infiltration of bone marrow, liver and spleen.
Splenomegaly is massive and hepatomegaly is less
common. Hairy cell can be identified on the peripheral
smear.
Prolymphocytic leukemiait is another variant of chronic
lymphatic leukemia in which there is massive
splenomegaly with little lymphadenopathy and a very
high WBC count. The characteristic cell is a large
lymphocyte with prominent nucleus.
Aleukemic leukemiait is the sub-leukemic form of
leukemia in which the WBC count of the peripheral blood
is normal or even subnormal and abnormal or immature
leucocytes may be present.
Dental Considerations
Topical treatmentto stop gingival bleeding, removal of
local irritants, direct pressure and use of absorbable
Myeloma
Multiple Myeloma
It is also called as myelomatosis. It is a malignant neoplasm
of plasma cells of the bone marrow with widespread
involvement of the skeletal system, including the skull and
jaws. It is thought to be multicentric in origin.
Origin
Proliferation of single clonenormal plasma cells are
derived from B-cells and produce immunoglobulin,
which contain heavy and light chain. In myeloma,
plasma cells produce immunoglobulin of single heavy
and light chain, a monoclonal protein commonly
referred as para-protein. There is proliferation of a single
clone of abnormal plasma cells in the bone marrow.
Bence Jones proteinuriain some cases, only light chains
are produced and these appear in urine as Bence Jones
proteinuria.
Clinical Features
Age and sexthe most common age group affected is
between 40 and 70 years with male to female ratio 4:1.
Siteusually the skull, clavicle, vertebrae, ribs, pelvis,
femur and jaws are involved.
Symptomsskeletal pain associated with motion or
pressure over the tumor masses, is an early symptom.
Pain in the involved bone may be aggregated by an
exercise and relieved by rest. Patient may complain of
vomiting due to increase in the serum calcium level.
Pathological fracturespontaneous pathological fracture
can also occur.
Bleeding tendencypatient may have bleeding tendency
and bruising of skin due to anemia and thrombocytopenia. The cause of bleeding is that the abnormal
globulins bind with coagulation factors which also
increase the viscosity of blood.
Signswelling over the areas of bone involvement may
be detectable. There is an increased susceptibility to
infection due to abnormal immunoglobulin production
by the plasma cells.
Hypercalcemiamobilization of calcium from the
skeleton may cause hypercalcemia resulting in
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Oral Manifestations
Radiographic Features
Diagnosis
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Plasmacytoma
Metastatic carcinomamultiple myeloma is, comparatively, more common than metastatic carcinoma.
The absence of definitive serum, characteristic history
of treatment for an earlier tumor indicates that the
disease is metastatic carcinoma.
Histiocytosis Xthe incidence of Histiocytosis X is most
common in children. The lesions of this disease have
ragged and vague margins.
Cherubismmultiple radiolucent lesions of cherubism
may be scattered throughout the jaws, commonly seen
in the first or second decades of life. Radiolucent lesions
may be multilocular or unilocular, elliptical without well
circumscribed or hyperostotic borders.
Advanced osteomyelitisshows the presence of visible
cause.
Simple bone cystit may be bilateral but they are usually
corticated in part and characteristically interdigitate
between roots of teeth in much younger population.
Clinical Features
Age and sexmean age of occurrence is in age of 51 years
and males are affected more commonly than females.
Sitenares, tonsil, palate tongue, gingivae and the floor
of mouth. They are also found in pleura, mediastinum,
thyroid, ovary, intestine, kidney and skin.
Symptomspain and swelling are the most common
complaints.
Signspathologic fractures are common.
Metastasisregional metastasis may develop in small
number of cases.
Management
Chemotherapeutic agentsgeneral disease is treated with
chemotherapeutic agents like melphalan and cyclophosphamide.
Management of anemia and hypercalcemiapatients who
present with anemia, hypercalcemia, and evidence of
renal damage require urgent management with
alkalization of urine with oral bicarbonates, high fluid
intake, corticosteroids and possibly mithramycin to
reduce calcium level.
Blood transfusionit may be required if hemoglobin is
less than 10 gm/dl.
Cell transplantationstem cell autotransplant may
improve quality of life and prolong survival.
Radiotherapythis is effective for localized pain not
responding to simple analgesics and for pathological
fractures.
Bi-phosphonate therapyit may reduce bone pain and
skeletal events.
Others drugsalpha interferons may prolong the
plateau phase. Inorganic fluoride phosphate to reduce
bone pain.
Solitary Myeloma
It can appear in any bone and remains for long period of
time. It usually involves single bone. The hematological
and biochemical changes seen in multiple myeloma are
not seen in solitary myeloma. Patient is not anemic and
serum protein level is normal. Others symptoms are same
as in multiple myeloma.
Oral Manifestations
Siteit is rare in jaws and can occur in mandible or
maxilla.
Appearancethe lesions are described as sessile or
polypoid reddish masses in mucous membranes, which
become lobulated as they enlarge but exhibits the
tendency to ulcerate.
Symptomspain is not prominent symptom unless bone
is invaded.
Signsthere may be bleeding and ulceration of oral
mucosa.
Radiographic Features
Formsit mainly occurs in two forms, one is purely
destructive lesion suggestive of metastatic carcinoma
and the other type is an expansible lesion, suggestive of
a giant cell tumor.
Destructive lesionthere is no new bone at the margins
or under the periosteum. The margins are clearly defined
or show evidence of infiltration. In the flat bone, solitary
myeloma extends along the bone and produce a saucershaped lesion, with undulating margins.
Expansible lesionan area of bone destruction is well
demarcated from the surrounding bone and sometimes
is corticated. If the bone is expanded, subperiosteal new
bone may form a complete bony covering of the tumor.
In the substance of the lesion, trabeculae vary
considerably in number and thickness. Some are thin
and delicate, while others are coarse.
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Diagnosis
Disadvantages
Osteoradionecrosisthere is risk of post-irradiation
osteoradionecrosis.
Effect on normal tissuethere is harmful effect on soft
tissue and salivary glands.
Retreatment not possiblein case of failure or recurrence,
re-treatment with radiation is not very successful.
Management
Indications
Types of Beams
Treatment Modalities of Oral Cancer
Electron Beam
Radiotherapy
Advantage of Radiotherapy
Avoiding surgical proceduredue to radiotherapy, major
surgical procedure is avoided.
No cosmetic and functional defectas surgery is avoided,
there is no cosmetic or functional defect.
Management of early metastasisearly metastatic spread
to cervical lymph nodes can be treated.
Proton Beam
Protons are much heavier than electrons and have a positive
charge. They have a finite range like electrons but at the
end of their range, Braggs peak occurs where they deliver
the maximum dose.
Protons have virtually no side scatter which adds to the
therapeutic ratio. By appropriately adjusting the proton
beam, Braggs peak can be positioned with the tumor almost
anywhere in the body, sparing the normal tissues; both
proximal and distal to the tumor.
Neutron Beam
Cancer cells that are hypoxic or that are in certain stages of
the cell cycle or that are proficient at repairing damage are
relatively resistant to be killed by photon or electron beam
irradiation.
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Teletherapy
This is the most common modality of radiation therapy.
The X-rays of different energies are used for diagnostic and
therapeutic purposes.
Superficial X-ray
Orthovoltage X-ray
These X-rays have energies between 250 KV to 350 KV and
these are used as most common treatment modalities. The
tissue penetration at 5 cm in depth is about 60%. The
maximum absorbed dose from single field is at the skin
surface and the deeper tissues are treated by using multiple
therapies. Orthovoltage radiations are still used for
palliative therapy where poor tissue penetration is of little
importance.
Megavoltage
It includes linear accelerators (Fig. 16-54) and betatrons.
These machines accelerate electrons across millions of volts
to provide a continuous X-ray spectrum, with the maximum
energy equal to the accelerating X-ray. These machines
normally operate at 4-8 MeV range and spare the skin.
The target in linear accelerator is small, which produces
a narrow penumbra compared to that of the cobalt unit. It
is more expensive to maintain (than the cobalt unit) and
requires staff trained in physics, as it requires daily
caliberation. It produces high energy beams with good
tissue penetration. The energy from these high energy beams
is absorbed by Compton Effect. The energy absorption is
not dependent on the average weight of the tissues. So, the
bones, cartilage and soft tissues receive the same dose and
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Field Arrangement
Multiple Field
Head and neck tumors are superficial and can be irradiated
by two fields, without compromising the depth, while
tumors of thorax and abdomen require 3 to 4 fields to
achieve an adequate concentrated tumor dose.
Most common form of multiple field treatment is with 4
fields, arranged two parallel and two opposed pairs (4 field
brick technique)) which produce good tumor localization
with a square volume.
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Tumor Volume
After the field position has been verified an outline of the
patient is taken through the center of the volume by
applying a pliable lead strip to the patient. This outline is
then transferred to a paper, with the field in center, the
patient in the midline of the couch surface and often a
reference point marked.
The tumor volume is calculated from orthogonal X-ray
films and put onto the transverse outline through the tumor
center. The coronal projections of tumor volume are
normally obtained from the anteroposterior films. The
lateral check films are used to calculate the sagittal
tumor volume. Tumor volume depends on several factors,
one of which is the experience and philosophy of the
radiotherapist.
Isodose Distribution
A treatment plan is a result of the addition of Isodose curves
of the entire field. This will produce an even dose across
the tumor volume with less than 5% variation. The dose of
surrounding tissues should be as small as possible.
Brachytherapy
In brachytherapy or intracavitary radiation therapy, the
radioactive source is close to the patients body as it is
contained in a custom fabricated carrier device and placed
directly on the surface of the tumor. Brachytherapy is
divided into three types:
Mould Treatment
Interstitial Therapy
It involves the insertion of a radioactive source into the
tumor.
Intracavitary Therapy
In it, radiation source is placed into the body cavity to
irradiate the surrounding tissues. The dose from the source
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Radioactive Isotopes
Iodine-131 (131I)
It is concentrated in thyroid follicular cells which can be
killed by I131 hence, it is useful in the treatment of
thyrotoxicosis and follicular adenocarcinoma. Physical
half life is 8 days but the biological half life is only 3 days.
Iodine-131 is given orally and the maximum dose is limited
to 200 mCi.
If the patient contains more than 30 mCi of I131, he should
be confined in an isolated room and the public contact is
allowed only when they got less than 15 mCi of I131, as
iodine is excreted in all body fluids. Precaution such as
special toilet facilities should be taken.
Phosphorus-32 (32P)
It is taken up by bone so, it can be used in the treatment
of polycythemia vera. These isotopes are pure beta
emitters and are not excreted readily in body fluids.
Radioprotection is much easier and doses above 10 mCi
are rarely necessary.
Yttrium-90 (99Y)
The isotopes are pure beta emitter and are available as
silicate colloid. It can be injected into the body cavity to
palliate malignant effusion. The surface dose is high but
falls to 50% at 1 mm depth.
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Hyperfractionation
Accelerated Fractionation
Most of the tumors have intermitotic intervals of few days
like acutely reacting tissue. The dose which increases injury
to acutely reacting tissue will increase the injury to
malignant cells. When the dose more than 200 rads per
day are used in a single fraction, the injury to the late reacting
tissues will increase. So, the accelerated radiation must be
delivered in multiple conventional fractions per day with
5-6 hours gap between successive irradiations. Thus, in
the accelerated fractionation, neither the fraction size is
reduced nor increased but, there is an increase in radiations
per day, normally with intervals of 5-6 hours.
Combined Strategies
A large number of possible permutations and combinations
of hypofractionation, hyperfractionation and accelerated
fractionations to treat the head and neck cancers are under
investigation.
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Complications of Radiotherapy
Osteoradionecrosis
Surgery
The surgical treatment of oral cancer as a primary modality
is ablative (excisional) in nature. All the clinically detectable
tumors must be excised with adequate margins of adjacent
normal tissue, to ensure that the residual elements of
microscopic disease do not remain within the surgical field.
Different types of surgeries may be performed as follows.
Surgical treatment has two distinctive phases: the resection
of the tumor and the reconstruction of the defect.
Enbloc Resection
In it, removal of the entire tumor along with adequate
margins of surrounding normal tissue in continuity, as
one intact specimen is carried out, without incision through
the involved tissue. Localized tumors without apparent or
suspected cervical lymphatic involvement are treated by
this method. Skin incisions are necessary to gain sufficient
access for larger lesion. Resection should proceed along
anatomical planes, whenever possible.
The extent of resection is determined by the margins of
carcinoma or potentially involved tissue and is not spared
to facilitate reconstruction. The surgeon must clear the site
of the tumor at the first attempt. The chance of resecting
residual tumor in a second operation is likely to be poor, as
the demarcation between normal and pathological tissue
becomes obscured by scarring and distortion of the
anatomy.
Commando Operation
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Reconstruction
Surgical Reconstruction
Reconstruction following resection or oral carcinoma is
designed both, to repair the cosmetic defect and to reestablish
the functions of the lost tissue. Conservation of lower border
of mandible should be attempted, whenever feasible.
Mandible bone can be replaced by a variety of natural
and alloplastic materials. Blocks of bone from hip or rib
have commonly been used. Metal implants have also been
used but suffer from problems of rejection and instability at
the site where they abut the bone.
Nowadays, free bone graft secured by microvascular
anastamosis has been used. In graft, bone remains viable
and the graft may include periosteum, muscle and skin.
Following hemimandibulectomy, some patients are
happy to tolerate a deformity. In these cases, direct soft
tissue closure is feasible. Scar contraction, which will result
in mandibular deviation, can be minimized by initial
intermaxillary fixation and then interdental traction with
training elastic bands.
Maxillofacial Prosthodontics
While surgeons can provide coverage of the defect following
resection of oral carcinoma, the return of function such as
speech and mastication and optimal cosmetic repair often
rely on the skills of the prosthodontist. Two phase of
prosthodontic care may be needed; the initial for the
provision of surgical splints and after sufficient healing,
definitive prosthetic appliance can be constructed and fitted.
Chemotherapy
It is described in Chapter 43: Anticancer Drugs.
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Intralesional Chemotherapy
Intra-arterial Chemotherapy
In this, drug is injected into the arteries which are supplied
to the tumor. This therapy can help to inhibit the tumors
growth with high remission rate. There is also low toxicity
reported.
Gene Therapy
It is defined as introduction of functional genetic material
into target cells to replace or supplement defective gene.
Principleprecise amount of genetic material is
transferred into each target cells allowing the expression
of the gene product without causing toxicity. It targets
dominantly on activated oncogenes on the cancer cells.
Gene addition therapythe role of p53, a tumor suppressor
gene in cell regulation cycle and apoptosis is well established. Hence p53 gene transfer is safe and well tolerated.
Antisense RNA therapygene expression can be inhibited
by RNA. The antisense RNA can prevent activity of several
known oncogenes. Such therapy can be directed towards
cancer cells inhibiting the expression of oncogenes.
Suicide gene therapyit involves the introduction of gene
into cell that enables a prodrug to be activated into an
active cytotoxic drug. Most commonly used are herpes
simples virus thymidine kinase which selectively targets
activity dividing cells.
Cancer Vaccines
Intensity Modulated Radiation Therapy (IMRT)
It is also called as tomotherapy. IMRT delivers planned,
specified doses of radiation therapy directly to cancer cells
at the targeted site. This will spare the surrounding healthy
tissue.
Principlein this, software is used to deliver a precise
radiation beam, to particular area of tumor. This will
decrease harmful doses to healthy tissue.
Componentit consists of image acquisition software,
treatment planning software, treatment simulator,
platinum medical linear accelerator, dynamic multileaf
collimator.
Advantageadvantage includes reduced xerostomia,
reduced risk of myopathy, and improved rate of tumor
control.
Immunotherapy
It is designed to repair, stimulate and enhance the bodys
immune response. Previous effort with interferon,
interleukins as immunomodulator got limited benefits.
Nowadays, newer therapies like immunologic gene
therapy and radioimmunotherapy are currently under trials.
Immunologic gene therapyin this, we are increased
immunogenic potential of tumor cells.
Radioimmunotherapyalso called as targeted radiotherapy. In this, radionucleotides are linked to antibodies
in order to deliver toxins directly to the tumor target.
Most commonly used radionucleotides are Yttrium-90
and Iodine-131. Radioimmunotherapy is effective for
treatment of lymphoma.
Suggested Reading
1. Anneroth G, Hansen LS, Silverman S Jr. Malignancy grading in
oral squamous cell carcinoma. J Oral Pathol 1986;15:162-8.
2. Arafat A, Ellis G, Adrian JC. Ewing Sarcoma of the jaw. Oral
Surg, Oral Med, Oral Pathol 1983;55:589-96.
3. August M, Dodson TB, et al. Nasopharyngeal carcinoma: clinical
assessment and review of 176 cases. Oral Surg, Oral Med, Oral
Pathol, Oral Radiol Endod 2001;91:205-14.
4. August M, Magennis P, Dewitt D. Osteogenic sarcoma of the
jaws: factors influencing prognosis. Int J Oral Maxillofac Surg :
1997;26:198-204.
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Introduction
Ulceration of the oral mucous membrane is a common
occurrence in patients and may challenge the diagnostic
acumen of the clinician. When observed in mouth, all
these lesions have a similar appearance. As texture of oral
mucosa is thin, mucosa is easily traumatized and infected
by foods and oral mucosa in their appearance is nonspecific
in the oral cavity. The ulcer is a Greek word meaning
wound or sore. It has focus of necrotic tissue on the surface
and a destroyed overlying epithelium.
An ulcer consists of margins, edges, floor and base.
A margin is the junction between normal epithelium
and the ulcer; so it is the boundary of the ulcer. An edge is
the junction between a margins and the floor of the
ulcer. Activity is maximum at the margins and edges of the
ulcer.
Five common types of ulcer edges are seen.
Undermined edgeit is mostly seen in tuberculosis ulcer.
The disease causing the ulcer spreads and destroys
the subcutaneous tissue faster than it destroys the skin.
The overhanging skin is friable reddish blue and
unhealthy.
Punched out edgeit is mostly seen in gummatous ulcer
or in deep tropic ulcer. The edges drop down at right
angle to the skin surface.
Sloping edgesloping edge is seen mostly in healing,
traumatic or venous ulcer which is reddish purple in
color and consists of new healthy epithelium.
Raised and pearly white, beaded edgeit is a feature of
rodent ulcer. This type of edge develops in invasive
cellular disease and becomes necrotic in the center.
Rolled out (everted) edgeit is a characteristic feature of
malignant ulcer. This ulcer is caused by fast growing
cellular disease, the growing portion at the edge of the
ulcer heaps up and spills over the normal skin to produce
an everted edge.
Formation of Ulcer
There are many ways by which ulcer develops. The simplest
and most frequent development is through the destruction
due to trauma. But many ulcers develop by systemic illness
and hence, their pathogenesis is different. These lesions
are preceded by the accumulation of fluid in subepithelial
regions with the consequent formation of small blisters
(vesicles) or large blisters (bullae) (Fig. 17-1). The presence
of fluid, thickness of the epithelium and proliferation of the
blister predispose to rupture; thus resulting in ulcer
formation, e.g. bullous form of erythema multiforme.
Oral ulcerations are preceded by intense accumulation
of inflammatory cells in the subepithelial regions, clinically
visible as macular or papular eruptions. They may break
down with resultant ulcer formation, as in certain cases of
recurrent ulcerative stomatitis. Rarely, ulcerative lesions
are preceded by an accumulation of fluid entirely within
the confines of the epithelium forming an intraepithelial
vesicle or bulla, as observed in pemphigus.
The life cycle of an ulcer consists of three phases (Fig.
17-2):
Extensionthe floor is covered with exudate and sloughs
while the base is indurated. The edge is sharply defined
and discharge is purulent or even blood stained.
Transitionit is occupied for preparation for healing.
The floor becomes cleaner, the slough separates;
indurations of base diminish and the discharge becomes
more serous. Small reddish areas of granulation tissue
appear at the floor and these unite until the whole
surface is covered.
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Classification of Ulcers
1st Classification According to Etiology and
Pathology
Traumatic
Due to mechanical irritation
Chemical irritant
Thermal burns
Radiation burns
Anesthetics necrosis
Oral trauma from sexual practice
Herpes zoster
Hand-foot and mouth disease
Herpangina
Chickenpox
Smallpox
Measles
Infectious mononucleosis
AIDSHIV
Bacterial infection
ANUG
Tuberculosis
Syphilis
Gonorrhea
Scarlet fever
Diphtheria
Fungal infection
Histoplasmosis
Blastomycosis
Mucormycosis
Cryptococcosis
Allergy
Local (stomatitis venenata)
Systemic
Secondary vaccinia
Acrodynia
Neoplastic
Squamous cell carcinoma
Malignant melanoma
Non-Hodgkins lymphoma
Systemic disorders
Infection
Blood disorder
Agranulocytosis
Cyclic neutropenia
Leukemia
Aplastic anemia
Viral infection
Herpes simplex infection
Nutritional deficiency
Scurvy
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Riboflavin deficiency
Pellagra
Protein deficiency
Malabsorption syndrome
Xerostomia
Hand-Schller-Christian disease
Letterer Siwe disease
Acrodermatitis enteropathica (Zinc deficiency)
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Blastomycosis
Mucormycosis
Etiology
Mechanical or physicalit includes biting, sharp or malposed teeth or roots, sharp food, stiff toothbrush bristles,
sharp margins of crown, fillings, denture, orthodontic
appliances and faulty instrumentation.
Self-inflictedthis is also one of the important cause of
traumatic ulceration.
Chemicalit results from caustic substances such as
silver nitrate, phenol, TCA, formocresol, eugenol,
eucalyptus oil, phosphorus and acetylsalicylic acid.
Thermalexcessive heat in the form of hot fluid or food,
on rare occasion the application of the dry ice, reverse
smoking and hot instrumentation.
Electrical currentapplication to the oral tissues may
result in destruction and consequent ulceration, e.g.
galvanism.
Othersradiation burns, self-inflicted and iatrogenic.
Clinical Features
Age and sexit occurs in persons of any age, with equal
frequency in both the sexes.
Siteit may involve any region of the mouth but common
on tongue, in mucobuccal fold, gingiva and palate.
Factors affecting appearance of ulcerthe appearance of
the traumatic ulcer varies markedly depending on the
site of the injury, the nature and severity of trauma and
the degree of secondary infection present.
Uncomplicated ulcer
Symptomsthere is tenderness and pain in the area
of lesion and it will be helpful to identify the cause of
lesion. It may persist for few days and may last for
weeks.
Size and shapethe most common variety of traumatic
ulcer is single uncomplicated ulcer. It is of moderate
size (from several millimeters to a centimeter or more
in diameter). Shape of ulcer is usually round, oval or
elliptical in shape and flat or slightly depressed
(Fig. 17-3).
Surfaceits surface consists of a serosanguineous or
grayish serofibrinous exudate. It may be composed of
a grayish necrotic slough which when removed,
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Progressusually the simple and uncomplicated traumatic ulcer heals uneventfully in 5 to 10 days after onset
and even without treatment. However, in the presence
of secondary infection or repetitive trauma, longer
healing period is required.
Diagnosis
Clinical diagnosisthere is adjacent source of irritation
present. History of the patient is also aid in coming to
diagnosis.
Differential Diagnosis
Management
Removal of causative agentcausative agent should
eliminate.
Persistent ulcertriamcinolone acetonide in emollient
base before bedtime and after meals. A persistent ulcer,
not responding to the foregoing regimen, should be
surgically excised and the entire tissue must be sent for
histopathological examination to rule out dysplastic
changes.
Pain reliefdyclonine HCL or hydroxypropyl cellulose
films can be applied for temporary pain relief.
Chlorhexidine gluconate (0.2%) ointment), chlorhexidine
mouthwash or even topical local anesthetic to relive
acute symptoms of pain.
Anesthetic Necrosis
In some cases, after administration of local anesthetics
ulceration and necrosis can occur at the site of injection.
Causes
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Diagnosis
Clinical diagnosisulceration and necrosis at the site of
injection will easily diagnose this condition.
Management
It is usually not required and lesion will heal on its
own.
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Drug Allergy
It is also called as drug idiosyncrasy, drug sensitivity and
stomatitis or dermatitis medicamentosa. Some patients have
greater susceptibility to drugs and manifest reactions more
readily than others.
Drugs which can most commonly cause drug reactions
are aminopyrine, barbiturates, gold, bromide, penicillin,
streptomycin, opioid and morphine derivative, amphetamine, etc. Drug allergy many time is caused by drug
abuse/misuse of the drugs. Many times, patient goes for
self-medication causing various types of drug sensitivity
reaction in the body. While diagnosing, drug abuse history
of patient should be carefully noted. In the history, patient
may give vague complaint or he may be polydrug user.
Clinical Features
Etiology
Fellatioin this, there is extravasation of erythrocyte
which results from soft palate elevation and tensing
against environment of negative pressure.
Cunnilingusas tongue is moved forwards taut frenum
rubs against the incisal surface of mandibular incisor.
Clinical Features
Locationit is more commonly seen on soft palate
(fellatio) and floor of mouth (cunnilingus).
Fellatio lesionin this, there is submucosal palatal
hemorrhage. Lesion appears as erythema, petechiae,
purpura or ecchymosis.
Cunnilingushorizontal ulceration with linear fibrous
hyperplasia can be seen.
Diagnosis
Clinical diagnosishistory of patient will give clue to the
diagnosis.
Management
No treatment is required in this condition and lesion is
resolved after some days.
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3
Fig. 17-8: Extensive area of erythema seen on the palate due to
drug allergy (Courtesy Dr Revent Chole).
Oral Manifestations
Symptomsxerostomia is most common complaint in
drug abuser. This may occur due to pharmacological
action on the salivary gland resulting in the
hypofunction of the gland. Another complaint includes
taste alteration, eating difficulties.
Signsin the early stages of reaction, vesicle or even
bullae may be found on the mucosa (Fig. 17-7).
Occasionally purpuric spots appear and angioneurotic
edema is seen.
Diagnosis
Fig. 17-7: Vesicles seen on the buccal mucosa in the patient
of drug reaction (Courtesy Dr Revent Chole).
Differential Diagnosis
Recurrent herpes simplex infectionit has got virus based
etiology, prodormal symptoms. Lesion occurs usually
in cluster.
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Management
Discontinuation of drugthe signs and symptoms of drug
allergy regress with discontinuing of the causative drug.
Antihistaminic drugsthe acute signs may be relieved by
administration of anti-histaminic drugs.
Topical corticosteroidlocalized reaction can be resolved
by using topical corticosteroid.
Management of anaphylactic stomatitisthis is managed
by administration of adrenaline to patient.
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Oral Manifestations
Acute contact stomatitisin this case, barely visible
redness is present. Edema may be present. If vesicle
present, it gets ruptured to form erosive lesion.
Chronic contact stomatitisin this, as allergen remains
more in contact with the oral mucosa, we can see white
hyperkeratotic lesion (Fig. 17-10).
Contact Allergy
It is caused by delayed type of hypersensitivity reaction to
topical antigen. On the skin, it is referred as dermatitis
venenata and oral lesions are referred as stomatitis venenata.
The oral mucosa is less sensitive as compared to skin as
saliva dilutes and removes many antigens. Another reason
is that period of contact with the oral mucosa is brief as
allergen is rapidly dispersed from the oral cavity. Oral
lesions are rare due to number of Langerhans cells, saliva
which dilutes the allergens and washes them from the
surface of the mucosa and digest with enzymes and a thin
layer of keratin present on the oral mucosa.
Etiology
Medicationit is caused by poison ivy, leather, rubber,
nickel, medication or other chemicals.
Dental amalgamcontact allergy to dental amalgam is
caused by mercury, which is released during
condensation.
Dental and cosmetic preparationit includes dentifrices,
mouthwashes, denture powder, lip stick, cough drop
and chewing gums.
Dental materialit includes vulcanite, acrylic, metal alloy
base.
Dental therapeutic agentsit includes alcohol, antibiotics,
chloroform, iodide, phenol, procaine and volatile oils.
Cinnamon flavoringcinnamon oil is used as flavoring
agents in ice cream, soft drinks, alcoholic beverage, gum,
candy, mouthwashes, and breathes freshener.
Clinical Features
Ageit has got more predilections of females as
compared to males.
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Diagnosis
Differential Diagnosis
Herpetic gingivostomatitisexanthemas on hand, feet and
mouth.
Erythema multiformelip changes, target or iris type of
skin lesions and malaise, in severe conditions.
Acute necrotizing ulcerative gingivitisstarting on tips of
papillae, mild fever and lymphadenopathy. Punched
out ulcerations covered with gray-yellow to gray-green
pseudomembrane.
Acrodynia
Management
Etiopathogenesis
Secondary Vaccinia
It is also called as vaccinia autonoculata. Undesired skin or
mucosal lesion, after smallpox vaccination, is caused by
transfer of the contents of vaccination pustule to other parts
of the body (Fig. 17-11). It is followed by formation of
secondary lesions usually with weaker reaction than the
one seen in case of primary inoculation.
Angioedema
It is also called as angioneurotic edema, Quinckes edema,
and giant urticaria. It is common form of edema which
involves subcutaneous and submucosal connective tissue.
Clinical Features
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Diagnosis
Clinical diagnosisclinical presentation is typical with
known antigenic stimulant.
Management
Removal of causewhen etiological agent such as food
can be discovered, its elimination from diet will prevent
recurrent attacks. If it is associated with ACE inhibitor,
the drug should be avoided in future.
Antihistamine drugsantihistaminic drugs (50 mg to 75
mg diphenylhydramine hydrochloride) can give prompt
relief. In case of severe attack, intramuscular epinephrine
should be administered.
Systemic Disorders
It is described in other respective chapters.
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Etiology
Immunological abnormalitiesmucosal destruction occur
due to T cell mediated immunological reaction. IgG and
IgM binding of the epithelial cells of the spinous layer of
oral mucosa is seen in patients suffering from recurrent
aphthous ulcer.
Genetic predispositionincreased susceptibility to RAS
is seen among the children of RAS positive parents.
Specific HLA antigen has been identified in RAS
patients. There is familial tendency for the occurrence of
the disease. It is associated with HLA histocompatibility
agents.
Microbial organisma pleomorphic transitional L-form
of -hemolytic streptococcus and streptococcus sanguis
has been implicated as the causative agent of the disease.
The reason for their occurrence is increased in antigenic
exposure of the patient. Other microbial agents which
are responsible are varicella zoster virus, adenovirus
and cytomegalovirus.
Systemic factorssmall percentage of patients with
recurrent aphthae have certain nutritional deficiency.
Presence of a deficiency allows the expression of an
unrelated, underlying tendency to ulceration. Other
systemic factors like celiac disease, cyclic neutropenia,
inflammatory bowel disease, MAGIC syndrome (mouth
and genital ulcer with inflamed cartilage) and Sweet
syndrome can also cause aphthous ulcer in oral cavity.
Precipitating Factors
Traumalocal trauma including self-inflicted bites, oral
surgical procedures, toothbrushing, needle injections
and dental trauma can cause aphthous ulceration. The
reason behind is that it decreases the mucosal barrier
locally.
Endocrine conditionsthere is some relation between
occurrence of aphthous ulcer and pregnancy,
menstruation and menopause. There is remission of
ulcers during pregnancy. Incidences of aphthae are
greatest during menstruation. Ulcerations are maximum
during postovulation period.
Stressacute psychological problems appear many
times, to precipitate the attacks of the disease. Stress and
anxiety can also precipitate the attack. You can see more
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Classification
Clinical Features
Age and sex distributionit usually occurs between
second and third decades of life. It is common in women
than men.
Sitesit occurs most commonly on buccal and labial
mucosa (Fig. 17-13), buccal and lingual sulci, tongue,
soft palate, pharynx and gingiva.
Diagnosis
Clinical diagnosisdiagnosis is made from clinical
presentation and exclusion of other disease.
Differential Diagnosis
BMMP and pemphigusabsence of vesicles and blebs.
Bednars aphthaethese are not aphthae as such but
traumatic lesions on the palatal mucosa of a newborn
which develop through careless wiping of the oral cavity.
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B
Figs 17-15A and B: Minor aphthous ulceration seen on labial
mucosa and gingiva. Size of ulcer is around 0.5 mm.
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Superficial ulceration
Deep ulceration
At any age
Slow development
Features
Recurrent aphthous
ulcer
Recurrent intraoral
herpes infection
Little or no pain
Age
Wide range
Thickened edges
Associated edema
Palpation noncontributing
Borders indurated
Location
Initial lesion
On freely movable
mucosa like lip, buccal
mucosa, tongue,
mucobuccal fold and
soft palate.
Erythematous macule or
papule which undergoes
central blanching
followed by necrosis
and ulceration.
Management
Number of
lesion
Occur single
Histology
Nonspecific ulcer
Erythematous halo
Very painful
Moderately painful
Recurring appearance at
different location
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Erythema Multiforme
It is acute inflammatory disease of the skin and mucous
membrane that causes a variety of skin lesions, hence the
term multiforme.
Etiology
Immune mediated disease that is indicated by the
deposition of immune complexes in the superficial
microvasculature of the skin and mucous membrane or
cell mediated immunity.
Drugs like sulfonamides, trimethoprin, nitrofurantion,
phenylbutazone, digitalis, birth control pills and penicillin.
Microorganismsmicroorganisms like mycoplasma
pneumoniae and herpes simplex virus.
Other factorsvaccination, radiation therapy and occasionally other disease like Crohns disease, ulcerative
colitis and infectious mononucleosis can also
predispose to this condition.
Types
Erythema multiforme minorit is self-limiting form and
is less severe form and lesion.
Erythema multiforme majorit is severe form may be
present as Steven Johnson syndrome.
Toxic epidermal necrolysisit is the most severe form of
erythema multiforme. It occur due to increased apoptosis
of the epithelial cells.
Clinical Features
Age and sexit is most frequently seen in children and
young adults and is rare after the age of 50. It affects
males more than females.
Oral Manifestation
Prevalenceit occurs along with skin lesions in 45% of
the cases.
Siteslip is prominently involved followed by buccal
mucosa, palate, tongue and face.
Appearanceoral lesions start as bullae, on an erythematous base and break rapidly into irregular ulcers.
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Differential Diagnosis
Fig. 17-20: Extensive lesion of buccal mucosa seen in
erythema multiforme
Herpetic gingivostomatitis
B
Figs 17-21A and B: Hemorrhagic crusting of lip seen in
erythema multiforme patient (Courtesy Dr Chole).
No skin changes
Acute onset
Self-limiting course
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Pemphigus
Pemphigus
Acute disease
Chronic disease
Pustulopapular vegetation
Diagnosis
Clinical diagnosisbulls eye lesion with hemorrhagic
crusting of lip is typical of erythema multiforme.
Laboratory diagnosisbiopsy shows subepithelial or
intraepithelial vesiculation.
Management
Topical steroidmild cases can be managed by topical
application of steroid.
Removal of causeif you are able to identify causative
drug, its use should be discontinued.
Rehydrationif patient is dehydrated due to pain then
intravenous rehydration should be carried out. Patient
should be given soft liquid diet.
Topical anesthetic mouthwashthis is given to manage
the pain in the oral cavity.
Systemic steroidin severe cases, systemic 30 mg/day
prednisone or methyl prednisone for several days should
be given. Dose should be tapered after the symptoms
subside (Fig. 17-22).
Acyclovirit is indicated in erythema multiforme
associated with HSV.
Management of toxic epidermal necrolysisthis patient is
managed in burn center. Administration of pooled
human immunoglobulin is also effective in TEN. The
reason behind is that it induced blockade of Fas ligand
which induce epithelial cell apoptosis.
Types
Pemphigus vulgaris
Pemphigus vegetans
Pemphigus foliaceous
Pemphigus erythematosus
Pemphigus Vulgaris
Mechanism
Epithelial cell separationbinding of IgG antibody to
Pemphigus antigen leads to epithelial cell separation
by triggering complement activity or plasminogen
plasmin system. Separation of cell takes place in lower
layer of stratum spinosum.
Associated factorspemphigus may be associated with
thymoma, myasthenia gravis or with multiple autoimmune disorders. It may be triggered by drug therapy
like penicillamine, penicillin, phenobarbitone and
captopril.
Clinical Features
Age and sexit is seen in 5th to 6th decades of life and
male to female ratio is 1:1, with whites more commonly
affected.
Sizethin walled bullae or vesicles varying in diameter
from few mm to several centimeters arise on normal skin
or mucosa (Fig. 17-23).
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Oral Manifestations
Prevalencein 90% of the cases, oral lesions develop and
in 60% cases, they occur first.
Sitesinitial lesion most frequently occurs on buccal
mucosa because the epithelium demonstrates
less intercellular substance and fewer intercellular
junctions making the area more susceptible to
acantholysis. Palate and gingiva are other common sites
of involvement.
Onsetoral lesions begin as classic bullae on noninflamed base with formation of shallow ulcers as bullae
break rapidly (Fig. 17-25).
Symptomslesions bleed easily and are tender on
palpation. The pain may be so severe that the patient is
unable to eat.
Signsthin layer of epithelium peels away in an irregular
pattern leaving denuded base.
Pemphigus Vegetans
Types
Neumann typeit is more common and early lesions are
similar to those seen in pemphigus vulgaris.
Hallopeau typein hallopeau type; pustules, not bullae,
are the initial lesions which are followed by verrucous
hyperkeratotic vegetations.
Clinical Features
Incidenceit occurs in 1% to 9% of the cases.
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Differential Diagnosis
Oral Manifestations
Granular or cobblestone appearancegingival lesions are
lace like ulcers with purulent surface on red base or
have granular or cobblestone appearance.
Diagnosis
Clinical diagnosispositive Nikolskys sign with
vesicular and bullous lesion seen on trunk, leg and oral
mucosa.
Laboratory diagnosisbasic defects are intraepithelial
and is demonstrated as acantholysis as in stratum
spinosum.
Tzanck smearit is done to demonstrate Tzanck cells
which often are found lying freely within the vesicular
space.
Indirect immunofluorescent antibody testantibodies
against intercellular substance can be seen. The titers of
No eye symptoms.
Painful lesions.
Management
Corticosteroidstopical or systemic prednisone. Systemic
prednisone is used to bring disease under control and
once the disease is under control, dose of prednisone is
reduced.
Combination therapyhigh dose of corticosteroids are
combined with immuno-suppressive drugs such as
cyclosporine or azathoprine.
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Bullous Pemphigoid
It is also called as para-pemphigus, or aging pemphigus. In
this, the initial defect is subepithelial in the lamina lucida
region of the basement membrane. It is associated with antibasement membrane antibodies which are detected in the
basement membrane.
Clinical Features
Age and sex distributionit occurs chiefly in adults over
the age of 60 is self-limiting and rarely lasts over 5 years.
Onsetpruritus is seen in patient which is followed by
develop of multiple bullae. Bullae do not extend
peripherally and remain localized; heal spontaneously.
Skin lesionskin lesions begin as generalized nonspecific rash, commonly on the limbs, which appear as
blisters on inflamed skin; itching precedes.
Progressit may persist for several weeks to several
months before ultimate appearance of vesiculo-bullous
lesions.
Signsthese vesicle and bullae are relatively thick walled
and may remain intact for several days (Fig. 17-27).
Rupture does not occur although it leaves raw eroded
areas which heal rapidly.
Diagnosis
Clinical diagnosisbulla present on skin which does not
extend peripherally. Ruptured bulla can be seen.
Laboratory diagnosisthe vesicle and bullae are subepidermal and non-specific. Epithelium appears normal.
The vesicle contain fibrinous exudate admixed with
occasional inflammatory cells.
Indirect immunofluorescence antibody testlesions will
demonstrate circulating IgG antibodies against
basement membrane antigen.
Tzanck smear negative to acantholytic cells.
Direct immunofluorescence testing and compliment fixation
testpositive specimen will demonstrate IgG and
complement in the basement membrane zone.
Management
Oral Manifestations
Sitesvesicles and ultimately erosion may develop not
only on the gingival tissue but any other area such as
the buccal mucosa, palate (Fig. 17-28), floor of the mouth
and tongue.
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Clinical Features
Age and sexit occurs more commonly in patients over
50 years of age and female to male ratio is 2:1.
Sitestypically, the vesiculo-bullous lesions occur on
the oral mucus membrane, conjunctivae and skin. The
other mucous membranes involved are those of nose,
larynx, pharynx, esophagus, vulva, vagina and penis.
Symptomsinvolvement of esophagus and trachea may
cause strictures leading to difficulty in swallowing or
breathing.
Eyesadhesions may develop between bulbar and
palpebral conjunctivae resulting in obliteration of the
palpebral fissure with opacity of the cornea, frequently
leading to blindness. Scarring can lead eyelid to turn
inward (entropion). This will cause eyelashes to rub
against cornea and globe (trichiasis).
Healingit may lead to scarring of affected area.
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Fig. 17-30: Same patient showing ulceration on inner aspect of lip.
Diagnosis
Clinical diagnosisdesquamative gingivitis with erosive
lesion seen in oral cavity with typical eye lesion will
diagnose these conditions.
Laboratory diagnosisthe vesicle and bullae are subepidermal rather suprabasilar and there is no evidence
of acantholysis. Low titers of serum antibody.
Direct immunofluorescent studyit will show positive
fluorescence for immunoglobulins and complement in
basement membrane zone, i.e. in intercellular substance
of prickle cell layer of epithelium.
Differential Diagnosis
Oral Manifestations
Sitesit occurs on gingiva, buccal mucosa and palate.
The mouth may be the only site involved.
Onsetthe mucosal lesions are also vesiculo-bullous in
nature, but appear to be relatively thick walled and for
this reason may persist for 24 to 48 hours before
rupturing and desquamation.
Appearancethere may be formation of ulcer, which
surrounded by zone of erythema. There may be erosion
on cheek (Fig. 17-29) and vesicles on palate and narrower
peripheral extensions.
Signsafter rupture of vesicle surface epithelium is lost
leaving raw red bleeding surface (Fig. 17-30).
Management
Topical steroid treatmentdisease can be controlled by
topical application of steroid many times daily. In case
of gingival lesion, flexible mouth guard may be fabricated
to use as carrier for the corticosteroid medication.
Systemic steroid and immunosuppressive therapyif topical
treatment is not successful, systemic corticosteroid with
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Mucous membrane
pemphigoid
Herpetic gingivostomatitis
Independent of age
No eye involvement
Clinical Features
Age and sexit is usually manifested during adolescent
or young life with no predilection for sex.
Sitesthe most common sites are flexure surfaces of the
axillae and groin, the neck and the genital area.
Appearancethe lesions develop as small groups of
vesicles appearing on normal or erythematous skin,
which soon rupture to leave eroded, crusted areas
Nikolskys signthey enlarge peripherally but heal in
center with Nikolskys sign positive.
Symptomstender and enlarged regional lymph nodes
may also be present.
Oral Manifestations
Eroded areaintraorally, there is presence of crops of
vesicle which ruptures very rupturing leaving raw
eroded areas.
Diagnosis
Clinical diagnosiscrops of vesicle seen on flexor surface
of hand with positive Nikolskys sign.
Laboratory diagnosisacantholysis is more extensive as
compared to other types of pemphigus. Characteristic
feature of this disease in occasional intercellular bridges
persist so that adjacent epithelial cells still adhere to
each other. This gives classic description of the
dilapidated brick wall effect.
Management
Antibiotics therapyit is generally effective in this lesion.
Topical antibiotics like clindamycin or erythromycin in
improvement of lesion.
Soothing ointmentsoothing ointment like aluminum
acetate will give some relief from symptoms.
Corticosteroidsthis should be used intermittently in this
disease.
Epidermolysis Bullosa
It is a dermatological disorder in which bullae or vesicles
occur on skin or mucous membrane surface spontaneously,
shortly after minor trauma. There is defect in attachment
mechanism of epithelial cells.
Classification
Epidermolysis bullosa simplex
Generalized form
Localized form (Weber-Cockayne syndrome, recurrent
bullous eruption of hands and feet)
Epidermolysis bullosa dystrophic, dominant.
Epidermolysis bullosa dystrophic, recessive.
Junctional epidermolysis bullosa (Epidermolysis bullosa
latalis, junctional bullous epidermatosis, Herlitzs
disease)it is severe form and many patient may die at
birth.
Epidermolysis bullosa acquista (acquired)it is similar to
dystrophic form of the disease but usually with an adult
onset. It is autoimmune rather than genetic in origin.
Clinical Features
Epidermolysis bullosa simplex
Ageit is inherited as autosomal dominant trait and
manifests at birth or shortly thereafter.
Sitesit is characterized by formation of bullae or vesicle
on the hands and feet at site of friction or trauma. The
knees, elbows and trunk are rarely involved and nails
are occasionally affected.
Healingwhen the blister heals within 2 to 10 days there
is no resultant scarring or permanent pigmentation.
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3
Fig. 17-33: Vesicular lesion seen on thigh of patient in
epidermolysis bullosa
Oral Manifestations
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Management
Sterile drainagelarge blisters should be pricked and
the blister fluid released. Dressing, to minimize reaction
may be helpful.
Antibioticssuper infections should be treated with
appropriate local or systemic antibiotics.
Plastic surgerymitten deformity of hand can be
corrected with plastic surgery.
Lip lubricantthis should be applied to prevent trauma
to lip.
Dermatitis Herpetiformis
It is also called as Duhring-Brocq disease. It is a rare, benign,
chronic, recurrent dermatologic disease of unknown
etiology.
Clinical Features
Age and sexit occurs between 20 to 55 years of age,
with males affected at least twice as frequently as females.
Sitesthese occur most frequently on buttocks,
extremities as well as on the face, scalp and sometimes,
the oral cavity.
Symptoms and signsthe first manifestation of the
disease is usually pruritis and severe burning followed
by the development of erythematous papules (Fig. 1735), vesicles, bullae or pustules. The patient usually
shows increased severity in summer months.
Diagnosis
Clinical diagnosisNikolskys sign is positive with vesicle
and bullous formation on skin, leg, thigh and face. The
diagnosis should be simple when the family history,
reaction to trauma and the lesions appearing most
profusely on the extremities are taken into consideration.
Laboratory diagnosisindividual cells become edematous
and show dissolution of organelles and tonofibrils with
displacement of the nucleus to the upper end of cells.
Oral Manifestations
Ulcerationvesicles and bullae rupture very rapidly in
oral cavity. This rupture of vesicle will result in formation
of superficial ulceration.
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Differential Diagnosis
Pemphiguschronic course, epithelial tag on the borders
of lesion, occurs in older patients.
Mucous membrane pemphigoiderosion, immunofluorescence, no necrosis, eye involvement, Tzanck test is
negative.
Erythema multiformeacute onset, most commonly seen
on the mucosa of lip, iris or target lesions, more frequent
in young patients.
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Diagnosis
Clinical diagnosisoccurrence of hemorrhagic bulla with
complaint of tightness will give clue to diagnosis.
Management
Patient should be given antiseptic mouthwash to control
infection. As blister spontaneously rupture and heals
rapidly, no other treatment is required.
Management
Dapsone100-200 mg per day will give prompt relief.
Gluten free dieta gluten free diet may help to reduce or
completely remove the disease.
Common Syndromes
Stevens-Johnson Syndrome
It is the severe form of erythema multiforme with
widespread involvement, typically involving skin, oral
cavity, eyes and genitalia.
Clinical Features
Clinical Features
Diagnosis
Etiology
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Clinical Features
3
Fig. 17-36: Stevens-Johnson syndrome showing extensive
lesion on the soft palate.
Oral Manifestations
Symptomsoral mucous membrane lesions may be extremely painful and so, mastication becomes impossible.
Signsmucosal vesicles or bullae occur, rupture and
leave a surface covered with thick, white or yellow
exudates (Fig. 17-36).
Pharynxerosions of the pharynx are also common.
Lipslips may exhibit ulcerations with bloody crusting
and are often painful.
Management
There is no specific treatment for this, although in some
cases, ACTH, cortisone and chlortetracycline have
shown promising results.
Behcets Syndrome
It is discovered by H. Behcet in 1937 as a tried of recurring
oral ulcers, recurring genital ulcer and eye lesion.
Etiology
Immunologicalit is caused by immune complexes that
lead to vasculitis of small and medium sized blood vessels.
It has got strong association with certain HLA type. There
may be inflammation of the epithelium caused by
immunocompetent T-lymphocytes and plasma cells.
Environmental antigenit may be associated with
environmental antigen such as bacteria (streptococci),
viruses, pesticides and heavy metal.
Classification
Mucocutaneousoral, genital and skin lesions.
Arthriticarthritis, in addition to mucocutaneous
lesions.
Diagnosis
Clinical diagnosisrecurrent oral ulcerations at least 3
times in 12 month period, plus at least two of the
following four manifestations:
Recurrent genital lesions.
Eye lesions including uveitis or retinal vasculitis.
Skin lesions including erythema nodosum,
pseudofolliculitis and papulo-pustular lesions.
Laboratory diagnosisthere is positive Pathergy test
(cutaneous hypertrophy to intra-cutaneous injection or
needle sticks (Pathergy) with the finding of pustule
forming 24 hours after needle puncture).
Management
Topical and intralesional steroidsoral mucosal lesions
be treated with topical or intralesional steroids.
Severe casespatients with life threatening or slight
threatening vasculitis are managed with combination
of immunosuppressive drugs and systemic corticosteroids. Immunosuppressive drugs which used are
cyclosporine, azathioprine and interferon alpha. Use of
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Reiters Syndrome
It is a disease of unknown etiology and is considered as an
important complication of non-gonococcal urethritis and
is often acquired sexually. Reiter syndrome can also be
found in HIV infected patient. Oral lesions occur in less
than 5% to about 50% of the patients with the disease.
It consists of tetrad of:
Urethritis.
Arthritis.
Conjunctivitis.
Mucocutaneous lesions.
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Diagnosis
Clinical diagnosisthe clinical finding of peripheral
arthritis which last longer than 1 month in association
with urethritis, cervicitis will diagnose this syndrome.
Laboratory diagnosisthere is leukocytosis, and elevated
ESR. Biopsy of lesion shows parakeratosis, acanthosis,
and polymorphonuclear leukocyte infiltration of
epithelium, sometimes with microabscess formation.
Differential Diagnosis
Etiology
Infectious agentsit may be due to pleuropnemonia like
organism. Variety of infectious agents like bedsonia,
mycoplasma, chlamydia, virus, etc.
Staphylococciit can be associated with staphylococci
and in that case, it is called as staphylococcal scalded skin
syndrome.
Clinical Features
Age and sexit is totally confined to men, usually
between the ages of 20 to 30 years.
Symptomsthe disease begins abruptly with diffuse
erythema and fever.
Signslarge flaccid bullae are formed which contain a
clear yellowish fluid. The bullae rupture very easily
leaving large areas of skin devoid of superficial epidermis.
Genital findingsthe urethral discharge is usually
associated with an itching and burning sensation.
Arthritisarthritis is often bilateral, symmetrical and
usually polyarticular.
Conjunctivitisconjunctivitis is often so mild as to be
overlooked.
Skin lesionthe skin lesions consist of red or yellow
keratotic macules which eventually desquamate.
Management
Spontaneous remissionmany patients undergo
spontaneous remission.
Antibioticsin case symptomatic patient, doxycycline
or minocycline may be given.
Analgesicsnonsteroidal anti-inflammatory drugs are
given to manage arthritis.
Immunosuppressive agentsimmunosuppressive agents
like azathioprine and methotrexate are given in cases of
most resistant cases.
Oral Manifestations
Clinical Features
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3
Fig. 17-37: Ulceration seen in palate after patient is given
chemotherapy for the malignancy,
Management
Topical anesthetictopical anesthetic such as elixir of
diphenhydramine or lidocaine combined with milk of
magnesia.
Tetracycline suspensionoral suspension of tetracycline
which is used as mouthwashes and then swallowed.
Suggested Reading
1. Akinson JC, Frank MM. Oral manifestation and dental
management of patient with hereditary angioedema. J Oral Pathol
Med 1991;20:139-42.
2. Allen CM, Blozis GG. Oral mucosal reaction to cinnamon-flavored
chewing gum. JADA 1988;116:664-7.
3. Allen CM, Camisa C. Paraneoplastic pemphigus: a review of
literature. Oral Dis 2000;6:208-14.
4. Autoo JW, Miller RL. Aphthous ulceration: a review of literature
on etiology, pathogenesis, diagnosis and treatment. JADA 1980;
101:803-08.
5. Bagan JB, Sanchis JM, et al. Recurrent aphthous stomatitis: a
study of clinical characteristic of lesion in 93 cases. J Oral Pathol
Med 1991;20:395-7.
6. Bagan JV, et al. Recurrent aphthous stomatitis: A study of clinical
characteristics of lesion in 93 cases. J Oral Path Med 1991;20(8):
395-7.
7. Barone CM, Bianchi MA, et al. Treatment of toxic epidermal
necrolysis and Steven Johnson syndrome in children. J Oral
Maxillofac Surg 1993;51:264-8.
8. Bolewska J, Hansen HJ, et al. Oral mucosal lesion related to silver
amalgam restoration. Oral Surg, Oral Med, Oral Pathol 1990;
70:55-8.
9. Brain JH, Paul BF, Assad DA. Periodontal plastic surgery in
dystrophic epidermolysis patient: a review and case report. J
Periodontal 1999;70:1392-6.
10. Brooke RI, Sapp JP. Herpetiform ulceration. Oral Surg, Oral Med,
Oral Pathol 1976;12:182-8.
11. Carroll MJ. Tissue necrosis following a buccal infiltration. Br
Dent J 1980;149:209-10.
12. Casiglia JM. Recurrent aphthous stomatitis: etiology, diagnosis,
and treatment. Gen Dent 2002;50(2):157-66.
13. Cohen L. Etiology, pathogenesis and classification of aphthous
stomatitis and Behcets syndrome. J Oral Path 1978;7:405-13.
14. Damm DD, White DK, Brinker CM. Variation of palatal erythema
secondary to fellatio. Oral Surg, Oral Med, Oral Pathol 1981;52:
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36. Mader CL. Lingual frenum ulcer resulting from orogenital sex.
JADA 1976;92:888-90.
37. Magesh K, Malathi N, Anandan S. Angina bullosa hemorrhagicaA case report. JIAOMR 2006;18(2):103-05.
38. Mattingly G, Rodu B, Alling R. Quinckes disease, non hereditary
angioneurotic edema of the uvula. Oral Surg, Oral Med, Oral
Pathol 1993;75:292-5.
39. Nolan A, Lamey PJ, et al. Recurrent aphthous ulceration: vitamin
B1, B2 and B6 status and response to replacement therapy. J
Oral Pathol Med 1991;20:289-391.
40. Rees SR, Gibson J. Angioedema and swelling of the orofacial
region. Oral Disease 1997;3:256-60.
41. Regezi JA, Zarbo RJ, et al. Oral traumatic granuloma:
characterization of the cellular infiltrate. Oral Surg, Oral Med,
Oral Pathol 1993;75:723-7.
42. Rennie JS, et al. Recurrent aphthous stomatitis. Br Dent J 1985;159:
361-7.
43. Robinson JC, Lozada-Nur F, Frieden I. Oral pemphigus vulgaris:
a review of literature and a report on the Management of 12
cases. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod
1997;84:349-55.
44. Roman C. Angina bullosa hemorrhagica:
http.www.emedicine.com.
45. Scully C, Carrozzo M, et al. An update on mucous membrane
pemphigoid: a heterogeneous immune related mediated
subepithelial blistering entity. Oral Surg, Oral Med, Oral Pathol,
Oral Radiol Endod 1999;88: 56-68.
46. Ship JA. Recurrent aphthous stomatitis: an update. Oral Surg,
Oral Med, Oral Pathol, Oral Radiol Endod 1996;81:141-7.
47. Stephenson P, Lamey PJ, et al. Angina bullosa hemorrhagica:
clinical and laboratory features in 30 patients. Oral Surg, Oral
Med, Oral Pathol 1987;63:560.
48. Titsas A, Ferguson MM. Impact of opoid use in dentistry. Aust
Dent J 2002;47(2):94-8.
49. Van Loon LAJ, Bos JD, Davidson CL. Clinical evaluation of fifty
six patient referred with symptoms tentatively related to allergic
contact stomatitis. Oral Surg, Oral Med, Oral Pathol 1992;74:5725.
50. Vincent SD, et al. Clinical historic therapeutic features of cicatrical
pemphigoid: A review of literature and open therapeutic trial
with corticosteroids. Oral Surg, Oral Med, Oral Path 1993;76(4):
453-9.
51. Vincent SD, Lilly GE. Clinical, historic and therapeutic features
of aphthous stomatitis, literature review and open clinical trial
employing steroid. Oral Surg, Oral Med, Oral Pathol 1992;74:7986.
52. Williams DM. Vesiculobullous mucocutenous disease: benign
mucous membrane pemphigoid and bullous pemphigoid. J Oral
Pathol Med 1990;19:16-23.
53. Wray D, et al. Nutritional deficiencies in recurrent aphthae. J
Oral Path 1978;7:418-23.
54. Wright JM. Oral manifestation of drug reaction. Dent Clin North
Am 1984;28:529-43.
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18
Orofacial Pain
Introduction
Pain and fear of pain continues to be the strongest
motivation for people to seek dental care. Pain is a personal
experience of the sufferer that cannot be shared and it
wholly belongs to the sufferer. The head and face are
subjected to chronic persistent or recurring pains more often
than any other portion of the body. The dentists responsibility in managing orofacial pain is twofold, first is the
diagnosis, and second is the therapy.
The most frequent source of orofacial pain is dental
disease and it has been estimated that toothache is a major
health problem. Many conditions manifest as only orofacial
pain with no other associated signs or symptoms. It has
been clear that successful diagnosis of orofacial pain
depend on (Fig. 18-1).
Historyan accurate and detailed history of the pain.
Clinical examinationa detailed clinical examination of
the face and associated organs.
Knowledgethorough knowledge of those conditions
which may produce orofacial pain.
Pain is derived from word poine meaning payment or
penalty, which certain segments of our religious heritage
have translated as being synonymous with punishment.
Definition
By IASP (international association for study of pain)it is
an unpleasant sensory and emotional experience
associated with actual or potential tissue damage or
described in term of such damage.
It is an unpleasant emotional experience initiated by
noxious stimuli and transmitted over a specialized
neural network to the central nervous system, where it
is interpreted as such.
It is more or less a sensation of discomfort, distress or
agony resulting from the stimulation of specialized nerve
endings.
It is a distressing sensation elicited by noxious stimuli
of sufficient intensity acting on nerve endings.
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Neurophysiology of Pain
Structure of nervenerve is a cord-like structure that
conveys nervous impulse. It consists of a connective
tissue sheath called as epineurium, which enclose
bundles of nerve fibers, each bundle being surrounded
by its own connective tissue sheath called as perineurium.
Within each bundle the nerve fibers are separated by
interstitial connective tissue called as endoneurium (Fig.
18-2).
According to Onset
Spontaneousif the pain occurs without being provoked.
Inducedwhen some provocation causes the painful
sensation.
Triggeredwhen evoked response is out of proportion
to the stimulus.
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Proprioceptors
Pain Conduction
Fig. 18-7: Interneuron present in the brain.
Sensory Receptors
Exteroceptors
They are stimulated by external environment and are thus
located so as to become exposed to the external environ
ment. Most impulses arising from these are sensed at
conscious level. For example
Merkels corpusclestactile receptors in submucosa of
tongue and oral mucosa.
Meissners corpusclestactile receptors of skin.
Ruffinis corpusclespressure and warmth receptors.
Krause s corpusclescold receptors.
Free nerve endingsperceive superficial pain and tactile
sensations.
Interoceptors
They are located in and transmit impulses from the cavities
of the body. Most impulses arising from these receptors are
involved in involuntary functions of the body and are
below conscious levels. For example
Resting state
Ion concentrationwhen the nerve is at rest, greater
amount of anions (-ve) are present inside the cell
membrane, whereas an equal number of cations (+ve)
are gathered outside the membrane. The positively
charged potassium ions are concentrated inside, while
sodium and chloride ions are concentrated outside the
membrane.
Creation of potential electrical differencethe difference in
respective ion concentrations across the nerve membrane
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Depolarization
Activation of membrane by stimuluswhen a stimulus of
sufficient intensity is applied to the nerve, the membrane
is activated by the increased permeability of sodium,
which diffuses through the membrane into the nerve
cell.
Sodium diffusionthe marked increase in the diffusion
of sodium into the cell is followed by the passage of
potassium out of the cell. This action is said to abolish
the resting potential and depolarize the membrane.
Liberation of acetylcholineas the nerve is stimulated;
there is a rapid passage of sodium into cell and a slower
passage of potassium out of it. The alteration in
permeability of cell membrane after the stimulus is a
result of liberation of transmitter substance, acetyl
choline, at the site of stimulation.
Repolarization
Change in permeabilityfollowing depolarization, the
permeability of the nerve membrane to sodium is again
decreased, while the high permeability of potassium is
restored.
Theories of Pain
Specificity Theory
In 1644, Descartes postulated this theory that pain system
is a straight channel from the skin to brain. It was thought
that this specific pain system carried message from the
receptors to pain center in the brain.
Pattern Theory
It was proposed by Goldscheiders. He emphasized that
stimulus intensity and central summation are the critical
determinants of pain. He proposed that the large cutaneous
nerve fibers comprise a specific touch system whereas the
small fibers converge on the dorsal horn cells, summate
their input and transmit a pattern to the pain receptors
which perceives the pain.
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A
B
Figs 18-9A and B: Gate control theorya diagrammatic
representation.
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Group 1
Flickering
Quivering
Pulsing
Throbbing
Beating
Pounding
Group 2
Jumping
Flashing
Shooting
Group 3
Pricking
Boring
Drilling
Stabbing
Lancinating
Group 4
Sharp
Cutting
Lacerating
Group 5
Pinching
Pressing
Gnawing
Cramping
Crushing
Group 6
Tugging
Pulling
Wrenching
Group 7
Hot
Burning
Scalding
Searing
Group 8
Tingling
Itchy
Smarting
Stinging
Group 9
Dull
Sore
Hurting
Aching
Heavy
Group 10
Tender
Taut
Rasping
Splitting
Group 11
Tiring
Exhausting
Group 12
Sickening
Suffocating
Group 13
Fearful
Frightful
Terrifying
Group 14
Punishing
Grueling
Cruel
Vicious
Killing
Group 15
Wretched
Blinding
Group 16
Annoying
Troublesome
Miserable
Intense
Unbearable
Group 17
Spreading
Radiating
Penetrating
Piercing
Group 18
Tight
Numb
Drawing
Squeezing
Tearing
Group 19
Cool
Cold
Freezing
Group 20
Nagging
Nauseating
Agonizing
Dreadful
Torturing
Neoplasmneoplasm of the parotid gland, nasopharynx and acoustic neuroma may cause pain.
Non-neuropathic painthis type of pain involves nerves
likely to be associated with the pain. It is subdivided into: Central originthis type of pain is caused by the
lesions affecting the cord (central nervous system) is
referred to as non-neuropathic pains of central origin.
Neuronal damagepain results from neuronal
damage in CNS.
Phantom limb painphantom limb pain and
causalgia (a persistence burning sensation
resulting form peripheral nerve trauma associated
with various other phenomenon and curable by
stellate ganglion block).
Brain tumor and central lesiontumor, vascular
lesion and other destructive lesions of the brain
stem, pons, thalamus and cerebrum should be
considered in the diagnosis of chronic orofacial
pain.
Other causeslike thalamic syndrome of Dejerine
and Roussy, tertiary neurosyphilis and multiple
sclerosis.
Extra-neural origin
Dentalthis includes dental caries, exposed dentin
and cementum, pulpal and periapical disease,
periodontal disease, pericoronitis, impacted food,
ANUG, faulty restorations, fractured teeth,
traumatic occlusion, tooth eruption and exfoliation, unerupted and impacted teeth, retained root,
dental cyst, post-surgical pain, post-injection pain,
and other direct trauma to the teeth and aerodontalgia.
Alveolar and adjacent tissue origindry socket,
sinusitis, various neoplastic and non-neoplastic,
osteolytic lesions, Pagets disease, multiple
myeloma etc.
MusculoskeletalTMJ arthritis, TMJ myofacial
dysfunction, myositis, muscle spasm and trismus,
cervical muscle spasm, osteoarthritis, arthralgia
of the cervical spine and tension headache.
Vascularvascular headaches including migraine
and cluster headache, toxic and metabolic vascular
headache, hypertensive vascular changes, arterial
diseases such as aneurysms, emboli, cranial
arteritis (including giant cell arteritis, polymyalgia
and immune arteritis ), thrombophlebitis and
carotidynia.
Pain referred from outside the orofacial areaotitis
media, inflammatory or neoplastic diseases of the
ear, diseases of major salivary glands (calculus,
cyst and tumor), lesions of nasal and sinus mucosa,
myocardial ischemia which may all cause pain in
the orofacial area, often at some distance from the
focus of disease.
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Deep pain
Odontogenic pain
Pulpal pain
Periodontal pain
Musculoskeletal pain
Muscle pain
Local muscle soreness
Muscle splinting pain
Neoplastic myofacial pain
Muscle spasm pain
Temporomandibular joint pain
Disc attachment pain
Retrodiscal pad pain
Capsule pain
Arthography pain
Soft connective tissue pain
Osseous pain
Vascular pain
Atypical facial neuralgia
Cranial arteritis
Visceral pain
True visceral pain
Reflex sympathetic dystrophy
Atypical neuralgias
Migraine
Spheno-palatine neuralgia
Migranous neuralgia
Ciliarys neuralgia
Petrosal neuralgia
Carotodynia
Cluster headache
Typical facial pain
Pain of extra-cranial origin
Dental disease
Ocular disease
Ear, nose and throat disease
Salivary gland disease
TMJ syndrome
Musculoskeletal disorders of the head and neck
Cranial arteritis
Thyroid disease
Angina pectoris
Pain of intra-cranial origin
Trigeminal neuropathy
Tumor of middle cranial fossa and Gasserian ganglion
Cerebellopontine angle tumor
Thalamic central pain syndrome
Trigeminal neuralgia in multiple sclerosis
Neurogenous
Traumatic neuroma pain
Neuritis pain
peripheral neuritis
herpes zoster
Neuralgia pain
Idiopathic neuralgia
Symptomatic neuralgia
Psychogenic pain
Psychogenic intensification pain
Conversion hysteria pain
Delusional pain
Acute Pain
Acute pain may be considered to be a protective mechanism
for the body, by stimulating the sympathetic nervous
system, is often accompanied by the automatic signs of
stress and anxiety. It serves as a diagnostic value to the
clinician in determining the nature and site of the
disturbance.
Chronic Pain
What is chronic pain?
It is persistent of pain after healing. Pain of more than 6
months duration may be considered as chronic pain.
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Pathophysiology
Inflammatory originmany orofacial pains of chronic
are inflammatory in origin. The inflammatory response
to tissue damage, results in the production of pain,
edema, local increase in temperature, redness and loss
of function.
Neuroplasticityneurons are capable of altering the
structure and function in response to stimuli. This will
result in new stimulus response relationship.
Reduction in stimulation thresholdthis will result in
activation of neurons without noxious stimulus.
Alteration in temporal patterndue to this transient
stimulus may lead to sustained burst of activity.
Greater responsethere is increase in general response of
motor neurons. This will result in more response to
noxious stimuli.
Expansion of receptive fieldthis will result in wider area
may get involve with the stimuli.
Clinical Manifestation
Hyperalgesiachanges in CNS result in the clinical
manifestation of hyperalgesia. Hyperalgesia is
characterized by spontaneous pain, decreased pain
threshold and an increased magnitude of perceived
pain for any given stimulus.
Allodyniathere is pain due to stimulus that does not
normally cause pain.
Psychosocial disturbancepatient suffers from the
depression, anxiety, and social isolation.
Dysfunctiondue to chronic pain normal activity of
patient is decreased.
Superficial Pain
Superficial pains have a bright, stimulating quality and
can be correctly located by the patient so that he is aware of
precisely where it hurts. He is able to describe the location
of the pain with anatomical accuracy and thus the site of
pain and site of origin are identical.
Superficial pain is primary hyperalgesia, i.e. the structure
is painful owing to lowered threshold from local cause.
The reaction is proportional to the intensity of the stimulus;
it lasts as long as the stimulus and there is no reference to
pain to other structures.
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Deep Pain
Sensory innervations of the deeper structures of the body
supply the cortex with constant inflow of information
regarding all internal functioning of the body. Deep pain
has a dull, depressing quality. Deep pain is less accurately
localized by the patient and the patients anatomical
description of where he feels the pain may be quite diffuse.
Deep pain may not be proportional to the stimulus.
Some deep pains respond rather faithfully to stimulus but
not as faithfully as superficial pain. One of the clinical
characteristic of the deep pain is central hyperexcitability.
Deep pain input tends to cause referred pain, secondary
hyperalgesia, localized autonomic effects and secondary
myospasm activity.
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Musculoskeletal Pain
Pain arising from musculoskeletal structures present
clinical characteristics by which they may be differentiated
from other causes of deep pain; the pain relates reasonably
and logically to use, movement and the demand of function.
The pain can be provoked or aggravated by manipulation
of the structure involved. The pain is usually but not always
accompanied by some dysfunction.
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Vascular Pain
Pain of this type occurs because of noxious stimulation of
the afferent nerve fibers that supplies sensation to blood
vessels. The characteristics of vascular pain can be
differentiated from other types of deep somatic and visceral
pain. They are:
Spontaneous painthe pain occurs spontaneously
without regard from the demand for function.
Exacerbations occur spontaneously and without any
provocation.
No pain on provocationprovocation of the site of pain
does not initiate or aggravate the pain.
Recurrent and periodic behaviorthe behavior of pain is
typically recurrent and periodic.
No dysfunctionno dysfunction accompanies the pain
other than the inhibitory influence of pain and the effect
of secondary muscle spasm as a central excitatory effect.
Wolf has indicated that there are several conditions that
cause discomfort in vascular pain syndrome. These are
dilatation of blood vessels, local edema at the painful site,
edema of the vessel walls and perivascular tissues, and
associated muscle pain especially in the occipital area.
The distinctive feature of vascular pain is its primary
pulsatile or throbbing quality. Greater the amplitude of
vascular dilatation, more pronounced the throbbing quality
of the pain. This quality may be very slight at times and
may be masked by muscle pain but is usually present
during exacerbation. Although not invariably, there is an
emotional factor that accompanies vascular pain
syndrome. Frustrations, fatigue, feeling of insecurity with
tension in the individual appears to set the stage for a
painful episode.
Migraine
It is also called as migraine syndrome or migraine headache.
Etiology
Trigeminovascular neuron activationthere is activation
of trigeminovascular neurons surrounding a cephalic
blood vessel due to vasoconstriction. This will lead to
cerebral ischemia followed by compensatory vasodilation with subsequent pain and cerebral edema.
Hereditaryit has got autosomal dominant inheritance
pattern.
Triggering factorsDiversity of factors is thought to be
triggering the attack. It includes dietary factor (chocolate,
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Types
Clinical Features
Age and sex distributionit begins at young age, and
primarily affects women in a ratio of four to one.
Locationheadache is unilateral and felt in temporal,
frontal, and orbital region. Rarely, it can be felt in parietal,
postauricular and occipital areas.
Onsetheadaches often begin immediately or soon after
awakening. The attack may be recurrent or episodic with
variable frequency, usually 1 to 4 in a month.
Nature of painit is started with mild headache which
later increases in severity. It is of throbbing quality at the
peak.
Associated symptomsthere are other symptoms like
nausea, vomiting, anorexia, sensitivity to light and
sound, and mood changes.
Diagnosis
Clinical diagnosispre-headache symptoms with
presence of trigger zone with throbbing type of pain.
Management
Severe attacksthese are controlled by ergotamine
tartarate combined with caffeine, aspirin, acetaminophen, belladonna and Phenobarbital.
Mild casestreated by methergine, beta adrenergic agents
and calcium channel blockers and serotonin receptor
agonists.
Drug therapydrug which is used in treatment of cluster
head are ergotamine (2 mg sublingual tablet), sumatriptan (50-100 mg tablet, agonist to 5-HTID) will give relief
from the symptoms. Another drug which can be used are
naratriptan (2.5 mg tablet), almotriptan (12.5 mg tablet),
rizatriptan (5-10 mg tablet), zolmitriptan (2.5 mg tablet).
Non-pharmacological managementnon-pharmacological
management includes diet control, stress management,
sleep regulation and pressure on ipsilateral carotid
artery.
Cluster Headache
It is also called as migranous neuralgia, sphenopalatine
neuralgia, histaminic cephalgia, periodic migraine and Horton
syndrome. It is an uncommon. It is the most severe headache
and has been referred to as suicide headache. It is called as
cluster as attacks occur in groups or cluster.
Etiology
Vascular causethis disease is caused by abnormal
hypothalamic function, head trauma, and abnormal
release from masts cells.
Triggering factorsheadache can be initiated by alcohol,
cocaine, and nitroglycerine.
Clinical Features
Age and sex distributionmore common in third to fourth
decade of life with strong male predilection.
Locationthe deep intense pain may last for 15 minutes
to 3 hours, which is unilateral and involves the periorbital area, often radiating to the ipsilateral temple and
maxilla including the teeth. Pain is present in the
distribution of ophthalmic nerve.
Nature of painpain is paroxysmal, burning, and
lancinating without trigger zone.
Alarm clock headacheAttack develops regularly, usually
once at day over prolonged periods and some patients
at same time in day for this reasons, is referred to as
alarm clock headache.
Associated featuresassociated symptoms, such as
lacrimation from the eye, nasal congestion, rhinorrhea,
forehead and facial sweating, miosis and eyelid edema,
may be seen. Paresthetic sensation of skin over the lower
half of the face has been also reported.
Diagnosis
Clinical diagnosisalarm clock headache without trigger
zone will diagnose this condition.
Management
Drug therapydrug which is used in treatment of
cluster head are ergotamine (2mg sublingual tablet),
prednisone, lithium carbonate, indomethacin, methylsergide maleate, and verpamil, sumatriptan ( 50-100 mg
tablet, agonist to 5-HTID) will give relief from the
symptoms.
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Diagnosis
Clinical diagnosispolymyalgia rheumatica with severe
headache in temporal region.
Management
Etiology
Tension Headache
Temporal Arteritis
Clinical Features
Age and sex distributionit occurs exclusively in
individuals over the age of 50 years. It affects women
more frequently than males.
Onsetonset may involve one or both temporal areas.
Symptomssevere throbbing headache that often has
abrupt onset and pain, usually being on one temple but
occasionally involve the whole side of face. Headache
may be associated with hyperesthesia. There is pain on
mastication, pain in teeth, jaws and zygoma region due
to involvement of internal and external maxillary artery.
Patient may feel pain on chewing and talking also.
Nature of painmoderate to severe headache of deep,
aching, occasional throbbing or burning quality may be
present.
Radiating pointpain present may radiate from the
temporal region to the neck, maxilla, mandible or face.
Polymyalgia rheumaticasometimes, there is aching and
stiffness of the muscle of the shoulders and hips which
is often termed as polymyalgia rheumatica.
Tongue involvementpain present in tongue associated
with blanching and even gangrene, which occurs
because of involvement of lingual arteries.
Associated featuresthere may be swollen and tender
scalp arteries, usually the superficial temporal artery.
Complicationif prompt treatment is not carried out, it
may result in eye pain, photophobia, diplopia and
blindness.
Etiopathogenesis
Psychophysiologic changesPsychophysiologic changes
like stress, anxiety, and depression may cause this type
of headache.
Masticatory muscle contraction abnormalitiesabnormalities of masticatory muscle contraction will also result
in tension type headache.
Clinical Features
Age and sex distributionthis is more commonly seen in
adults and women are affected more commonly than
male.
Nature of painthe pain is episodic, which is thought to
be due to psychological or physical stressful events or of
chronic type related to stressful daily life. It is usually
slow budding pain. Pain is bilateral, dull, aching
sensation, of mild to moderate intensity, with a pressing
or tightening quality.
Physical activityunlike migraine, physical activity does
not worsen the pain and nausea is absent.
Tender areaspatients often have tender areas on the
scalp and neck and palpation may reveal tender nodules
in the cervical and trapezius muscle groups. These
nodules may be trigger points and have the capacity to
refer to the face and head area.
Diagnosis
Clinical diagnosisby looking at the symptoms, it is easy
to make diagnosis of tension type headache.
Management
Psychological managementsimple counselling,
hypnosis, relaxation and biofeedback measure are
helpful.
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Clinical Features
Age and sex distributionit is more commonly seen in
adulthood and more common in female.
Onsetit has rapid onset characterized by unilateral
head pain lasting for minute to hours.
Site of paintemporal and orbital region are site of pain.
Jaw and face are also affected.
Associated symptomsthere is also lacrimation,
rhinorrhea, nasal stuffness and swelling of painful area.
Fig. 18-10: Facial pain may be very distressing for the patient.
Diagnosis
Clinical Features
Differential Diagnosis
Cluster headacheit is an attack with same characteristics
of pain and associated symptoms and signs of a cluster
headache, but they are shorter lasting, more frequently,
occur in females, and there is absolute effectiveness of
indomethacin.
Management
Indomethacinit is given in dose of 25 to 150 mg daily. It
is effective in all cases of chronic paroxysmal
hemicranias.
Diagnosis
Management
Carotidynia
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Neurogenous Pain
Characteristics of Typical Neurogenous Pains
Bright qualitythe pain has a bright stimulating quality.
Exact location of site of painthe site of pain is accurately
localized by the patient.
Analgesic blockingsite of pain does not necessarily
identify the site of origin (except traumatic neuroma).
Site of pain bears a precise anatomical relationship to
the site of origin, so that analgesic blocking is useful
diagnostically.
Intense painpain is extremely intense compared to the
degree of stimulation.
No central excitatory effectthere is no central excitatory
effect like referred pain or secondary hyperalgesia.
Presence of trigger zonespresence of trigger zones is
the most important characteristic feature of true
neuralgia.
Painful Neuritis
Neuritic pain occurs as a result of inflammatory influence
on pain conduction fibers and is felt in the peripheral
distribution of the affected fibers. The inflammatory process
alters the relative activity of the fibers that mediate pricking
and burning pain elevating the threshold of pricking pain
but lowering it for burning pain. This gives the pain of a
characteristic burning quality.
Sensory effects such as hyperesthesia, paraesthesia,
dysesthesia, and anesthesia may be seen. If motor efferent
fibers are affected, then muscular signs such as muscular
tic, weakness or paralysis may be seen.
Etiology
Dental pathosisdental pathosis is believed by some
investigators to be involved with the onset of trigeminal
neuralgia.
Excessive tractionsecondary to excessive traction on the
various divisions of the fifth nerve, being influenced by
maxillo-mandibular relationship.
Allergicit can be secondary to an allergic and hypersensitivity reaction causing edema of the trigeminal nerve
root.
IschemiaWolf thought that ischemia at various portions
of the trigeminal pathway might be responsible for the
paroxysms of pain.
Compression distortion phenomenonJannetta and others
have shown subtle changes of a compression- distortion
phenomenon which is usually caused by arterial loops
of atherosclerotic vessels. Vessels become elongated with
advancing age and with atherosclerotic involvement
gain abnormal positions by wedging into the space
between the pons and trigeminal nerve. It is postulated
that with progressive material elongation, fascicles of
adjacent nerves later suffer myelin injury and pain
results.
Mechanical factorslike pressure due to aneurysms of
the intrapetrous portion of the internal carotid artery
that may erode through the floor of the intracranial fossa
to exert a pulsatile irritation on the ventral side of the
trigeminal ganglion.
Anomalies of superior cerebellar arteryit is the most
recently blamed cause for trigeminal neuralgia. It lies in
contact with the sensory root of the nerve and implicated
as a cause of demyelination. Surgical elevation of artery
or decompression of the sensory root has high success
rate in relieving paroxysmal pain in case of idiopathic
trigeminal neuralgia.
Secondary lesionconditions such as carcinoma of the
maxillary antrum, nasopharyngeal carcinoma, tumors
of peripheral nerve root, intracranial vascular anomalies,
and multiple sclerosis may be presented with trigeminal
pain.
Trigeminal Neuralgia
It is also called as Tic Douloureux (painful jerking), Trifacial
neuralgia or Fothergills disease. The term Tic douloureux is
only applied when the patient suffers from spasmodic
contractions of the facial muscles.
Trigeminal neuralgia is an extremely painful condition
as it is unique to humans. It is a syndrome in which
symptoms are sufficiently distinctive to permit a reliable
diagnosis solely on the basis of history. It is seriousness of
these disorders that it has one of highest cause for suicide
rates of any disease.
Clinical Features
Age and sex distributionit usually occurs in middle and
old age, the disease seldom occurs before 35 years of
age. Incidence increases with age due to degenerative
changes of the nerve fibers. It most frequently occurs in
women.
Siteit is more common on the right side and the lower
portion of the face is more frequently affected.
Nature of painthe pain is paroxysmal, lasting only a
few seconds to a few minutes and is usually of extreme
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Diagnosis
Clinical diagnosisabrupt onset of pain with trigger
point, pain is extreme in nature with less time duration.
Pain is localized to known distribution of trigeminal
nerve. Spontaneous remission can occur.
Differential Diagnosis
Migrainea very common condition mistaken for
trigeminal neuralgia is migraine or migranous neuralgia
((Hortons syndrome, histamine headache, histamine
cephalgia), but this severe type of periodic headache is
persistent, at least over a period of hours, and it has no
trigger zone.
Sinusitispain is not paroxysmal and no trigger zone
present.
Toothachethis can be easily identified by examining
the oral cavity.
Multiple sclerosisit occurs because of autoimmune
process. Specific clinical features are Charcots triad, i.e.
intention tremor, nystagmus and dysarthria or scanning
speech.
Tumors of nasopharynxtumors of the nasopharynx can
also produce similar type of pain, manifested in the lower
jaw, tongue and side of the head with associated middle
ear deafness. This complex lesion is called as trotters
syndrome. Here the patient exhibits asymmetry and
defective mobility of the soft palate and affected side. As
the tumor progresses, trismus of internal pterygoid
muscle develops, and patient is unable to open the
mouth. Here, the actual cause of pain is the involvement
of mandibular nerve in the foramen ovale.
Post herpetic neuralgianeuralgia occurs after attack of
herpes zoster virus. Pain is usually involved in the
ophthalmic division. The history of skin lesion prior to
the onset of the neuralgia usually aids in the diagnosis.
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Glossopharyngeal Neuralgia
Clinical Features
Clinical Features
Diagnosis
Clinical diagnosispain in ear, tongue, and soft palate
with vesicle formation may give clue to the diagnosis.
Management
Diagnosis
Occipital Neuralgia
Management
Topical anestheticspatient may get pain relief after
applying topical anesthetics to tonsil and side of
pharynx on side of pain.
Other therapyother therapy like carbamazepine,
oxcarbazepine, baclofen, phenytoin, lamotrigine and
resection of glossopharyngeal nerve can also be initiated.
Post-herpetic Neuralgia
It is discussed in Chapter 31: Viral Infections.
Geniculate Neuralgia
Symptomatic Neuralgia
Causes
Characteristics
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Types
Classic typethe classic type occurring after tonsillectomy resulting from surgical exposure of the styloid
process. Scar formation will result in pressure on nerve
causing the pain while swallowing.
Carotid artery syndromethe carotid artery syndrome
resulting from calcifications of the stylohyoid ligament
and elongated styloid process which encroaches the
external or internal carotid vessels produce vascular
pain.
Traumatic Eagles syndromeit develops after fracture of
mineralized stylohyoid ligament.
Clinical Features
Ageit is more commonly seen in adults.
Signsometime, elongated styloid process can be
visualized in pharyngeal area.
Symptomspain in the lateral pharyngeal wall and side
of the lower face and neck. It may mimic glossopharyngeal neuralgia.
Associated symptomsassociated symptoms include
difficulty in swallowing, sore throat, glossodynia, and
headache and dull to severe hemifacial pain. Blurred
vision and vertigo have also been seen.
Characteristic signpatients with Eagles syndrome will
characteristically rotate their head slowly to avoid
provoking pain. The pain can be demonstrated when
pressing the pharyngeal wall against the styloid process
and when swallowing or opening the mouth wide.
Radiological Features
Elongation can be seen radiographically. It is more
commonly seen panoramic radiograph. Mineralization
is also noticed on the radiograph (Fig. 18-12).
Diagnosis
Clinical diagnosispain in lateral pharyngeal wall,
blurred vision will aid in diagnosis.
Radiological diagnosiselongated styloid process can be
seen radiologically.
Management
Topical anesthesiaapplication of topical anesthesia will
not relieve pain but infiltration of a local anesthetic
around the styloid process will provide relief.
Surgicalit is treated by surgical segmentation or
resection of the elongated styloid process.
Corticosteroid injectionlocal injection of corticosteroid
sometimes provides relief.
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Psychogenic Pain
Pain that originates in the mind refers to this pain disorder,
for which, there is no apparent physiologic or organic basis
and in addition, the patient has a definite history of
psychological problems or it implies the presence of
emotional or personality disorder.
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Delusional Pain
It is created in the subjects mind as a hallucination and is
symptomatic of serious psychiatric problems. Delusional
pains of the mouth and face is a manifestation of
schizophrenic hallucination which is very rare.
Etiology
Local factors
Contact allergysubstances in denture material can be
allergic like monomer methyl methacrylate, epoxy resin
and glycol.
Chronic mechanical traumachronic mechanical trauma
may occur due to denture, clasp etc.
Habitsoral habits like clenching, grinding, and chronic
tongue thrust habit may be causative factors.
Infectioninfection with Candida albicans, fusospirochetal infection.
Xerostomiaxerostomia due to irradiation, immunological deficiency, systemic causes, mediation focal
disease.
Otherother factors like TMJ dysfunction, geographic
tongue, oral submucus fibrosis, esophageal reflux,
angioedema, trauma to lingual nerve, and acoustic nerve
neuroma may cause burning mouth syndrome.
Systemic Factors
Nutritional deficiencyvitamin deficiency like pernicious
anemia, other B complex vitamins, folic acid, iron
Clinical Features
Age and sex distributionit occurs in 5.1% of the general
population and patients older than 50 years of age.
Females are affected more as compare to males.
Sitetongue is most frequently affected followed by
denture bearing areas, buccal mucosa, throat and floor
of the mouth.
Nature of painpain is present in the morning and it can
persist and become aggravated during the day with
maximum intensity being in the evening. Half of the
patients have continuous pain which may be mild,
moderate or severe. Some patients exhibit waxing and
waning pattern that occurs several days and week.
Associated featuresheadache, insomnia, lethargy,
decreased libido, mood changes (irritability, depression,
and decreased desire to socialize).
Aggregative and relieving factorsaggregative factors
include tension, fatigue, and hot foods. Sleeping, eating
and distraction reduce intensity.
Scaled mouth syndromethis is the term used for patient
who suffers from burning due to angiotensin converting
enzyme (ACE).
Diagnosis
Clinical diagnosiswaxing and waning pattern
presented for many days. Pain is mild with increasing
intensity throughout the day.
Management
Removal of causeany cause which is casing the burning
mouth syndrome should be removed. For example
denture adaptation, allergy control, habit control,
consulting.
Nutritional supplementnutritional supplement like
ferrous sulfate 300 mg TDS, iron sulfate 2.5 ml/day IM,
cyanocobalamin 250 mg/day, pyridoxine HCl 25 to 100
mg/day, riboflavin 10 mg /day, thiamin HCl 5 to 30
mg/day, folic acid 0.1 to 34 mg/day should be given.
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Mood altering drugsmood altering drug like chlordiazepoxide shows improvement in patients.
Other drugsother drugs like amitriptyline, clonazepam,
alpha lipoic acid, hydrocortisone locally, nystatin oral
suspension, ketoconazole, and diphenylhydramine HCl
for rinsing.
Adjuvant Drugs
Several pharmacological agents are useful for palliative
and cause-related therapy.
Analgesic balmsit gives soothing palliative relief from
inflammatory pain of both superficial and deep somatic
category when applied topically on exposed or ulcerated
area. Aloe Vera juice is an ancient variety used for superficially generated pain. Balsam of Peru and eugenol are
well known balms. They are applied in various forms
like ointment, liquid, and adhesive dressings.
Anticonvulsantsphenytoin has capability of suppressing pain of paroxysmal neuralgia in about 20% of
cases. Carbamazepine which can be used in trigeminal
neuralgia is effective in 70% of cases.
Antidepressantssome patients with vascular pain and
chronic pain may respond to antidepressant medication.
Some antidepressants like tricyclic and MAO
(monoamine oxidase) inhibitors are helpful in managing
chronic pain syndromes.
Antihistaminicantihistaminic counteract the vasodilator effect of histamine by blocking certain histamine
receptors. They may be useful in allergic conditions and
some vascular pain syndromes. A direct analgesic effect
is reported by use of several antihistaminics like
diphenylhydramine.
Antimicrobials and antiviral agentsantinociceptive
benefits of such agents related to resolution of infection
that cause pain.
Dietary supplementsthe chief relationship between
diet and pain appear to be with L-tryptophan which
converts into serotoxin. Brain and spinal cord serotoxin
neuron are actively involved in nociceptive response.
The synthesis of brain serotoxin is dependent on
deposition of plasma tryptophan, 90% of which is bound
to albumin and must compete with other amino acids at
blood-brain barrier. The use of tryptophan and other
amino acids as dietary supplement appear to be a valid
approach to otherwise refractory chronic pain problems
Adequate dose of 4 mg /day with low protein, low fat,
high carbohydrate diet should be given.
Neurolytic agentsthe most commonly used is 95% ethyl
alcohol, although effective, neurolysis does not produce
regeneration of peripheral axons and gives only
temporary relief. The hazards include extensive local
fibrosis and deafferentation effect restrains its use.
Nor-epinephrine blockersin analgesic, blocking of the
stellate ganglion for the control of causative pain about
orofacial region norepinephrine blockers are used.
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Relaxation
To an extent, tension and stresses are etiological factors
in pain. Following techniques are used to provide
relaxations.
Autosedationit has been demonstrated that some
functions are automatic and beyond the voluntary
influence. However, it can be manipulated by conscious
mental procedure. There are a number of relaxation
techniques that involve mental discipline and selftraining like yoga. Modulating effects of conscious
mental autosuggestion is very reactive and should be
actively utilized in pain management. Sometimes music
may be helpful in relaxation techniques.
BiofeedbackEMG feedback has been found to be
useful in reducing hyperactivity of masticatory
muscles in individuals who are prone to clench their
teeth during day time. EMG biofeedback apertures
include pair of surface electrodes made up of silicon
rubber, voltmeter with amplifier and visual and auditory
display. In training muscle relaxation, the electric
potential of masticatory muscles can be recorded and
displayed on digital voltmeter so that patients can
observe the amount of tension and try to relax. EMG
feedback training aims at teaching the patient to become
aware of the tension in the masticatory muscle and to
learn to relax it.
Occlusal disengagementocclusal disengagement
induces substantial beneficial effects on discomfort of
TMJ disorders. Disengagement sets occlusion at rest and
causes the masticatory system to relax. Occlusal
disengagement can be accomplished by
Voluntarily disengagementpatient is asked to
voluntarily leave its teeth apart.
Chewing gumvariety of simple habit training as by
placing thin parts of chewing gum between molar
teeth.
Muscle relaxantwe can also use muscle relaxant for
the occlusal disengagement.
Counseling
Armed with good understanding of nature of pain and
how it is modulated, the doctor can use counseling as a
powerful tool in the management of pain.
Emotional stressdue to anxiety and fear, a person in
pain may be emotionally upset which accentuates his
suffering. An accurate explanation of pain should be
given to the patient in a language that can be understood
by him. It will boost the patients confidence and hope.
Honest words of assurance can allay fear and diminish
anxiety thus reducing the level of suffering.
Evaluation of consequenceapprehension concerning the
consequent damage and expecting future threat to ones
well-being cause psychological intensification of painful
experience. This can be reversed by open discussion on
realistic consequences that exist.
Inhibitory influencethe excitatory influence of attention
directed towards the complaint can be countered with
distraction by directing the mind towards thinking that
is more positive.
Coping strategiesattention and tender loving care
should reward illness behavior. Severe pain may be
made tolerable by replacing the suffering with something
better to do like doing something that benefits others,
activities that direct attention away from self or constitute
occupational therapy.
Hypnotherapyanti-nociceptive methods can be used,
provided that the pain is not due to psychoneurosis.
Some suffering is too valuable to the patient to be given
up. Personality, disintegration may follow withdrawal
of pain. Effects depend on susceptibility of the patient to
suggestion. Hypnosis is effective in large number of
patients presenting symptoms of severe pain of organic
origin.
Psychotherapyit is needful in mainly chronic pain
syndromes like conversion hysteria and delusional
pain. Pain behavior may be unlearned by manipulation
of consequences such as withdrawing positive
reinforcement and rewarding better behavior. It requires
full knowledge and cooperation not only of the patient
but also of those in close personal contact which
includes family members, doctors, nurses and the
therapist.
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Physiotherapy
Sensory Stimulation
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Local Anesthesia
Analgesic blockingto arrest the pain of myospasm by
analgesic blocking has marked therapeutic effect. It is
preferable to block nociceptive pathway than muscle
proper.
Interruption of pain cycleon the basis of clinical evidence,
a cycling mechanism appears to be implicated in several
pain syndromes that occur in the orofacial region. Such
cycling is effectively interrupted by local anesthetic
blockage of nociceptive impulses at the primary source
or somewhat along its mediating pain pathway.
Remission of pain outlasts the period of anesthesia.
Trigger point therapyinjection of short acting local
anesthetics of low myotoxicity at myofacial trigger point
located in muscle tissue effectively resolves the referred
pain syndrome. This therapy is required when triggered
point are located in the muscle tendon.
Sympathetic blockagethe diagnostic analgesic blocking
of afferent sympathetic pathway to identify mediation
by such neuron. Stellate ganglion analgesic block is as
effective as amitidine for treatment of reflex sympathetic
dystrophy. Other syndromes in which it is effective are
herpes zoster and post-herpetic neuralgia.
Suggested Reading
1. Benoliel R, Biron A et al. Trigeminal neurosensory changes following
acute and chronic paranasal sinusitis. Quintessence Int 2006;37:
437-43.
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19
Infections of
Oral Cavity
Introduction
Facial infections are relatively a common presentation to
both, general medical and dental practice. Most originate
in superficial structures (skin, subcutaneous tissue, etc.)
and are often easily diagnosed and treated.
Infections originating in deeper structures can be severe,
rapidly progressive and may cause prolonged morbidity,
long-term complications as well as potentially endanger
life. Efficient treatment requires accurate diagnosis, early
aggressive medical treatment and in most cases, urgent
decisive surgical management.
Infection is a clinicopathological entity involving
invasion of the body by pathogenic microorganisms and
reaction of the tissues to microorganisms and their toxins.
Soft tissue infections of head and neck are commonly
encountered in routine practice in dentistry. These
infections may be odontogenic or non-odontogenic in origin.
Once the infection extends past the apex of the tooth the
pathophysiology of the infectious process can vary, depending upon the number and virulence of the microorganisms,
the host resistance and anatomic geography.
These odontogenic infections can become severe, life
threatening facial space infections. These infections have
the potential to spread through facial planes of head and
neck thereby compromise the vital structures in these
regions, e.g. intracranial odontogenic infection leading to
necrotizing fascitis of head and neck. Most odontogenic
infections can be managed successfully with minimal
complications. The key to successful management is sound
surgical principles.
Local Defense
Epithelial liningit is the first line of defense. It physically
hinders the penetration of surface bacteria into deeper
tissues. When there is a break in the continuity of the
anatomic barriers, the microbes find an easy way into
deeper tissues. In the oral cavity, the bacterias find way
through deep periodontal pockets and necrotic dental
pulp.
Secretory and drainage systemthis system assists host
defense by physical and chemical action. The mucociliary activity, peristaltic motion and flushing action,
that all result in drainage and mechanical removal of
bacteria. Obstruction and impairment of drainage
almost always result in infection. Secretion of the oral
cavity, i.e. saliva and swallowing mechanism helps to
remove the food particles and also prevents stagnation
of microbial flora at one site. Chemical constitution of
saliva changes as the pH changes. This favors the growth
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Humoral Factor
Immunoglobulinthe host synthesizes specific protein
molecules, with antibody activity, in response to
antigenic stimulation. These proteins are derived from
B lymphocytes and plasma cells and are called as IgA,
IgM, IgD, IgG and IgE. Secretory IgA and IgE antibodies
directly prevent the attachment of pathogenic bacteria
or parasites to epithelial receptor cells, which is very
crucial in preventing colonization and subsequent
infection. By direct action, antibodies can neutralize
viruses and microbial toxins.
Complement systemthis consists of group of serum
proteins, which by a series of reactions produce and
release byproducts whose functions are to initiate
inflammatory reaction, regulate and enhance phagocyte
function and attack the bacterial cell membrane. The
activation of complement system by either pathway
results in generation of cytolytic activity, chemotatic
factor and mediator, anaphylactic toxin, opsonising and
phagocyte enhancing activity, and immune adhered
activity.
Cellular Component
Polymorphonuclear leukocytesPMNs are the first
phagocytes to respond to the chemotactic factor elaborated by complement system. Thus, they predominate
in acute infection, which persists for about one week.
Their function is to clear up the battle field.
Lymphocyteit consists of two types of cellsB
lymphocyte and T lymphocyte. Both T cells and B cells
produce lymphokinin hormone that plays several vital
roles in resistance to infection. Primarily they regulate
the action of phagocytic cells. Thus lymphocytes are
responsible for modulation and control of phagocytic
cells.
Microbial Factors
Pathogenicity
Definitionpathogenicity is the ability of a microbial
species to produce disease.
Mechanismit involves subversion of host cell
metabolism, and production of host cell lytic factor.
Toxinproduction of potent toxins which systemically
act on the host. To set up an infectious process, a
microorganism must be able to do the following:
To enter the host
To multiply in host tissues
To resist host defense
To damage the host.
Virulence
Definitionit is the term applied to the properties in
particular strain microorganisms. Virulence is the sum
total of several determinants such as adhesion,
toxigenicity and communicability.
Exaltation and attenuationenhancement of virulence is
known as exaltation and reduction of virulence is known
as attenuation.
Adhesionthe initial event is the attachment of bacteria
to the body surface. This attachment is not a chance
event, but it is a specific reaction between the surface
receptors on the epithelial cells and the adhesive
structures on the surface of the bacteria.
Invasivenessthis refers to the ability of a pathogen to be
spread in the host tissue after establishing infection.
Highly invasive pathogens cause generalized infections
and less invasive one causes localized infections.
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Oral Microflora
The microbial flora that is characteristic of a particular site
in majority of the population is referred as the indigenous
flora or normal flora. The oral microflora at birth is aerobic
and after eruption of teeth, anaerobes are also established.
The intrinsic source of microorganisms in the oral cavity is
gingival crevice material, pus cells and epithelial cells
undergoing degradation and salivary component.
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Spread of Infection
Direct Invasion or Extension (Table 19-1)
It is the propagation of an infection between the layers of
fascia; from one area to fascia of another area. It can occur
secondary to distension and pressure on the body. This
will force contents of infection through facial layers by
hydrostatic pressure.
Spread of infection within the bone
Alveolar bonethe bone of the alveolar process is quite
similar to the dental structure, in terms of response to
infection. The alveolar bone consists of interconnecting marrow spaces delimited by unyielding calcified
tissue, all of which are enclosed circumferentially by
layers of cortical bone of varying thickness.
Invasion of bacteria in marrowthe invasion of bacteria
from marrow space triggers the process of inflammation and cause some consequences of edema,
Involved
teeth
Usual exit
from bone
Relation of
muscle
attachment
to root apices
Site of
localization
Upper
central
incisor
Labial
Above
Oral vestibule
Upper
lateral
incisor
Labial
palatal
Above
Oral vestibule
Palate
Upper
canine
Labial
Above
Below
Oral vestibule
Canine space
Upper
premolars
Buccal
palate
Above
Oral vestibule
Palate
Upper molars
Buccal
Palatal
Above
Below
Oral vestibule
Buccal space
Palatal
Lower incisors
Labial
Above
Below
Submental
space
Oral vestibule
Lower canine
Labial
Below
Oral vestibule
Lower premolars
Buccal
Below
Oral vestibule
Buccal
Below
Above
Below
Oral vestibule
Buccal space
Sublingual
space
Below
Above
Below
Above
Oral vestibule
Buccal space
Sublingual
space
Submandibular
space
Above
Submandibular
or
pterygomandibular space
Lingual
Lower
second
molar
Buccal
Lingual
Involve teeth
Usual exist
Lingual
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Pathophysiology of Infection
Cardinal signthe bodys response to infectious agent
is inflammatory, which is essentially a protective
phenomenon. Hence, the cardinal signs of inflammation
are present, to some degree, in nearly all patients with
infection.
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Principles of Management of
Odontogenic Infection
The primary treatment of odontogenic infection does not
end with extraction of offending tooth. It also includes
establishment of adequate drainage and administration of
appropriate antibiotics along with maintenance of airway,
when indicated.
Proper assessment of airwayoften this becomes difficult
due to limited mouth opening, which frequently
accompanies these facial space infections. To assess it
properly, mouth opening should be measured; tongue
mobility and elevation of floor of mouth should be
checked lateral pharyngeal edema and deviation of
uvula should also be checked. If the airway compromise
is recognized early, then an awake fibro-optic
laryngoscopy of blind nasal intubation should be used.
If intubation can not be performed while the patient is
awake, tracheostomy should be considered.
Evaluation of vital parameterspulse, temperature and
respiration should be recorded. If temperature is more
than 103 degree Fahrenheit, then it is a cause of concern.
In such cases, besides employing local and systemic
Sequelae of Pulpitis
(Pulpoperiapical Abscess)
Causes of pulpitiscauses for pulpitis is due to irritating
inflammatory products. Various factor like host
resistance, number and virulence of bacteria, amount of
antigenic material, and degree of tooth function and
extent of other trauma also play a vital role.
Local inflammatory responsethese products escape from
pulp canal and initiate local inflammatory response.
The pulp is non-vital in such cases.
Periapical lesionif none of the irritating products of pulp
necrosis reach the periapical tissue, then no periapical
pathos is induced. If infection reaches the periapical
tissue then in some cases host defense effectively combats
and localizes the resultant inflammation in circumscribe
area.
Acute periapical abscessteeth with contaminated
gangrenous pulp have large number of bacteria passing
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Radiographic Considerations
Lamina durathere are variations in lamina dura from
person to person and region to region. Lamina dura is
not continuous in case of periapical pathology.
Amount of bone destruction30 to 60% bone destruction
required for radiographically detectable changes.
Radiographic changes can not be detected without
involvement of junctional and cortical bone.
Root resorptionexternal root resorption is caused by
orthodontic movement, inflammation or infection of bone
and benign and malignant tumor.
Jaws
Cyst and tumorsit can develop cysts or tumors that can
range from odontogenic to either primary or secondary
malignancy. Most are derived from the dental apparatus
and although benign, can nevertheless continuously
grow and become secondarily infected on breaching the
surrounding bone.
Osteomyelitis, although rare, can be the result of chronic
infection, as mentioned before.
Osteoradionecrosis occurs readily in irradiated jaws
subjected to further trauma (such as extractions).
Bacterial infectionthese are tuberculosis, actinomycosis
and syphilitic osteomyelitis.
Most jaw fractures in the tooth bearing segments are
defined to be compound to the oral cavity and can easily
be infected by the oral microbes.
Extraction sites, again are comparable to compound
fractures and it is surprising that infection in such cases
are relatively rare.
Paranasal Sinuses
It may be primarily infected, obstructed and result in facial
swelling. It may become infected, secondary to infected
teeth protruding into the maxillary sinus (upper premolars
and molars often exhibit close proximity to sinus). Tumors
or cysts may become infected. Fractures such as the orbital
floor, are by definition compound to the exterior and
may result in orbital cellulitis.
Teeth
Decay (caries) reaching the dental pulppulpitis, this in
turn spreads to supporting bone, resulting in periapical
abscess, which in turn may spread subperiosteally.
Periapical abscess may occur in seemingly intact but
devitalized teeth (trauma, cracks or decay under fillings).
Periapical and periodontal abscess may form as a result
of chronic gingivitis and supporting bone and soft tissue
loss (periodontal disease).
Erupting teeth (especially partially impacted lower third
molars) can result in inflammation and infection of the
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Pathogenesis
Microorganismstreptococci viridans and staphylococci
are frequently associated with abscess formation. They
produce the enzyme called coagulase which causes
fibrin deposition and thus helps in walling off the lesion.
Coagulase promotes virulence by inhibiting phagocytosis.
Bacterial invasionbacterial invasion of pulp canal takes
place. Canal contains large number of virulent bacteria
that rapidly spread to periapical tissues, causing acute
periodontitis, tender tooth and alveolar swelling.
Necrosis of periapical tissuewhen inflammatory response
may extend into adjacent periapical alveolar bone, it
will initiate necrosis of periapical tissue.
Abscess formationnecroses tissue coalesces and
enlarges, compressing the surrounding fibrous connective tissue. Thus an abscess is generated, which is a
collection of pus surrounded by a wall of fibrous
connective tissue.
Progress of abscessenlarging dentoalveolar abscess
contains purulent material that is under pressure due to
the production of pus. The purulent material travels
along path of least resistance, until it reaches the surface,
where due to limitation of periosteal layer, it temporally
forms subperiosteal abscess. Eventually, it erodes
through the periosteum and penetrates the soft tissue,
again, following the path of least resistance. Path of least
resistance is determined by the location of breakthrough
in the bone and the anatomy of muscles and fascia plane
in the area.
Sinus formationwell circumscribed lesion may form
sinus due to:
Inability of the body to completely contain or localized
the causative organisms.
Increase in number of causative organisms.
Lowering of patients general resistance.
Trauma or surgical intervention.
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Fig. 19-1: Periapical abscess showing swelling in palatal surface.
Clinical Features
Acute periapical abscess
Locationit develops in the periapical region of the tooth
as sequelae to necrosis of pulp (Fig. 19-1).
Symptomspain is severe and of throbbing type.
Periapical abscess may confine to osseous structures
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B
Figs 19-5A and B: Cutaneous sinus showing extraoral opening.
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Radiographic Features
Acute periapical abscess
Periodontal ligament space wideningswelling of
periodontal ligament space force the tooth slightly from
its socket, creating widening of periodontal ligament
space (Fig. 19-6).
3
Fig. 19-7: Chronic periapical infection in upper first molar showing
loss of lamina dura (Courtesy Dr Ashok L).
Diagnosis
Clinical diagnosispositive tenderness, carious tooth,
sinus formation, non-vital teeth will give clue to the
diagnosis.
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Management
A
B
Figs 19-9A and B: Loss of bone density seen in periapex of the
tooth due to chronic periapical infection.
Etiology
Differential Diagnosis
Periodontal abscessit is an accumulation of pus along
the root surface of a tooth. It is associated with periodontal pocket with mild pain. It is usually associated
with vital, rather than pulp less teeth.
Periapical osteofibrosisit is associated with vital tooth.
There may be persistence of lamina dura in the periapical
osteofibrosis, even in the presence of well marked bone
destruction.
Foraminain it, lamina dura is intact. If foramens
are exactly superimposed on the roots, then
Clinical Features
Locationinflammation is restricted to periodontal
ligament.
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Radiographic Features
PDL space wideningwidening of periodontal ligament
space is caused by edema (Fig. 19-10).
Etiology
The peri-radicular area may react to noxious stimuli form a
diseased pulp with chronic peri-radicular disease. At times,
because of an influx of necrotic product from a diseased
pulp or because of bacteria and there toxins, this apparently
dormant lesion may react and cause an acute inflammatory
response.
Clinical Features
Symptomspatient complains of intense pain, local
swelling and possibly associated cellulitis (Fig. 19-11).
Signsat the onset, tooth may be tender to touch.
Surfacemucosa over the radicular area may be sensitive
to palpation and may appear red and swollen.
Historythe patient has history of traumatic accident
that turned the tooth dark after a period of time or of
postoperative pain in a tooth that had subsided until
the present episode of pain.
Vitality testlack of response to vitality test points to
diagnose necrotic pulp.
Diagnosis
Clinical diagnosistender tooth without abscess formation and secondary to trauma will give clue to diagnosis
Radiological diagnosisperiodontal ligament (PDL)
space widening is present.
Laboratory diagnosisan inflammatory reaction occurs
in the apical periodontal ligament. The blood vessels
are dilated. Polymorphonuclear leukocytes are present
and an accumulation of serous exudate distends
the periodontal ligament and extrudes the tooth
slightly.
Radiological Features
Management
Diagnosis
Clinical and radiological diagnosispositive tenderness
with radiological finding of chronic periapical infection
will diagnose this condition.
Laboratory diagnosisarea of liquefaction necrosis with
disintegrating polymorphonuclear neutrophils and
cellular debris. These are surrounded by infiltration of
macrophages and some lymphocytes.
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Fig. 19-12: Phoenix abscess showing same appearance
as that of chronic periapical abscess.
Differential Diagnosis
Acute alveolar abscessvitality test; it will react to electrical
pulp test and application of cold, as compared to acute
exacerbation of chronic infection.
Management
Drainageeither via the root canal or by incision, if there
is localized swelling.
Antibiotics and anti-inflammatory drugsthis should be
given to the patient.
Pericoronal Abscess
It is also called as pericoronitis. It is the infection of soft
tissues surrounding the crown of a partially erupted tooth.
Clinical Features
Locationthe most common type of pericoronal infection
is found around the mandibular 3rd molar.
Symptomspain, malaise is present. Pain may radiate
to throat, ear or floor of mouth.
Sequelae of pericoronitisit may result in cellulitis and
muscular trismus. There is also regional lymphadenopathy, submaxillary and pharyngeal abscess.
Signsoperculum may get traumatized by opposing
teeth during mastication (Figs 19-13 and 19-14). Edema,
visible in both submandibular area and peritonsillar
region. There is extreme tenderness on palpation of the
abscess.
Pericoronal infection of infancypericoronal infection of
infancy is often associated with the supra-dental tissue,
involving the superior portion of the follicle and the
overlying mucoperiosteum, which may become
Radiographic Features
Appearancedefect in bone on mesial or distal side which
appears as the step like distortion of crypt wall distal to
the crown (Fig. 19-15).
Lower 3rd molar areain cases of lower third molar,
there is circumferential bone resorption around the
tooth.
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Superficial Abscess
The yellow color is imparted by accumulation/pooling of
pus in the enlarging abscess, covered by thin, stretched
skin (Fig. 19-16). Fistula, if formed, drains the pus and no
yellow color will be imparted.
It appears as raised sessile swelling with smooth,
frequently reddened mucosa, over yellow pus. The most
common presenting symptoms, is pain which may be slight
or severe. Fluctuant swelling and when aspirated, yield
pus. Surface may be ulcerated.
Fig. 19-15: Distal bone loss seen in association with 3rd molar
suggestive of pericoronitis.
Diagnosis
Clinical diagnosisinflammation of pericoronal tissue
around 3rd molar with pain and trismus will give clue
to the diagnosis.
Radiological diagnosisthere is semilunar shaped distal
bone loss.
Management
Antibioticsimmediately, antibiotics should be started.
Most commonly use antibiotics are phenoxylmethyl
penicillin 250 mg four times daily. In pericoronitis due
to ulceromembranous gingivitis metronidazole 200 gm
three times daily for 7 days is given.
Drainagecareful probing should be done around the
3rd molar, which permits entry into the expanded follicle
and allows evacuation of pus and other septic material.
Extractionwhen the symptoms become sub-acute, the
impacted 3rd molar should be extracted.
Operculectomysometimes when the retention of 3rd
molar is necessary, the inflamed tissue surrounding the
occlusal portion of the tooth should be excided.
Extraction of maxillary 3rd molarmaxillary 3rd molar
can be a contributing factor to the pericoronal infection
of the mandibular 3rd molar. In such cases, especially
when the mandibular 3rd molar is fully erupted in
Cellulitis
It is also called Phlegmon. Occasionally, the infectious
process progress out of the bone, despite the use of
supportive therapy and the patient develops cellulites,
either in vestibular region or extraorally. It is a potential
complication of acute dental infection.
Cellulitis may be defined as a non-suppurative
inflammation of the subcutaneous tissues extending along
the connective tissue planes and across the intercellular
spaces. It occur when abscess is not able to drain through
surface of skin.
Bacteriology
Hemolytic streptococcithe alpha hemolytic streptococci
are the classic etiologic agent. They produce enzymes
like streptokinase and hyaluronidase. These enzymes
break down fibrin, connective tissue ground substance
and cellular debris, thus facilitating rapid spread of
bacterial invaders.
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Fig. 19-17: Cellulitis showing diffuse involvement of buccal space.
Clinical Features
Symptomsthere is widespread swelling, redness and
pain without definite localization.
Signsthere is presence of tenderness on palpation.
Tissues are grossly edematous. There is marked
induration, hence tissues are firm to hard an palpation.
Tissues are often discolored; temperature is elevated with
malaise and lethargy. Usually massive cellulitis (Fig.
19-17) will ultimately suppurate, particularly if bacteria
are staphylococcal.
Evacuation of pusdepending upon the location and
proximity to anatomic structures that guide the progress,
the pus may evacuate into nose, maxillary sinus, and
oral vestibule, floor of mouth, infra-temporal fossa and
into fascial spaces.
Maxillary infectioninfections arising in maxilla may
perforate the outer cortical layer of bone, above the
buccinator attachment and, cause swelling of upper half
of face. If infection in mandible perforates the outer
cortical palate, below the buccinator attachment, there
is diffuse swelling of the lower half of face, which then
spreads superiorly as well as cervically.
Eyeif maxillary tooth is involved, there may be redness
of eye (Fig. 19-18).
Diagnosis
Clinical diagnosisdiffuse edematous swelling with
positive tenderness will give clue to diagnosis.
Laboratory diagnosisESR and white cell count are
raised. Biopsy shows diffuse exudation of polymorphonuclear leukocytes and occasional lymphocytes, with
considerable serous fluid and fibrin, causing separation
of connective tissue or muscle fibers. It presents only a
nonspecific picture of diffuse acute inflammation.
Management
Surgical incision and drainageit is performed when the
presence of pus is diagnosed. In case of large cellulites,
a superficial erythematous spot develops, which is
pathognomonic of pus near the superficial surface.
These superficial fluctuant areas can be incised and
drained under local anesthesia. Usually ring block of
peripheral skin, as a wheel is made for skin anesthesia.
Knife is introduced in the most inferior portion of the
fluctuant area. A small sinus forcep is introduced in the
wound, opened in several directions and pus is drained.
A rubber drain is placed in the deepest portion of the
wound, so that just 12 cm lie above the source of the
skin, where it is sutured. A large dressing is applied.
When no superficial spot is present, fluctuance is more
difficult to determine, particularly if deep pus is
suspected.
Antibioticsheavy antibiotics should be given to the
patient. Usually antibiotics in the cephalosporin family
should be given.
Extractionextraction of the offending tooth should be
carried out.
Ludwigs Angina
It is a condition which was first described by Ludwig in
1936. The word angina means sensation of choking or
suffocation. It is the most commonly encountered neck
space infection.
It is a rapidly swelling cellulitis of the sublingual and
submaxillary spaces, often arising from infection of the
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Etiology
Odontogenic infectionit is usually an extension of
odontogenic infection from mandibular molar teeth into
the floor of mouth. The 2nd and 3rd molars are the teeth
most commonly involved.
Traumait may also be caused by oral soft tissue
laceration and punctured wounds of the oral floor.
Sialadenitissubmandibular gland sialadenitis and
infected malignancy may be sometimes contributory to
Ludwigs angina.
Calculisalivary calculi or from intravenous injection
of the internal jugular vein, especially in drug abusers.
Osteomyelitisosteomyelitis in compound mandibular
fracture.
Bacteriology
Streptococci are the most commonly reported organism
from the culture. Other microorganisms are hemolytic
streptococci, bacteroides, Klebsiella, Fusiform bacilli and E
coli.
Clinical Features
There are three typical appearances of Ludwigs angina.
First
Brawny indurationit is characterized by brawny
indurations. Tissues are board like and do not pit on
pressure. No fluctuation is present.
Gangrenous tissuethe tissues may become gangrenous
and when cut, they have a peculiar lifeless appearance.
Limitation between infected and normal tissuea sharp
limitation is present between the infected tissues and
surrounding normal tissues.
Second
Spaces involvethree facial spaces are involved
bilaterally, i.e. submandibular, submental and sublingual. If the involvement is not bilateral, the infection
is not considered a typical Ludwigs angina.
Third
Open mouth and respiratory obstructionthe mouth is
opened (Fig. 19-19) and the tongue is lifted upwards
and backwards, so that it is pushed against the roof
of the mouth and the posterior pharyngeal wall; when
this occurs, acute respiratory obstruction is likely to
occur.
Other Features
Signsswelling is firm, painful and diffused, with no
sign of localization. Floor of mouth appears erythematous
and edematous. Stiffness in tongue movement generally
develops. The patient develops a toxic condition and
speech becomes impaired. Larynx and glottis become
edematous. As the disease continues the swelling starts
involving the neck.
Symptomsthe patient always has fever and there is
considerable salivation, as the patient is unable to
swallow. There are chills accompanied with fever. There
is an inability to swallow and to eat. Respiratory distress
is common. There is also neck pain, redness of neck,
weakness, fatigue, excessive tiredness, confusion or
other mental changes, difficult breathing and earache.
There is an intense pain on tongue movement and the
patient may be severely dehydrated, owing to inability
to take anything by mouth. If the swelling has spread
into the pterygoid region, then there is difficulty in
opening the mouth.
Woody tonguedue to involvement of sublingual space,
there is elevation, posterior enlargement and protrusion
of tongue. This is called as woody tongue.
Bull neckthere is enlargement and tenderness of
neck above the level of hyoid bone due to submandibular gland involvement. This is called as bull neck
(Fig. 19-20).
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Fig. 19-20: Bull neck seen in Ludwigs angina patient
(Courtesy Dr Bhaskar Patle).
Fatal Complications
Respiratory obstructionthe infection of Ludwigs angina
tends to spread through the connective tissues which
cover the small muscles of the larynx and between the
muscles of the floor of mouth. The epiglottis and larynx
become edematous along with the posterior aspect of
the tongue. The tongue gets elevated and gets pressed
upward and backward, causing pressure on the larynx.
Therefore, dyspnea occurs in paroxysm. Ultimately,
death occurs due to respiratory embarrassment.
Generalized septicemiathis can occur due to spread of
infection.
Erosion of the carotid arterylate spread of infection to
lateral pharyngeal space can also cause erosion of the
carotid artery.
Cavernous sinus thrombosis with subsequent meningitis
may be sequelae of it.
Othersmediastinum extension, pharyngomaxillary
space extension, osteomyelitis and airway obstruction.
Impetigo
It is also called as non-bullous impetigo or impetigo vulgaris.
It is acute superficial, purulent infection of the skin. It is
caused by Streptococcus pyogenes.
Predisposing Factors
Management
Clinical Features
Diagnosis
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Etiopathogenesis
Entry of microorganismthe microorganisms are thought
to enter the tissues through a small break in the mucosa
or the skin, such as fissure, abrasion, erosion or
excoriation.
Post-surgical erysipelaspost-surgical erysipelas is
caused by transmission of streptococci from the nose,
throat, or hands of the patient or from, the attendant or
visitors.
Predisposing factorsnephrotic edema, lymphedema,
dysgammaglobulinemia, malnutrition and alcoholism
are known predisposing factors.
Clinical Features
Diagnosis
Clinical diagnosisred itchy sopt with typical stuck on
appearance is characteristic of impetigo.
Management
Erysipelas
It is an acute, superficially spreading infection of the
dermis, usually of the face, with a well demarcated, slightly
indurated erythema and progressive lymphangitis. It is
caused by Beta hemolytic streptococci. It is sometime also
called as saint Anthonys fire (as the wall of Saint Anthonys
fire is that of same color of erysipelas).
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Oral Manifestations
Diagnosis
Clinical diagnosissnail track ulceration with
cobblestone appearance may give clue to the diagnosis.
Laboratory diagnosisbiopsy shows papillary projections
with tiny areas of focal necrosis and micro abscess
formation, either intraepithelial or sub-epithelial.
Management
Diagnosis
Clinical diagnosishigh fever with red and swollen skin
with lymphadenopathy will aid in diagnosis.
Management
Antibioticspenicillin is the drug of choice and if
sensitive to penicillin, erythromycin can be given.
Pyostomatitis Vegetans
It is an uncommon inflammatory disease of the oral cavity.
It is unusual oral expression of inflammatory bowel disease.
The name is given as there is a similarity between it and the
skin lesions in a dermatologic disease known as pyodermatitis vegetans. It may occur due to intestinal
disturbances.
Clinical Features
Age and sexit occurs in any age with no sexual
predilection.
Sitethis lesion may occur in any area of oral cavity,
except in tongue. It is multiple in numbers.
Appearanceoral lesions consists of large number of
broad base papillary projections, tiny abscess or
vegetations developing in areas of intense erythema.
Symptomsit painless but in some cases, oral discomfort
may be present.
Signsthese small projections are red or pink in color,
but on careful examination may show tiny pustules
beneath the epithelium, which liberate a purulent
material when ruptured. Buccal and labial mucosal
lesions have many folds and papillary projections may
develop on these folds.
Snail track ulcerationafter vesicle is rupture ulceration
is present which may coalesce into larger areas of
necrosis.
Cobblestone appearancebuccal mucosa show
cobblestone appearance, while vestibular lesions
Maxillary Sinusitis
It is described in chapter of paranasal sinus.
Etiology
Slow carious exposureslow progressive carious exposure
of the pulp is the cause.
Chronic low grade infectionfor the development of a
hyperplastic pulp, a large open cavity, a young resistant
pulp and a chronic low grade stimulus is necessary.
Mechanical irritationmechanical irritation from chewing
and bacterial infection often provides the stimuli.
Clinical Features
Siteteeth most commonly involved are deciduous
molars and first permanent molars as they have an
excellent blood supply because of a large root opening,
and this coupled with high tissue resistance and
reactivity in young persons accounts for unusual
proliferative properties of the pulp tissue.
Ageit is seen only in teeth of children and young adults.
Symptomsit is asymptomatic and there may be feeling
of pressure when masticator forces are applied.
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Etiopathogenesis
Prolonged irritationit occurs as a response to intense
and prolonged irritation from infected root canals
producing extension of chronic apical periodontitis
beyond the periodontal ligament.
Release of inflammatory mediatorsinsult from diseased
pulp represents broad spectrum of inflammatory
mediators like prostaglandins, kinin and endotoxins.
Elevated level of IgG in pulpoperiapical lesion.
Replacement of bone by granulation tissuethe expanding
inflammation and increased vascular pressure result in
abscess formation and resorption of the bone in the
affected area, which in period of time is replaced by
granulation tissue.
Fig. 19-23: Chronic hyperplastic pulpits presenting as reddish mass
in third molar region (Courtesy Dr Tapasya).
Radiographic Features
It will show a large open cavity with direct access to the
pulp chamber.
Diagnosis
Clinical diagnosisFleshy pulpal mass in pulp chamber
with negative thermal test will aid in diagnosis.
Differential Diagnosis
Proliferating gingivitisone should raise and trace the
stalk of the tissue back to its origin, i.e. the pulp chamber.
Management
Pulp extirpationelimination of polypoid tissue,
followed by extirpation of the pulp. After removing the
hyperplastic tissue, bleeding can be controlled by
pressure.
Extractionextraction of tooth can also be done.
Periapical Granuloma
It is the most common type of pathologic radiolucency
encountered in dentistry. It is a growth of granulation
Clinical Features
Symptomsmild pain can be occasionally experienced
while biting or chewing on solid foods.
Signstooth may be darker in color, because of the
blood pigments that diffuse into the dentinal tubules.
There is, seldom, swelling or expansion of the overlying
cortical bone. Tooth may feel to be slightly elongated in
the socket.
Vitality testthe tooth is non-vital, i.e. it does not respond
to thermal and electric pulp test.
Sensitivitysensitivity occurs due to hyperemia, edema
and inflammation of the apical periodontal ligament.
Radiographic Features
Lamina duraperiapical area is radiolucent with loss of
lamina dura (Fig. 19-24).
Sizeradiolucency is less than 1.5 cm in diameter (Fig.
19-25).
Marginsthere may or may not be hyperostotic borders.
It may or may not have well defined borders.
Teethinvolved tooth may show a deep restoration,
extensive caries, fracture or a narrow pulp canal with
non-vital pulp.
Multiple periapical granulomain some cases, multiple
periapical granuloma may be present (Fig. 19-26).
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Differential Diagnosis
Management
Root canal therapyroot canal therapy is treatment of
choice.
Extraction of teethif the tooth is unrestorable then
extraction of the involved tooth should be carried out.
Curettagecurettage of apical tissue can be carried out.
Causes of failure of treatmentlesion may heal due to
inadequate endodontic, vertical foreign material,
associated periodontal disease, and cysts formation.
Periapical Scar
It is a possible end point of healing. It is composed of dense
fibrous tissue and is situated at the periapex of pulp less
tooth, in which usually, the roots canal have been
successfully filled.
Fig. 19-25: Periapical granuloma presenting as
radiolucency in relation with two teeth.
Formation of Scar
Irritant substanceconfined in the periapical area, which
leads to accumulation of chronic inflammatory cells.
Granuloma formationyoung fibroblasts, endothelial
cells and capillaries proliferate, which lead to granuloma
formation.
Scar formationafter endodontic treatment, the granuloma resolves, but in some cases, granulation tissue
gets slowly organized with the production of more and
more collagen fibers, which in turn leads to scar
formation.
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Etiology
Fig. 19-27: Periapical scar seen as radiolucency at the
apex of central incisor (Courtesy Dr Mody).
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis.
Radiological diagnosisradiolucency at the apex of
endodontically treated tooth.
Laboratory diagnosisbiopsy shows spindle shaped
fibroblast scattered throughout the dense collagen
bundles, which show advanced degree of hyalinization.
Pathogenesis
Management
There is no treatment necessary for this disease
Osteomyelitis
Osteomyelitis is the inflammation of the bone marrow that
produces clinically apparent pus and secondarily affects
the calcified components. It is infection of the bone that
involves all the three components viz. periosteum, cortex,
and marrow.
It may be defined as an inflammatory condition of the
bone that begins as an infection of medullary cavity and
the haversian system and extends to involve the periosteum
of the affected area.
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Microbiology of Osteomyelitis
Microorganismmicroorganism responsible for osteomyelitis are Staphylococcus aureus, Staphylococcus albus,
hemolytic streptococci, gram-negative organisms like
Klebsiella, pseudomonas, protease, E coli, anaerobic
microorganisms like pepto-streptococci, bacteroides and
fusobacteria. Some specific forms like Mycobacterium
tuberculosis, treponema palladium and A. israeli.
Following parameters should be used for recognition of
pure anaerobic or mixed anaerobic infection:
Presence of foul smelling exudate.
Sloughing of necrotic tissues or gas in the necrotic
tissue.
Gram stain revealing multiple organisms of different
morphological character.
Presence of sequestra.
Classification
According to anatomic location of infectious process
Intramedullary
Subperiosteal
Periosteal
According to duration and severity
Acuteit occurs initial infection with the microorganism
Chronicit can be primary or secondary
Primaryvirulence of the microorganism is low
and the host resistance is high. This type is not
preceded by an episode of acute symptoms.
Secondaryit is secondary to incompletely treated
acute osteomyelitis.
Depending upon the presence or absence of suppuration
Suppurative:
Acute suppurative osteomyelitis
Chronic suppurative osteomyelitis
Infantile osteomyelitis
Nonsuppurative:
Chronic nonsuppurative
Focal sclerosing
Diffuse sclerosing
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Clinical Features
Occurrence
Sexit is more common in men, than women.
Sitesit occurs in mandible in premolar area because:
The cortical plate of the bone in time mandible is dense.
It takes longer time for sinus formation and release of
pits and hence, the infection gets directs into spongiosa and spreads.
Removal of posterior mandibular teeth is attended by
more damage to the bone.
Mandible is less vascular than maxilla.
Thin cortical plates and relative paucity of medullary
tissue in the maxilla precludes confinement of
infection within the bone and permits dissipation of
edema and pus into the soft tissues and paranasal
sinuses.
Acute
Initial symptomsit has rapid onset and course. Patient
complaint of severe pain, paresthesia or anesthesia of
the mental nerve.
Initial signsat this stage, the process is truly intramedullary, therefore swelling is absent, teeth are not
mobile and fistulae are not present.
Late symptomsthere is deep intense pain, anorexia,
malaise, fever, and regional lymphadenopathy. Patient
also complain of soreness of involved teeth which become
loose within 10 to 14 days. There is also fetid oral odor.
Late signspus exudtes around the gingival sulcus or
through mucosal and cutaneous fistula. There is firm
cellulitis of cheek and abscess formation with localized
warmth and tenderness on palpation. The patient feels
toxic and dehydrated.
Chronic
Onsetit has insidious onset with slight pain, slow
increase in jaw size and a gradual development of
sequestra without fistula.
Symptomsit is painless unless there is an acute or subacute exacerbation.
Necrotic bonein some cases, necrotic bone may be visible
inside the oral cavity (Figs 19-29A and B).
Sinusintraorally and extraorally sinus develops (Figs
19-30A and B) intermittently and drains small amount
of pus and then gradually heals. Sinus extends from
medullary bone, through cortical plate, to mucous
membrane or skin. Sinus may be at a considerable
distance from the offending infection.
Signslocal tenderness and swelling develop over the
bone in the area of abscess (Fig. 19-31).
Lymph nodesregional lymphadenopathy is present.
Radiographic Features
Acute
Radiodensityabout 10 days after acute infection, the
density of trabeculae will be decreased, with blurred and
fuzzy. For the radiographs to reveal any changes, there
must be a loss of from 30 to 60% in the calcium content.
Trabecular patternthe earliest radiographic change is
that trabeculae in the involved area are thin, of poor
density and slightly unsharp or blurred. The trabeculae
soon loose their continuity as well as the little density
present. Individual trabeculae become fuzzy and
indistinct.
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A
A
B
Figs 19-29A and B: Necrotic bone seen in osteomyelitis.
B
Figs 19-30 A and B: Extraoral discharging sinus seen in
osteomyelitis ( Courtesy Dr Bande).
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A
A
B
Figs 19-32A and B: Sequestration seen as horizontal radiopaque
structure in the mandibular bone.
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Features
Osteomyelitis
Carcinoma
Age
Usually under
40 years
Progression
Fast
Slower
Extent of involvement
Large involvement
and sporadic
occurrences
Relatively
continuous
destruction
Sequestrum
Yes
None
None
Periosteal formation
Generally none
except in some
sarcoma
Residual small
bony fragment
None
Formation seen
within the lesion
Bone scintigram
Negative uptake
at the sequestration
Strong positive
uptake seen
Management
Diagnosis
Clinical diagnosispain, swelling, fever is present.
Radiological diagnosisloss of lamina dura, saucer
shaped destruction, sequestrum formation and moth
eaten appearance will give clue to the diagnosis.
Laboratory diagnosisthe medullary spaces are filled
with inflammatory exudate that may or may not progress
to the actual formation of pus. The inflammatory cells
are chiefly neutrophilic polymorphonuclear leukocytes,
but may show occasional lymphocytes and plasma cells.
Investigation to be carried out in osteomyelitis
investigation like gram staining, culture and sensitivity,
WBC count and complete hemogram, blood sugar,
Mantoux test, radiographs, scintigraphy and computerized tomography.
Differential Diagnosis
Pagets diseaseit affects multiple bones and the complete
involvement of individual bone.
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in the prevention and adjunctive treatment of osteomyelitis, osteoradionecrosis and certain soft tissue
infections. The partial pressure of oxygen in osteomyelitis bone is significantly decreased, compared with
normal bone. The oxygen tension of normal bone is
between 40 to 45 mm of Hg. The oxygen tension in
osteomyelitis bone involves a combination of factor, but
it oxygen tension in osteomyelitis bone varies from
10-20 mm of Hg. In osteomyelitis, bone has increased
consumption of oxygen may be because of greater
inflammatory response, cellular exudation and
respiration of phagocytes. Secondary to infection,
infective organisms also consume more oxygen.
Rationale behind oxygen therapyadequate tissue
oxygen is necessary for fibroblast proliferation.
Fibroblast lay down collagen, which provides a
framework for capillary formation. The most
important aspect of HBO is its positive enhancement
of neoangiogenesis in the aerobic portion of the
proliferative phase of wound healing. Under the
influence of hyperbaric oxygen therapy, endothelial
proliferation is seen, which obliterates avascular and
ischemic pieces. Free oxygen radical is formed during
hyperbaric oxygen therapy that is toxic to many
pathogenic anaerobes. HBO is bactericidal for many
anaerobic microorganisms. Besides these, the
endotoxin liberated by pathophysiological activity
of microorganisms is rendered inert by exposure to
elevated partial pressure of oxygen. HBO enhances
lysosomal degradation potential, by enhancing the
development of intracellular halides in leukocytes
and oxygen radicals, which are a major component
of catabolic enzymes of the macrophage lysosomes.
Formation of this enzyme is depressed or decreased
in hypoxic environment, such as that found in
osteomyelitis foci. Thus, leukocytic bactericidal
ability is enhanced. Patient usually experiences relief
from pain within 3 to 5 sittings treatment of with rapid
closure of draining fistulae. Sequestra get localized
and there is rapid progression to osseous reconsolidation and fibrous union.
Procedurescrubbing the exposed bone with
antiseptic solution such as acminoacridine. Purulent
wound should be covered with neomycin dressing.
An antibiotic, preferably penicillin, erythromycin or
tetracycline, is administered orally. Vitamin E is also
given (100 gm) daily to decrease oxygen seizure
susceptibility. Patient is placed in multiplace/
monoplace chamber and a concentration of 100% O2
is given. Duration of treatment is of 1.5 to 2 hours for
5 to 6 days in a week, for a total of 60 treatments.
Daily wound irrigation and debridement are often
required. After 6 months ten additional 2 hour
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Management
Endodontic treatmentendodontic treatment should be
carried out with affected tooth. This will resolve the
lesion.
Extractionif the tooth is unrestorable extraction of tooth
should be carried out.
B
Figs 19-37A and B: Condensing osteitis showing radiopacity
at the apex of tooth (Courtesy Dr Ashok).
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Actinomycotic Osteomyelitis
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis.
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Chronic Tendoperiostitis
Clinical Features
Radiological Features
Locationit is seen in anterior region of mandibular
angle and posterior region of mandibular body.
Sclerosissclerosis is limited to the one quadrant only.
There is radiolucent zone inside the radiopacity.
Erosionerosion of inferior border of mandible can be
present.
Diagnosis
Fig. 19-39: Moth eaten type of appearance seen in mandible due to
osteomyelitis with history of tuberculosis in this patient.
Radiation Osteomyelitis
It is on infection of the irradiated bone. It occurs after
exposure to radiation (40 to 80 Gy), bone undergoes marked
decreased in vascularity. Such bone has poor defensive
process and susceptible to traumatic injury. It draws
infection from extraction wound and infected pulp, severe
periodontitis and denture stomatitis. It will cause death of
bone cells and result in progressive obliterative arteritis.
This results in aseptic necrosis of the portion of bone directly
in beam of radiation, with compromised vascularity in the
adjacent bone.
Pathogenic organisms are introduced into this irradiated
bone through odontogenic infections, compound fractures
of the jaws and mucosal lacerations. The organisms most
commonly found are Staphylococcus aureus, Staphylococcus
epidermidis. Higher incidences in jaw are necroded due to
higher degree of infections and frequent trauma to which
these bones.
Osteomyelitis can occur in irradiated jaw. Intense pain
and facial fistula develop from the subperiosteal tissues.
Spread is diffuse and throughout with signs of inflammation and swelling.
Management
Muscular relaxation methodthis is carried out by
rotational exercise, myofeedback, soft diet should be
given.
Muscle relaxant durgsmuscle relaxant drugs like
diazepam, mefenoxalon should be given.
Occlusal splintocclusal splint should be given to the
patient to control parafunctional habits.
SAPHO Syndrome
SPAHO syndrome includes Synovitis, Acne, Pustulosis,
Hyperostosis, and Osteitis. It occurs due to unknown cause.
Genetic predisposition is present in this case.
Clinical Features
Age and sex distributionpatient affected in the age group
of 50 to 60 years.
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Radiological Features
Appearanceosteolytic areas are scattered in the
randomly in the sclerotic bone.
Periosteal bone reactionit is present in many cases. There
is no perforation of bone.
External bone resorptionexternal bone resorption of
mandible is common in this condition.
Scintigraphyit will show involvement of multiple site
of bone deposition.
Diagnosis
Clinical diagnosisit is easy to make clinical diagnosis
by 5 typical features of this syndrome.
Radiological diagnosisperiosteal bone reaction with
multiple sites of bone deposition.
Laboratory diagnosisbiopsy shows bone remodelling,
there is also interconnecting trabeculae of vital reactive
mixed with fibrous connective tissue.
Canine Space
Anatomy
Locationone of the potential spaces that is frequently
the seat of infection is the canine fossa. This space
actually lies between the anterior surface of the maxilla
and the overlying elevator muscle of upper lip.
Contentthe fossa contains considerable amount of
connective tissues and fat, which allow the accumulation of tissue fluid and pus.
Boundariesit is bounded by:
Superiorlyby levator labii superioris alequae nasi.
Anteriorlyby orbicularis oris.
Posteriorlyby buccinator.
Clinical Features
Management
Steroidal and non-steroidal anti-inflammatory drugsthese
are most effective agents to relive the symptoms.
Decorticationthis is effective in some cases of SPAHO
syndrome.
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Buccal Space
Anatomy
Origin of Infection
Blood born infectionmost of the infections are blood
borne or occur as retrograde infection through the parotid
duct.
Retrograde extensionit reaches from the lateral
pharyngeal space or by retrograde extension along the
parotid gland.
May break into lateral pharyngeal spaceprimary
infections of parotid space break into lateral pharyngeal
space readily because the fascia is thin over the deep
portion of the parotid space.
Clinical Features
Clinical Features
Location of swellingswelling extent from lower border
of mandible to level of zygomatic arch (Fig. 19-41).
Swelling arises due to infection from mandibular or
maxillary molar or premolar, if apex is above the
attachment.
Symptomsfacial swelling with little trismus.
Signswelling is dome shaped and in some cases
periorbital edema develops.
Parotid Space
Anatomy
Contentit is a compartment formed by splitting of
investing layer of deep cervical fascia. It contains parotid
gland as well as extra-glandular and intra-glandular
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Spread
Spread to cavernous sinusinfra-temporal infection
can extend via the plexus of veins, through the inferior
orbital fissure into the terminal part of inferior
ophthalmic vein and then, through the superior orbital
fissure into cavernous sinus.
Spread to pterygomandibular spacethe infection from this
space can extend into pterygomandibular space.
Origin
Fracture or direct extensioninfection may arise from
fracture or by direct extension from the floor of mouth,
lateral pharyngeal spaces and masticator space.
Dental, periodontal or blood borninfection may be dental,
periodontal or vascular in origin.
Clinical Features
Location of swelling due to infection from incisor, canine and
cuspid teethswelling can be present in different location,
according to origin of infection. Infection from incisors,
cuspid or bicuspid teeth also can cause infection of space
of the body of mandible.
Outer cortical plate involvementif outer cortical plate
is involved then there is induration or fluctuation of
the labial sulcus.
Inner cortical plate involvementwhen the inner cortical
plate is involved, the infection is restricted to the floor
of mouth (Fig. 19-43).
Clinical Features
Locationextraoral swelling over the region of sigmoid
notch and TMJ joint area and intraorally swelling is
usually in the tuberosity area.
Symptomsthe patient may exhibit trismus and
sometimes swelling of eyelids, if there is involvement of
post-zygomatic fossa.
Signsentire cheek may be swollen, if the buccal space
is also involved.
Pharynx involvementthe involvement of pharynx may
cause dysphagia and severe pain or a feeling of pressure
in the general area of infection.
Fig. 19-43: Swelling seen floor of mouth due to space for body of
mandible infection
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Submental Space
Anatomy
Origin
Odontogenic infection of this space is caused by 2nd and
3rd mandibular molars.
Clinical Features
Clinical Features
Sublingual Space
Anatomy
Submandibular Space
Anatomy
Locationit lies lateral to submental space.
Contents of this spaceit contains superficial part of
submandibular salivary gland and its lymph nodes, the
facial artery deep to the gland, proximal portion of the
Whartons duct, the lingual and hypoglossal nerve as
they coarse deep to the gland and facial vein superficial
to the gland.
Boundariesit is bounded by:
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Origin
The infection may arise directly from perforation of the
lingual cortical plate, above the mylohyoid attachment or
by extension from other spaces, primarily submandibular
space.
Clinical Features
Location of swellingbrawny erythematous tender
swelling of the floor of mouth is present. Swelling is
close to mandible and spreads towards midline or
beyond (Fig. 19-46).
Symptomselevation of the tongue may be noted in late
cases. Dysphasia and dyspnea may be the related
complains.
Clinical Features
Location of swellingthe swelling may be either external
or internal, or both.
External swellingthe external swelling consists of
brawny induration over the ramus and angle of
mandible (Fig. 19-47).
Internal swellinginternal swelling may predominate in
some cases. Such swelling involves the sublingual
region and the pharyngeal wall. The pharyngeal
swelling pushes palatine tonsils towards midline.
Symptomspain is excruciating and often radiates to
the ear. Dysphagia may be present, especially when the
swelling is internal.
Trismusclinically masticatory space infection is likely
to be marked by severe trismus because of irritation of
masseter and medial pterygoid. It can be so severe that
the mouth opening is restricted only to half a centimeter.
Lateral pharyngeal wall, behind the palatine tonsil, is
not swollen, which will help to differentiate between it
and lateral pharyngeal space infection.
Submasseteric Space
Anatomy
Locationit includes sub-periosteal region of mandible
and facial sling, containing ramus of mandible and
muscles of mastication. This space is formed by splitting
of the investing layer of deep cervical fascia. The splitting
occurs as the fascia is attached to the lower border of the
mandible.
Content of spaceit contains muscles of mastication,
internal maxillary artery and mandibular nerve.
Boundariesit is bounded by:
Anteriorly by body of mandible.
Posteriorly by parotid space.
Mediallylateral pharyngeal space.
Temporal Space
Anatomy
Locationthese are the facial spaces in relation to
temporalis muscle. They are two in number, i.e. superficial and deep.
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Clinical Features
Location of swellingin case of infection with superficial
temporal space, swelling is limited below by the
zygomatic arch and laterally, it is limited by the outline
of superficial and temporal line (Fig. 19-48). A deep
temporal abscess produces less swelling than one
involving the superficial temporal space. Since it lies
deep to temporalis muscle, fluctuance is difficult to
elicit.
Dumble shaped appearancewhen it is associated with
buccal space infection, the swelling has a characteristic
dumble shaped appearance caused by the lack of swelling
over the zygomatic arch.
Symptomsdue to limited distentibility of temporal
fascia, the pain is severe.
Trismusit is a common finding.
Pterygomandibular Space
Anatomy
Locationit is a well defined space between the
mandibular ramus and pterygoid muscle.
Contents of spaceit contains variable amount of fat,
inferior alveolar nerve and maxillary artery.
Boundariesit is bounded by:
Lateral wallits lateral wall is formed by inner surface
of ramus of mandible.
Medial wallits medial wall is formed by medial
pterygoid muscle.
Roofits roof is formed by inferior head of lateral
pterygoid muscle.
Frontal sectionin frontal section the pterygomandibular space is a triangular space narrowing downward, where medial pterygoid converges with the
mandible.
Posteriorposteriorly, with retromandibular space
containing parotid gland.
Anterioranteriorly, the pterygomandibular space is
accessible between the deep tendon of temporal
muscle, which is attached to the temporal crest of the
mandibular ramus and anterior border of pterygoid
muscle.
Clinical Features
Location of swellingthere is no external evidence of
swelling. Intraoral examination reveals an anterior
bulging of half of the soft palate.
Signsdeviation of tongue to the affected side.
Symptomssevere trismus and difficulty in swallowing.
Anatomy
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Origin
The source of infection is 3rd molars and sometimes, 2nd
molars, particularly by way of infection in the submandibular space or by direct extension the tooth.
Clinical Features
Location of swellingif the infection is confined to the
anterior compartment, external swelling occurs anterior
to the sternocleidomastoid muscle. The swelling is first
seen at the angle of mandible and in the submandibular
region.
Symptomsthere is severe pain on the affected side of
throat. Pain is sometimes referred to the ears. Infection
of space occurs with abscess formation, which may
impinge on pharynx and result in pain while swallowing and making it impossible. Patient also complaint
of trismus irritation of medial pterygoid muscle.
Signsinternally, the anterior part of lateral pharyngeal
wall is swollen and it pushes the palatine tonsils
together, with the soft palate towards the mid line.
Posterior compartment involvementwith infection of
posterior compartment, the clinical picture is marked by
septicemia.
Complicationrespiratory paralysis resulting from acute
edema of larynx. There is also thrombosis of internal
jugular vein and erosion of internal carotid artery. The
lateral pharyngeal space communicates with the
mediastinum by prevertebral fascia, so the infection may
reach to this area as direct extension.
Origin
Infection result due to medial extension of infection in the
lateral pharyngeal space.
Clinical Features
Agethese infections are classically seen in children
less than 5 years.
Causethese are generally due to otitis media and
pharyngitis.
Symptomspatient will have pain, dysphagia and
nuchal rigidity.
Signsthere is bulging of posterior pharyngeal wall.
Prominence is noted on one side due to adherence of
median raphe or prevertebral fascia.
Radiographic findingit will show widened retropharyngeal space. Computed tomography can be used
to diagnose this condition (Fig. 19-49).
Complicationinfection may be spread to mediastinum,
causing mediastinitis.
Retropharyngeal Space
Anatomy
Locationit is situated between the posterior walls of
pharynx and prevertebral fascia, extending from the base
of the skull to mediastinum.
Boundariesit is bounded by
Laterallyit is bound by lateral pharyngeal space and
on each side by carotid sheath.
Anteriorlyby the wall of pharynx.
Posteriorlyby prevertebral fascia.
Danger spaceinfections in this region are dangerous
because of ease of spread to mediastinum and for this
reason, this space is termed as danger space.
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the other leg also flexes) and cheek sign (pressure against
cheek below zygoma will cause reflex flexion at elbow
with upward jerking of the arm) are positive.
Diagnosisdiagnosis is made by lumbar puncture and
CSF examination.
Microorganisms responsibleStaphylococcus, Streptococcus,
pneumococci, Proteus, Klebsiella and H influenzae are
common pathogens causing meningitis secondary to
head and neck infection.
Diagnosis
Clinical diagnosispositive Kernigs and Brudzinskis
sign is positive.
Laboratory diagnosisdiagnosis is made by lumbar
puncture and CSF examination.
Management
It is a medical emergency and prompt intravenous
antibiotics should be started, after antibiotic sensitivity
testing.
Brain Abscess
It can develop from bacteremia associated with odontogenic
infections.
Pathogenesis
Bacterial Meningitis
Clinical Features
Clinical Features
Symptomsheadache, chills, fever and nausea. Pain in
back and stiffness of neck.
SignsKernigs sign (restriction of knee movement when
hips are flexed due to spasm of hamstring) and
Brudzinskis sign like neck sign (on flexing neck there is
flexion of the hips and knee), leg sign (on flexing one leg,
Diagnosis
Clinical diagnosispapilloderma, convulsion dysphagia
can give clue to diagnosis.
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Management
Bacteriology
Anatomy
Locationthey are paired sinuses situated on either side
of sella turcica on lateral slopes of sphenoid bone. Each
sinus is an irregularly shaped space within the dura,
between the body of the sphenoid bone and medial
border of middle cranial fossa.
Extentit extends from superior orbital fissure to the
apex of petrous portion of temporal bone. It has
anastomosis anteriorly and inferiorly with pterygoid
plexus through foramen of vasallus, foramen ovale and
foramen lacerum.
Nerve passing through sinusthe oculomotor and trochlear
nerves, the ophthalmic and maxillary divisions of
trigeminal nerve passes through the sinus on the lateral
wall. The abducens nerve and internal carotid artery,
with its surrounding sympathetic plexus, is suspended
in the sinus between the lateral wall and sphenoid bone.
The blood in the sinus flows around these structures, but
are separated from each other by fibrous sheath.
Clinical Features
Symptomsthere is high spiking fever.
Signssigns of meningeal irritation including severe
headache, stiffness of neck, ocular palsy and facial
weakness.
Eyeproptosis or protrusion of eye is seen as a result of
decreased venous drainage, chemosis and edema of
eyelid, which is secondary to venous stasis.
Cranial nerve involvementlimitation of extraocular
movements because of involvement of 3rd, 4th and 6th
cranial nerves.
Cranial nerve palsycranial nerve palsy of 3rd, 4th and
6th nerve is usually evident due to irritation caused by
pressure of venous congestion.
Progressrapid progression of signs and symptoms from
one eye to other eye, due to spread of infection through
inter-cavernous sinus.
Diagnosis
Clinical diagnosiscranial nerve palsy, eye involvement,
limitation of extraocular movement will give clue to the
diagnosis.
Laboratory diagnosislumbar puncture should be made.
CSF shows neutrophils, decreased glucose concentration and elevated protein concentration.
Management
Etiopathogenesis
Infection of maxillary premolar and molar teethinfection
from tooth may perforate buccal cortical plate. Then
infection reaches to the maxillary sinus, pterygopalatine
space, reaching the orbit via inferior orbital fissure. After
this, infection can spread to cavernous sinus at cranial
vault and results in cavernous sinus thrombosis.
Infection from maxillary anterior teethin this, infection
spread to sinus through canine space.
Septic embolibacteria can reach cavernous sinus in
septic emboli through venous and arterial systems. Septic
thrombophlebitis of emmissary veins can directly lead
to this phenomenon.
Infratemporal space infectionit can also result from direct
extension through skull, by an abscess located in deep
spaces such as in infratemporal space.
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Etiology
Mediastinitis
Clinical Features
Progressprogress of orbital infection posteriorly may
involve the superior orbital fissure and spread to cavernous sinus via superior ophthalmic vein (Fig. 19-50).
Symptomsit may result in temporary loss of visual
acuity. Long-term ophthalmologic sequelae include
permanent loss in visual acuity, residual proptosis,
diplopia and blindness.
Signsswelling is seen in orbital region.
CNS involvementwhen later CNS is involved, hemiparesis, seizures and death have also been reported.
Pathogenesis
The process occurs because it gives a pathway for spread
of pus and infection from submandibular region, floor of
mouth and from all the related spaces in neck, beneath the
investing layer to deep cervical fascia.
Following this pathway, infection can come into close
relationship with trachea, larynx and great vessels and
eventually reach the mediastinum.
The most common anatomic pathway is lateral
pharyngeal space, through visceral space inferiorly, which
may occur causing weakening and rupture of pleura.
Clinical Features
Symptomspatient complaint of face swelling,
swallowing difficulty. Usually, there is chest pain and
severe dyspnea with intermitting fever and evidence of
swelling on the lateral aspect of neck of the affected side.
Involvement of one or two facial spaces is usually
preceded by these signs and symptoms.
Signsprogressive septicemia, mediastinal abscess,
pleural effusion, empyema, compression of mediastinum
veins with decreased venous return to heart and
pericarditis may occur, with death as the final step.
Hemorrhagehemorrhage secondary to erosion of
internal carotid artery or one of its branches is the most
common cause of death in deep space infection.
Radiological Features
CT scansthis is more precise and accurate method than
conventional radiography. On CT scan extent of necrosis
can be determined.
Fig. 19-50: Swelling seen in orbital region
due to odontogenic infection of molar.
Diagnosis
Clinical diagnosistemporay loss of visual acuity with
swelling in orbital region.
Management
Antibioticwhen orbital infection is suspected, early
aggressive antibiotic therapy and surgical intervention,
following appropriate consultation, should be initiated
to prevent serious ocular complications and CNS
involvement.
Management
Airway managementutmost priority is to be given for
airway control. In such cases, either emergency tracheostomy or cricothyroidectomy may be performed.
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Necrotizing Fasciitis
This condition was first recognized in 1924 by Meleney. It
is defined as rapidly progressing necrosis of subcutaneous
tissue and fascia, usually sparing the muscles and accompanied by toxicity, high fever and apathy. Necrotizing
Fasciitis is an inflammation of the connective tissue, which
may be caused by streptococcal or other types of infection,
an injury, or an autoimmune reaction.
Etiopathogenesis
Microorganismthe usual cause is a mixture of aerobic
and anaerobic organisms. Streptococcus A group is
responsible.
Extension of organism to the subcutaneous tissuethe
organisms reach the subcutaneous tissue by extension
from a contiguous infection or trauma to the area,
including surgery.
Dermal gangrenethere is widespread damage to the
surrounding tissue, and occlusion of small subcutaneous vessels leads to dermal gangrene.
Risk factorsthe presence of diseases such as diabetes
mellitus, malignancy and drug addiction, are significant
risk factors.
Clinical Features
Symptomsthe classic warning signals are unusually
severe pain at the site of a wound or cut, or in the lymph
nodes, and flu-like symptoms, surfacing a few hours
after an injury or surgical operation.
Signsa tender erythematous cellulitis with ill defined
margins develop. The affected area of skin becomes
anesthetic, secondary to cutaneous nerve destruction,
which can occur before clinical gangrene.
Progressthe progression of disease can alarmingly
rapid with skin color changing from red blue to grey in
as early as 36 hours leading to frank cutaneous gangrene
due to thrombosis of nutrient vessels, usually by 4th or
5th day.
Skinskin bullae may develop, but lymph adenitis is
usually not seen. Skin death subsequent to subcutaneous
necrosis is common (Fig. 19-51).
Diagnosis
This problem is diagnosed both clinically by an experienced
clinician, based upon the rapid and severe progression of
an infection, and by culturing the offending bacteria.
Management
Antibioticsspectrum of antibiotics should include
drugs active against anaerobic organisms such as
metronidazole.
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Clinical Features
Diagnosis
Clinical diagnosishistory of severe pain lasting from a
few minutes to a few hours, followed by complete and
sudden cessation of pain.
Laboratory diagnosisthere is necrotic pulp tissue, cellular
debris and microorganisms may be seen in the pulp
cavity. The periapical tissue may be normal or slight
evidence of inflammation of the apical periodontal
ligament may be seen.
Management
Root canal treatmentpreparation and obturation of root
canals.
Pulp Calcifications
Various forms of pulp calcifications are found within the
pulp which may be located in the pulp chamber or in the
root canals. It can occur in any sex and in any teeth in the
dental arch.
Etiology
Types
Classification
Pulpal Infection
Necrosis of Pulp
It is the death of pulp. It may be partial or total depending
on whether a part or the entire pulp is involved.
Etiology
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Clinical Significance
Symptomssometimes, it may cause pain from mild
pulpal neuralgia to severe excruciating pain resembling
that of tic douloureux as the denticle can impinge on the
nerve of the pulp.
Difficulty in root canal treatmentdifficulty may be
encountered in extirpating the pulp during root canal
therapy.
Radiographic Features
Appearancethey are seen as radiopaque structures
within the pulp chamber (Fig. 19-52), in the root canals
or extending from pulp chamber into root canals.
Shapethey may be round or oval. Their outline varies
from sharply defined to more diffuse margins.
Locationthey may occur as single dense mass or several
opacities.
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis
Radiological diagnosisround or oval shaped radiopacity in the pulp chamber will diagnose this condition.
3
Fig. 19-52: Pulp stone seen as radiopacity in the pulp chamber.
Management
It is not required.
Focal Infection
Focus of infection refers to circumscribed area of tissue, which
is infected with exogenous pathogenic microorganisms and
which is usually located near a mucous or cutaneous
surface. Focal infection refers to metastasis from the focus of
infection, of organisms or their products that are capable of
injuring tissue.
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Suggested Reading
1. Adekeye EO, Cornah J. Osteomyelitis of jaw: a review of 141
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2. Allan BP, Egber MA, Myall RWT. Orbital abscess of odontogenic
origin: a case report. J Oral Maxillofac Surg 1991;20:268-70.
3. Balcerak RJ, Sisto JM, Bosack RC. Cervicofacial necrotizing
fascitis: report of three cases and literature review. J Oral
Maxillofac Surg 1988;46:450-9.
4. Bhaskar SN. Periapical lesion: types, incidence, and clinical
features. Oral Surg, Oral Med, Oral Pathol 1966;21:657-71.
5. Calobrisi SD, Mustasim DF, McDonald JS. Pyostomatitis
vegetans associated with ulcerative colitis: temporary clearance
with fluocinonide get and complete remission after colectomy.
Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1995;79:
452-4.
6. Chan SWY, Scully C, et al. Pyostomatitis vegetans: oral
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7. Cogan MIC. Necrotizing mediastinitis secondary to descending
cervical cellulitis. Oral Surg 1973;36:307.
8. Demidovich CW, Wittler RR,, et al. Impetigo: current etiology
and comparison of penicillin, erythromycin and cephalexin
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9. Dolan RW, Chowdhury K. Diagnosis and treatment of
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10. Eliasson S, Halversson C, Ljungheimer C. Periapical condensing
osteitis and endodontic treatment. Oral Surg, Oral Med, Oral
Pathol 1984;57:195-9.
11. Eversole LR, Stone CE, Strub D. Focal sclerosing osteomyelitis/
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12. Felsberg GJ, Gore RL, Schweitzer ME. Sclerosing osteomyelitis of
garre (periostitis ossificans). Oral Surg, Oral Med, Oral Pathol,
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13. Ficarra G, Cicci P, et al. Oral Crohns disease and Pyostomatitis
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14. Groot RH, van Merkesteyn JP, et al. Diffuse sclerosing osteomyelitis
(chronic tendopeiostitis) of the mandible: an 11 year follow-up
report. Oral Surg, Oral Med, Oral Pathol 1992;74:557-60.
15. Hutchinson IL, James DR. New treatment for Ludwig angina. Br
J Oral and Maxillofac Surg 1989;28:189-93.
16. Ida M, Tetsumura A, et al. Periosteal new bone formation in the
jaw: A computed tomographic study. Dentomaxillofac Radiol
1997;26:169-76.
17. Jacobsson S, Hollender L. Treatment and prognosis of diffuse
slcerosin osteomyelitis (DSO) of the mandible. Oral Surg, Oral
Med, Oral Pathol 1980;49:7-14.
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26. Ochs MW, Dolwick MF. Facial erysipelas: a report of case and
review of literature. J Oral Maxillofac Surg 1991;49:1116-20.
27. Ogundiya DA, Keith DA, Mirowski J. Cavernous sinus thrombosis
and blindness as complication of an odontogenic infection. J Oral
Maxillofac Surg 1989;47:1317-21.
28. Sakamoto H, Aoki T, et al. Descending necrotizing mediastinitis
due to odontogenic infection. Oral Surg, Oral Med, Oral Pathol,
Oral Radiol Endod 2000;89:412-9.
29. Suel Y, Taguchi A, Tanimoto K. Radiographic evaluation of
possible etiology of diffuse sclerosing osteomyelitis of the
mandible. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod
1997;84:571-7.
30. Tonder KJH. Vascular reaction in the dental pulp during
inflammation. Acta Odontol Scand 1983;41:247-56.
31. Van Merkesteyn JPR, Bakker DJ, et al. Hyperbaric oxygen
treatment of chronic osteomyelitis of jaw. Int J Oral Surg 1984;13:
386-95.
32. Van Merkesteyn JPR, Groot RH, et al. Diffuse sclerosing
osteomyelitis of the mandible: a new concept of its etiology. Oral
Surg, Oral Med, Oral Pathol 1990;70:414-9.
33. Wood RE, Nortje CJ, et al. Periostitis ossificans versus Garres
osteomyelitis: Part I: what Garres really say. Oral Surg, Oral
Med, Oral Pathol 1988;65:773-7.
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Oral Pigmentation
Introduction
Pigments are the colored substances, some of which are
normal constituents of cells (e.g. melanin), whereas others
are abnormal and collect in cells only after under special
circumstances. Pigments can be exogenous, coming from
outside in the body, or endogenous, synthesized within the
body itself. Exogenous pigmentation is commonly due to
foreign-body implantation in the oral mucosa.
Endogenous pigments include melanin, hemoglobin,
hemosiderin and carotene.
In the course of disease, the oral mucosal tissues can
assume a variety of discolorations blue, brown, and black
discolorations constitute the pigmented lesions of the oral
mucosa, and such color changes can be attributed to the
deposition of either endogenous or exogenous pigments.
The most important endogenous factor causing pigmen
tation in the oral cavity is melanin. It is derived from the
Greek (Melas-black), is an endogenous, non-hemoglobin
derived, brown-black pigment formed when the enzyme
tyrosinase catalyzes the oxidation of tyrosine to dihydroxyphenylalanine in melanocytes. Melanin in the melanosome,
the specialized epidermal melanin-bearing organelle, is
responsible for the color variation of human skin.
There are generally considered to be two types of melanin
pigmentation which form normal skin color. Constitutive
skin color implies the genetically determined color of healthy
unexposed skin such as observed on habitually sunshielded areas like the buttock and inner upper arm;
facultative skin color applies, for example, to tanned skin
and reflects the genetic capacity of the skin to darken in
response to ultraviolet radiation exposure.
Three types of melanin have been demonstrated.
Eumelaninit is brown-black melanin which is found
in ellipsoid melanosomes which impart brown-black
color to skin and hair.
Pheomelaninit is yellowred melanin in spherical
melanosomes which are the basis of yellow-red hair.
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Classification
It is discussed in Tables 20-1 to 20-3.
Etiology
It is often congenital in nature and usually but not
invariably follows a benign course. Some authorities believe
Color
Focal
Diffuse
Multifocal
Blue/purple
Varix,
Hemangioma
Hemangioma
Kaposis sarcoma,
Hereditary hemorrhagic telangiectasia
Brown
Melanotic macules,
nevus, melanoma
Ecchymosis, melanoma,
drug induced, hairy tongue,
petechiae
Gray black
Metal ingestion
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Focal
Early onset
Red blue purple
Physiologic pigmentation
Blanching
Peutz-Jeghers syndrome
Hemangioma
Predominantly adults onset
Varix
With systemic signs and symptoms Non-Blanching
Addisons disease
Thrombus
Kaposis sarcoma
Hematoma
Heavy metal pigmentation
Blue gray
No systemic signs and symptoms
Amalgam tattoo
Smokers melanosis
Other foreign body
Drug-induced pigmentation
tattoos
Post inflammatory pigmentation
Blue nevus
Brown
Oral melanotic macule
Pigmented nevus
Melanoacanthoma
Melanoma
Pigment
Color
Disease process
Hemoglobin
Blue, red,
purple
Hemosiderin Brown
Melanin
Brown,
black, gray
Differential Diagnosis
the lesion, particularly the congenital form, is not the true
neoplasm, but rather a developmental anomaly or
hamartoma.
Clinical Features
Signsthe earliest sign of a hemangioma is blanching
of the involved skin, often followed by fine telangiectases
and then a red macule.
Hemangioma in childrenrapid growth during the neonatal period is the hallmark of hemangiomas, occurring
characteristically beyond the growth rate of the infant.
The hemangiomas of childhood are found on the skin,
in the scalp, and within the connective tissue of mucous
membranes. Approximately 85% of childhood-onset
hemangiomas spontaneously regress after puberty.
Diascopydiascopy usually shows blanching on
pressure. This procedure is performed by pressing gently
on the lesion with a glass slide or a glass test tube. A
positive diascopy result (blanching) generally indicates
that the blood is within vascular spaces and is displaced
out of the lesion by pressure. However, lack of blanching
does not exclude the possibility of a vascular lesion.
Management
Sclerosing techniquesclerosing agents such as sodium
tetradecyl sulfate can be used intralesionally.
Cryosurgeryit can be useful in treating hemangioma.
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Definition
Varicespathological dilatation of vein or venules are
varices or varicosity.
Varixfocal dilatation of group of venules or vein is
known as varix.
Etiology
Trauma plays an important role in the development of a
varix. The traumatic event probably damages and weakens
the vascular wall and result in dilation.
Clinical Features
Locationit is commonly found on the tongue, lip or
cheek, mainly in the seventh decade of life.
Colororal varix is characterized as a red to purple
papule or nodule.
Margins and shapeit has sharply delineated borders
and a smooth, rounded surface contour.
Caviar tonguewhen many of sublingual veins are
involved it is called caviar tongue (Fig. 20-2).
Management
Surgical approachthe lesion can be excised or removed
by other surgical methods, including electrosurgery and
cryosurgery.
Intralesional injection of sclerosing solutionintralesional
1% sodium tetradecyl sulfate injection is effective as well,
yet it is usually more painful than simple excision. This
sclerosing agent should be injected directly into the
lumina with a tuberculin syringe (depositing 0.05 to 0.15
mL/cm3).
Thrombus
A thrombus, or blood clot, is the final product of the blood
coagulation step in hemostasis. It is achieved via the
aggregation of platelets that form a platelet plug, and the
activation of the humoral coagulation system (i.e. clotting
factors). A thrombus is physiologic in cases of injury, but
pathologic in case of thrombosis.
Specifically, a thrombus is a blood clot in an intact blood
vessel. A thrombus in a large blood vessel will decrease
blood flow through that vessel. In a small blood vessel,
blood flow may be completely cut-off resulting in death of
tissue supplied by that vessel. If a thrombus dislodges and
becomes free-floating, it is an embolus.
Etiology
Differential Diagnosis
Difference between hemangioma and varixthe varix
resembles the hemangioma both clinically and histologically, yet it is distinguished by two features: the
patients age at its onset and its etiology. A hemangioma
Clinical Features
Colorif the varix contain the thrombus, it presents as a
firm bluish purple nodule that does not blanch under
pressure.
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Management
Heparin and warfarinthese are often used to inhibit the
formation and growth of existing blood clots, thereby
allowing the body to shrink and dissolve the blood clots
through normal method.
Kaposis Sarcoma
Synonyms: Multiple idiopathic hemorrhagic sarcoma of Kaposis,
Angioreticuloendothelioma.
Kaposis sarcoma is an unusual and uncommon disease
of blood vessels which occasionally manifests in the oral
cavity: Classical (sporadic) Kaposis sarcoma was described
by Moritz Kaposi in 1872 in central Europe among elderly
persons of Mediterranean or Jewish origin as a multiple
pigmented sarcoma of the skin. Kaposis is most accurately
described as a multifocal angioproliferative neoplasm that
primarily involves the skin in non-HIV infected person. KS
is a neoplasm now most commonly a manifestation of
infection with the human immunodeficiency virus (HIV),
that frequently affects the oral cavity.
Although KS interaction with HIV infection remains
unexplained, the epidemic occurrence of KS in patient with
AIDS clearly supports a causal relationship between the
immune deficiency and the appearance of this neoplasm.
Pathogens or factors suspected to be associated with KS
include human herpes virus type 6, cytomegalovirus,
human immunodeficiency virus, mycoplasm penetons, sex
hormones and nitrate inhalants. However, solid evidence
of etiologic association among any of these agents with
AIDS or non-AIDS KS has not been established yet.
This vascular neoplasm may present as cutaneous, oral
or visceral lesion either independently or synchronously.
The frequency is higher in homosexual and bisexual male
than in other risk group for HIV infection. There is also an
increased incidence of Kaposis sarcoma among transplant
patients, which can resolve after immunosuppression drug
therapy is halted. Some investigators believe that KS is a
form of vascular hyperplasia responding to endothelial
growth factors rather than a malignant neoplasm.
Clinical Features
Age distribution and sex distributionKS may occur at
any age, but is most common in the fifth, sixth and
seventh decades. There is marked male predilection with
a gender ratio of 20 to 1.
Appearancethe tumor begins as a multicentric
neoplastic process that manifests as multiple red/purple
(vascular appearing) macules and in more advanced
types, nodules, occurring on the skin or mucosal areas.
Oral Manifestation
Locationthe lesions of the oral mucosa are identical in
appearance with cutaneous nodules. KS can involve any
oral site but most frequently involves the attached
mucosa of the palate, gingiva and dorsum of tongue.
Appearanceoral KS lesions occur as red to purple
nodules and macule with mucosal ulceration in some of
the more mature cases.
Symptomsthe lesions result in pain, dysphagia, difficulty with mastication, bleeding, and may be cosmetically
displeasing. This is particularly true with the progression
from the flat to the nodular form, which has been associated with increasing grades of immunocompression.
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Management
Blue Nevus
Nevus is defined as a congenital, developmental tumorlike malformation of the skin or mucous membrane. It is a
true mesodermal structure composed of dermal melanocytes
which only rarely undergo malignant transformation.
The Blue nevus represents a localized proliferation of
dermal melanocytes. It is an uncommon pigmented tumor
of dermal melanocytes that has traditionally been classified
into common and cellular variant. It is usually a skin tumor
in adults but can become apparent in early childhood or
even present at birth. Malignant blue nevus is a rare
melanocytic tumor of the skin arising from a preexisting
cellular blue nevus.
Differential Diagnosis
Etiology
Dermal arrestalthough definitive experimental
evidence is lacking, blue nevi are believed to represent
dermal arrest in embryonal migration of neural crest
melanocytes that fail to reach the epidermis.
Genetic predispositionbecause of the variation of blue
nevi in different populations, a genetic predisposition
has been suggested. However, familial cases of blue nevi
are exceedingly rare.
Clinical Features
Age and sex predilectionblue nevi are twice more
common in women than in men. Blue nevi may develop
at any age but are usually noticed in the second decade
of life or later.
Siteit occurs chiefly on buttocks, on the dorsum of feet
and hands, on the face and occasionally on other area.
Colorthe lesion is smooth, exhibits hairs growing from
its surface and varies in colors from brown to blue or
bluish black.
Appearancethe common blue nevus is a flat to slightly
elevated, smooth surfaced macule, papule, or plaque that
is gray-blue to bluish black in color.
Tyndall effectthe clinically noted blue color is due to
the depth of melanin in the epidermis and has the
Tyndall effect. The Tyndall effect is the preferential
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Differential Diagnosis
The differential diagnosis includes traumatic tattoo,
pigmented basal cell carcinoma and melanoma.
Fig. 20-3: Racial pigmentation seen on the gingiva.
Management
Surgical excisionsimple excision is the treatment of
choice.
Etiology
Geneticcontroversy exists on the pathogenetic
mechanism that leads to the development of melanotic
macules and it is not clear if they represent a physiologic
or a reactive process. Some authors reported a positive
family history and a genetic predisposition has been
hypothesized.
Racialif arising in children, it is most likely racial in
origin, in which case it may be called racial pigmentation
(Fig. 20-3) or physiologic pigmentation; no treatment is
necessary.
Clinical Features
AgeThe solitary oral melanotic macule is seen in
middle aged adults. Females are more affected than
males.
Siteit is attributed to actinic exposure and therefore
occurs on vermilion border of the lower lip. Sometimes it
can also occur on gingiva, palate and buccal mucosa.
Color and appearancethe melanotic macule is typically
a well circumscribed flat area of pigmentation that may
be brown, black, blue or gray in color.
Sizemost of the lesions are less than 1 cm in diameter,
although in occasional cases, they may be larger in size.
Shapelesions are oval or irregular in outline.
Differential Diagnosis
Melanoplakiathey are larger and occur in black
individuals.
Amalgam tattooassociated with juxtaposed amalgam
filling.
Ecchymosis patchit has got brownish color and it
usually disappears within few days.
Superficial spreading melanomaIt is seen in older age
group and spreads by circumferential growth. Men are
more affected and palate is commonly affected site.
Flat nevi and lentigoare very rare in the oral cavity.
Focal melanosisit is not seen as pigmented lesion.
Management
Surgical excisionexcision with adequate borders
should be carried out.
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Pigmented Nevus
Etiology
Pigment cellsthe origin of nevus cells is not completely
known. It has been postulated that they are derived from
pigment cells that migrate from the neural crest to the
epithelium and dermis (submucosa) or that may develop
from altered resident melanocytes.
Clinical Features
Agethey usually appear shortly after birth and
throughout childhood.
Siteit is most frequently encountered on the palate,
gingiva, buccal mucosa and lip.
Color and appearanceintraoral nevi are rare that may
occur at any age. It is characterized by a plaque or domeshaped sessile nodule with blue or black pigmentation
(Fig. 20-4).
Signspigmented nevi do not blanch on pressure. They
generally reach a given size and then growth becomes
static.
Management
Excisional biopsyjunctional nevi in adult may evolve
into malignant melanoma. For this reason, all nevi should
be excised. Since their size is generally less than 1 cm,
excisional biopsy would be usually indicated.
Melanoacanthoma
The term melanoacanthoma was first used by Mishima and
Pinkus in 1960 to describe a benign mixed skin tumor
composed of basal and prickle cell keratinocytes and
pigment-laden dendritic melanocytes. Oral melanoacanthoma is a rare, benign pigmented lesion, similar to
cutaneous melanoacanthoma, characterized by proliferation of dendritic melanocytes scattered throughout the
thickness of an acanthotic and hyperkeratotic surface
epithelium.
Etiology
The pathogenesis of oral melanoacanthoma is not clear,
although its clinical behavior is suggestive of a reactive
origin.
Clinical Features
Sex predilectionthe lesion occurs almost exclusively in
blacks and has a female predilection.
Siteit is seen most frequently on the buccal mucosa,
which may be related to greater frequency of trauma in
this area in 20-40-year-old persons. But can occur at any
oral site like lip, palate and gingiva and at any age.
Appearanceit is usually presenting as a single smooth,
flat or slightly raised, dark brown to black macule.
Sizethe lesion often demonstrates an alarmingly
rapid increase in size and occasionally will reach a
diameter of several centimeters within a period of a few
weeks.
Symptomsit is asymptomatic and not indurated.
Differential Diagnosis
Vascular lesionsthese include hematoma, varix, and
hemangioma. Hematoma is ruled out by history and
varix and hemangioma are ruled out by diascopy
(compression) method. These vascular lesions blanch
on pressure.
Differential Diagnosis
Melanomathis lesion has a tendency to enlarge rapidly,
which raises the possibility of a malignant process in
the clinical differential diagnosis. However, its tendency
to occur in young black females distinguishes it from
melanoma, which is uncommon in this age and racial
group.
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Differential Diagnosis
Melanoplakia
This term is applied to a flat, localized or widespread, black
or brownish discoloration of the oral mucosa due to
increased amount of melanin.
Melanin is produced by dentrite melanocytes in basal
cell layer of epidermis and is formed by oxidation of tyrosine,
a reaction that is catalyzed by copper containing enzyme
tyrosinase and mediated by melanocytes stimulating
hormone from anterior pituitary.
Management
Biopsybiopsy is done if the pigmented patch appears
recently rather than from birth or during childhood. It
becomes elevated in part or whole lesion and increases
in size and undergoes color changes and surface
ulceration.
Etiology
Smokers Melanosis
Clinical Features
Racedark complexioned people frequently have
macular pigmentation of various sizes on their oral
mucosa.
Colorit varies from light brown (Fig. 20-5) to blue
pigmentation depending on amount of melanin present
and depth of lesion.
Etiology
Nicotinesmokers melanosis may be due to the effects
of nicotine (a polycyclic compound) on melanocytes
located along the basal cells of the lining epithelium of
the oral mucosa (Fig. 20-6). Nicotine appears to directly
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Clinical Features
Race and sex distributionthis condition is most evident
in whites because of a lack of physiologic pigmentation
in the oral mucosa of this population, but some darkskinned individuals who smoke will have more
prominent pigmentation in many oral sites. Females are
affected more than males, which may be explained by
the additive effects of estrogen in female smokers.
Increases in estrogen levels observed during pregnancy
and the use of birth control pills are linked to other
hyperpigmentation conditions (e.g. melasma).
Agethe incidence of smokers melanosis increases with
age, suggesting that the longer a person smokes, the more
likely he or she will develop the condition. Some authors
noticed a significant increase in gingival melanosis of
children with parents who smoke.
Locationsmokers melanosis has been mostly observed
at the anterior mandibular gingiva; however, it can also
be seen in other parts of the oral cavity. Other part
involved is palate (Fig. 20-7), buccal and commissural
mucosa, and inferior surface of tongue and lip mucosa.
Management
With cessation of the smoking, improvement is expected
over the course of months to year. Smokers melanosis,
appears to be little significance. It may, however, potentially
mask other lesions or may be cosmetically objectionable.
Differential Diagnosis
Other entities to consider in differential diagnosis are racial
melanosis, melanosis due to medications, Peutz-Jeghers
syndrome, Addisons disease and early melanoma.
Smokers melanosis is benign and not considered to be
precancerous, but a biopsy may be indicated to rule out
more serious conditions, in particular melanoma.
Melanoma
It is also called as melanocarcinoma. Melanoma is the
malignant neoplasm of melanocytic origin that arises from
a benign melanocytic lesion or de novo from melanocytes
within otherwise normal skin or mucosa. It is the third
most common cancer of skin but they may develop at any
site where melanocytes is present.
Primary malignant melanoma of the oral mucosa is
extremely rare tumor, representing 0.2 to 8% of all
melanomas. Amelanotic malignant melanoma accounts for
only 2.3% of all melanomas. Amelanotic malignant melanoma was defined as a tumor composed of nonpigmented
melanocytes. However, another report, a tumor that lacks
pigmentation clinically and has melanin pigmentation
histopathologically is also included in this category. It is
neoplasm of epidermal melanocytes.
Growth Phase
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Types
Based on clinical featuresthe clinical appearance of the
tumor is variable and may be divided into the following
five types based on clinical features:
Pigmented nodular type
Nonpigmented nodular type
Pigmented macular type
Pigmented mixed type
Nonpigmented mixed type.
Clinicopathologic typesfour clinicopathologic (skin)
types of melanoma have also been described.
Superficial spreading melanomasuperficial spreading
melanoma is the most common form of melanoma. It
accounts for 65-70% of cutaneous melanomas. It exists
in a radial growth phase which has been called as
premalignant melanosis or pagetoid melanoma in
situ.
Nodular melanomanodular melanoma represents 1315% of cutaneous melanomas. It apparently has no
clinically recognizable radial growth phase, existing
solely in a vertical growth phase.
Lentigo-maligna melanomait accounts for 5-10% of
cutaneous melanomas. It exists in a radial growth
phase which is known as lentigo-meligna or melanotic
freckle of Hutchins. It predominantly occurs on sun
exposed skin of elderly person. It is characterized by
an extensive radial growth phase which may last up
to 25 years before connective tissue invasion takes
place.
Acral lentiginous melanomaIt is the most common
form of melanoma in blacks and also the most common
form of oral melanoma. It typically develops on the
palms of the hands, soles, feet, subungual area and
mucous membrane.
Oral Manifestations
Siteoral melanoma exhibits definite predilection for
the palate and maxillary gingiva.
Color and appearancean oral lesion typically begins as
a brown to black macule with irregular borders. The
macule extends laterally and a lobulated exophytic mass
develops once the vertical growth is initiated.
Signsulceration may develop early (Fig. 20-8) but many
lesions are dark, lobulated, exophytic masses without
ulceration at the time of diagnosis.
Clinical Features
Age and sexit can occur at any age group, but it is
extremely rare in ages below 30. The age range for patient
with oral melanoma is from 40-70 years, the average age
being 55 years. It is more common in men.
Sitethe most frequent oral sites of occurrence are the
palate and the maxillary gingiva, accounting for 80% of
all melanomas. The most frequent head and neck site of
occurrence of mucosal melanoma are the conjunctiva,
followed by the upper respiratory tract and the oral
cavity.
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Radiological Features
Differential Diagnosis
Oral melanotic maculebecause of many clinical
similarities exist between melanoma and its counterpart,
the melanocytic nevus, an ABCD system of evaluation
has been developed to help distinguish a melanoma
clinically from a melanocytic nevus. Asymmetry (because
its uncontrolled growth pattern), Borders irregularity
(often with notching), Color variation (which varies from
shades of brown to black, white, red and blue, depending
upon amount and depth of melanin pigmentation) and
Diameter often greater than 0.5 cm.
Melanotic neuroectodermal tumor of infancyoccurs in
infants.
Ecchymotic patchit disappears within few days.
Melanoplakiait is firm and occurs in infancy or puberty
without change.
Intramucosal compound or blue nevussame as oral
melanotic macule.
Pigmented fibromahistopathological diagnosis should
be done.
Drug-induced Pigmentation
A number of medications may induce oral mucosal
pigmentation. Direct deposition on oral surfaces, local
accumulation after systemic absorption, stimulation of
melanin related pathways, bacterial metabolism, alone or
in combination, may result in oral pigmentations. Several
antimalarial drugs are known to be capable of inducing
intraoral melanin pigmentation. These drugs include:
quinacrine, chloroquine, and hydroxychloroquine. Long
term use may cause pigmentation of the oral mucosa.
Clinical Features
Color of pigmentationthe pigmentation of the oral
mucosa is described as slate-gray in color, bearing
some resemblance to pigmentation caused by silver
arsphenamine.
Locationthey are usually located on hard palate.
Amodiaquine has been used to manage autoimmune
disease and oral pigmentation occur in 10% of patient
taking the drug on long term basis.
Minocycline pigmentationminocycline is a synthetic
tetracycline that is commonly used in the treatment of
acne vulgaris. Although tetracycline causes
pigmentation of bones and teeth, minocycline alone is
also responsible for soft tissue pigmentation. It is usually
seen as brown melanin deposits on the hard palate,
gingiva, mucous membranes, and the tongue.
Management
Surgical excisionthe treatment for cutaneous malignant
melanoma is surgical excision. Although regional lymph
node dissection is indicated when nodes are involved;
prophylactic lymph node dissection is very controversial.
Radiotherapyradiotherapy is applied mainly on
patients unable to undergo surgical treatment or as an
adjuvant to surgery.
Preoperative chemotherapypreoperative chemotherapy
is occasionally used to reduce the size of the melanoma
and improve surgical management. The first line
chemotherapeutic agent is dimethyltriazeno, imidazole
carboxamide solely or in combination with vincristine
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Differential Diagnosis
The diffuse distribution of pigment in drug induced lesion
is similar to that seen in Addisons disease and, in the
palate, to early superficial spreading melanoma. The history
is, of course, of prime importance and biopsy is recommended.
Treatment
Withdrawal of the medication is recommended, although
the pigmentation may persist for as long as one year after
cessation of medication.
Physiologic Pigmentation
Oral pigmented lesions are usually caused by increased
amount of melanin deposition. Physiologic pigmentation
is one of these lesions and is defined as localized, symmetric
hyperpigmentation which is commonly seen on attached
gingiva.
Etiopathogenesis
Geneticphysiologic pigmentation is probably genetically determined.
Mechanical, chemical and physical stimulationDummett
suggested, that degree of pigmentation is partially related
to mechanical, chemical, and physical stimulation.
Activity of melanocytesin darker skinned people, oral
pigmentation increases, but there is no difference in the
number of melanocytes between fair-skinned and darkskinned individuals. The variation is related to differences in the activity of melanocytes.
Age factorsthere is some controversy about the
relationship between age and oral pigmentation.
Steigmann and Amir et al stated that all kinds of oral
pigmentation appear in young children. Prinz, on the
other hand, claimed that physiologic pigmentation did
not appear in children and was clinically visible only
after puberty.
Clinical Features
This type of pigmentation is symmetric and persistent and
does not alter normal architecture, such as gingival
stippling.
Age distributionthis pigmentation may be seen in
patient at any age and is without gender predilection.
Differential Diagnosis
Clinical differential diagnosis would include smoking
associated melanosis, the syndrome associated with oral
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Treatment
Post-inflammatory Pigmentation
Long-standing inflammatory mucosal diseases, particularly lichen planus (Figs 20-12 and 20-13), can cause
mucosal pigmentation.
Etiology
The pathogenesis of post-inflammatory pigmentation
remains unclear.
Addisons Disease
Clinical Features
This is seen more frequently in dark-skinned individuals.
Clinically, multiple brownblack pigmented areas are noted
adjacent to reticular or erosive lesions of lichen planus.
Cyanosis
Causeit is caused by substantial decrease in proportion
of reduced hemoglobin to oxygenated hemoglobin in
blood. It becomes apparent when reduced Hb is less
than 5 g/100 ml.
Etiology
Tuberculosisit was the leading cause of Addisons
disease until the antibiotics were introduced that
successfully treated TB.
Autoimmune disordersnowadays, the major cause is an
autoimmune disorder in which the bodys immune
system makes antibodies which attack the cells of the
adrenal cortex and slowly destroys them. This can take
months to years.
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Pathogenesis
It has been shown that ACTH and melanocytes stimulating
hormone (MSH) are similar in structure, and ACTH is
believed to have some degree of melanocytes stimulating
activity. Normally, the pituitary gland produces ACTH
which causes the adrenal cortex to produce glucocorticoids
(such as hydrocortisone), which in turn are secreted into
the circulation. When the glucocorticoids reach a certain
concentration in the blood, they cause the anterior pituitary
to cease production of the ACTH. In Addisons disease,
however, the defective cortex is unable to produce much
glucocorticoid, so this feedback mechanism is not activated
and the pituitary continues to produce ACTH. As a result
of the increased production of melanin changes, the color
of the skin is a smoky tan or a chestnut brown.
It may take one of the two forms, the more usual being a
deep tanning of the skin and mucous membrane with
heavier deposits of melanin over pressure points. The
cheek is the most common site for this pigmentation in
the oral mucosa. More infrequently, the increased
melanocytic activity is expressed by the development of
distinct brownish macule on the oral mucosa and the
skin.
Color of pigmentationbluish black to pale brown or deep
chocolate spreading over the buccal mucosa from the
angle of the mouth (Fig. 20-14) or developing on the
gingiva, tongue and lips.
Diagnosisif Addisons disease is suspected, tests
measuring cortisol and aldosterone blood and urine
levels must be performed to make a definitive diagnosis.
The diagnosis of the Addisons disease is based on the
clinical sign as well as on characteristic changes in the
blood sodium and chloride levels.
Clinical Features
Signs and symptomsthe signs and symptoms of
Addisons disease are generally non-specific and
include fatigue, weakness, weight loss, nausea,
abdominal pain, diarrhea, and vomiting and mood
disturbances. These symptoms steadily worsen over time
due to the slowly progressive loss of cortisol and
aldosterone production.
Skin signsThe following skin signs may be indication
of Addisons disease and should take prompt further
investigations and appropriate tests.
Generalized darkening of the skin (hyperpigmentation) that may look like an inappropriate tan on a
very ill person.
Hyperpigmentation is most evident on areas exposed
to light, but also affects the body folds, sites of pressure
and friction, and in the creases of palms and soles
Hyperpigmentation may also appear prominent on
the nipples, armpits, genitals and gums (buccal
mucosa).
Women may have loss of androgen-stimulated hair,
such as pubic and underarm hair
Pigmentationpigmentation usually appears early
and is one of the most prominent signs of the disease.
Differential Diagnosis
HyperpituitarismAddisons disease may be distinguished from hyperpituitarism by the use of urine test:
levels of 17-ketosteroids in the urine are decreased in
the former but elevated in latter condition. A history of
silver ingestion identifies argyria.
Peutz-Jeghers syndrome, Albrights syndrome and von
Recklinghausens diseasethe macular type of discoloration that occasionally develops in place of the
more generalized tanning might be mistaken for PeutzJeghers syndrome, Albrights syndrome, or von
Recklinghausens disease; however, the attending
feature these individual syndromes should preclude any
such confusion.
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Management
It is done by adequate corticosteroid maintenance therapy
provided by an average daily dose of 25 to 40 mg cortisone.
Peutz-Jeghers Syndrome
Etiology
To date, it has not been possible to determine the gene,
although germline mutations have been detected on the
LKB1 (STKI11) gene on chromosome 19pl3.3. These are
nonsense, frameshift and mis-sense mutations and all
inactivate LKBl gene which encodes a threonine kinase
and behaves like a tumor suppressor gene.
Inactivation of this gene by germline mutations or loss
of normal allele can result in hamartomatous polyps. Apart
from the role of beta-cathenice, adenomatous polyposis coli,
K-ras and p-53 gene mutations have also been investigated.
The mucocutaneous pigmentations caused by melanin
aggregation can be seen in 93% of patients even in infancy.
They are generally located around the mouth, nose, cheek
mucosa, hand, foot and sometimes perianal and genital
areas.
Clinical Features
Agegenerally, it is of childhood onset with no sex
predilection.
Intestinal polypsthe major manifestation of PJS is the
intestinal polyps that are found anywhere in the
gastrointestinal tract, but most frequently in the small
bowel especially in the jejunum. The number and the
rate of growth of these polyps are variable.
Symptomsthe polyp usually becomes symptomatic
between the ages of 10 and 30, and may cause ulceration
with bleeding, obstruction, diarrhea, and intussusceptions. Patient may be anemic from chronic blood loss.
The polyps are usually benign, but malignant transformation may occur. Peutz-Jeghers syndrome has been
accepted as a precancerous syndrome, with cancers
being seen in 50% of patients.
Tuberous sclerosistuberous sclerosis is a frequent
neurologic problem in PJS patients and it is characterized
by hamartomatous polyp, mental retardation, and
epilepsy and adenoma cebaceum.
Pigmentationit is also characterized by multifocal
macular melanin pigmentation in perioral location. It
manifests itself as freckle like macules about the hands,
Management
Referral to a gastroenterologist is recommended. No
treatment is required for oral lesions.
Neurofibromatosis
It is also called as Von Recklinghausens disease. It is
transmitted as autosomal dominant trait. In it, multiple
neurofibromas of the skin along with brown spots are seen.
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Radiographic Features
Differential Diagnosis
Basal cell syndrometumor is restricted to skin of face,
neck and chest. Pigmentation is not feature.
Gardeners syndromepigmentation is not seen.
Management
Surgical excisionsurgical excision of individual
lesion.
Albrights Syndrome
Oral Manifestation
Siteareas of melanin pigmentation are seen on oral
mucosa with lips being the common site of involvement.
Intraoral growththere is presence of intraoral growth
inside the oral cavity (Fig. 20-17).
Differential Diagnosis
Addisons diseasediscrete macules are seen in adrenal
insufficiency.
Peutz-Jeghers syndromepigmented macules on skin
restricted to areas surrounding the body orifices, on finger
and both.
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They are purpuric submucosal and subcutaneous hemorrhages (Fig. 20-18). Petechiae are minute pinpoint
hemorrhages while ecchymosis is larger than 2 cm in
diameter.
Management
Surgery, after detection of disease.
Clinical Features
Sitecommon on lips and face.
Causesit occurs immediately following traumatic event
and erythrocyte extravasation into submucosa.
Colorit appears as bright red macule (Fig. 20-19) or
swelling, if hematoma is formed. After hemoglobin is
degraded to hemosiderin, lesion assumes brown color.
It does not blanch on pressure.
Fluctuant swelling, as hemorrhage is slow and no
sufficient blood to pool.
Differential Diagnosis
Amalgam tattoo, oral melanotic macule, junctional nevus,
melanoma and telangiectasia in Rendu-Osler-Weber
syndrome in all of the above, history of recent trauma,
change from bluish brown to green to yellow and then
disappearing lesion within 4 to 5 days indicate
petechiae.
Trauma from fellatiodisappear in few days after passing
through blue to green to yellow color changes to be taken.
Careful history should be taken.
Trauma from vomiting and coughingbroad linear red or
bluish bruise.
Carotenemia
Causeschronic excessive levels of carotene pigments due
to long and continuous consumption of food containing
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Clinical Features
Jaundice
Yellow or green discoloration of the skin and mucous
membrane with bile pigments. Oral mucosa presents a
yellowish discoloration. Tongue is heavily coated.
Hematoma
Hematoma is a localized collection of blood, usually clotted,
in a tissue or organ. Lingual hematoma has been
documented as a result of maxillofacial trauma causing
tongue laceration, post-extraction complication, severe
hypertension, unusual complications of anticoagulant
therapy, and surgical implant placement. Although not
recorded in the dental literature, periodontal flap
procedures may also affect hematoma formation. While a
relatively uncommon sequelae of surgical therapy, the
broad spectrum of events resulting in hematoma necessitates
the dental practitioners familiarity with its diagnosis and
treatment. The floor of the mouth hematoma can be more
problematic because of the facial planes are involved and
the anatomical structures at this site.
Etiology
Differential Diagnosis
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Treatment
Exogenous Pigmentation
It is defined as a pigmentation which arises as a result of
introduction of metal/drugs into the body via mucous
membrane, intestinal tract and skin.
Iatrogenic Pigmentation
Amalgam Tattoo
It is also called as localized argyrosis. Dental amalgam
tattoos are relatively common intraoral pigmented lesions,
with an estimated incidence of 8%. It is characterized by
the deposit of restorative debris composed of a mixture of
silver (Ag), mercury (Hg), tin (Sn), zinc (Zn), and copper
(Cu) in subepithelial connective tissue.
Etiology
Restorative workit may be condensed in the abraded
gingiva during routine amalgam restorative work.
Removal of old fillingit may enter the mucosa lacerated
by rotary instruments during removal of old amalgam
fillings or crown and bridge preparations of teeth with
large amalgam restorations.
During extractionbroken pieces may be introduced into
the socket or beneath the periosteum during extraction
of the teeth.
Retrograde amalgam fillingparticles may enter the
surgical cut during root canal treatment with retrograde
amalgam filling. There may be chances of corrosion of
retrograde amalgam filling.
Classification
Clinical Features
Accidental Pigmentation
Foreign substances are embedded in the gingival tissue. It
may be due to:
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Clinical Features
Radiological Features
Oral Manifestations
Differential Diagnosis
Superficial hemangiomait blanches on pressure while
amalgam tattoo does not.
Nevus and melanomarare in oral cavity. It has brown
color as compared to tattoo which has blue black color.
Management
Surgical excisiononce present, the amalgam tattoo
remains indefinitely, and occasional lesions slowly
enlarge over time, presumably as amalgam-laden
histiocytes try to move the material out of the local site.
No treatment is necessary, but excisional biopsy is often
performed in order to rule out melanoma or another
pigmented lesion. Lesions visible on radiographs are
usually not biopsied and those occurring on the visible
vermilion border of the lips are usually removed for
aesthetic reasons. There is no malignant potential for
this lesion.
Management
Removal of causeStoppage of use of bismuth.
Oral hygiene maintenancedentist should establish and
maintain oral hygiene of the patient.
Topical anestheticsmanagement of painful ulcerative
lesions should be done by topical application of
lignocaine hydrochloride gel.
Bismuthism
It is systemic metallic intoxication due to bismuth
compound.
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Etiopathogenesis
Clinical Features
Nervous systemlead has high affinity for cells in central
as well as peripheral systems. In acute poisoning,
demyelination and axon degeneration occurs. Lead
encephalopathy, cerebral palsy, mental retardation,
seizures, wrist or foot drop and fatigue can occur.
Gastrointestinal tractthere may be serious gastrointestinal disturbances like nausea, constipation,
vomiting, and colic.
Bonewhen incorporated in the bone, it can interfere
with cellular metabolism and changes are seen in the
rate of bone resorption and apposition.
Oral Manifestations
Symptomsthere is a metallic taste which is accompanied by excessive salivation and dysphagia.
Burtonian linewhen exposure to lead is very high and
oral hygiene is very poor, a line known as burtonian
line is seen which is gray black in color (Fig. 20-23) and
is present along the gingival margin. Lead line is more
diffuse than bismuth line.
Signsthere is pallor of lip, poor muscle tone and the
face appear ashen in color because of associated anemia.
Tremor of tongue may present on thrusting.
Parotid glandthere is bilateral parotid gland hypertrophy.
Radiological Features
Lead linelead line can be seen in the long bones and
skull. It represents deranged calcium metabolism that
results from the activity of lead on osteoclastic activity
and calcium resorption.
Management
Chelating agentslead can be removed from body by
using a chelating agent such EDTA (calcium disodium
ethylenediaminetetraacetate). But nowadays, other
chelating agents DMSA (2, 3-dimercapto-succinic acid)
and DMPS (2, 3-dimercaptopropane-1-sulfonate) are
used.
Mercurialism
It is also called Pink disease, Swifts disease, Dermatopolyneuritis, and Acrodynia. It is an uncommon disease
caused due to a mercurial toxicity reaction, either actual
mercury poisoning or, more likely, an idiosyncrasy to the
metal.
Etiology
Medicinal usemercury can be used in teething powder,
cathartic agents and antihelminthics preparation.
Mercury in dental amalgamimproper use of dental
amalgam alloy which contain mercury can also cause
mercurialism. But there is no documented literature on
the mercury toxicity occurring due to dental amalgam.
Mercury in paintmercury hazards exist in paints
containing mercurial salts such as phenylmercuric
propionate.
Mercurial diureticsprolonged administration of
mercurial diuretics can also result in mercurialism.
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Clinical Features
Ageit occurs most frequently in young infants before
the age of 2 years although children can be occasionally
affected up to age of five years or six years.
Gastrointestinal symptomsintestinal colic and diarrhea.
There is also pharyngitis, dysphagia, nausea, abdominal
pain.
Nervous symptomslong continued exposure to mercury
vapor can result in permanent neurological changes.
Headache, insomnia, tremors of fingers and tongue and
mental depression.
Renal symptomssevere intoxication and it can be the
cause of death.
Color of pigmentationhands, feet, nose and cheeks
assume pink color.
Hair and nailsthe nails are shed at the same time with
teeth lost prematurely and alopecia is also present. The
children will frequently tear their hair out in patches.
Raw beef appearancethe skin of hands, feet, nose, ears
and cheek becomes clammy red or pink and has a cold
clammy feeling. The appearance is described as
resembling raw beef.
Skinthe skin over the affected area peels frequently
during the course of the disease. The patients also have
maculopapular rash which is extremely pruritic.
Others findingsevere sweating, extreme irritability,
photophobia with lacrimation, insomnia, muscular
weakness, tachycardia and hypertension.
Radiographic Features
Appearancechanges occurring in the jaw are similar to
the changes seen in osteomyelitis except that changes
may be localized at first and gradually extend until large
portion of bone involved.
Irregular bone destructionthere is irregular area of bone
destruction with loss of cortex of the follicle of the affected
tooth.
Management
Supportive measurebed rest and suitable dietary regimen
should be adjusted for renal damage.
Control of salivary flowatropine or belladonna can be
prescribed to lessen the salivary flow.
Chelating agentsadministration of chelating agents
BAL- British anti-lewisite (2,3-dimercaptopropanol) is
recommended. But nowadays, as side effect of BAL is
more, another chelating agents DMSA (2, 3-dimercaptosuccinic acid) and DMPS (2, 3-dimercaptopropane-1sulfonate).
Oral Manifestations
Etiology
Clinical Features
Siteexposed body surfaces, nail-beds are commonly
involved.
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Oral Manifestations
Etiology
Medicinal usegold is useful for the treatment of
rheumatoid arthritis, lupus erythematous and leprosy.
Management
Removal of causesource of contact should be eliminated.
Clinical Features
Arsenism
It occurs due to arsenic poisoning.
Etiology
Industrial exposurearsenic exposure from industrial use
can lead to arsenic poisoning.
Medicinal usearsenic is used to treat asthma and
dermatose such as psoriasis.
Clinical Features
Symptomschronic gastritis and colitis, keratosis of
palms of the hand and soles of feet.
Hyperpigmentationdiffuse macular hyperpigmentation
is seen on the skin of the patient. This occurs due to
increase in melanin production.
Arsenical keratosisthese are the premalignant skin
lesion which can occur in arsenic poisoning.
Other complicationpatient can also notice palmar and
plantar hyperkeratosis, basal cell carcinoma and
cutaneous squamous cell carcinoma.
Oral Manifestations
Symptomsoral tissues are extremely painful and patient
may complain of excessive salivation.
Severe gingivitisgingiva become intensely inflamed.
Necrotizing ulcerative stomatitislocal contact with
arsenic trioxide often produces ulceration which can
become necrotic.
Dorsal hyperkeratosis of tonguethis occurs in patient in
past, who has taken arsenic for syphilis treatment.
Color of pigmentationtissues are deep red in color.
Management
Anesthetic ointmentsurface anesthetic ointment or rinses
such as lidocaine or dyclonine solution can be given to
control pain occurred due to salivation.
Oral Manifestation
Siteit includes buccal mucosa, lateral border of tongue,
palate and pharynx.
Symptomspatient gets metallic test in the oral cavity
before the development of stomatitis.
Stomatitisit is the most common complaint of the
patient who is receiving gold therapy.
Signvesiculation and ulcerations of the oral mucosa.
Management
Removal of causepatient should be advised to
discontinue of gold therapy.
Alkaline mouth washthis should be prescribed to treat
oral stomatitis.
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Summary
Pigmentation is the both normal and abnormal discoloration of oral mucous membrane. Pigmentation has
multifactorial etiology. Most of the pigmentation is
physiologic but sometimes it can be a precursor of severe
diseases. Melanin pigment irregularities and color changes
of the oral tissues could provide significant diagnostic
evidence of both local and systemic disease. Evaluation of
a patient presenting with a pigmented lesion should include
a full medical and dental history, extraoral and intraoral
examinations, and laboratory tests. The history should
include the onset and duration of the lesion, the presence
of associated skin hyperpigmentation, the presence of
systemic signs and symptoms (e.g. malaise, fatigue, weight
loss), use of prescription and nonprescription medications,
and smoking habits. Pigmented lesions on the face, perioral
skin and lips should be noted. The number, distribution,
size, shape and color of intraoral pigmented lesions should
be assessed. In general, benign pigmented lesions show
regular borders and are small, symmetric and uniform in
color. They may be either flat or slightly elevated. In contrast,
irregular borders, color variation, and surface ulceration
suggest malignancy. Clinical tests such as diascopy,
radiography and laboratory investigations such as blood
tests can be used to confirm a clinical impression and reach
a definitive diagnosis. However, because it is not always
possible to distinguish between a benign pigmented lesion
and an early melanoma on the basis of clinical features
alone, biopsy is usually recommended for focal oral
pigmented lesions that cannot be explained by local factors.
The recognition, identification, and clinical assessment of
pigmentation is of great importance because of the possible
risk of serious systemic disease, such as melanoma, various
syndromes, and the side effects of drugs.
Clinical Features
Vision problemsalbinism is associated with vision
problems and has low vision. Vision problems in
albinism result from abnormal development of the
retina and abnormal patterns of nerve connections
between the eye and the brain. It is the presence of these
eye problems that define the diagnosis of albinism.
Therefore, the main test for albinism is simply an eye
examination.
Skin problemswhile most people with albinism are fair
in complexion (Fig. 20-24). Skin or hair color is not
diagnostic of albinism. People with many types of
albinism need to take precautions to avoid damage to
the skin caused by the sun such as wearing sunscreen
lotions, hats and sun-protective clothing. In less
pigmented types of albinism, hair and skin are creamcolored.
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Suggested Reading
3
Fig. 20-25: Hypopigmented region of face in albinism.
Management
Skin protectionuse appropriate skin protection, such
as sunscreen lotions, higher and opaque clothing, and
people with albinism can enjoy outdoor activities even
in summer.
Avoid social stigmafamilies and schools must make an
effort not to exclude children with albinism from group
activities.
Vitiligo
It is localized type of hypopigmentation. It is progressive
symmetric areas of complete pigment loss. It is most
commonly seen area around mouth (Fig. 20-26). lip, nose,
nipples and anus. Color of pigmentation is chalk white.
Management is done by topical glucocorticoids, PUVA
therapy.
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21
Dental Caries
Introduction
Dental caries is a microbial disease of the calcified
tissues of the teeth, characterized by demineralization of
the inorganic portion and destruction of the organic
substance of the tooth. It is one of the most common
infectious diseases affecting the human race. Cariogenic
plaque contains 2 108 bacteria per milligram weight and
pH of 5.5 is critical threshold for the demineralization. The
initial lesion appears as opaque white or brown spot
beneath the plaque layer. As the caries process results in
demineralization, the affected area of the tooth appears
more radiolucent than unaffected area. Carious area
attenuates less radiation than intact tooth substance so
that the area of the film on which remnant beam from the
deminerlized area falls, it receives higher exposure and
thus appears more darker on the processed radiograph.
The disease process begins with the concentration of
Streptococcus mutans at specified tooth surfaces and lead to
white spot formation or even cavitations. The development
of dental caries is a dynamic process of demineralization
of the dental hard tissues by the products of bacterial
metabolism, alternating with periods of remineralization.
Etiology
Dietary factorcarbohydrates with types like monosaccharides, disaccharides or polysaccharides and the
amount consumed and whether it is between meals.
Microorganismsacidogenic Streptococcus mutans and
Actinomycosis viscosus.
Systemic factorshereditary, pregnancy and lactation
factors have been suggested as etiological factors for
dental caries.
Host factorpoor oral hygiene and improper brushing
technique can lead to dental caries.
Pathogenesis
Fermentation of oral microorganismwhenever carbohydrate is consumed, oral microorganisms rapidly begin
fermentation producing organic acids like lactic acid,
acetic acid and formic acid. This leads to fall in pH of
the oral fluids.
Demineralizationthese organic acid attack the tooth
structure, resulting in loss of tooth minerals specially
calcium and phosphate ions, which leach out from
hydroxyapatite. This process is known as demineralization.
Remineralizationafter a period of 30 minutes, due to
salivary buffering by bicarbonate ions and ammonia
production from salivary proteins, there is an increase
in pH of the oral fluids. The acid is neutralized and the
condition now favors precipitation of calcium and
phosphate ions into tooth surface. This process is called
as remineralization and is hastened if fluoride is present
in a small amount in either plaque fluid or saliva.
Further demineralizationthe microorganism which is
of primary concern in the pathology of dental caries is
Streptococcus mutans. It forms insoluble, sticky
extracellular polysaccharides which help in further
colonization and increases the contact of the acids with
the tooth structure, leading to further demineralization
which ultimately leads to cavitations.
Formation of cariesthe balance between the caries
causing and caries protective factors is very delicate. It
is only when repeated attacks of demineralization occur
that there is a net loss of minerals from tooth and caries
results. The surface layer of enamel overlying the lesion
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Theories of Cariogenesis
Proteolytic Theory
Proteolysis can play a role in dental caries process,
particularly in lesions that develop on exposed root
surface.
Acidogenic Theory
It is generally agreed that dental caries is caused by acid
resulting from action of microorganisms on carbohydrates.
It is characterized by decalcification of the inorganic portion
and is accompanied or followed by a disintegration of the
organic substance of the tooth. The cariogenicity of
carbohydrate varies with the frequency of ingestion,
physical form and chemical composition, route of
administration and presence of other food constituents.
Sticky solid carbohydrates are more caries producing than
those consumed as liquids.
Most commonly associated microorganisms are L.
acidophilus and Streptococcus mutans which are found in
caries susceptible individuals. Acids are produced due to
enzymatic breakdown of the sugar and the acids formed
are chiefly lactic acid and butyric acid.
Autoimmunity
Jackson and Bunch suggest that zones or regions of
odontoblasts in specific sites with the pulp of specific
teeth are damaged by an autoimmune process so that the
defense capacity of the overlying dentin and enamel is
compromised and concluded that caries should be regarded
as a degenerative process.
Initially disease event corresponds to a form of somatic
gene mutation in central growth control stem cells.
Descendent mutant cells synthesize autoantibody which
damage specific groups of odontoblasts and thus determine
the sites of caries susceptibility.
Classification
First Classification
Based on Location of the Lesion (see Fig. 21-4)
Pit and fissure caries
Occlusal
Buccal or lingual pit
Smooth surface caries
Proximal
Buccal or lingual surface
Root caries
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Second Classification
Site
Site 1includes lesions on the pit and fissure of the
posterior teeth and on other surfaces, these include the
buccal grooves of the mandibular molars, palatal grooves
of the maxillary molars and erosion on the incisal edges.
Site 2includes lesions in the contact areas of posterior
and anterior teeth.
Site 3includes lesions originating in the gingival third
of all teeth.
Size
Size 1(mild)includes lesions which have progressed
just beyond remineralization.
Size 2 (moderate)includes larger lesions with adequate
tooth surface to support the restoration.
Size 3 (enlarged)includes lesions in which the tooth
structure and the restoration are susceptible to fracture.
Size 4 (severe)it includes lesions which have destroyed
a major portion of the tooth structure.
Explorer
Sensitivity of testthe sensitivity of the explorer is also
reported to be low in diagnosing occlusal dentinal
lesions. Use of sharp explorers in probing has been
questioned by several authors. It is reported that it may
cause damage or create a cavity at the site of a superficial
carious lesion.
How to do itusing explorer in the intraoral examination
may not improve diagnostic accuracy. Sticking probe
may not be indicating caries but only be a sign of local
anatomical features.
Disadvantagealso probing a sterile fissure after an
infected one may inoculate pathogenic microorganisms
and infect the sterile fissure. However, in a study which
lasted as long as 11 years in which the same children
were examined repeatedly as often as six times with
vigorous probing of pits and fissures but it didnt show
any evidence that probing increases caries. In some parts
of the world, especially in Scandinavian countries,
applying pressure with sharp explorer is not approved
because of the damage, it would create change in the
surface integrity and possible implantation of
microorganisms. There are some controversial results
in this issue but the evidence suggests that an explorer
should be used lightly or not at all on occlusal surfaces.
In most cases when there is a cavitation on the enamel
surface, dentinal involvement is also there.
Radiographic Method
Clinical Method
Visual Inspection
Sensitivity of testvisual inspection is a traditional
diagnostic method and it appears to have a very low
sensitivity and high specificity in diagnosing caries.
Dry and clean teeththe teeth should be clean, dry and
well illuminated during a visual examination to obtain
maximum information.
Visual examinationin detecting occlusal caries has a
limited sensitivity. Black or brown discolorations and
fissure morphology are not reliable for definitive
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Fig. 21-1: Bite wing radiography is useful method for the diagnosis
of dental proximal caries.
Fluorescence
Acid dissolution of the structure results in a local decrease
in fluorescence in area of acid exposure (Fig. 21-3). This
has been used in detection of dental caries.
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Fig. 21-3: Decreases fluorescence seen in proximal caries area
Clinical Features
Opaque chalky regionit takes 3 to 4 years to manifest
clinically as loss of enamel transparency resulting in
opaque chalky region (white spot). In some cases, it
Fig. 21-5: Proximal caries seen with second premolar and first
molar in proximal contact area.
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Fig. 21-8: Fractured tooth due to carious process.
Radiological Types
Incipient cariesradiographically, this caries susceptible
zone has vertical dimension of 1.0 to 1.5 mm. There is
loss of normal homogeneity of the enamel shadow (Figs
21-9A and B). It appears as a radiolucent notch on the
outer surface of teeth. Magnifying glass should be used.
Moderate cariesinterproximal incipient lesion that
develops and involves more than outer half of enamel
but that do not radiographically extends into DEJ may
B
Figs 21-9A and B: Incipient proximal caries showing loss of
enamel homogeneity (Courtesy Dr Fusan Yasser).
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A
B
B
Figs 21-10A and B: Moderate caries seen
in incisor region
D
Figs 21-11A to D: Advanced caries showing extension
in dentin (Courtesy Fusun Yasser),
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Clinical Features
Locationit usually extends from the area opposite to
the gingival crest occlusally to the convexity of the tooth
surface. It extends laterally towards the proximal
surfaces and on occasion extends beneath the free margin
of the gingiva.
Cervical lesionit usually occurs in cervical area and
the typical cervical lesion is a crescent shaped cavity
(Fig. 21-13). Beginning as slightly roughened chalky area
which gradually becomes excavated.
Buccal pitthis again one of common type of caries
which occur as pit on the buccal surface of tooth
(Fig. 21.14).
C
Figs 21-12A to C: Severe carious lesion involving
more than half of dentin (Courtesy Fusun Yasser).
Severe carieswhen carious lesion is seen radiographically to have penetrated through more than half of
dentin (Figs 21-12A to C) and is approaching the pulp
chamber, it is categorized as severe. It reveals a narrow
path of destruction through enamel, the expansion of
the radiolucency at DEJ and extends its development
toward pulp chamber. It may or may not appear to
involve pulp. Force of mastication will cause the
undermined enamel to collapse leaving very large cavity
or hole in the tooth (Fig. 21-12D).
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Radiographic Features
Fig. 21-16: Deep pits and fissure more prone for carious tooth.
Clinical Features
Locationit usually occurs in pits and fissures with high
steep walls and narrow bases.
Appearanceit appears brown or black (Figs 21-17A
and B) and feels slightly soft and catches a fine explorer
point. The enamel directly bordering the pit and fissure
may appear opaque, bluish white as it becomes undermined.
Spreadthe lateral spread of caries at the dentinoenamel
junction as well as penetration into the dentin along the
dentinal tubules may be extensive without fracturing
away the overhanging enamel. Thus, there may be large
carious lesion with only a tiny point of opening.
Radiological Features
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Figs 21-17A and B: Pit and fissure carious lesion brown black
discoloration of tooth.
Root Caries
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Clinical Features
Radiographic Features
Radiographic Features
Appearancethe carious process is best described as
scooping out which result in radiographic appearance
usually described as ill-defined saucer-like crater. If
peripheral surface area is small, the appearance of
carious lesion will be notched rather than saucer-like.
Recurrent Caries
Dental caries that occurs immediately adjacent to the
restoration is referred to as recurrent caries (Fig. 21-21). It
may be caused by inadequate extension of restoration and
there has not been careful and complete excavation of
original carious lesion.
Clinical Features
Incidence16% of restored teeth have recurrent caries.
Causerestoration will show poor margins which
permit leakage and the entrance of both bacteria and
substrate.
Pathogenesis
The reasons for this are that the child is put on bed at
afternoon nap time or at night with nursing bottle
containing milk or a sugar containing beverage. The child
fall asleep and the milk or sweetened liquid becomes pooled
around the maxillary anterior teeth. The carbohydrate
containing liquid provides an excellent culture medium
for acidogenic microorganisms. Salivary flow is decreased
during sleep and clearance of the liquid from the oral cavity
is slowed. Lactose content of human milk, as well as that of
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Figs 21-22A to E: Recurrent caries seen below the
restoration (Courtesy Fusan Yasser).
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Clinical Features
Radiation Caries
It is a rampant form of dental decay that may occur in
individuals who receive a course of radiotherapy that
includes exposure of the salivary glands.
Prevention
Clinical Features
Radiological Features
Appearanceradiographically it appears as dark
radiolucent shadow appearing at necks of teeth most
obvious on mesial and distal aspects.
Rampant Caries
It is defined as a suddenly appearing, widespread, rapidly
burrowing type of caries, resulting in early involvement of
the pulp and affecting those teeth usually regarded as
immune to ordinary decay. Some believe that the term
rampant caries should be applied to those carious lesions
with 10 or more new lesions per year. It usually occurs in
children with poor dietary habits.
Etiology
B
Figs 21-23A and B: Nursing bottle caries seen in maxillary anterior
teeth (Courtesy Dr Shetty).
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Clinical Features
Radiological Features
Pre-eruptive Caries
Radiographic Features
Appearanceit demonstrate severe advanced carious
lesions especially of mandibular anterior teeth.
Arrested Caries
It has been described as caries which becomes static or
stationary and does not show any tendency for further
progression.
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Radiographic Differential
Diagnosis of Dental Caries
Erosion cavitysince these cavities are saucer shaped
and have sloping margins in radiographs, they may
resemble carious cavities. Clinical examination is
necessary to rule out erosion cavity.
Non-opaque fillingif carious cavities are filled with nonopaque filling material then it may resemble caries. But
sharpness of the margin surgically prepared suggests
the presence of filling.
Cervical burnoutfollowing is the difference between
cervical burnout and cervical caries
Cervical burnout is located at the neck of the teeth,
demarcated above by the enamel cap or restoration
and below by the alveolar bone level while caries have
no apparent upper and lower demarcating borders.
It is triangular in shape, gradually becoming less
apparent towards the center of the tooth while caries
is saucer shaped and becomes more apparent toward
center of tooth.
In cervical burnout axial border fades or follows
anatomic contour while in case of cervical caries
sharp delineation and ragged contour is present.
Peripheral outline of cervical burnout appear intact
as compared to caries where it is cavitated.
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Suggested Reading
1. Ast DB, Chase HC. The clinical study of caries prophylaxis with
zinc chloride and potassium ferrocyanide. JADA 1950;41:437-9.
2. Atchinson KA, White SC, et al. Assessing the FDA guidelines for
ordering dental radiographs. JADA 1995;126:1372-83.
3. Espelit I, Tveit AB. Diagnosis of secondary caries and crevices
adjacent to amalgam. International Dental Journal 1991; 41:35964.
4. Flack VF, Atchinson KA, et al. Relationships between clinical
variability and radiographic guidelines. J Dent Res 1995;16:77582.
5. Goaz PW, White SC. Oral Radiology Principles and Interpretation.
Chapter 15 Dental Caries (3rd edn), Mosby 1994;306-26.
6. Haak R, Wicht M. Grey-scale reversed radiographic display in
the detection of approximal caries. Journal of Dentistry 2005;33:
65-71.
7. Haak R, Wicht MJ, et al. The validity of proximal caries detection
using magnifying visual aids. Caries Res 2002;36:249-55.
8. Huysmans MC, Longbottom C. The challenges of validating
diagnostic methods and selecting appropriate gold standards. J
Dent Res. 2004;83 Spec No C:C48-52. Review.
9. Idem. Effect of stannous fluoride dentifrice in children residing in
during three year study period. JADA 1962;64:216-9.
10. Katz RV, Hazen SP, et al. Prevalence and distribution of root
caries in an adults population. Caries Res 1982;16:265.
11. Kidd EAM, Beighton D. Prediction of secondary caries around
tooth-colored restorations: a clinical and microbiological study. J
Dent Res 1996;75(12):1942-6.
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Diseases of Tongue
Introduction
The tongue makes up a large part of the oral cavity and can
be affected by numerous lesions. The tongue may be affected
as a part of oral disease or as a signs of a systemic disease.
The word tongue is derived from the Latin word lingua
and Greek word glossa. It is partly oral (anterior 2/3rd of
tongue) and partly pharyngeal (posterior 1/3rd of tongue).
It is composed of body (movable oral part) and base
(attached part).
Anatomy of Tongue
The tongue is a muscular organ situated in the floor of
mouth, associated with the function of deglutition, taste
and speech. Tongue has a base, body and a tip. It has two
surfaces, a dorsal and a ventral surface. The dorsal surface
is divided into an oral and pharyngeal part and the ventral
surface is confined to the oral cavity only.
Surface
Sulcus terminalisit lies partly in the mouth (oral part),
which comprises the anterior 2/3rd and in the pharynx
(pharyngeal part), which comprises the posterior 1/3rd.
Both the parts are separated by the inverted V shaped
sulcus called the sulcus terminalis. At the apex of sulcus
terminalis, there is a depression, called the foramen cecum.
Anterior partin the anterior part of the tongue the
mucous membrane is thin with reduced lamina propria
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Papillae
Circumvallate papillaethey are usually 8 to 12 in number
and are the largest of the papillae. They are situated in a
row parallel to and close to the sulcus terminalis.
Papillae are 1 to 3 mm in diameter and are flattened
with a circular depression. They are surrounded by a
moat-like trough.
Fungiform papillaethey are smaller than the vallate
papillae and are distributed over the dorsal surface of
the tongue, being most numerous on the anterior part.
They are round and mushroom shaped and is distinguished from the filiform papillae by their larger size
and bright red color. Their number is about 100/cm2 on
the tip and 50/cm2 in the middle. They carry taste buds.
Filiform papillaethese are smallest, but most numerous
and are evenly distributed over the dorsum and are often
Muscle
Types of musclethe muscles of tongue are grouped into
two sets: an extrinsic set and an intrinsic set. The
extrinsic muscles include genioglossus, hyoglossus,
styloglossus and palatoglossus.
Genioglossusit is the largest and arises from the upper
mental spine and spread in a fan-like fashion and is
inserted into the tongue from its tip to the root. It draws
the tongue forward and acting together. This muscle is able
to flatten the tongue, making a concavity from side-to-side.
Hyoglossusit is a flat, quadrilateral muscle arising from
the hyoid bone. It runs as thin plate upward, connect
with fibers from the styloglossus and enter the tongue
lateral to the genioglossus. It depresses the tongue.
Styloglossusit originates from the styloid process,
passes downwards and forwards and inserts into the
side of the tongue, connecting with fibers from the
hyoglossus. The styloglossus draws the tongue upwards
and backwards.
Palatoglossusit originates from the palate and runs in
the palatoglossus arch, continuing into the side and
dorsum of the tongue.
Intrinsic musclesthese are situated inside the tongue
and constitute a greater part of the organ. They are
divided into the superior longitudinal, inferior
longitudinal, transverse and the vertical muscles.
Superior longitudinalit arise from submucous fibrous
layer close to the epiglottis and from the median fibrous
septum. If runs forward to the edges of tongue, some
of its fibers being inserted into mucous membrane. It
shortens the tongue and makes the dorsum concave,
by turning the tip and side of the tongue upward.
Inferior longitudinalit is a narrow band lying close
to the inferior surface of tongue, between genioglossus
and hyoglossus. It extends from the root apex of the
tongue, some of its posterior fibers being connected
with the body of hyoid bone. In front, it blends with
the fibers of styloglossus. It shortens the tongue and
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Arterial Supply
Lingual arterythe lingual artery, a branch of the external
carotid, is the main vessel supplying the tongue. Before
the artery reaches the posterior edge of the hyoglossus
muscle, it gives off a branch to the hyoid bone area.
Lingual dorsal arteryin its course below the hyoglossal
muscle, it gives off a lingual dorsal artery, which runs
steeply upward dividing into many branches supplying
the base of tongue and posterior part of the dorsum.
Ascending pharyngeal artery and tonsillar arterythe root
of the tongue is also supplied by the ascending
pharyngeal artery and tonsillar artery.
Sublingual arteryat the lower border of the anterior part
of the hyoglossal muscle, the lingual artery gives off the
sublingual artery, which supplies the sublingual region
medial to the sublingual gland.
Venous Drainage
Lingual veindeep lingual vein is the largest and the
principal vein of the tongue. Deep lingual vein originates
near the tip of the tongue and runs backward, close to the
mucous membrane on the ventral surface of the tongue.
Vena comitansit joins the sublingual vein, at the
posterior border of the hypoglossal muscle to form the
vena comitans of the hypoglossal nerve, which drains to
the facial or internal jugular vein.
Dorsal lingual veinthe dorsal lingual vein drains into
the dorsum and sides of the tongue. It joins the sublingual
veins, which follow the artery deep to the hypoglossal
muscle and enter the internal jugular vein, near the hyoid
bone.
Nerve Supply
Hypoglossal nerveall the muscles of the tongue, except
the palatoglossus are supplied by the hypoglossal nerve.
The palatoglossus is supplied by the pharyngeal plexus.
Lingual branch of mandibular nerve is nerve for general
sensation for anterior 2/3rd of tongue.
Lymphatic Drainage
Submental nodesthe tip of the tongue drains bilaterally
into the submental nodes.
Submandibular lymph nodesright and left halves of rest
of the anterior 2/3rd of the tongue, drain unilaterally to
submandibular lymph nodes. A few central lymphs
drain laterally into the same nodes.
Jugulodigastric nodessome of the lymph vessels, from
the lateral margins of the tongue, drain to the jugulodigastric nodes.
Jugulo-omohyoid nodesthe posterior 1/3rd of the tongue
drain bilaterally to the jugulo-omohyoid nodes, in which
most of the lymphs drain from the tongue.
Functions of Tongue
Speechit is the result of interaction between different
organs. Even small changes in the position or shape of
the tongue may cause disturbance in speech. Tongue is
one of the organs in the oral cavity, which interrupts the
air passage through mouth or pharynx thereby
producing consonants. Certain consonants like c, d, j, i,
n, t, z, l, g, etc. require movement of tongue.
Masticationthe tongue has a direct crushing effect on
food by pressing it against the hard palate. The tongue
pushes the food onto the occluding surfaces and helps
to mix in the saliva. The sensory ending on the tongue
enable to select those parts of the food mass are
sufficiently well masticated to be ready for swallowing.
Deglutitionwhen the food bolus is placed on dorsum
of tongue, it is pressed lightly against the hard palate
just behind the incisors. It is a coordinated muscular
activity involving the tongue and constrictor muscle of
the pharynx, to close the palatal vault and the epiglottis.
It allows the passage of the bolus into the esophagus,
without regurgitation into the nose or lower respiratory
tract. The process is initiated by the voluntary action of
collecting food onto the tongue and propelling it
backwards into the pharynx. The muscles involved in
this process are the mylohyoid and the pharyngeal
constrictors. Bolus is pushed backwards by raising the
back of tongue. Food bolus is sucked from mouth into
pharynx, by creating a negative pressure, while airways
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Adenoma
Hemangioma
Lymphangioma
Malignant
Squamous cell carcinoma
Adenocarcinoma
Transitional cell carcinoma
Verrucous carcinoma
Mucoepidermoid carcinoma
Reticular cell carcinoma
Metastatic lesions from
Kidney
Liver
Stomach
Lung
Fissured tongue
Congenital
Syphilis
Amyloidosis
Melkersson-Rosenthal syndrome
Papillon-Lefevre syndrome
Traumatic bite
Lymphosarcoma
Angiosarcoma
Kaposis sarcoma
Melanoma
Red and white lesions
Leukoplakia
Erythroplakia
Lichen planus
OSMF
Candidiasis
Psoriasis
Focal epithelial hyperplasia
White sponge nevus
Pemphigus
Clinical Features
Symptomspatient encounters difficulty in eating and
speaking.
Signspatient may have high arched palate and a
narrow constricted mandible.
Airway problemsthere may be an airway obstruction,
due to negative pressure generated by deglutition and
inspiration.
Syndrome associatedoromandibular limb hypogenesis
syndrome (hypodactylia) and hypomelia and Pierre
Robin syndrome.
Diagnosis
It can diagnose on clinical examination.
Management
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Non-keratotic lesion
Thrush
White sponge nevus
Vesiculobullous and other desquamative disorders
Keratotic white lesions
Lichen planus
Leukoplakia
Depapillation and atrophic lesions
Chronic trauma
Nutritional deficiency
Hematological abnormalities
Medication
Peripheral vascular disease
Diabetes and chronic candidiasis
Tertiary syphilis and interstitial glossitis
Pigmentation
Ulcer and infectious disease
Superficial vascular disease
Disorders affecting body of mandible
Amyloidosis
Infection
Tumors of tongue
Squamous cell carcinoma
Benign
Dermatomyositis
Diabetes
Syphilis
Zoster infection
Tuberculosis
Neurological disease
Glossodynia
Dyskinesia
Paralysis
Oropharyngeal dysphagia
Cyst
Anterior median lingual cyst
Bronchogenic cyst
Epidermoid and dermoid cyst
Gastric mucosal cyst
Parasitic cyst
Thyroglossal duct cyst
Benign tumor
Fibroma
Glomus tumor
Granular cell tumor
Leiomyoma
Rhabdomyoma
Plasmacytoma
Pre-malignant lesion and conditions
Leukoplakia
Lichen planus
Oral submucus fibrosis
Malignant tumor
Squamous cell carcinoma
Malignant lymphoma
Malignant melanoma
Metastatic tumor
Sarcoma
Miscellaneous
Pigmentation of tongue
Phlebectasia
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Classification
Congenital
Acquired
Hypertrophicin it, muscles of the tongue are hypertrophic. It usually occurs in mentally retarded patients.
Inflammatoryit may involve the tongue partially or
completely. It is due to various causes like syphilitic,
Ludwigs angina, etc.
Neoplasticit can be based on benign and malignant
tumors.
Relative macroglossiait is a condition, in which a normal
sized tongue appears abnormally large, if it is particularly enclosed within a small oral cavity.
Apparent macroglossiait is a condition where the tongue
appears large due to poor muscular control of the tongue,
although there is no increase in the bulk of tongue tissue.
Etiology
Congenitalit includes hemangioma, lymphangioma
and lingual thyroid. Other congenital disorders which
can cause macroglossia are cretinism, Down syndrome,
neurofibromatosis and multiple endocrine neoplasia
type 2B
Inflammatoryinflammatory causes include tuberculosis, actinomycosis, dental infection, syphilitic
gumma, Riga disease, ranula and sublingual calculus.
Traumatictraumatic causes include dental irritation,
hematoma and postoperative edema.
Neoplasticthe neoplastic causes can be divided into
malignant and benign lesions; with the malignant
lesions including carcinoma and sarcoma. The benign
lesions include granular cell tumor, neurofibroma,
leiomyoma and lipoma.
Metabolicmetabolic causes are myxedema, amyloidosis,
lipoid proteinosis, chronic steroid therapy and
acromegaly.
Muscular hypertrophyover development of musculature, this may or may not be associated with generalized muscular hypertrophy or hemihypertrophy.
Clinical Features
Agemacroglossia is most prominent in infants, but
tongue size may remain above normal in childhood and
adolescence. As hyoid descends with age, macroglossia
may improve.
Symptomspatient complaint of noisy breathing, drooling
of saliva and difficulty in eating. Patient may get recurrent
upper respiratory tract infection as tongue is usually
protruded (Fig. 22-1) and mucosal drying occurs. The
enlargement is generalized and may cause variety of
difficulties with speech, feeding and airway problems.
SignsIt may produce displacement of teeth and
malocclusion, due to the strength of muscles involved
and pressure exerted by the tongue on teeth.
Crenated lateral bordercrenation or scalloping of the
lateral borders of the tongue; the tips of scalloping fit
into the interproximal spaces between the teeth.
Syndrome associatedit is associated with syndromes like
Beckwiths hypoglycemic syndrome which includes
neonatal hypoglycemia, mild microcephaly, umbilical
hernia, and fetal visceromegaly and postnatal somatic
gigantism.
Diagnosis
Clinical diagnosislarge size of the tongue can be
clinically diagnosed.
Management
Orofacial therapyit uses a palatal device to stimulate
muscular tone and proper tongue position.
Surgical managementmajority of the cases of
macroglossia are treated surgically. Indications for
surgery include airway obstruction, speech difficulties,
dysphagia and cosmetics. The procedure of choice is
partial glossectomy. Surgical goal is to reduce the tongue
size and thus improve the condition.
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Ankyloglossia
Types
Completefusion of tongue and the floor of mouth.
Partialshort lingual frenum.
Clinical Features
Symptoms
Restricted tongue movementit may limit the movement
of the tongue.
Feeding problemsIn extreme cases of ankyloglossia,
nursing and feeding problems can occur. Poor sucking
and inability to chew some food also occurs.
Speech defectit was felt that tongue-tie was
associated with speech abnormalities, especially
lisping and inability to pronounce certain sounds
and words viz t, d, n, l, as, ta, te, time etc.
Tongue bitingin some cases, recurrent tongue biting
is also reported.
Signs
V shaped notchwhen there is an attempt to stick the
tongue out, there may be a V shaped notch at the tip
(Fig. 22-2). Physical examination will easily
demonstrate the short or anteriorly placed lingual
frenulum (Fig. 22-3).
Anterior open bitepatients have midline mandibular
diastema and inability to clean the teeth and lick the
lips with tongue.
Periodontal problemsdue to high frenum attachment
some patient may face periodontal problems.
Syndromes associatedankyloglossum superius
syndrome, Rainbow syndrome, Frasers syndrome and
orofacial digital syndrome.
Diagnosis
Clinical diagnosisit can be easily diagnosed clinically.
Management
Counsellingphysician education, parental education
and reassurance should be given to the patient.
Surgeryindications for surgery, i.e. frenectomy are as
follows:
If complete fusion of tongue is present then it requires
surgery.
When nursing and feeding become a problem, surgery
is indicated.
Children between 2-4 years, with poor development
of speech and anxious parents desire for the
necessary treatment.
In cases where tongue-tie has recurred after snipping.
Complications of surgery
Injudicious cutting of the frenum in a newborn can
cause hemorrhage and the tongue may become too
mobile and may be swallowed, causing asphyxia.
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Pathogenesis
Lingual Varices
Cleft Tongue
Clinical Features
Incidencecompletely bifid or cleft tongue is rare. It is
due to lack of merging of lateral swellings of the organ.
Appearancepartially cleft tongue is manifested as deep
grooves in the midline of dorsal surface (Fig. 22-4).
Symptomsfood debris and microorganisms may collect
in the base of cleft and cause irritation.
Syndromes associatedseen with orofacial-digital
syndrome, with thick fibrous bands in lower anterior
mucobuccal fold, which eliminate the sulcus and is
associated with clefting of hypoplastic mandibular
alveolar process.
Pathogenesis
Diagnosis
Clinical diagnosiscleft can be seen clinically.
Management
Regular cleaning of the tongue should be carried out.
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Clinical Features
Age and sex distributionfemales are more affected as
compared to males in a ratio of 7:1. The reason for
occurrence in female is due to hormonal influence. The
age of onset ranges from birth to the 6th decade, with a
peak in the 2nd decade.
Sitebase of the tongue is the most common site of
undescended thyroid gland. It is present in midline.
Symptomsthere may be complaints of dysphagia
(difficulty in eating), dysphonia (difficulty in speaking),
dyspnea (difficulty in breathing), hemorrhage with pain
or feeling of tightness or fullness in the throat. In some
cases pain may be referred to ear.
Appearanceit is manifested as a nodular mass in or
near the base of the tongue (Fig. 22-6), in general vicinity
of the foramen caecum. It is often but not always, in the
midline.
Signsthe mucosa covering the swelling is thin, smooth
and with prominent vascular marking.
Diagnosis
Clinical diagnosismass seen in vicinity of foramina will
give clue to the diagnosis.
Radiological diagnosisScintigraphy with iodine will
locate the lingual thyroid nodules.
Management
Suppressive thyroxinsuppressive thyroxin should be
given for 6 months. This will reduce the size of swelling.
Surgical excisionwhen it causes difficulty to the patient
in spite of thyroxin therapy, excision or ablation with
radioiodine is indicated.
Surgical excision with reimplantationwhen thyroid gland
is absent in the neck, surgical excision with reimplantation can be carried out.
Laserit can be used as an alternative to scalpel surgery.
Tongue Thrusting
Positioning of tongue between the anterior teeth during
swallowing, speaking or at rest. It is an infantile swallowing pattern. It may be associated with macroglossia. In
these cases, anterior open bite is present.
Radiological Features
ScintigraphyScintigraphy with 131I and 99Tc can be
useful to locate normal and ectopic thyroid tissue.
Thyroid radioactive uptake can be determined after
administration of 131I.
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Clinical Features
Age and sexit usually occurs in young persons with no
sex predilection.
Siteit is seen above the thyroid, in vicinity of the hyoid
bone, in midline of the neck.
Symptomsin some cases, dysphagia may occur.
Signsit is a firm cystic mass in which formation of
fistula may take place. It is compressible.
Aspirationit yields yellow fluid on aspiration.
Diagnosis
Clinical diagnosisdysphagia with firm cystic mass in
midline of neck will give clue to the diagnosis.
Laboratory diagnosisthe cyst is lined by columnar,
respiratory or stratified squamous epithelium. Follicle
of thyroid is frequently located in juxtaposition to the
cyst lining.
Management
Types
Foliaceus
Cribriform
Plicated.
Etiology
Reactive Lymphoid Aggregate
The lingual tonsils, one of the largest oral lymphoid
aggregates, are located on the posterior portion of the
tongue on the dorsolateral aspect. They are reported to
occur on the gingiva, buccal mucosa, tongue and floor of
mouth.
Clinical Features
Lingual Cyst
It is a rare lesion, located anteriorly in the midline of the
tongue (Fig. 22-7). It is movable and compressible. It arises
as a result of epithelial entrapment during fissural closure
of the lateral lingual processes. Surgical excision is
recommended.
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Management
Maintenance of tongue hygieneyou have to clean the
debris with brush.
Pathogenesis
Failure of tuberculum imparit is a congenital abnormality
of the tongue which is due to failure of tuberculum impar
to retract or withdraw before fusion of lateral halves of
the tongue, so that a structure devoid of papilla is
interposed between it.
Etiology
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Management
Etiology
Hypersensitive patientin patients with geographic
tongue, there is a high frequency of history of asthma,
eczema and hay fever.
Other factorsgeographic tongue can be seen in
immunological reaction, emotional stress, hereditary
factors, infections, and nutritional deficiencies.
Classification
Type Ilesion confined to the tongue, with both active
and remission phases. No other lesion elsewhere in the
oral cavity.
Type II as type one with similar lesions elsewhere in
the mouth.
Type IIIlesions on the tongue are not typical and may
be accompanied by lesions elsewhere in the mouth. It
consists of two forms:
Fixed forma few areas of the tongue are affected, but
no movement is observed. They may disappear only
to recur at the same area.
Abortive formsthis form starts as yellow-white
patches, but disappear before acquiring the typical
appearance of geographic tongue.
Type IVno tongue lesions are present, but geographic
areas present elsewhere in the mouth.
Fig. 22-12: Median rhomboid glossitis
(Courtesy Dr Amit Parate).
Diagnosis
Clinical diagnosisrhomboidal shaped lesion seen in
posterior part of tongue will diagnose the lesion.
Laboratory diagnosisbiopsy shows loss of papillae with
varying degrees of hyperparakeratosis. There is
proliferation of spinous layer with elongation of rete
pegs, which may branch and anastomose.
Clinical Features
Age and sexit is common in young and middle aged
adults, with an age range of 5 to 84 years with a
predilection for females.
Sitelesion confines to dorsal surface (Fig. 22-13) and
lateral border of the tongue, but may occur on the ventral
surface.
Sizeit is extremely variable in size and diameter and it
may be single or multiple (Fig. 22-14).
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Fig. 22-13: Geographic tongue seen on dorsal surface of tongue
(Courtesy Dr Parate).
Diagnosis
Clinical diagnosismultiple areas of desquamation on
dorsal surface of tongue.
Laboratory diagnosisbiopsy shows loss of filiform
papillae with hyperparakeratosis and acanthosis. There
is also presence of Monros abscess, near the surface.
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Management
For control of burningtopical local anesthetic agents
like lidocaine, dyclonine hydrochloride or diphenhydramine can be given.
Otherbland diet, elimination of irritants and psychological reassurance is useful.
Topical therapytopical corticosteroids and topical
application of salicylic acid and tretinoin (retinoic acid
or Vit A) for external use.
Zinc supplementrecent study suggests that zinc
supplement is effective in symptomatic geographic
tongue.
Hairy Tongue
It is also called as lingua villosa, lingua nigra, black hairy
tongue. It designates an overgrowth of the filiform papillae
on the dorsum of the tongue, giving the tongue a superficial
resemblance as that of hairiness. There is marked
accumulation of keratin on the filiform papillae of the dorsal
tongue. There may be delayed shedding of the horny layer
of the filiform papillae or there may be an increase in the
rate of formation of keratin.
Etiology
Fungal and bacterial overgrowthovergrowth of fungal
organisms like Candida albicans and certain bacterial
organism can lead to hairy tongue.
Use of certain drugsoral use of certain drugs (sodium
perborate, sodium peroxide and antibiotics like penicillin
and Aureomycin).
Radiationextensive X-ray radiation around head and
neck for the treatment of tumors.
Poor oral hygienePatients who are unable to maintain
oral hygiene can lead to accumulation of keratin in the
tongue.
After surgeryit also occurs in patient with intermaxillary fixation and with disturbed orophysiology,
due to recent surgery in the oral cavity.
Lowered pHa lowered pH of oral secretion, which
blocks the normal desquamation of epithelial cells
covering the filiform papillae.
Clinical Features
Sitethe lesion involves the dorsum, particularly the
middle and posterior one-third.
Symptomspapillae which are of considerable length
will occasionally brush the palate and may produce
gagging or bad taste.
Signsthere is hypertrophy of filiform papillae. The
papillae may reach a length of 2 cm. Papillae can be
elevated by using dental instrument.
Appearancethe elongated papillae have an appearance
of hair. The hyperplastic papillae then become
pigmented by the colonization of chromogenic bacteria,
which can impart a variety of colors ranging from green
to brown to black to yellow. This gives it a coated or
hairy appearance and retains debris and pigments from
substances such as food, tobacco, smoke and candy.
Color can be imparted by tobacco, certain food and
medicines.
Earthy or encrusted tongueextreme degree of coating
occurring in dehydrated, debilitated and terminally ill
patient can lead to a very thick, leathery coating on the
tongue which is referred to as earthy or encrusted
tongue. It is heavily coated with bacteria and fungi and
forms a thickened malted layer.
Diagnosis
Clinical diagnosishyperplastic papillae with green to
brown color will give clue to the diagnosis.
Laboratory diagnosisthere is elongated papillae with
mild hyperkeratosis and inflammatory cells.
Management
Maintenance of tongue hygienebrushing of the tongue
twice daily for 2 minutes, making gentle movements over
the involved area towards the tip of the tongue.
Elimination of predisposing factorsall the predisposing
factors which are responsible for hairy tongue should
be eliminated.
Topical keratolytic applicationthe topical application of
keratolytic agent such as podophyllum in acetone and
alcohol suspension seems to be quite effective. It will
produce desquamation of hyperkeratotic papillae.
Crenated Tongue
The term is applied to a condition in which indentations of
teeth are observed at the lateral margins of the tongue. It
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Foliate Papillitis
Clinical Features
Age and sex distributionit is more common in women,
usually in the second half of life.
Symptomssymptoms may be partly due to upper
respiratory tract infection and partly due to irritation.
Soreness, tenderness, pain and occasionally, a sour or
metallic taste.
Locationthe condition may be bilateral with a duration
varying from few weeks to many years.
Signsfoliate papillae frequently become inflamed and
enlarged, so that it is clinically evident (Fig. 22-17).
Diagnosis
Clinical diagnosisinflamed and enlarged foliate
papillae with pain will aid in diagnosis.
Management
Elimination of irritating factorsit consists of elimination
of irritating factors such as sharp edges of teeth and
dentures.
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Fig. 22-19: Chronic atrophic candidiasis causing
depapillation of tongue.
Systemic Disease
Iron deficiency anemiainhibition of epithelial reproduction, secondary candidiasis and chronic xerostomia.
There are atrophic changes on the dorsum of the tongue
(Fig. 22-20). It first appears at the tip and lateral borders
with loss of filiform papilla. In extreme cases, the entire
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Neurological Disorders
Glossodynia
Terminology
Glossalgiathe term glossalgia is used to describe painful
tongue.
Glossopyrosisthe term glossopyrosis is used to describe
burning sensation in the tongue.
Lingual paresthesia or dysesthesiawhen just discomfort
is felt, it is called as lingual paresthesia or dysesthesia.
Stomatodyniawhen the entire oral cavity is involved,
the terms stomatodynia, stomatopyrosis and oral
dysesthesia are used.
Etiology
Local factors
Habitsoral habits such as excessive use of tobacco,
excessive drinking, frequent uncontrolled movements
of the tongue or bruxism.
Dental causeslocal dental causes such as dentures,
irritating clasps or a recently fixed bridge.
Referred painreferred pain from infected teeth or
tonsils, Moellers glossitis and periodontal disease.
Sensitizersit may be caused by peppermint oil in
sweets (since it is a volatile oil) and primary and
secondary sensitizers.
Local tongue disordersgeographic tongue, plicated
tongue, lichen planus and median rhomboidal
glossitis.
Electrogalvanic dischargeelectrogalvanic discharge
due to dissimilar metallic restoration.
Atherosclerotic changesatherosclerotic changes in
the lingual arteries have also been a cause for
glossodynia.
Allergyallergy to denture base material, metallic
restoration and particular food, medication, mouthwashes and dentifrices.
Systemic factorssystemic diseases like multiple myeloma,
amyloidosis, muscular tension, hypoestrogenism,
pernicious anemia, pellagra, diabetes, vitamin B
deficiency can cause glossodynia. Gastric disturbances
such as hyperacidity or hypoacidity, angioneurotic
edema, mercurialism. Prolonged antibiotic therapy,
psychological problems, xerostomia, and hypothyroidism may be responsible for glossodynia.
Neurological factorstrigeminal neuralgia, damage of
lingual nerve after surgery, glossopharyngeal neuralgia.
Cerebrosclerosis and subclinical cerebrovascular
accidents can possibly cause pain in the tongue.
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Clinical Features
Nature of painthe description varies from patient to
patient, some refer it as pain and others as burning,
tingling or numbness in the tongue. It may occur as an
isolated features or it may be one from group of oral
symptoms.
Changes in tongueit may occur with clinically observable changes in tongue or without observable changes.
Management
Removal of local causethis is best management treatment
for glossodynia.
Muscle relaxanttreatment of muscular problems by
correction of malocclusion or by muscle relaxants such
as diazepam.
Management of systemic problemstreatment of the
systemic cause should be done.
Surgicalsurgical exploration of glossodynia with
neuropathy.
Topical treatmentuse of topical analgesics 0.5% of
Diphenhydramine alone or mixed with 0.5% of
dyclonine or lidocaine.
Dyskinesia
It is defined as an impairment of voluntary motion, causing
movements that are incomplete or only partial.
Paralysis
It is also called as glossoplegia. It usually occurs due to
unilateral injury of the nucleus in the medulla or the
peripheral hypoglossal nerve. There is paralysis and
atrophy of the muscles of one-half of the tongue.
Causes
It may be caused by acute anterior poliomyelitis, infectious
polyneuritis, neurofibromatosis, syringobulbia, irradiation
of head and neck and compression by a tortuous internal
carotid artery in the neck.
Clinical Features
Signsthe affected tongue deviates towards the
paralyzed side when protruded. The movement towards
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Causes
Local factorslocal factors like oral candidiasis, oral
galvanism, periodontitis, oral lichen planus, and
xerostomia.
Systemic factorssystemic factors like vitamin deficiency,
nutritional deficiency, food allergy, Sjgren syndrome,
liver dysfunction, Crohns disease, depression, alcoholism, temporal arteritis, migraine, upper respiratory
tract infection, chronic gastritis and radiation therapy
to neck and head may cause dysgeusia.
Pharmacological agentspharmacological agents like
anticoagulant, antihistamine, antihypertensive,
antimicrobial, antipsychotic drugs can cause dysgeusia.
Clinical Features
Onsetonset of dysgeusia is sudden and is distinguished promptly by the patient.
Symptomspatient may told altered taste as metallic,
foul, rancid.
Stimulusstimulus require for altered taste like certain
food and liquids.
Management
Removal of underlying causeif underlying cause is
removed, taste function will return to normal.
Oropharyngeal Dysphagia
It is caused by weakness of the tongue. Symptoms are
aspiration while swallowing, regurgitation of food into
nose, pharyngeal pain on swallowing and inability of the
tongue to move the bolus of food into the pharynx. Dilatation
or atony of the pyriform sinuses and pharynx with retention
of contrast media in the valleculae is the characteristic
radiographic findings.
Clinical Features
Siteit is confined to the anterior 2/3rd of the tongue
(Fig. 22-23). It gradually spreads on the dorsum.
Appearancethe surface may become fissure and
cracked, due to contraction of the underlying scarred
tissue by chronic inflammation.
Signsthe affected area of the tongue shows milky-white
patches with cracks and fissures (Fig. 22-22). In course
of time atrophy tends to succeed hypertrophy, the
thickened papillae disappear and the white membrane
is worn off. The surface becomes smooth and red.
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Malignant Tumor
Squamous Cell Carcinoma
It is the most common oral carcinoma with 60% cases
arising from the anterior 2/3rd of the tongue and remainder
from the base. Carcinoma of tongue is caused by physical
trauma, alcohol, tobacco smoke, candidiasis, syphilis,
sepsis, chronic dental trauma and chronic superficial
glossitis.
Clinical Features
Symptoms
Painless mass or ulcerthe most common presenting
signs of carcinoma of tongue is a painless mass or
ulcer (Fig. 22-25), although in most patients the
lesion ultimately becomes painful, especially when it
becomes secondarily infected.
Salivationexcessive salivation gradually appears
along with the growth. In late stages, saliva becomes
blood stained.
Foetor orisas the patient is unable to swallow saliva,
offensive smell in the mouth occurs due to bacterial
stomatitis.
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Fig. 22-25: Ulceration seen on lateral
border of tongue in carcinoma.
B
Figs 22-27A and B: Induration seen in malignancy of tongue
(Courtesy Dr Chole).
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Management
Surgeryif the growth is less than 1 cm in diameter, it
should be removed along with a wide margin of mucosa,
not less than 1 cm. If it is localized to anterior 2/3rd of
the tongue, partial glossectomy or subtotal glossectomy
should be carried out. When the growth reaches within
2 cm of jaw, hemimandibulectomy may be required with
excision of the growth.
Radiotherapywhen the growth is more than 1 cm in
diameter in anterior 2/3rd, the preliminary treatment is
radiotherapy in the form of interstitial radiotherapy.
Prognosisthe 5 years survival rate of cancer tongue is
not more than 25%.
Other malignant tumors of the tongue are rare and are discussed
in detail in Chapter 16: Malignant Tumor of Jaw.
Pigmentation of Tongue
The tongue may exhibit various patterns of racial melanin
pigmentation (Figs 22-28A and B).
Endogenous pigmentation is rarely identifiable on the
dorsum of tongue because of the thickness of the epithelium,
but jaundice may be apparent under the thinner ventral
mucosa.
Exogenous pigmentation of filiform papillae of the
normal and coated or hairy tongue is very common and
result from microbial growth, metabolic products, food
debris and dyes from candy, beverages and mouth rinses.
Pigmentation of the tongue has been described by a
commonly used anti-chemotherapeutic agents doxorubicin
B
Figs 22-28A and B: Pigmentation seen in tongue
due to melanin deposit.
Suggested Reading
1. Aguirre A, Piedra M, Ruiz R. Ectopic thyroid tissue in the submandibular region. Oral Surg, Oral Med, Oral Pathol, 1991; 71:73-6.
2. Alexander RW, James RB. Melkersson-Rosenthal syndrome: a
review of literature and report of case. J Oral Surg 1972;30:599.
3. Avery JK. Oral development and histology (1st edn), BC Decker
Inc, Philadelphia, 1988.
4. Banoczy J, Szabo L, Csiba A. Migratory glossitis. Oral Surg
1975;39:113.
5. Baughman RA. Llingual thyroid and lingual thyroglossal tract
remnants: A clinical and histopathological study with review of
the literature. Oral Surg, Oral Med, Oral Pathol 1972;34:781-99.
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Diseases of Lip
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Diseases of Lip
Anatomy
Developmental
Congenital lip pits
Commissural lip pits
Double lip
Cleft lip and cleft palate
Cheilitis
Glandular cheilitis
Granulomatous cheilitis
Angular cheilitis
Contact cheilitis
Eczematous cheilitis
Actinic cheilitis
Exfoliative cheilitis
Plasma cell cheilitis
Cheilitis due to drugs
Carcinoma of lip
Miscellaneous
Chapping of lips
Actinic elastosis
Lip ulcers due to caliber persistent artery
Development of Lip
In the sixth week of intrauterine life, two medial nasal
processes merge in midline. This will form intermaxillary
segment which will give rise to center of upper lip.
In adult, center of upper lip forms philtrum. Philtrum is
bound laterally by two vertical ridges under the nostril.
Lateral part of upper lip fissure presents in maxillary
process. This may lead to cleft formation if it is not covered
by epithelium and fused. Upper lip is thus formed from onethird medial nasal process and two-third maxillary process.
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Etiopathogenesis
Hereditaryit is inherited as an autosomal dominant
trait.
Notching of lipthere is notching of lips at an early stage
of development with fixation of tissues at the base of the
notch.
Incomplete unionit may occur due to failure of complete
union of embryonic sulci of the lip, resulting in persistent
lateral sulci on the embryonic mandibular arch.
Clinical Features
Sex predilectionit is more commonly seen in females.
Siteit is common on vermilion border of either side of
midline. It is most commonly seen on lower lip. Lip pits
or fistula is unilateral or bilateral depression.
Sizeit may be upto 3-4 mm in diameter and may extend
as deep as 2 cm.
Appearancelips, some times appear swollen, accentuating the appearance of the pit.
Palpationon palpation, sparse mucus secretion may
be visible from the base of the lip-pit which occurs due
to involvement of underlying minor salivary glands.
Syndromes associatedcongenital lip pits may occur in
association with Van der Woudes syndrome (cleft lip, cleft
palate and congenital lip pits). Another syndrome is
associated with it is popliteal pterygium syndrome which
also includes Popliteal webbing (pterygia), cleft lip/cleft
palate, genital abnormalities and congenital bands
connecting the upper and lower jaws (syngnathia).
Diagnosis
Clinical diagnosisunilateral or bilateral depression on
vermilion border of lip will diagnose these conditions.
Management
Surgical excisionit is done for cosmetic purpose.
Commissural Pits
Commissural lip pits are mucosal invagination occurring
at the vermilion border of lip.
Pathogenesis
They occur due to failure of normal fusion of embryonal
maxillary and mandibular processes. It is transmitted as
autosomal dominant transmission.
Clinical Features
Sex distributionit is more common amongst males and
black people are affected more than white people.
Siteif it is unilateral, it occurs on the right side of the
lip.
Appearancecommissural pit appears as a unilateral or
bilateral pit at the corner of the mouth on the vermilion
surface.
Sizesize ranges from a shallow dimple to a tract
measuring 4 mm in length and tissue slightly raised
above the opening.
Palpationin squeezing of the lip pit, small amount of
saliva can come out.
Differential Diagnosis
Congenital lip pitit may be associated with facial or
palatal cleft.
Management
Surgical excisionit is indicated only in severe condition,
where salivary secretion excessive and secondary
infection can occur.
Double Lip
It is an anomaly characterized by a fold of excess tissue on
the inner mucosal surface of the lip. It may be congenital or
acquired because of trauma to the lip.
Pathogenesis
It occurs in 2nd or 3rd week of gestation due to persistent of
the sulcus between the pars glabrosa and pars villosa of
the lip.
Clinical Features
Siteit usually occurs on inner aspect of upper lip.
Cupid bow appearancewhen upper lip is tensed, double
lip resembles cupid bow.
Syndromes associatedit is associated with Aschers
syndrome which consists of double lip, blepharochalasis (it is drooping of the tissue between eyebrow and
edge of the upper eyelid so that it hangs loosely over the
margin of the lid) and non-toxic thyroid enlargement.
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Diseases of Lip
Diagnosis
Clinical diagnosiscupid bow appearance is typical.
Management
Surgical excision.
Definition
Cleft lipit is a birth defect that results in a unilateral or
bilateral opening in the upper lip between the mouth and
the nose. It is also called as harelip. It is wedge shaped
defect resulting from failure of two parts of the lip to fuse
into a single structure.
Cleft palatecleft palate is a birth defect characterized by
an opening in the roof of the mouth caused by a lack of
tissue development.
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Etiology
Development of Cleft
In general, patients with clefts have a deficiency of tissue
and not merely a displacement of normal tissue.
Unilateral cleft lipA cleft lip occurs when an epithelial
bridge fails, due to lack of mesodermal delivery and its
proliferation from the maxillary and nasal processes. It
results from failure of maxillary process on one side to
meet and fuse with medial nasal process. This will lead
into the division of lip into medial and lateral part. It
again occurs due to absence or deficiency of mesodermal
masses or their failure to penetrate the ectodermal
grooves lead to breakdown of the ectoderm, causing cleft
formation. In unilateral cleft lip, the floor of the nose
communicates freely with the oral cavity, maxilla on the
cleft side is hypoplastic, columella is displaced to the
normal side and the nasal ala on the cleft side is laterally,
posteriorly and inferiorly displaced.
Bilateral cleft lipin this, medial mass interposed
between two maxillary processes grows down from
lateral areas form above the maxillary process. In bilateral
cleft lip, the central portion of the alveolar arch is rotated
anteriorly and superiorly.
Median cleft lipit results from partial and complete
failure of the medial nasal process to merge. The cleft of
lip occurs earlier and inhibits tongue migration, which
may then prevent horizontal alignment and fusion of
the palatal shelves.
Median cleft of mandibular lipit occurs due to failure of
mesenchymal masses of mandibular process to merge
together at 5 weeks of intrauterine life.
Classification
First Classification
Unilateral incomplete.
Unilateral complete.
Bilateral incomplete.
Bilateral complete.
Second by Veaus
Cleft lip
Class IA unilateral notching of vermilion border
and it is not extending into the lip.
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Fig. 23-1: Unilateral cleft lip also involving the cleft palate.
Clinical Features
General
Sexit is more common in males as compared to females.
But incidence of isolated cleft palate is seen more in
females.
Siteit is more frequently seen on the left side than on
the right side. Left side is involved in 70% of the cases.
Cleft of mandibular lip or jaws are rare.
Appearancea typical patient with cleft palate, cleft lip
and ridge exhibits a large defect with a direct opening in
the nasal cavity (Fig. 23-1).
Teethdisturbances in the dental structures are seen in
this region so that teeth may be missing, deformed,
displaced or divided, thus producing supernumerary
teeth.
Cleft lip
There is nasal distortion as lip and nasal tissue pulls
towards the attached side.
Hare lipthis term is used to apply for only median cleft
lip. Hare lip is derived from the rabbit who normally
have cleft in the middle of their lip.
B
Figs 23-2A and B: Unilateral cleft lip present on the
left side of upper lip.
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Fig. 23-4: Incomplete cleft lip present on right side which is not
extending upto to nostril.
B
Figs 23-3A and B: Bilateral cleft lip seen in child patient.
Fig. 23-6: Complete cleft lip which extends towards the palate.
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Fig. 23-7: Cleft palate extending all the way towards the palate.
Radiographic Features
Fig. 23-8: Cleft of palate showing involvement of hard and soft palate.
Diagnosis
Clinical diagnosiscleft can be seen clinically on lip and
palate.
Radiological diagnosiscleft palate involving alveolus
is seen clearly on radiography.
Management
The complete rehabilitation of the condition requires a
multi-disciplinary approach.
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Diseases of Lip
Cheiloplastyit is surgical closure of the lip. A general
rule of tens is used in determining optimal timing of
lip closure, i.e. 10 weeks of age, 10 pounds of body weight
and 10 gm of Hb. At the time of lip closure, when an
infant is under general anesthesia, an impression is
made for the new obturator.
Obturatorbetween 3rd and 9th months of age, an
obturator is used to provide cross-arch stability, support
and to prevent collapse of maxillary arch.
Palatoplastyit is performed to close an opening in the
palate. Surgeons may close the palate in one surgery,
when the child is about one year of age or the palate may
be closed in two stages, the soft palate is closed first
followed by the hard palate.
Bone graftingsometimes, closure of palatal cleft may
be done by bone grafting.
Orthodontic therapyorthodontic therapy is done to
correct malocclusion.
Cleft rhinoplastyto improve nasal function and correct
the distortion.
Speech therapyspeech therapy is given to improve
pronounciation of the words.
Psychotherapypsychological management is necessary.
Feeding plateto overcome initial feeding problems,
feeding plate is used which acts as an obturator to
prevent nasal reflux.
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Deep suppurative type (cheilitis glandularis apostematosa, myxadenitis labialis)deep seated infection
with abscess and fistula tract that eventually forms a
scar.
Clinical Features
Ageit is more common in adults but sometimes, it can
also occur in children.
Sitelower lip is involved more often than the upper
lip.
Symptomsenlargement of labial salivary glands occurs
which can be nodular.
Signsorifices of secretory ducts are inflamed and
dilated appearing as small red macules over the mucosa.
Palpationviscid mucous secretion may seep from these
openings of everted hypertrophic lips after pressure
given on the lip.
Volkmanns cheilitisit is more severe suppurative form
of glandular cheilitis. The lip is considerably and permanently enlarged and is subjected to episodes of pain,
tenderness and increased enlargement. The surface is
covered by crust (Fig. 23-10) and scales beneath which
the salivary duct orifice may be discovered.
Cheilitis
It is inflammation of lip. Various types of cheilitis are
described below.
Glandular Cheilitis
It is also called as cheilitis glandularis. It is an uncommon
condition in which lower lip becomes enlarged, firm and
finally everted.
Fig. 23-10: Severe form of glandular cheilitis showing crust formation
Etiology
Sun exposureglandular cheilitis can occur due to
chronic exposure to sun.
Hereditaryfamilial occurrence, suggesting a hereditary
pattern is also present in glandular cheilitis.
Salivary gland inflammationinflammation of enlarged
heterotopic salivary glands can also be causative factors.
Othersdust, tobacco use and emotional disturbances
also been reported in this patients.
Types (Historical)
Simplemultiple, painless, pinhead sized lesions with
central depression and dilated canals are present.
Superficial suppurative type (Baelzs disease)it is
characterized by painless swelling, induration, crusting
and superficial ulceration of lip.
Diagnosis
Clinical diagnosiseverted hypertrophic lip with
secretion after pressure on lip.
Management
Vermilionectomy or lip shavedue to high incidence of
associated malignancy, a vermilionectomy or surgical
stripping of lips has been recommended. It will give
satisfactory cosmetic results.
Surgical excisionif the lips are grossly enlarged,
excision of an elongated ellipse of tissue may be required.
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Granulomatous Cheilitis or
Orofacial Granulomatosis
It is also called as Mieschers syndrome or cheilitis
granulomatosa. This condition is described in 1945 by
Miescher. It is a condition of unknown etiology that is not
related to chelitis glandularis except by the similarity in
the clinical appearance of the two diseases.
Etiology
Local causes
Chronic oral/dental infection
Embedded foreign material
Allergy to cosmetics, foods, oral hygiene products and
dental restorative materials.
Systemic causes
Chronic granulomatous disease
Crohns disease
Sarcoidosis
Tuberculosis
Diagnosis
Clinical diagnosissoft swelling of lip with fever,
headache and vesicle can be seen.
Differential Diagnosis
Clinical Features
Age and sexit is seen in adults as well as in children
and there is female predilection.
Symptoms
There is diffuse swelling of the lips, especially the
lower lip (Fig. 23-11).
In some cases, an attack is accompanied by fever and
mild constitutional symptoms including headache
and even visual disturbances.
Enlarged lip can create cosmetic problems, difficulty
during eating, drinking or speaking.
Management
Corticosteroid injectionrepeated injection of triamcinolone into the lips every few weeks may be effective.
Before giving steroids, topical anesthetics gels was
applied over the lesion and then 0.1% of triamcinolone
acetonide injection is given. This injection should be
given weekly for 7 to 10 weeks.
Cheiloplastysurgical stripping of lip can be done.
Angular Cheilitis
It is also called as Perleche, Angular cheilosis Cheilocandidiasis.
Causes
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Clinical Features
Ageit occurs in young children as well as in adults.
Symptomsit is characterized by feeling of dryness and
a burning sensation at the corners of the mouth.
Appearanceit is usually a roughly triangular area of
erythema (Figs 23-12A and B) and edema at one or more,
commonly both the angles of mouth.
Signsepithelium at the commissures appears wrinkled
and somewhat macerated (Fig. 23-13). In time, wrinkling
becomes more pronounced to form one or more deep
fissures or cracks which appear ulcerated but do not
tend to bleed, although a superficial exudative crust may
form.
Diagnosis
Clinical diagnosistriangular area or erythema with
wrinkled macerated mucosa at angle of mouth.
Management
Removal of the causeunderlying primary cause should
be identified and treated.
Nutritional supplementa course of vitamin B and iron
supplements are useful in these cases.
Fusidic acid ointmentit is used in staphylococcal
infection. The lesions should be swabbed first and then
fusidic acid ointment or cream should be applied at least
four times a day.
Miconazolemiconazole may be preferred, if angular
cheilitis is due to candidiasis (cream applied locally
together with an oral gel).
Gentian violet applicationin some cases, it is useful.
Eczematous Cheilitis
B
Figs 23-12A and B: Triangular area of erythema seen at the angle
of mouth in angular cheilitis.
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Contact Cheilitis
Definition
Contact cheilitis is an inflammatory reaction of the lips
provoked by the irritants or sensitizing action of chemical
agents in direct contact with them.
Causes
Actinic Cheilitis
It is also called as Actinic cheilosis. Some other terms which
use are Farmers lips or Sailors lip as these people are more
exposing to sunlight.
Definition
It is a pre-malignant squamous cell lesion resulting from
long-term exposure to solar radiation and may be found at
the vermilion border of lip as well as other sun exposed
surfaces.
Etiology
Chronic sun exposureit is the main cause, so it usually
occurs in hot, dry regions, in outdoor workers and in
fair skinned people.
Clinical Features
Clinical Features
Diagnosis
If acute eczematous changes are obviously present, the
diagnosis of contact cheilitis presents no difficulty. If an
allergic reaction is suspected, patch test can be carried
out.
Management
Topical steroids will give symptomatic relief but the
offending substance must be traced and avoided. Most
commonly used topical steroids use is 1% triamcinolone
acetonide.
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Diagnosis
Clinical diagnosisredness, edema with history of
chronic sun exposure will give clue to diagnosis.
Management
Exfoliative Cheilitis
It is also called as Factitious cheilitis. It is a chronic superficial
inflammatory disorder of the vermilion border of lips characterized by persistent scaling and flaking (Fig. 23-17).
Fig. 23-16: Actinic cheilitis showing ulceration of
upper lip in female patient.
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Causes
Chronic injurythese cases may occur due to repeated
lip sucking, chewing or other manipulation of the lips.
Personality disordersemotional disturbance, psychological difficulties and stress can also lead to exfoliative
cheilitis.
Clinical Features
Management
It responds to topical application of powerful steroids or to
intradermal injection of triamcinolone.
Diagnosis
Clinical diagnosisScaling, crusting with perioral skin
erythema will aid to diagnosis.
Management
Reassurance and psychotherapythis is done to overcome
personality disorders. After this, many patients get relief.
Topical steroidshydrocortisone cream is useful in
resolving some chronic cases in some patients.
Combinationhydrocortisone can be combined with
iodoquinol (antibacterial and antimycotic) cream can
be used in chronic cases of exfoliative cheilitis.
Others therapyit includes topical silver nitrate, salicylic
acid, antibacterial and antifungal formulation.
Clinical Features
Siteit can affect penis, vulva, lips, buccal mucosa,
palate, gingiva, tongue, epiglottis and larynx.
Signit presents as circumscribed patches of erythema
(Fig. 23-18), usually on the lower lip in elderly persons.
Diagnosis
Clinicalnot possible.
Laboratoryon histopathological examination plasma
cell can be seen.
Drug-induced Cheilitis
Hemorrhagic crusting of the lips is a feature of Steven
Johnson syndrome which is commonly caused by drugs
but, cheilitis can occur as an isolated feature of a drug
reaction- either as a result of allergy or a pharmacological
effect.
The aromatic retinoids, etretinate and isotretinoin cause
dryness and cracking of lips in most patients.
Carcinoma of Lip
Squamous cell carcinoma is the commonest malignancy to
affect the vermilion zone. It occurs in light skinned people
who have chronic exposure to sunlight.
Clinical Features
Age and sex distributionthere is peak appearance in 6th
and 7th decade of life. It is more common in males as
compared to females.
Siteit is most common on the lower lips of fair skinned
people and persons who work in outer climate.
Onsetit usually begins on vermilion border of the lip
to one side of the midline and it may be covered with
crust due to absence of saliva.
Actinic cheilitisit is preceded by actinic cheilitis which
is characterized by innocuous looking white plaque on
the lip.
Symptomspatient may complain of difficulty in speech,
difficulty in taking food and inability to close the mouth.
There is also pain, bleeding and paresthesia.
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Diseases of Lip
Signs
It often commences as a small area of thickening,
induration and ulceration or irregularity of the surface
(Fig. 23-19).
In some cases, it commences as a small warty growth
or fissure on the vermilion border of the lip.
Crater like lesion having a velvety red base and rolled
indurated borders.
As the lesion enlarged, it takes papillary or an
ulcerative form.
In untreated cases, there is total destruction of lip
(Fig. 23-20) and invasion of cheek, the gums and the
mandible.
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Diagnosis
Clinical diagnosisulcerative growth with destruction
of lip is present.
Laboratory diagnosisit is mainly well differentiated
malignancies.
Management
Surgicalprognosis is good if the treatment is done
before metastasis.
The best results are seen when being obtained when the
entire lip mucosal field is removed for early lesion.
Miscellaneous Disorders
Chapping of the Lips
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Management
Fig. 23-22: Chapping of lip showing crack in lower lip.
Actinic Elastosis
It is also called as Solar elastosis or Senile elastosis.
Suggested Reading
Causes
Clinical Features
Siteit is seen on the labial mucosa exposed to sun.
Ageit occurs in elderly population.
Signswhite area of atrophic epithelium develops with
underlying scarring of the lamina propria.
Appearanceit includes leathery appearance, laxity with
wrinkling and various pigmentary changes.
Clinical typesclinically, it is manifested in three forms:
Cutis rhomboidalisthickened skin with furrow
giving an appearance of rhomboidal network.
Dubreuilhs elastomadiffuse plaque like lesions.
Nodular elastoidosisnodular lesion.
Clinical Features
Age and sex distributionit is more commonly seen in
adults as in adults there is loss of tone in the connective
tissue.
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Diseases of Lip
19. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology
(2nd edn) 2004: Saunders Elsevier.
20. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology
(2nd edn), 2004: Saunders Elsevier.
21. Ohman SC, Dahlen G, et al. Angular cheilitis: a clinical and
microbial study. J Oral Pathol 1986;15:213-7.
22. Ohman SC, Dahlen G, Moller, A, et al. Angular chelitis: a clinical
and microbial study. J Oral Pathol 1986;15;213-7.
23. Oliver ID, Pickett AB, cheilitis glandularis. Oral Surg, Oral Med,
Oral Pathol 1980;49:526-9.
24. Patton DW, Ferguson MM, et al. Orofacial granulomatosis: a
possible allergic basis. Br J Oral Maxillofac Surg 1985;23:235-42.
25. Reade PC, Sim R. Exfoliative cheilitis: factitious disorders. Int J
Oral Maxillofac Surg 1986;7:146-51.
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26. Reichart PA, Weigal D, et al. Exfoliative chelitis in AIDS: association with candida infection. J Oral Pathol Med 1997;26: 290-3.
27. Sholapurkar A, VIneetha R, et al. Cheilitis granulomatosa-report
of two cases with clinical signs and diagnostic implication.
JIAOMR 2006;18(4):218-23.
28. Williams PM, Greenberg MS. Management of cheilitis
granulomatosa. Oral Surg, Oral Med, Oral Pathol 1991;72(4):
436-9.
29. Winnie R, DeLucke DM. Melkersson-Rosenthal Syndrome: review
of literature and case report. Int J Oral Maxillofac Surg 1992;
21:115-7.
30. Zecha JJ, van Dijk, et al. Cheilitis granulomatosa (MelkerssonRosenthal syndrome). Oral Surg, Oral Med, Oral Pathol
1976;42(4):454-60.
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24
Introduction
Gingival and periodontal diseases, in their various forms,
have been affecting humans since the dawn of history.
Periodontal diseases have been implicated as a major cause
of tooth loss besides dental caries.
A review of literature on epidemiology of periodontal
disease has concluded that:
Periodontal disease appears to be a major global public
health problem affecting a majority of adult population
after the age of 35-40 years.
The disease starts as gingivitis in young age which, if
left untreated, leads to progressive periodontitis.
More than 90% of the variance of the periodontal severity
in the population can be explained by age and oral
hygiene.
This concept of periodontitis prevailed until late 1970s.
However, the recent studies emphasized on extent of the
dentition affected by destructive disease (i.e. the percentage
of tooth sites involved), and the severity of the defects (the
amount of lost tissue support). The global distribution of
one or several deeper pocket depths (6 mm) ranged
between 1% and 74% in Africa, 8% and 22% in North and
South America, 2% and 36% in Eastern Mediterranean, 2%
and 40% in Europe, 2% and 64% in South East Asia and
1% and 22% in Western Pacific area.
Normal Periodontium
The periodontium (periaround, odontostooth) consists
of gingiva, periodontal ligament, cementum and alveolar
bone.
Gingiva
It is the part of the oral mucosa which covers the alveolar
process of the jaws and surrounds the neck of the teeth.
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Alveolar Process
It is the portion of maxilla and mandible that forms and
supports the tooth sockets. It is formed with eruption of
tooth. It provides an osseous attachment to the forming
periodontal ligament and disappears after the tooth is lost.
Alveolar process may be defined as the part of the
maxilla and mandible that forms and support the socket of
the teeth. It is made up of alveolar bone proper, cribriform
Periodontal Ligament
Width of periodontal ligamentthe width of periodontal
ligament in function is 0.25 to 0.40 mm. Just below the
epithelial attachment, there are usually a small number
of lymphocytes present.
Connective tissue fibersa few connective tissue fibers of
the periodontal ligament, i.e. the free gingival group
fibres project from the cementum of the tooth root into
the gingiva without attachment to bone.
Compositionthe periodontal ligament is made up of
collagen fibers, oxytalan fibers, fibroblasts, amorphous
ground substance and interstitial tissue, cementoblasts,
osteoblasts and osteoclasts, epithelial rests of Malassez,
thin wall blood vessels, lymphatic vessels and tactile
sensory nerves.
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Gingival diseases
Dental plaque-induced gingival diseases*
Non-plaque-induced gingival lesions
Chronic periodontitis**
Localized
Generalized
Aggressive periodontitis**
Localized
Generalized
Gingival Diseases
Hereditary Gingival Fibromatosis or Fibromatosis
Gingiva
It is also called as Elephantiasis gingivae, Congenital
macrogingivae. Hereditary gingival fibromatosis is an
uncommon condition characterized by diffuse gingival
enlargement (Fig. 24-5), sometimes covering major parts or
total tooth surfaces. The enlargement develops irrespective
of effective plaque removal.
Hereditary gingival fibromatosis may be an isolated
entity or part of a syndrome, associated with other clinical
manifestations such as hypertrichosis, mental retardation,
and epilepsy, hearing loss, growth retardation and
abnormalities of extremities. Most cases are related to an
autosomal dominant trait. The most common syndrome of
hereditary gingival fibromatosis includes hypertrichosis,
epilepsy and mental retardation.
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A
Fig. 24-5: Fibromatosis gingivae showing diffuse overgrowth
(Courtesy Dr Parate).
Clinical Features
Ageit may be present at birth or may become apparent
with eruption of deciduous or permanent teeth.
Appearanceit is manifested as dense smooth diffuse or
nodular overgrowth of gingival tissue of one or both
arches that usually occurs at the time of eruption of
teeth (Figs 24-6A and B). It has a characteristic
pebbled surface. In some cases, surface has a nodular
appearance.
Colortissue is of normal or pale color. In some cases, it
may appear pink.
Consistencyit is often so firm, leathery and dense that
it prevents normal eruption of teeth.
Symptomsit is not painful and shows no tendency for
hemorrhage.
Extentextent may be such that the crown of fully
erupted teeth may be hidden.
Significancethe dense firm gingival swelling results in
varying spacing between the teeth and change in profile
and facial appearance.
Radiological featuresin the radiograph, significant bone
loss can be present. At the same time, soft tissue is also
visible (Fig. 24-7).
B
Figs 24-6A and B: Fibromatosis gingivae preventing eruption of
teeth in the oral cavity.
Diagnosis
Clinical diagnosisdiffuse fibrous overgrowth is seen
clinically and it is readily diagnosed.
Laboratory diagnosisepithelium is thickened with
elongation of rete pegs, although the bulk of the tissue is
composed of dense fibrous connective tissue. Bundles
of collagen fibers are coarse and show few interspersed
fibroblasts or blood vessels.
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Management
Surgicalsurgical removal of excessive tissue with
exposure of teeth is necessary. However, recurrences are
common.
Extraction of teethdramatic improvements in gingival
enlargements have been observed following extraction
of teeth.
Gingivitis
It is the inflammation of the gingiva.
Classification
Gingivitis can be classified on the basis of:
Course and duration:
Acute gingivitisit is of sudden onset and of short
duration and can be painful. A less severe form of
acute gingivitis has been termed subacute.
Recurrent gingivitisrecurrent gingivitis reappears
after having been eliminated by treatment or
disappearing spontaneously.
Chronic gingivitischronic gingivitis is slow in onset
and is of long duration. It is painless unless
complicated by acute or subacute exacerbations.
Distribution:
Localized gingivitisit is confined to the gingiva of a
single tooth or a group of teeth (Fig. 24-8).
Generalized gingivitisgeneralized gingivitis involves
the entire mouth (Fig. 24-9).
Marginal gingivitismarginal gingivitis involves the
gingival margin and may also involve a portion of
the contiguous attached gingiva.
Papillary gingivitispapillary gingivitis involves the
interdental papilla and often extends into the adjacent
portion of the marginal gingiva (Fig. 24-10).
Diffuse gingivitisdiffuse gingivitis involves the
gingival margin, the interdental papilla and the
attached gingiva.
Stages of Gingivitis
Stage I gingivitis (the initial lesion)the first manifestation of gingival inflammation is vascular changes,
consisting essentially of dilation of capillaries and
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3
Fig. 24-13: Deep bite causing gingival disease.
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Management of Gingivitis
Removal of local irritantthe local irritants should be
removed at this stage.
Plaque controlthorough plaque control should be done
with scaling and polishing.
Chlorhexidine mouth washuse of chlorhexidine, on a
short-term basis.
Clinical Features
Sexit is more frequently in women and young adults.
Siteit is located on the oral aspect of the attached
gingiva and therefore, differs from plaque induced
gingivitis.
Symptomspatients may complain of a sore and burning
mouth, scaling of lips and angular cheilitis.
Appearanceentire free and attached gingiva is edematous, friable, granular, bright red (Fig. 24-16) and
bleeds on slightest provocation.
Management
Cessation of exposurecessation of exposure to allergen
resolves the lesion.
Gingival Enlargement
Classification
Inflammatory enlargementit can be acute or chronic .
Drug inducedmay occur due to dilantin, nifedipine or
cyclosporine.
Combinedit is combination of (inflammatory + fibrotic).
Enlargement due to systemic diseasemany systemic
diseases like leukemia, Crohns disease can cause
gingival enlargement.
Neoplastic enlargementbenign and malignant tumor of
gingiva can cause enlargement.
Clinical Features
Siteit is limited to the marginal gingiva or the
interdental papilla (Fig. 24-17).
Onsetit is localized, painful, rapidly expanding lesion
that is usually of sudden onset.
Appearancein early stages, it appears as a red swelling
with a smooth, shiny surface. Within 24 to 48 hours, the
lesion usually becomes fluctuant and pointed with a
surface orifice, from which an exudate may be expressed.
Teeththe adjacent teeth are sensitive to percussion.
Diagnosis
Clinical diagnosisbright red color inflammation with
history of some allergen.
Laboratory diagnosislamina propria is infiltrated by
plasma cells.
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Diagnosis
Clinical diagnosisred swelling with shiny surface
associated with pain will give clue to the diagnosis.
Laboratory diagnosisit consists of a purulent focus in
the connective tissue, surrounded by a diffuse infiltration of polymorphonuclear leukocytes, edematous
tissue and vascular engorgement.
Management
Incisionafter topical anesthetic is applied, the fluctuant
area of the lesion is incised with a blade and the incision
is gently widened to permit drainage. The area is
cleansed with warm water and covered with a gauze
pad. After the bleeding stops, patient is instructed to
rinse every 2 hours with a glassful of water.
Clinical Features
Sitethe enlargement is generally papillary or marginal
and localized or generalized.
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Management
Removal of local factorsall the factors which are
responsible for enlargement should be removed.
Antibioticsantibiotics should be given. The most
commonly used antibiotics is metronidazole.
Flap surgeryperiodontal flap surgery is done if
necessary.
Clinical Features
Onsetgingival hyperplasia may begin as early as two
weeks after dilantin therapy.
Sitethe hyperplasia is generalized throughout the
mouth, but it is most severe in maxillary and mandibular
anterior region.
Appearancethe first change noted is a painless bead
like enlargement of the gingiva, starting with one or
two interdental papillae (Figs 24-21A and B). The
surface of gingiva shows an increase in stippling and
finally, a cauliflower, warty or pebbled surface. As the
enlargement increases, the gingival tissue becomes
lobulated and clefts are seen between each enlarged
gingiva.
Palpationpalpation reveals that the tissue is dense,
resilient and insensitive. It shows little tendency to bleed.
Significancethey may develop massively, covering a
considerable portion of the crown. They may interfere
with occlusion. The presence of an enlargement makes
plaque control difficult, resulting in a secondary
inflammatory process that complicates the gingival
hyperplasia. In hyperplasia associated with Dilantin
sodium the presence of dental plaque does not seem to
initiate the enlargement. Additional studies have
demonstrated that oral hygiene procedures may limit
the severity of the lesion but are unable alone to lead to a
reversal of the condition.
B
Figs 24-21A and B: Dilantin-induced gingival enlargement showing
bead-like enlargement.
Cyclosporine
It is a potent immunosuppressive agent used to prevent
organ transplant rejection and to treat several diseases of
autoimmune origin.
Clinical Features
Clinically, it is similar to that induced by Dilantin.
Sitegrowth starts in the interproximal papillae, more
frequently in anterior facial areas, partially covering the
crown.
Appearancethe tissue is usually pink, dense and
resilient, with stippled or granular surface and little
bleeding tendency (Fig. 24-22).
Nifedipine
Actionit is a calcium channel blocker that induces
direct dilatation of the coronary arteries and arterioles,
improving the oxygen supply to the heart muscles. It is
used in the treatment of acute and chronic coronary
insufficiency.
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Fig. 24-22: Drug-induced gingival enlargement showing pink resilient
surface due to cyclosporine administration.
Diagnosis
Clinical diagnosisenlargement of the gingiva with
history of drugs will diagnose the condition (Fig. 24-23).
Laboratory diagnosisthe stratified squamous epithelium
covering the tissue is thick and has a thin keratinized
layer. The rete pegs are extremely long and thin,
sometimes called as test tube pegs, with considerable
confluence. Mitotic figures are seldom seen.
Clinical Features
Fig. 24-23: Nifedipine-induced gingival enlargement.
Management
Surgical excisionIf hyperplasia interferes with function,
surgical excision is recommended.
Discontinue the drugdiscontinuing the drug will result
in gradual diminution of the bulk of the gingiva.
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Clinical Features
Age and sexit occurs in both, males and females in
pubertal age group. It also appears in areas of local
irritants.
Siteit involves mainly the marginal gingiva and
interdental gingiva.
Appearanceit is characterized by prominent bulbous
interproximal papillae (Fig. 24-27). Sometimes, only
facial gingivae are enlarged, as the mechanical action of
the tongue prevents heavy accumulation of local irritants
on the lingual surface.
Diagnosis
Clinical diagnosismushroom like enlargement in
pregnancy will diagnose this condition.
Laboratory diagnosisthe connective tissue consists of
numerous, diffusely arranged, newly formed and
engorged capillaries, lined by cuboidal endothelial cells.
The epithelium exhibits some degree of intracellular or
extracellular edema with prominent intercellular bridges
and leukocytic infiltration.
Diagnosis
Clinical diagnosisbulbous enlargement at the onset of
puberty will give clue to the diagnosis.
Laboratory diagnosismicroscopic picture is that of
chronic inflammatory cells with prominent edema and
associated degenerative changes.
Management
Removal of local irritantafter puberty, the enlargement
undergoes spontaneous reduction, but does not
disappear until local irritants are removed.
Management
Maintenance of oral hygienemost gingival enlargement
during pregnancy can be prevented by the removal of
local irritants and institution of a fastidious oral hygiene.
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Etiology
Clinical Features
Ageit is most commonly seen in the age group of 16 to
30 years, but can be seen in children from a low
socioeconomic group, in underdeveloped countries.
Symptomsonset is sudden with pain, tenderness, profuse salivation and peculiar metallic taste. Spontaneous
bleeding from gingival tissue occurs. There is also a loss
of sense of taste and diminished pleasure from smoking.
The typical fetid odor ultimately develops, which may
be extremely unpleasant.
Signsteeth seem slightly to be extruded and are
sensitive to pressure or have a woody sensation. They
are slightly movable and the patient is unable to eat
properly. Gingiva may become superficially stained with
brown color. There is blunting of interdental papillae
(Fig. 24-28).
Appearancea typical lesion consists of necrotic punched
out, crater like ulcerations are developed most commonly
on the interdental papillae and marginal gingiva (Fig
24-29). Removal of the lesion leaves raw surface. The
surface of gingival crater is covered by a gray, pseudomembranous slough, demarcated from the reminder of
the gingival mucosa by pronounced linear erythema. In
some cases, ulceration may develop on cheek, lip, tongue,
palate and pharyngeal area. If untreated, it may result
in progressive destruction of the periodontium and
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ANUG
Etiologyinteraction
Specific viral etiology
between host and bacteria,
most probably fusospirochetal
Necrotizing condition
Diffuse erythema
No definite duration
Duration of 7 to 10 days
Differential Diagnosis
ANUG, presenting as an isolated phenomenon, must be
differentiated from severe systemic diseases and in
condition where acute inflammation of gingival and
periodontal regions are the only associated symptoms.
Agranulocytosisblood picture shows evidence of a
systemic disease and due to diminished immunity lesion
is not marked by a severe inflammatory reaction.
Gingival changes due to cytostatic and immunosuppressive
therapyhistory is relevant.
Benign mucus pemphigoiderosion, no necrosis and seen
in elder adults.
Pemphigusit follows a chronic course with classical
histological picture. It occurs in older patients and skin
changes are seen.
Pemphigoid lichen planusno acute course, no bad breath,
whitish changes and skin symptoms.
Gonococcal stomatitisthe oral mucosa is covered with a
grayish membrane that sloughs off in areas, to expose
an underlying raw bleeding surface.
Syphilitic gingivitisprimary lesion seldom on gingiva,
does not spread to neighboring surfaces.
Gingivostomatitis due to Candidawhitish deposits that
can be wiped off, no bad breath, less acute picture and
demonstration of fungi.
Tubercular ulcerless acute picture.
Streptococcal gingivostomatitisit is characterized by a
diffuse erythema on the posterior areas of the oral
mucosa. But in these cases, necrosis of gingiva is not a
feature.
Management
Removal of pseudomembranethe involved areas are
isolated with cotton rolls and dried. A topical anesthetic
is applied and after 2 to 3 minutes, the areas are gently
swabbed with a cotton pellet to remove the pseudomembrane and nonattached surface. After the area is
cleansed with warm water, the superficial calculus is
removed.
Diphtheria
Secondary stage of
syphilis
Caused by
fusospriochetes
Caused by
corynebacterium
diphtheriae
Caused by treponema
pallidum
Affect marginal
gingiva
Rarely affects
marginal gingiva. Any
site of the oral cavity
can be affected
Membrane
removal easy
Membrane removal
difficult
Membrane not
detachable
Painful condition
Less painful
Minimal pain
Serological
findings are
normal
Serological findings
are normal
Doubtful
contagiousity
Contagious
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Non-plaque-induced Gingival
Disease
Bacterial Origin Gingival Disease
Herpes Zoster
Organismvaricella-zoster virus causes varicella
(chickenpox) as the primary self-limiting infections
which occur mainly in children and later activation of
the virus in adults causes herpes zoster (shingles).
Appearancethe intraoral ulcers usually involves
gingiva, tongue and palate. The diagnosis is generally
obvious due to unilateral occurrence of the lesions
associated with severe pain. Healing of lesions take place
in 1-2 weeks.
Managementtreatment consists of soft or liquid diet,
rest, atraumatic removal of plaque and diluted
chlorhexidine rinses. This may be supplemented by
antiviral drug.
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Gingival Recession
Types of Gingival Recession (By Miller)
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Fig. 24-34: Class III gingival recession.
Clinical Features
Radiographic Features
Typesthere are, radiologically, three types of bone
destruction, i.e. permeated type, moth eaten type and
pressure type.
Permeated typebone destruction with ill-defined
margins. Permeated means permeation of water into
sand, with ragged ill-defined borders. It also destroys
the mandibular canal.
Moth eaten typeit resembles moth eaten image with
remnants of bony fragments.
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Periodontal Disease
Periodontitis is defined as an inflammatory disease of the
supporting tissues of the teeth caused by specific
microorganism resulting in progressive destruction of the
periodontal ligament and alveolar bone with pocket
formation, recession or both.
The clinical feature that differentiates periodontitis from
gingivitis is presence of clinically detectable attachment
loss. The clinical classification was simplified to describe
the three general clinical manifestations to describe the three
general clinical manifestations of periodontitis: chronic
periodontitis, aggressive periodontitis and periodontitis
as a manifestation of systemic disease.
Diagnosis
Clinical diagnosisulcerative growth on the gingiva with
history of tobacco habit may give clue to the diagnosis.
Radiological diagnosiscomparison between periodontitis and carcinoma of gingiva is described below in
Table 24-5.
Laboratory diagnosisbiopsy show features suggestive
of squamous cell carcinoma.
Table 24-5: Comparison between periodontitis and
carcinoma of gingiva
Features
Periodontitis
Carcinoma of gingiva
Sclerotic bony
findings
No sclerotic finding
Size
Localized finding
Management
Surgerylocalized lesions, of less than 3 cm in diameter,
were cured in 80% of the cases by surgical excision.
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Pathogenesis of Periodontitis
It is an inflammation of the supporting structures of the
teeth. It starts out as gingivitis that then spreads down to
the root surface causing alveolar bone resorption and
pocket formation. It can eventually lead to alveolar bone
loss and damage to the periodontal ligament then can result
in tooth loss. Other complications include periodontal
abscess and osteomyelitis of the jaws.
Periodontal Pockets
Classification
Gingival pocket (relative or false)it is formed by gingival
enlargement, without destruction of the underlying
periodontal tissues. The sulcus is deepened because of
the increased bulk of the gingiva (Fig. 24-38).
Periodontal pocket (absolute or true)there is destruction
of the supporting periodontal tissue; progressive pocket
deepening leads to destruction of the supporting
periodontal tissues and loosening and exfoliation of the
teeth.
Suprabony pocket (supracrestal or supra-alveolar)in it,
bottom of the pocket is coronal to the underlying alveolar
bone.
Infrabony (intrabony, subcrestal or intra-alveolar)in it,
bottom of the pocket is apical to the level of the adjacent
alveolar bone.
Clinical Features
Signsgingival bleeding or/and suppuration, tooth
mobility and Diastema formation may be present. In some
cases, pus may be expressed by applying digital pressure.
Symptomspatient may complain of localized pain or
deep pain in the bone. When explored with a probe, the
inner aspect of the periodontal pocket is generally
painful.
Colorthere may be bluish red, thickened marginal
gingiva and a bluish red vertical zone from the gingival
margin to the alveolar mucosa.
Radiographic Findings
Pathogenesis
Diagnosis
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Fig. 24-39: Periodontal pocket is examined
with the help of periodontal probe.
Management
Pocket irrigationdevices like squeeze bottles and blunt
hypodermic needles can be used to irrigate the pocket
with chemotherapeutic agents.
Flap surgeryit is done to eliminate pockets.
Periodontal Abscess
It is usually culmination of a long period of chronic
periodontitis.
Pathogenesis
Pre-existing periodontal pocketit usually occurs in preexisting periodontal pocket. When such pocket reaches
sufficient depth of about 5 to 8 mm, the soft tissues,
around the neck of the tooth may approximate the tooth
so tightly that orifice of the pocket is occluded.
Multiplication of bacteriabacteria multiply in the depth
of pocket and cause sufficient irritation to form an acute
abscess, with exudation of pus into this area. It results
in sufficient swelling to destroy the cortical plates of
bone.
Diagnosis
Clinical diagnosissevere pain with swelling in the
apical region will give clue to the diagnosis.
Laboratory diagnosisthere is central cavity filled with
pus walled off on one side by the root and on the other
side by connective tissue.
Management
Clinical Features
Locationit starts at the gingival crevice and extends
down on one or more surface of the root, frequently as
far as apical region.
Symptomsacute episode usually has sudden onset
with extreme pain. There is also distension and
discomfort.
Signsthey are associated with swelling of the soft
tissues overlying the surface of the involved root (Figs
24-40A and B). Tooth is tender and mobile. Pus usually
exudes from the gingival crevice.
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Chronic Periodontitis
Classification
It is classified according to extent and severity of diseased
sites
According to extent of disease:
Low1 to 10 sites.
Medium11 to 20 sites
HighGreater than 20 sites.
According to severitythis can be differentiated to the
degree of clinical attachment loss.
Mild1-2 mm clinical attachment loss.
Moderate3-4 mm clinical attachment loss.
Severemore than 5 mm clinical attachment loss (Fig.
24-41).
Etiology
Many risk factors have been associated with initiation of
chronic periodontitis or once contracted then the
progression of the disease.
Microbial plaqueit is a crucial factor in inflammation of
the periodontitis is largely governed by host-based risk
factors.
Agethe prevalence of periodontitis increase with age
as a result of cumulative effects of disease over a lifetime.
Smokingsmoking has been positively associated with
progression of periodontitis. The risk attributed to
tobacco for chronic periodontitis is between 2.5 and 7.0.
It is not only the risk for developing the disease, but also
the response to periodontal therapy is impaired to
smokers.
Host-related factors
PMNreduction in number and/or function of
PMNs.
Drugsdrugs like Phenytoin, nifedipine and cyclosporine predispose to gingival overgrowth and thus
may modify preexisting chronic periodontitis.
Hormoneschanges in circulating hormones during
pregnancy, puberty, and menopause can modify
gingival response to plaque.
Immunosuppressant drug therapyimmunosuppressant drug therapy and any disease resulting in
suppression of inflammatory and immune processes
(such as HIV infection) may predispose the individual
to periodontal tissue destruction.
Nutritional deficiencynutritional deficiencies in
animals have shown effects on periodontal tissues
but have been proven in human studies. Vitamin C
deficiency has been consistently associated with
increased gingival bleeding.
Diabetes mellitusperiodontitis severity goes hand in
hand with poorly controlled diabetes mellitus. On
the other hand, periodontitis may also exacerbate
diabetes as it may decrease glycemic control.
Psychogenic disordersstress and other psychosomatic disorders may have direct anti-inflammatory
and/or immunosuppressive effects which are
relevant to the etiology of chronic periodontitis and
necrotizing ulcerative gingivitis.
Geneticgingivitis is a general and ubiquitous
response to plaque accumulation whereas risk of
chronic periodontitis has a high inherited component.
The focus of researcher is on the polymorphisms
associated with genes involved in cytokine production. An increased risk for chronic periodontitis has
been associated with polymorphisms of genes
involved in cytokines production but these findings
are yet to be confirmed.
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Fig. 24-43: Gingival recession seen in lower anterior region due to
periodontal problems.
Radiological Features
Bone resorptionthere is blunting of the alveolar crest
due to beginning of bone resorption. Bone loss may occur
horizontally, vertically (Fig. 24-44) or sometimes, in
furcation area.
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Diagnosis
Clinical diagnosisgingival recession, pocket formation
with mobility of tooth will diagnose the condition.
Radiological diagnosishorizontal and vertical bone loss
is present.
Laboratory diagnosisthe enlarged free marginal gingiva
is densely infiltrated with lymphocytes and plasma cells.
The apical borders of the inflamed area approach the
crest of the alveolar bone and the crestal fibers of the
periodontal ligament.
Management
Oral prophylaxisscaling and curettage can be done.
Flap surgerythis is the treatment of choice.
Aggressive Periodontitis
Aggressive Periodontitis is a group of diseases which was
previously defined on the basis of age of onset and was
hence named early onset periodontitis. But at the 1999
international classification workshop has clubbed a group
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Classification
Aggressive Periodontitis was sub-classified at the
international workshop into localized and generalized
forms. The following were the observed feature:
Localized aggressive periodontitis (LAP):
Circumpubertal onset.
Localized first molar/incisor presentation with
interproximal attachment loss on at least two permanent teeth, one of which is first molar and involving
no more than two teeth other than first molars and
incisors.
Robust serum antibody response to infecting agents.
Generalized aggressive periodontitis (GAP) (Fig. 24-47):
Usually affecting persons under 30 years of age, but
patients may be older.
Generalized interproximal attachment loss affecting
at least three permanent teeth other than first molar
and incisors.
Pronounced episodic nature of the destruction of
attachment and alveolar bone.
Poor serum antibody response to infecting agents.
It is important to underline that, in the present state of
uncertainty regarding both the causative agents and the
genetic and environmental susceptibility to Aggressive
periodontitis; it is possible that LAP and GAP may simply
represent phenotypic variations, of a single disease entity.
Conversely, it is possible that different Aggressive
periodontitis forms may manifest themselves with a
Clinical Features
Agethe age of onset of the disease ranges from the
middle to late teens and till 30 years of age
Sitethe lesions are more generalized and all or most of
the teeth are affected, without any definite pattern of
distribution.
Signsgingiva is acutely inflamed, often proliferated,
ulcerated and fiery red (Figs 24-48A and B). Bleeding
may occur spontaneously, or on slight provocation. In
some cases, gingiva appears pink and free of inflammation; but in spite of this, deep pockets can be revealed
on probing.
Systemic featuressome patients may have systemic
manifestations like weight loss, mental depression and
general malaise.
Diagnosis
Clinical diagnosisrapid loss of periodontal structure
with systemic features may suspect this disease.
Management
Antibioticsif microflora contains gram-positive
microorganisms, then it should be treated with 250 mg
amoxicillin and 125 mg potassium clavulunate three
times daily, for 14 days, along with scaling and root
planning. If flora is gram-negative, then clindamycin
should be given with dose of 150 mg, four times a day,
for 7 days, along with scaling and root planning.
Prepubertal Periodontitis
It is a very rare condition which starts during, or
immediately after the eruption of primary teeth. There are
functional defects of neutrophils and monocytes. It is
transmitted as an autosomal recessive trait. It is associated
with Papillion-Lefevre syndrome.
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A
Fig. 24-49: Prepubertal periodontitis showing
involvement of primary teeth.
Tooth Mobility
Tooth has a slight degree of physiologic mobility, which
varies from different teeth and at different times of the day.
Mobility beyond the physiologic range is termed as
abnormal or pathologic mobility.
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A
Radiographic Features
PDL space wideningthere is a widening of periodontal
ligament space and a single root may develop an
hourglass shape. In multi-rooted teeth widening of
periodontal ligament space at apices and in region of
furcation is seen.
Angular bone lossbone loss which surrounds the tooth
is also present (Fig. 24-51).
B
Figs 24-52A and B: Papillion-Lefevre syndrome showing hyperkeratosis of palms with severe destruction of periodontium.
Papillion-Lefevre Syndrome
It is an autosomal recessive and inherited disorder. It is a
triad of:
Hyperkeratosis of palms of the hand and soles of feet
(Fig. 24-52A).
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Diagnosis
Management
Periodontal managementflap surgery, oral prophylaxis
should be done.
Limitations of Radiography
Overlappinginability of the viewer to perceive bony
defects that are overlapped by existing bony walls.
Mild lesionearliest mild destructive lesions in the bone
do not cause sufficient alteration in the density to be
detectable.
Root superimpositiondensity of the root superimposed
with the image of the defect, tends to obscure bone height.
Bone loss in furcation areas may be obscured by an
overlying root or bony shadow.
Early Periodontitis
There are areas of localized erosion of the alveolar bone
crest.
In the anterior region, there will be blunting of the
alveolar bone. In some cases, it presents chisel edge, due to
greater destruction of bone at the sides than at the summit.
In posterior areas there is loss of the sharp angle between
the lamina dura and alveolar crest and it appears rounded
off, with irregular and diffuse borders.
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Osseous defects
It is a type of bony lesion that may be seen in moderate
periodontitis, other than horizontal bone loss. It is difficult
to locate on radiographs. There are various types of osseous
defects.
Inter-proximal craterit is the most common type of bony
deformity. It is a trough like depression that occurs in
the crest of inter-proximal septal bone between two
adjacent teeth. It consists of two side walls vestibular
and lingual cortical plates. The image of the side walls
that is projected more coronally will be reduced in
density, in relation to the image of apical side wall which
is superimposed over the other side wall. If two walls
are exactly superimposed, the inter-proximal crater may
appear as an irregular linear area of reduced density
between the adjacent teeth. Craters that are radiographically detected are about 1 mm or more in depth. The
apical margin of the defect will not be sharply
demarcated and will be such that relatively radiolucent
image of the crater will gradually blend with the normal
bone is apical to it.
Proximal intrabony defectit is a vertical defect within
the bone. It extends apically, from the alveolar crest and
is surrounded by three walls of bone, i.e. hemisepta and
two marginal walls (lingual and vestibular) roots of the
affected tooth is the fourth wall.
Hemiseptait is the bone of the interdental septum that
remains on the roots of uninvolved adjacent tooth after
destruction of either distal or mesial portion of the
interproximal bone septum (Fig. 24-56). It occurs as a
result of occlusal trauma which is complicated by
inflammation. It is more common on distal surfaces of
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Fig. 24-57: Bony pocket seen in relation with the mandibular first molar.
Advanced Periodontitis
It is defined as the bone loss which is so extensive that the
remaining teeth show excessive mobility, drifting and are
in jeopardy of being lost due to inadequate support
B
Figs 24-58A and B: Severe bone loss seen in furcation area of
molar teeth.
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Alveolar Dehiscence
It results when the marginal bone chips apically and
exposes the length of the root surface. The defect is wide
and irregular and extends as far as the apex of affected
teeth (Fig. 24-59). It occurs on either lingual or vestibular
side of the tooth. On radiographs, it will appear as a faint
radiopaque line representing its apical extension.
Suggested Reading
1. Armitage GC. Development of classification system for periodontal disease and conditions. Annals Periodontol 1999; 4:1.
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25
TMJ Disorders
Introduction
TMJ is a unique joint in which translatory as well as
rotational movements are possible and where both the ends
of bone articulate, in the same plane, with that of other
bone. It is also called as ginglymodiarthrodial type of joint,
meaning that it has a relatively sliding type of movement
between bony surfaces, in addition to hinge movement,
common to diarthrodial joint.
Anatomy of TMJ
The TMJ is located between the mandibular fossa (glenoid
fossa), the inferior surface of temporal bone and condylar
process of the mandible. It is a synovial type of joint and
it is distinguished from most of the joints by following
points.
Fibrocartilagearticulating surface of the bones is covered
by avascular, fibrous connective tissue, which may
contain variable number of cartilage cells. Thus called
as fibrocartilage.
Point of closurethe two articulating surface complex of
bone carry teeth, whose shape and position influence
the movement of joint. It is the only joint with rigid end
point of closure.
Articulationit has bilateral articulation with cranium,
so both the joints must function together. TMJ is a complex
joint as it has an articular disc interposed between the
condyle and the temporal bone (Figs 25-1A and B).
Joint Proper
Glenoid Fossa
The mandibular condyle articulates at the base of the
cranium with the squamous portion of the temporal bone.
This is called as the glenoid fossa.
B
Figs 25-1A and B: Normal positioning of disc in temporomandibular
jointfront and lateral view.
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TMJ Disorders
Squamous tympanic fissureposterior to the glenoid fossa,
there is a squamous tympanic fissure, which extends
mediolaterally.
Post-glenoid processthe posterior part of the fossa is
elevated to form a ridge called the posterior articular
ridge. This ridge increases in height laterally to form the
thickened cone shaped prominence called the postglenoid process, immediately anterior to the external
acoustic meatus.
Entaglenoid processthe lateral border of the fossa is
usually raised to form a narrow crest joining the articular
tubercle in front, with the post-glenoid process behind.
Medially, the articular fossa narrows and is bounded
by a bony wall, the entaglenoid process.
Roofthe roof of the glenoid fossa is always thin and
even translucent in many skulls. There is clear evidence
that the articular fossa is not a stress bearing functional
part of TMJ articulation.
Articular eminencethe articular eminence is strongly
convex in an anteroposterior direction and somewhat
concave in a transverse direction. The degree of convexity
varies, with the radius of the curvature varying from 5 to
15 mm.
Mandibular Condyle
Dimension and shapethe condyle is about 15 to 20 mm
long and 8-10 mm thick. Its long axis lies at right
angle with the plane of the ramus. The condyle is
usually quite convex anteroposteriorly and only
slightly convex mediolaterally. The mediolateral
convexity is often irregular, with medial and lateral
slopes divided by a more or less prominent anteroposterior ridge.
Polesthe articular surface of the mandible is seated on
its ovoid condylar process. From the anterior view, it
has medial and lateral projections called poles.
Lateral polethe lateral pole of condyle is roughened
and often bluntly pointed.
Medial polethe medial pole is usually rounded and is
more prominent than the lateral pole.
Lateral viewin lateral view, the condyle appears
tilted forward at the mandibular neck, with its articular
surface on its anterosuperior aspect. The articular
surface thus faces the posterior slope of the articular
eminence, when the jaw is held with teeth in complete
occlusion.
Articular surfacethe articular surface continues
medially down and around the rounded medial pole of
the condyle. Medial articular surface faces the
entaglenoid process of the temporal bone, when the jaw
is held in an occluded position.
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Articular Disc
It is composed of dense fibrous connective tissue devoid of
any blood vessels or nerve fibers.
Intermediate zonein the sagittal plane, it can be divided
into three regions according to thickness. The central
area is the thinnest and is called as intermediate zone.
Both anterior and posterior to the intermediate zone, the
disc becomes considerably thicker. The posterior border
is generally slightly thicker than the anterior border.
Anterior viewfrom the anterior view, the disc is
generally thicker medially than laterally. The precise
shape of the disc is determined by the morphology of the
condyle and mandibular fossa. During movement, the
disc is somewhat flexible and can adapt to the functional
demands of the articular surface.
Retrodiscal tissue and laminathe articular disc is
attached posteriorly to an area of loose connective tissue
that is highly vascularized and innervated it is called as
retrodiscal tissue. Superiorly, it is bordered by the lamina
of connective tissue, which contains many elastic fibers,
the superior retrodiscal lamina. This gives necessary
freedom for anterior movement of the disc. Since this
region consists of two areas, it is called as bilaminar
zone.
Attachmentthe articular disc is attached to the capsular
ligament anteriorly, posteriorly as well as medially and
laterally. This divides the joint into two distinct cavities;
the upper or superior cavity which is bordered by the
mandibular fossa and superior surface of the disc and
the lower or inferior cavity, which is bordered by the
mandibular condyle and inferior surface of the disc.
Synovial fluidthe internal surface of the cavity is
surrounded by specialized endothelial cells that form
the synovial lining. This lining along with a specialized
synovial lining located at the anterior border of the
retrodiscal tissue produce the synovial fluid, which fills
both the joint cavities. Thus, TMJ is referred to as a
synovial joint.
Ligamentous Structures
Functional Ligament
Collateral ligaments (Fig. 25-2)the collateral ligaments
attach the medial and lateral borders of the articular
disc to the poles of the condyle. It is commonly called as
discal ligament and are two in number. The medial one
attaches the medial edge of the disc to the medial pole of
the condyle and the lateral one, attaches to the lateral
edge of the disc to the lateral pole of the condyle. These
ligaments are responsible for dividing the joint
mediolaterally into the superior and inferior joint
cavities. Their function is to restrict the movement of the
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Accessory Ligaments
Sphenomandibular ligamentit is attached to the spine of
the sphenoid bone and extends downwards and
laterally to the small bony prominence on the medial
surface of the ramus of the mandible, called the lingula.
It does not have any significant effect on mandibular
movement.
Stylomandibular ligamentit arises from the styloid
process and extends downward and forward to the
angle and posterior border of the ramus of the mandible.
It becomes taut when mandible is protruded but is most
relaxed when the mandible is opened. Its function is to
limit the excessive protrusive movements of mandible.
Mandibular malleolar ligamentactually, the mandibular
malleolar ligament consists of fibroelastic tissue with
some ligamentous qualities. It originates from the neck
and anterior process of malleus and is inserted on the
medioposterior and superior part of the capsule,
interarticular disc and sphenomandibular ligament.
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TMJ Disorders
Synovial Fluid
Volumethe passive volume of upper and lower joint
cavity is 1.2 and 0.8 ml respectively. A small amount of
a clear, straw colored viscous fluid is found in the
articular spaces, which is known as synovial fluid.
Sourceit is secreted by synovial membrane lining the
articular disc, the capsule and also by retrodiscal tissue
lining.
Propertiessynovial fluid is characterized by well
defined physical properties of viscosity, elasticity and
plasticity. It contains small population of varying cell
type such as monocytes, lymphocytes, free synovial cells
and occasionally polymorphonuclear leukocytes. The
chemical composition of synovial fluid indicates that it
is dialysate of plasma, with some added protein and
mucin.
Gelationwhen the TMJ movements are reduced or
restricted due to some reasons, the synovial fluid becomes
viscid; its lubricating qualities are seriously impaired, a
condition clinically referred to as gelation.
Functions of synovial fluid
Lubricantit is a lubricant and reduces the mechanical friction between the condyle and the articular
disc and the mandibular fossa and articular disc.
Nutritional fluidit is also a nutritional fluid for the
vascular tissues covering the condyle and the
articular tubercle and also for the disc. It is elaborated
by diffusion from the rich capillary network of the
synovial membrane, augmented by mucin secreted
by the synovial cells.
Liquid environmentit provides liquid environment
for the joint surface.
Cleaning of jointsynovial fluid is also considered to
be responsible for the removal of entraneous material
shed into the joint cavity. The intimate cells have been
demonstrated to possess marked phagocytic
properties.
Joint Innervations
Vascular supplyit comes from the branches of the
superficial temporal arteries, deep auricular arteries,
anterior tympanic arteries and ascending pharyngeal
arteries.
Nerve supplyit is innervated by the branches of
auriculotemporal nerve, masseteric nerve and the
posterior deep temporal nerve, which are branches of
the mandibular portion of the trigeminal nerve.
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Diagnostic Studies
Radiography
It is the most important diagnostic aid in distinguishing
among the disorders that may affect the temporomandibular
joint. Routine radiographic examination includes
conventional radiography like Transcranial, Transorbital
and Transpharyngeal view, etc. But main limitation is that
it only shows osseous component and hence, the disease is
diagnosed much later.
Computed tomographytomograms are superior to
conventional radiography because of their ability to
depict a greater portion of the joint. By providing the
series of radiograph, tomography can reproduce small
changes in the central portion of the TMJ and therefore
decreases the false-negative interpretation (Fig. 25-5).
Arthrographywith increasing interest in soft tissue
derangement of the TMJ arthrography has assumed an
important role in the diagnosis of joint disorders. Defect
in the position or structure of the joint disc and its
attachment can be determined using arthrography.
Arthrography is performed by injecting the contrast
media into the joint space and then after radiograph is
taken.
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Intracapsular
Degenerative joint diseases
Osteoarthritis
Inflammatory
Rheumatoid arthritis (and other collagen disorders)
Psoriatic arthritis
Infection
Gonorrhea
Spread from contiguous sites
Tuberculosis
Syphilis
Developmental
Condylar hyperplasia
Condylar hypoplasia
Agenesis
Traumatic
Condylar fracture
Ankylosis
Dislocation
Disc displacement
Metabolic
Gout
Neoplasia
Benign
Malignant
Drug induced
Steroid
Extracapsular
Psycho-physiologic (MPD)
Iatrogenic
Traumatic
Those referred from local dental origin
Infection
Otologic
Neoplastic
Causes
Prenatal growth disturbances
Hereditaryhereditary anomalies like chromosomal
anomalies, achondroplasia, mandibulofacial dysostosis, progeria, Larsens syndrome and Goldenhar
syndrome can lead to hypoplasia of condyle.
Non-hereditarynon-hereditary disease like Pierre
Robin syndrome, radiation to fetus, Mobius syndrome
are also causative factors.
Postnatal growth disturbances
Endocrinehypothyroidism and hypopituitarism
causes decrease in secretion of growth hormone
resulting in hypoplasia of condyle.
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TMJ Disorders
Traumait is the most common cause of hypoplasia.
Trauma may occur in infancy or childhood.
Nutritional factorsdeficiency of vitamin A and some
other nutritional deficiency in the early infancy and
childhood can lead to hypoplasia of condyle.
Infectionrheumatoid arthritis can cause inhibition
of growth of a component of the joint.
Irradiationradiation upon the face during the period
of growth and extent of the change in the size of the
condyle depends to some extent on the amount of
radiation that is applied and the age at that time.
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Radiological Features
Condylecondylar process is short and it tends to
assume a more posterior position in the glenoid fossa
(Fig. 25-6). The neck of the condyle is slender.
Clinical Features
Unilateral
In this, only one side is involved. Following features can
be present in unilateral hypoplasia.
Appearance of faceon the unaffected side, there is
elongation of the body of mandible and flat
appearance of the face. Body of mandible is short on
affected side.
Shifting on affected sidemandible shift towards the
affected side on opening.
Malocclusionmalocclusion is present. There may be
cross bite on the affected side.
Eruption of teetheruption of teeth may be delayed in
case of hypoplasia of the condyle. In some cases, it
will cause impacted and unerupted teeth.
Earthere may be deficiency of some parts of the
adjacent auditory apparatus. The external ear may
be small, deformed, partially or completely absent.
Bilateral
In this, both the condyle are affected. Following features
are present in this type.
Mandiblewhen there is bilateral arrest of condylar
growth, there is usually symmetrical lack of growth
of the mandible.
Micrognathiadue to lack of mandibular growth,
micrognathia with the chin retruded to the level of
hyoid bone occurs.
Eruptionthere is delayed eruption of teeth on the
both side.
Class II malocclusionpatient is having Class II
malocclusion. It occurs as the mandibular ramus does
not increase in height sufficiently to open the space
between the upper and lower jaws into which the
teeth erupt with concomitant growth of alveolar
process. Another reason for this is that posterior
growth of the ramus is affected, so the length of the
body of the mandible is diminished and the last
molars are left within the ramus.
Diagnosis
Clinical diagnosismalocclusion, elongation of body of
mandible on unaffected side will give clue to the
diagnosis.
Radiological diagnosissize of condyle is easily
diagnosed on radiograph.
Management
Surgicalsurgical procedures commonly used in
unilateral deformities are directed towards contributing
bulk and increasing the length by means of bone,
cartilage and soft tissue grafts. Most commonly graft is
costochondral rib graft.
Orthodontic treatmentit is done to correct malocclusion.
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Clinical Features
Radiological Features
Absence of condyleabsence of condyle is easily detected
on radiograph.
Diagnosis
Clinical diagnosiseccentric movement with asymmetry
of face.
Radiological featuresabsence of condyle can be seen
radiologically.
Management
Maintenance of dental healthdental intervention can aid
by establishment of an acceptable plane of occlusion,
maintaining the oral health and offering palliative
treatment for discomfort.
Osteoplastyif the derangements are severe, osteoplasty
is advocated.
Causes
Developmentalit may occur due to trauma during the
birth.
Neoplasticsome tumors like chondroma, osteochondroma or osteoma of condyle can lead to hyperplasia of
condyle.
Bone diseasefibrous dysplasia, Pagets disease which
affects the bones, may affect the condyle leading to its
overgrowth.
Hereditarythis is also suggested the cause for condylar
hyperplasia. Condylar hyperplasia can be seen in
hereditary syndrome like Klinefelter syndrome.
Endocrineendocrine disorders like gigantisms as it
affects the whole body, it can also affect the condyle
causing its overgrowth.
Clinical Features
Age and sex distributionit occurs in either sex and there
is no predilection for any side. Most common age of
occurrence is 15 to 19 years.
Unilateral typeit can affect only one condyle. Following
features are present in unilateral type:
Mandibular enlargementthere is progressive
enlargement of the mandible on the affected side.
Facial asymmetryenlargement on the affected side,
give rise to facial asymmetry on that side.
Shift in midlinedue to facial asymmetry, shifting of
the midline of chin to the unaffected side.
Malocclusionunilateral type will result in cross bite,
open bite, and asymmetric protrusion on the affected
side.
Bilateralin this both the condyle are affected. Following
features are present in bilateral type:
Anterior cross bitemandible is larger on both side
and is placed more forward than the maxilla. This
will result in anterior cross bite (mandibular teeth are
anterior to the maxillary teeth).
Signsobtuse mandibular angle and the sigmoid
notch form an arc of a larger circle of mandible.
Relative microdontiaas there is definite disproportion
between normal size of crown of teeth and larger size
of jaw bones, teeth appear to be smaller as compared
to large size of jaw.
Radiological Features
Ramusthe vertical ramus is increased in vertical depth
as well as in its anteroposterior diameter. It will result in
prevention of occlusion of the posterior teeth.
Body of mandiblebody of the affected side of mandible
are larger as compared on unaffected side.
Condylethe condylar enlargement is sometimes
symmetrically distributed throughout the whole process.
It may retain its normal shape or it may assume a conical,
spherical, pear shaped or an uneven and lobulated
shape (Figs 25-7 and 25-8). The neck of the condyle may
retain its integrity, be enlarged or absorbed into the
enlarged head of the condyle.
Articular eminencethe articular eminence is shallower
than the opposite normal side, with the distal surface
slightly evacuated.
Displacement of condylehyperplasia of condyle may
result in displacement of condyle from the mandibular
fossa.
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Differential Diagnosis
Hemifacial hyperplasiait is associated with soft tissue
and teeth enlargement.
Management
Surgeryunilateral condylectomy should be performed
to improve function and esthetics of the patient.
Maxillary osteotomysome time, there may be occurrence
of compensatory maxillary growth. In these cases,
maxillary osteotomy should be performed.
Orthodontic therapythis is done to treat cross bite of the
patient.
Cause
Fig. 25-7: Large size of condyle seen on the computed tomogram
(Courtesy Dr Avinash Kshar and Dr Umarji).
Clinical Features
Fig. 25-8: Note large size of condyle on right side (arrow) as compared
to on left side (Courtesy Dr Avinash Kshar and Dr Umarji).
Diagnosis
Clinical diagnosisenlargement of mandible with shift
in midline will give clue to diagnosis.
Radiological diagnosisenlargement of condyle can be
seen radiologically.
Radiological Features
Bilobed appearanceradiographs will show bilobed
appearance of the condyle (Fig. 25-9).
Separate glenoid fossathere may be two separate glenoid
fossa.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosisbilobed appearance can be seen.
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Diagnosis
Clinical diangosisnot so specific.
Radiological diagnosiscoronoid growth can be seen
radiologically.
Management
Coronoidectomyit is carried out to remove the elongated
process of coronoid.
Management
Surgicalas such no treatment is necessary, but if it is
causing some problems surgical approach is carried out.
Coronoid Hyperplasia
It is rare developmental disorder affecting the coronoid
process of mandible.
Causes
Endocrineas most of the cases are seen in puberty in
the males, some sort of endocrine influence is suggested
as the cause of coronoid hyperplasia.
Hereditarysome cases are reported in sibling as hereditary factors may also play some role in coronoid
hyperplasia.
Tumorstumors like osteoma and osteochondroma can
also cause unilateral enlargement of the coronoid.
Osteoarthritis
It is also called as osteoarthrosis or degenerative arthritis. It
is primarily a disorder of movable joints characterized by
deterioration and abrasion of the articular cartilage with
formation of new bone at the joint surface. There is
destruction of the soft tissue component of the joint and
subsequent erosion with hypertrophic changes in bone.
There is breakdown of the connective tissue covering the
condyle, articular eminence and the disc. Recently, there
are some evidences suggesting that there are some
inflammatory components present in osteoarthritis.
Clinical Features
Age and sex distributionit is seen in 2nd decade of life
and most commonly encounter in males in the ratio of 5:1.
Unilateral coronoid hyperplasiain unilateral type, there
is restriction of mandibular movement. It occurs due to
enlarged coronoid may impinge on the zygomatic surface
causing reduction in the mandibular movement. There is
also deviation of mandible on the affected side.
Bilateral coronoid hyperplasiain this, limitation of
movements occur which become more severe as the age
progress.
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TMJ Disorders
Deterioration of functional capacity of jointthere may be
normal load to the joint but functional capacity is reduced
as a part of aging. This occurs due to:
Slower replacement of chondroblastsas age advances
there is slower replacement of chondroblasts and
chondrocytes in the joint.
Susceptible fibersthe cartilage matrix turns over less
rapidly resulting in available fibers to work for longer
period of time. This will make them susceptible to
fatigue.
Poor nutrition to jointas matrix contain less water,
the marrow blood flow diminished which results in
poor nutrition to the joint. This will make joint
desiccated and brittle.
Remodelling theoryby another theory, bone growth does
not cease completely after puberty and remodelling of
the joint progresses under functional demands.
Degenerative joint disease may develop when the
remodelling rate of bone exceeds that of the cartilaginous
repair. The gross evidence of these changes is the
formation of marginal osteophytes with development of
new bone in the area adjacent to the cartilage.
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Radiographic Features
Locationdegenerative changes located on the lateral
and anterolateral wall of the fossa.
Erosion of condylefirst evidence of erosion of condyle
on a radiograph occurs on an average, 6 months after
the onset of TMJ pain. This will result in enlargement
and shallowing of mandibular fossa (Fig. 25-11).
Types
Primaryit is generally described as a condition due to
wear and tear and is more common with increasing age.
It is commonly seen in patients more than 50 years of
age.
Secondarythe joint changes occur in response to
recognizable local or systemic factors. It is more
commonly seen in young persons.
Clinical Features
Age and sexit occurs in patients older than 40 years of
age and 85% of them are older than 70, with a mean age
of 53 years. Females are affected 6 times as frequently as
males.
Joints involvedit is common in many joints, but it is not
frequently found in TMJ.
Symptomsthere is unilateral pain over the joint, which
may be sensitive to palpation. Patient also experience
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Diagnosis
Clinical diagnosisswollen joint in elderly patient with
limitation of jaw movement may give clue to the
diagnosis.
Radiological diagnosisElys cyst, osteophytes
formation, joint mice, sclerosis, condylar erosion are
typical of osteoarthritis
Laboratory diagnosisbiopsy shows cells clumping
together and become unevenly distributed throughout
the fibrous matrix. It will also show loss of articular
surface.
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Management
Elimination of the causeit includes occlusal adjustment
or replacement of the missing teeth and ill fitting prosthesis, grinding, treatment of caries and periodontal disease.
Relieving the pressure on jointocclusal adjustment and
occlusal splints may reduce pressure on joint and relieve
the symptoms.
Analgesic and anti-inflammatory drugsfor the relief of
pain, nonsteroidal anti-inflammatory drugs and
analgesics should be given.
Physiotherapyheat therapy, diathermy and ultrasonic.
Myotherapymuscle exercises, injection of local
anesthetic in TMJ.
Arthroscopic lavagearthroscopic lavage may give relief
in some patients.
Doxycyclinenowadays, low dose doxycycline
(collaganase inhibitor, anti matrix metalloproteinase) is
giving relief in many patients.
Other therapyglucosamine, chondroitin sulfate have
also shown some success in osteoarthritis of TMJ.
Etiopathogenesis
Phase oneit result from some systemic infection, which
evokes an inflammatory response within the joint.
Phase twoas an autoimmune reaction to the antigen
generated by the initial inflammation itself or it may be
associated with derangement of the immune response
to the exogenous antigen.
Active phasein the active phase, TMJ may get involved
bilaterally. Bony components of the TMJ are affected
secondary to the granulomatous involvement of its
synovial membrane that subsequently spreads to the
articular surface of the condyle. The joint space enlarges
with synovial effusion which attacks the fibrocartilage
and ultimately produces erosion of the underlying bone.
This causes pain, stiffness and limitation of movement.
Chronic phasechronic phase may follow after active
phase. Here, there is proliferation of the synovial
membrane due to inflammation this is called as pannus
formation. This pannus then encroaches the joint space
and causes destruction of the articular cartilage. In this
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Clinical Features
General
Age and sex distributionit more commonly occurs in
temperate climate and has its highest incidence in
women from 20 to 50 years of age.
Sitesin typical cases, small joints of fingers and toes
are the first to be affected. Swelling of the proximal but
not the distal, interphalangeal joints give the finger as
like spindle appearance and swelling of the metatarsophalangeal joints results in broadening of feet.
Symptomssymptoms include bilateral stiffness,
crepitus, tenderness and swelling over the joint. Fever,
malaise, fatigue, weight loss, pain and stiffness in the
limb are also evident.
Polyarthritispolyarthritis develops subsequently, large
and weight bearing joints are frequently affected.
Subcutaneous or rheumatoid nodulesthere is formation
of subcutaneous nodules on the pressure points, sites of
friction and various vascular lesions, both necrotizing
and obliterative types. Severe deformities of extremity
can occur as a result of joint collapse, tendon rupture
and muscle involvement.
Signsthe joint may become red, swollen and warm to
touch. Muscle atrophy around the joint is common.
Handsin hands, it may produce an ulnar drift. Bursitis
can also occur.
TMJ involvement
Acute casein acute cases, there is bilateral stiffness, deep
seated pain, tenderness on palpation and swelling over
the joint. There is limitation in opening of mouth.
Referred painpain on biting is referred to the temporal
region, ear and angle of mandible.
Chronic casesin chronic cases, crepitus is the most
frequent finding. Functional disturbances like deviation
on opening and inability to perform lateral excursions
are common.
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Radiological Features
Diagnosis
Clinical diagnosissubcutaneous nodule, bilateral
involvement and pain on biting. Many joints are
involved at the same time.
Radiological diagnosissharpened pencil appearance,
with flattening of articular eminence.
Laboratory diagnosisbiopsy shows proliferation of
synovial lining cells with intense infiltration of
lymphocytes, plasma cells and polymorphs. Rice bodies
are seen histopathologically. Rose Waller test is positive
in 70% of the patients with rheumatoid arthritis. There
is elevation of RF factor. Antinuclear antibodies are
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detected by indirect immunofluorescence. Analysis of
synovial fluid is essential for the immediate diagnosis
of joint infection, inflammation and degenerative
disease.
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Psoriatic Arthritis
It is a chronic disease of unknown etiology characterized
by skin lesions and sometimes joint involvement.
Etiopathogenesis
Management
Supportive treatmentadequate rest to the joint, soft diet
is advocated.
Intra-articular corticosteroid injectionslocal injection of
long acting steroids such as methyl prednisone acetate
(20-80 mg for large joint and 4-10 mg for small joint) or
triamcinolone hexa-acetomide (10-40 mg for large joint
and 2-6 mg for small joint) are given.
Non-steroidal anti-inflammatory drugsthese drugs are
inhibitory to prostaglandins. These are used for
symptomatic relief. Salicylates (for pain) and antiinflammatory agents like phenyl butazone, indomethacin,
ibuprofen, diclofenac and piroxicam can be used.
Immunomodulatorazathioprine is found to be effective
in both, high and low doses.
Slow acting anti-rheumatic drugsthese are the
antimalarials like hydroxyl chloroquine sulphate,
sulphasalazine (500 mg/day) and methotrexate (DPenicillamine and parenteral gold).
Local treatmentit is done with heat, diathermy, jaw
exercise or a mouth stretcher. Muscle strengthening
exercise and hydrotherapy.
Medical synovectomysynovial obliteration is achieved
with osmic acid or variety of radiocolloids, if pain is
present even after injection of steroids. Erbium acetate is
used for small joints, while yttrium silicate is used for
large joints.
Surgical synovectomyit accounts for removal of synovial
membrane which is responsible for enzymatic
destruction of cartilage.
Clinical Features
General
Locationskin lesions are found on the trunk, arms, face
and scalp.
Appearanceskin lesions exhibit broad irregular papules
or plaques, which are dull red to brownish in color and
are usually covered with a layer of fine silvery scales.
Auspitzs signwhen scraped, they leave behind small
bleeding points: this is called as Auspitzs sign.
Exacerbationexacerbation occurs after exposure to ultraviolet light.
TMJ involvement
Symptomspreauricular pain, which is usually
unilateral. There is difficulty in opening the mouth.
SignsTMJ is tender. Crepitus, deviation towards the
affected side and in small proportion of cases, deformities
are seen.
Radiological Features
Articular surfacegeneralized appearance of irregularity
of condylar articular surface.
Osteoporosisgeneralized osteoporosis can occur.
Joint spacesproliferative changes with diminution of
joint space.
Diagnosis
Clinical diagnosispositive Auspitzs sign with tender
TMJ will give clue to the diagnosis.
Radiological diagnosisgeneralized irregularity of the
bone is present.
Management
DrugsSystemic drugs like salicylates should be given.
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Infective Arthritis
It is also called as septic arthritis. It may be acute or chronic.
Etiology
Microorganismsit is caused by direct spread of
organisms like staphylococci, streptococci, pneumococci and gonococci, from an infected mastoid process,
tympanic cavity or via blood.
Traumait may also be caused by trauma directly to the
joint or infection from a maxillary molar and parotid
gland.
Osteomyelitis and middle ear infectionit is acute in nature.
It can be caused by osteomyelitis and suppurative
middle ear infection.
Brucellosisbrucellosis can also cause infective arthritis
usually of chronic type but acute infection can occur.
Pathogenesis
Dilatation of blood vessels of synovial membraneearly
dilatation of blood vessels of the synovial membrane
with serous exudate is accompanied by the usual stages
of inflammation. This is followed by suppuration, with
formation of pus and ulceration of the synovial membrane.
Erosion of articular discthe articular disc is eroded and
partly destroyed. The cartilage of the head of the condyle
and the fossa are similarly affected.
Radiographic Features
Acute
Locationerosion usually seen on anterior and superior
aspect of the condyle.
Joint spacein early stages, width of joint space may be
increased by inflammatory distension in early infective
period. This will cause hazy appearance in radiographs.
Articular cortexarticular cortex of the condyle may
become slightly radiolucent. Discontinuities and subtle
irregularities of anterior cortical surface may be seen
(Fig. 25-18).
Osteoporosisthere is considerable osteoporosis of
adjacent parts of the condyle and it may extend to whole
of the ascending ramus.
Sequestrumin some cases, there is formation of
sequestrum, which if persistent may lead to some added
bone destruction.
Chronic
Condensing osteitisin chronic cases, there may be
peripheral condensing osteitis and approximation of
the joint surface, as the articular cartilage is eroded.
Bonethere may be frank bone destruction.
Condylea small cup shaped excavation on the anterior
face of the condyle, having a smooth or irregular base is
seen. In rare cases, whole of the condyle may be lost
with varying amount of eminence.
Clinical Features
Age and sex distributionit usually occurs in young
children with no sex predilection.
Locationit is always unilateral. In some cases of chronic
variety bilateral involvement can occur.
Symptomsthere is severe pain on jaw movement, with
an inability to place the teeth in occlusion, due to
presence of infection in the joint.
Signsredness and swelling over the joint. In some
cases, swelling may be fluctuant and extend beyond the
region of the joint.
Lymph nodestender cervical lymph nodes on the side
of infection. This helps to distinguish septic arthritis
from other TMJ disorders.
Chronic casesit may follow an acute infection, but
usually it is chronic. In these cases ankylosis of the joint
or facial asymmetry (if the growth centers are involved),
may occur.
Diagnosis
Clinical diagnosissevere pain in the joint, with sign of
inflammation over the joint will give clue to the diagnosis.
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Radiological diagnosisdestructive change in the condyle
will give clue to the diagnosis.
Management
Rest to jointadequate rest to the joint should be given
and patient is asked to do limited movements of joint.
Liquid dietpatient should be kept on liquid diet.
Antibiotics and analgesicsappropriate antibiotics and
analgesics should be given to patient.
Surgicalif there is suppuration, incision and drainage
should be carried out.
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Diagnosis
Clinical diagnosisjoint stiffness associated with
forward and stooped posture of the spine joint.
Radiological diagnosisflattening of joint surface.
Management
AnalgesicsNSAID should be given to the patient to
relieve pain and inflammation.
Ankylosing Spondylitis
Condylar Fracture
Clinical Features
Classification
Radiographic Features
Flatteningthere is flattening of the articular surface of
the TMJ (Fig. 25-19).
Osteophytesosteophytic formation is common.
Erosionin some cases, erosion of condylar head is seen.
Intracapsular Fracture
Articular surface fracturefractures involving articular
surface.
High condylar fracturefractures above or through the
anatomical neck, which may be termed as high condylar
fracture.
Injury to capsule, meniscus and ligamentfractures
associated with injury to the capsule, ligament and
meniscus.
Extracapsular Fracture
High condylar fracturethe fracture runs from the lowest
point of the curvature of the sigmoid notch, obliquely
downwards and backwards below the surgical neck of
the condyle, to the posterior aspect of the upper part of
the ramus.
Low or subcondylar fracturethe fracture is influenced in
its site and its direction by the insertion of part of
masseter muscle and TMJ ligament, the fracture taking
the line of least resistance. Such a fracture may be termed
as low or subcondylar fracture.
Combined fracturevery nearly the condylar head may
be split in the anteroposterior or sagittal plane; the split
extending through the neck and producing a combined
intra- and extracapsular fracture.
Etiology
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Clinical Classification
No displacementcrack/fracture is present without
tearing of periosteum or of ligament and without
significant alteration in the normal relationship of the
condylar head to glenoid fossa or neck of the condyle to
the ramus.
Deviationangulations exist between the condylar neck
and ramus.
Displacementoverlapping occurs between the condylar
processes and the surgical fragment lies lateral to ramus.
Comminuted fracturemay occasionally be encountered.
They are usually associated with a fracture of the
zygomatic arch and coronoid process, due to severe road
accidents and gun shot wounds.
Greenstick fractureit is seen in cases of children. If the
blow is not severe, this type of fracture occurs with medial
and anterior angulations, which tend to correct itself
spontaneously with the natural growth.
Dislocationfractured dislocation of the condylar head
occurs due to pull of the muscle.
Clinical Features
General
Incidencecondylar fracture accounts for 18% of
mandibular jaw fractures.
Locationunilateral fracture of the condyle is more
common as compared with bilateral but both occur with
or without injury. Fracture is more often associated with
dislocation if it is bilateral.
Associated fracturemost of the fractures of condyle are
associated with fracture of the opposite side of the
mandibular body.
Complicationcomplication like arthrosis, arthritis,
ankylosis and open bite deformity will occur.
Unilateral fractures (Fig. 25-20)
Symptomspain on the affected side; it is increased when
movement is attempted. Patient complains that his teeth
do not occlude in the normal fashion. Patient is also not
able to bring the jaw forward.
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Paresthesia of lower lipparesthesia of lower lip can occur
in some cases. It occurs as hemorrhage from the condylar
region, tracks across the base of the skull and exerts
pressure on the mandibular division of the trigeminal
nerves as it emerges from the foramen ovale.
Signssmall localized swelling over the injured TMJ.
There is tenderness over the condylar area of the affected
TMJ. There is also occasional crepitus and deviation of
the mandible to the affected side.
Earthere is bleeding from the ear on the affected side
which results from laceration of the anterior wall of the
external auditory meatus, caused by violent movement
of condylar head against the skin in this region.
Ecchymosishematoma surrounding the fractured
condyle may track downwards and backwards below
the external auditory canal. It gives rise to ecchymosis
below the external auditory meatus.
Limitation of jaw movementthere is painful limitation of
lateral excursion towards the normal side.
Gaggingthere is gagging of the ipsilateral molar teeth.
Bilateral Fractures (Fig. 25-21)
Gagging on molar teethall the above signs plus variable
degree of gagging of the occlusion on the molar teeth.
Restricted mandibular movementoverall mandibular
movements are more restricted, than in unilateral
fracture.
Forward displacement of mandiblemandible is displaced
forwards in case of bilateral fracture.
Fracture Dislocation
Absence of condyleall the above findings plus a definite
absence of condyle in the glenoid fossa (Fig. 25-22).
Unilateral dislocationif the condylar head is dislocated
medially and all edema has subsided due to passage of
time, it may be possible to observe a characteristic hollow
over the region of the condylar head.
Bilateral dislocationif there is a bilateral dislocation,
then there is an anterior open bite present.
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Fig. 25-22: Fracture dislocation showing absence of condyle in the
glenoid fossa (Courtesy Dr Datarkar).
Radiographic Features
View takendisplaced condylar fracture is well
demonstrated on AP and lateral projection. Nondisplaced fracture is well seen on AP view (Fig. 25-23).
Increased width of fracture condylewhen fracture occurs,
contraction of the lateral pterygoid muscle rotates the
transverse axis of the condylar head, so that the medial
end moves anteriorly, thus increasing the apparent
width of the fractured condyle.
Complete fracture dislocationin complete fracture
dislocation, the condylar head may be inclined medially
at an approximate 45 angle to the vertical axis of the
ramus.
Anterior displacement of the condyleif the condylar head
has been displaced anteriorly and turned at 90 angle to
the vertical axis of the ramus as viewed from the lateral
aspect, then only the articular surface of the condylar
head will be seen; this will appear as a narrow
radiopaque bar situated in the infratemporal fossa.
Condyle splitthe condyle may split with little or no
displacement of the fragments, or some portion may be
separated from head of the bone. Rarely, the whole of
the articular portion is crushed and flattened.
CT scanin difficult cases, CT scan has been
demonstrated to show changes in the relationship of
the condyle to the mandibular fossa more precisely than
the conventional radiographic examination (Fig. 25-24).
It is also claimed that it can demonstrate fine bony
alterations at the fractured site.
Fracture linethe fracture line is often transverse but
usually oblique, starting in the base of the mandibular
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Management
A simple crack fracture without displacement will not
require fixation. Patient should be kept under observation
and heavy masticatory forces are to be avoided.
A fracture with slight displacement reduction and
immobilization of the mandible for a period of 4 weeks.
Unilateral fractures with dislocationmandible should be
immobilized in normal occlusion for ten days then the
fixation is released and movement is encouraged.
Patients are kept under observation.
Bilateral fractures with dislocationarch bar is fitted and
reduction is achieved by traction in the incisor area. The
mandible is immobilized in normal occlusion for 4 weeks.
Gunning splintsfor edentulous patients gunning splints
should be used.
Early treatmentto avoid fibrous ankylosis early
movement of TMJ are to be achieved.
Other treatment includes relief of acute symptoms,
restoration to proper anatomic relation, intermaxillary
fixation for restoration of occlusion and early mobilization to minimize scarring.
Ankylosis
It is also called as stiff joint. Ankylosis, a Greek word means
fusion of body part. It is an abnormal immobility and
consolidation of the joint.
Types
Etiology
False
Myogenicthe most common problem associated with
muscle origin is fibrosis, which may result from chronic
infection of the elevator muscles of mastication. Myositis
ossificans can also produce limitation of opening.
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Fig. 25-25: Reduced mouth opening seen in patient with ankylosis of
temporomandibular joint.
General
Ageit is seen primarily in a young age or between 1 to
10 years.
Symptomspain and trismus which is directly related
to the duration of ankylosis. Patient also complaint of
reduced mouth opening (Fig. 25-25).
Oral problemsdepending upon the duration, there may
be poor oral hygiene, carious teeth and periodontal
problems malocclusion (Fig. 25-26).
Unilateral
Incidenceunilateral ankylosis is more common than
bilateral ankylosis.
Bilateral
Bird face appearanceface is symmetrical with micrognathia. There is bird face appearance (Fig. 25-29).
Clinical Features
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Fig. 25-27: Fullness of face seen on affected side (left)
due to ankylosis of TMJ.
Radiographic Features
Fibrous ankylosis
Appearancein some cases, there is transverse or oblique
dark line, irregular in outline, crossing the mass of dense
bone (Fig. 25-32). When a dark line is present, the
possibility of fibrous ankylosis is more.
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Bony ankylosis
Joint spacejoint space is completely or partially obliterated with dense sclerotic bone (Fig. 25-33). Sometimes,
large mass of new bone may be seen, radiographically
obscuring the condyle and joint space.
B
Figs 25-35A and B: 3D CT of ankylosis of temporomandibular joint.
Diagnosis
Clinical diagnosisin bilateral case, bird face appearance
or anterior open bite is present. In unilateral cases,
deviation of mandible, shifting of midline is present.
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Management
Dislocation
It results when condyle is forcefully displaced anteriorly
(by failure of muscular co-ordination) out of the articular
fossa but remains within the capsule of joint. The direction
of condyle is almost always anterior, beyond the articular
eminence.
Classification
Anteriorit is more common than other two.
Posteriorit is rare and results from the severe injuries
which are sustained at the point of the chin or at the
inferior border of the body of the mandible.
Centralsame as the posterior dislocation
Medial or lateralit occurs due to injury to the neck of
condyle with its fracture. It is very rare.
Etiology
Extrinsic forceit can occur under G.A. following
extraction of teeth or the use of mouth gag, when muscle
relaxant is used.
Intrinsicthese are related to attempts of excessive
opening of the mouth during eating or yawning and
occasionally singing. These types of dislocation are
sometimes called as spontaneous dislocations.
Occlusal disharmonyin cases of recurrent dislocation, the
etiologic factor is different, like occlusal disharmony
producing muscle spasm.
Phenothiazineoccasionally, action of phenothiazine
group of drugs produces spontaneous dislocation of the
mandible or spasm of the facial musculature.
Other causes like epileptic seizure, yawning, taking too
large bite of an apple and rarely, followed sneezing.
Clinical Features
Anterior dislocation
Siteanterior dislocation may be unilateral or bilateral.
In acute dislocation, there is a history of injury, gagging
of molar teeth and anterior open bite.
Symptomspatient has great difficulty in swallowing
and saliva drools over the chin. Pain in the region of
temporal fossa and there is a depression where the
condylar head is normally situated.
Signsthe mandible is postured forward and movement
is extremely limited. The condyle becomes locked anterior
to the articular eminence and is prevented from sliding
back by muscular spasm. When unilateral dislocation
occurs, the teeth will be gagged posteriorly on the side of
dislocation and the chin will be deviated towards the
normal side.
Central dislocation
Causethe head of the condyle is forced through
the floor of the articular fossa, into the floor of middle
cranial fossa. In this case, there may be damage to
the articular surface of the condyle and fracture of the
neck.
Neurological signsneurological signs like the cerebral
contusion, facial nerve paralysis, deafness and bleeding
from the ear may also be present.
Posterior dislocation
Causeit results from severe injury, which forces the
mandible backwards, so that the condyle penetrates the
tympanic plate of the temporal bone. When the upward
and backward thrust is applied to the chin, posterior
dislocation occurs.
Ageit is more common in elderly people as they have
increased gonial angle, which leads to more posterior
displacement of the condyle than in the case of an
individual having a smaller angle.
Symptomsthere may be tenderness over the affected
TMJ, limited mouth opening, anterior open bite and
laterognathism.
Radiographic Features
Anterior dislocationit is difficult to detect radiographically, as there is a wide variation in anterior condylar
movements. Condyle is locked in front of the articular
disc. Condyle is high on the anterior surface of the
eminence and is well up in the infratemporal fossa and
stayed there when the patient have closed their mouth.
Central dislocationradiologically, the anatomy of the
articulation is seen to be altered, so that neck of condyle
occupies a too high position in relation to the articular
fossa.
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Posterior dislocationradiologically, the anterior portion
of the articular fossa is empty and the condyle is seen
too far posteriorly. The neck of the condyle may appear
short, if the head of condyle maintain its abnormal
position. In such a case, the condyle may be seen partly
covered by the more radiolucent external auditory canal.
In cases when there is posterior dislocation into the
tympanic plate, but has been subsequently reduced, it
may be possible to identify the damage to the plate in
good quality radiograph.
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Etiology
Management
Clinical Features
Diagnosis
Radiological Features
Excessive excursion of the condyle from rest position to the
position when jaw is opened wide (Fig. 25-36).
Diagnosis
Subluxation (Hypermobility)
It is the unilateral or bilateral positioning of the condyle
anterior to the articular eminence, with repositioning to
normal accomplished physiologic activity. It is self reducing
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Management
Classification
Anterior displacement with reduction (Fig. 25-37)In it, as
the condyle moves forward, it snaps under the posterior
edge of disc producing an audible click and on closing
the condyle may again snap under the posterior edge of
the disc producing another click.
Anterior displacement without reductionThere is no
reduction of condyle in the mandibular fossa in closed
position.
Posterior disc displacementcondyle slip over anterior rim
of disc during opening.
Disc displacement with intermittent locking.
Disc displacement with perforation.
Etiology
Articular surface remodellingit occurs due to
combination of articular surface remodelling, disc
deformation and displacement of either the condyle or
the disc from an ideal relationship, which leads to
jamming of the disc.
Pathogenesis
Early changesIncreased muscle tone of the lateral
pterygoid it tends to pull the meniscus anteromedially
to the condylar head the meniscus will move anterior
to the condylar head a click or pop will then occur on
early opening as the condylar head reseats into the thin
central portion of the meniscus this type of joint noises
occur in early stages of joint disease and can be corrected
by relieving the muscle spasm.
Creation of freely moving discdiscal ligaments are not
elastic and hence once elongated; they generally remain
at that length the elongated discal ligament and the
continuous muscle pull due to spasm results in freely
moving disc on the articular cartilage.
Alteration of joint functionif the posterior border of the
disc becomes thinned and the retrodiscal laminae and
lateral discal ligament becomes elongated the disc
can be translated across the articular surface of the
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Clinical Features
Anterior disc displacement with reduction
Symptomsduring the disc dislocation, the condyle may
articulate on the retrodiscal tissue and may cause pain.
Signson physical examination, the joint is tender and
reciprocal audible clicking is heard. The jaw is deviated
towards the side of the click, till the click occurs and
then returns to the midline (Figs 25-38A and B).
B
Figs 25-38A and B: Deviation of jaw on right side in disc
displacement with reduction.
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Radiographic Features
Plane radiographythey are not diagnostic; except in
cases of perforation of the disc, where there is evidence
of degenerative changes in the joint.
Arthrogramarthrogram is useful in studying the
changes.
MRIin anterior disc displacement, posterior band of
the disc located anterior to the superior portion of the
condyle is seen in closed mouth sagittal image. In some
cases bone marrow edema can be seen (Figs 25-39 and
25-40).
Diagnosis
Clinical diagnosisclicking sound while opening and
closing the mandible with pain in TMJ area.
Radiological diagnosisMRI is useful in the diagnosis of
disc displacement.
B
Figs 25-39A and B: (A) Axial section, closed mouth, anteriorly
displaced disc. (B) Axial section, open mouth, anteriorly displaced
disc, but normal disc condyle relationship (Courtesy Dr Avinash Kshar
and Dr Umarji, Government Dental College and Hospital, Mumbai).
Management
Bite plane applianceit involves one of the bite plane
appliances that position the mandible so that the mouth
remains slightly open vertically and is placed anteriorly
to maintain the disc in a normal relationship to the
condyle. Maxillary and mandibular appliances can be
used for maintaining the disc reduction during function.
The evaluation and adjustment in the appliance should
be made monthly, till the condyle return to normal hinge
position. TMJ should be stabilized in the position for
two months by maintaining the patient on splints.
Occlusal adjustment, restorative and orthodontic treatment
next phase is of occlusal adjustment, restorative
treatment and orthodontics or all the three can be done.
Surgical treatmentit is indicated in those patients who
have chronic internal derangement, have failed to
respond to non-surgical treatment. It includes
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B
Figs 25-40A and B: Coronal section, closed mouth, laterally displaced
disc (Courtesy Dr Avinash Kshar and Dr Umarji, Government Dental
College and Hospital, Mumbai).
Adhesions
The movements between healthy articular surfaces occur
without friction. Changes in the articular surfaces and
synovial fluid can drastically change this frictionless
system. This sticking of articular surfaces has been called
Metabolic Disorders
Gout
It is a chronic metabolic disorder characterized by acute
exacerbations of joint pain and swelling associated with
an elevated blood uric acid and deposition of crystals of
monosodium urate.
Various drugs like thiazide diuretics, operations, trauma,
alcohol and rapid weight loss can predispose to this disease.
Clinical Features
Age and sex distributionseen in middle age with equal
sex distribution. It has a hereditary tendency.
Sitesinitially, metacarpophalangeal joints are
commonly involved. Later foot, ankles, hand, wrist and
elbow may be affected.
Symptomsthere is excruciating pain, which may be
worsen at night. Sometimes, it is associated with
anorexia, fever and general malaise.
Progressjoint returns to normal after few days, with
desquamation of the overlying skin.
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Radiological Features
Appearancethere is bony mass protruding from the
condyle (Figs 25-42 and 25-43).
Radiographic Features
Punched out lesionpunched out areas in the carpal bone
of the hands. In TMJ also, punched out radiolucency
can be seen on the condylar cartilage.
Destruction of cartilagesevere destruction of the cartilage
can also be seen in some areas.
Calcification in the jointthere is calcification within the
joint spaces which may be subtle or massive.
Diagnosis
Clinical diagnosismultiple joint involvements.
Tenderness on the TMJ area can diagnose the disease.
Radiological diagnosispunched out lesion with
calcification in the joint.
Laboratory diagnosisarticular cartilage reveals white
chalky deposits. This deposit is also often found in the
synovial and adjacent tissues. The cartilage may be
fragmented. Crystalline deposits of uric acid are seen.
This is followed by small accumulations (microtophi)
with surrounding granulomatous foreign body reaction.
Management
Dietdiet should be low in uric acid and fat, i.e.
sweetbread, meat, extract peas, beans.
Uricosuric agentsincreased elimination of uric acid by
uricosuric agents like colchicine 0.5 mg every 2 hourly,
to a maximum of 6 mg in 24 hours.
Management
Neoplastic Disorders
Benign Tumors
Malignant Tumors
Clinical Features
Types
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TMJ Disorders
Clinical Features
Age and sexage of incidence from 17 months to 68 years
with male to female ratio being 1:1.
Symptomspain on full opening of the mouth and
diminished hearing. Swelling of the TMJ is present.
Swelling may be huge to cause facial asymmetry.
Signsthe tumor may be fixed to deep structures.
Deviation of the mandible to the unaffected side. There
is also malocclusion (Fig. 25-44).
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Miscellaneous Disorders
Synovial Chondromatosis
It is a benign chronic progressive metaplasia that will not
resolve spontaneously. Although it is non-neoplastic, it
may resemble a malignant condition histologically. It is
also called chondrometaplasia. It denotes the condition
whereby a cartilaginous focus develops within the
synovial membrane of the joint.
Pathogenesis
Predisposing factorstrauma may be a predisposing
factor, other factors are malocclusion, occlusal habits,
and subluxation or tension sites.
Metaplasia of mesenchymal cellthis is generally believed
to occur through metaplasia of mesenchyal cell rests in
the underlying connective tissue of the membrane.
Formation of metastatic focithere is formation of
metastatic foci.
Detachment of metastatic focifoci are detached from the
affected membrane and become cartilaginous, and forms
mobile bodies within the joint cavity.
Calcification of cartilaginous focimany of these
cartilaginous foci then undergo calcification. These joint
bodies acquire a perichondrium, which enables them to
grow by proliferation of chondrocytes.
Fig. 25-44: Huge swelling seen on right side of
patient due to chondrosarcoma of condyle.
Radiological Features
Appearanceirregular destruction of bone in condylar
region is present (Fig. 25-45).
Management
It can be treated by surgery, chemotherapy, radiotherapy
and combination therapy.
Clinical Features
Age and sexfemale to male ratio is 3:1 with greatest
incidence at 40-60 years of age.
Sitethis affect large joints like knee, elbow, hip and
shoulder. This disease is also present in temporomandibular joint.
Symptomsfacial pain, limitation of motion and
deviation towards the affected side.
Signscrepitus, preauricular swelling, enlarged joint
with effusion and local tenderness.
Radiographic Features
Loose bodiesthis consists of rounded/irregular shaped
radiopaque structure in the joint (Fig. 25-46).
Joint spacethere is irregularity in the joint space. Joint
space is also widened.
Condylecondylar head is also irregular.
Diagnosis
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3
Fig. 25-46: Loose bodies seen as rounded shaped
in arthroscopic view (Courtesy Dr Honda).
Management
Surgicalloose bodies should be removed.
Synovectomytotal synovectomy can be done to prevent
recurrence.
Removal of metaplastic foci and synovectomy are the
preferred treatment.
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TMJ Disorders
to chronic para-functional habits or over-closure due to
bilateral loss of molar teeth result in TMJ dysfunction
syndrome.
Pathogenesis
During muscle contraction, the energy is released there
is formation and accumulation of lactic acid which
in turn causes changes in osmolality which results in
decrease in the pH it make the muscle receptor prone
to impulse excitation as their critical firing level is
impaired decrease in pH and lactic acid itself causes
infusion and effusion of histamine, bradykinin and
serotonin and other amines into the area it causes
pathological muscular derangement these particular
areas of muscular derangement are called as trigger
zones it is a hypersensitive area from which impulse
bombards the CNS and gives rise to referred pain.
Classification
Spasm of lateral pterygoid muscleit occurs when the teeth
are brought into maximum intercuspation and with
extended translatory movement. Pain reduces on biting
against a separator (as it prevents the intercuspation
required to stretch the spastic muscle). It is accompanied
by acute malocclusion expressed as anterior displacement of the mandible.
Spasm of elevator muscles- it occurs when biting and
chewing efforts are made and while opening the mouth.
Pain is not decreased on biting on a separator and is
accompanied by trismus with little or no restriction of
excursive movements.
Spasm of lateral pterygoid and elevator musclesin it, pain
occurs while biting, chewing, opening, maximum
intercuspation and extended translatory movement.
Pain is not affected by biting against a separator, except
for some decrease of pain with maximum intercuspation
and is accompanied by acute malocclusion, trismus but
with little or no restriction of excursive movements.
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Pain refers to
Temporalis
Clinical effect
Masseter
Mandible, maxillary
molar, TMJ, ear
Same as above
External
pterygoid
TMJ
Contralateral deviation
of the mandible, protrusion
of condyle, acute
malocclusion
Internal
pterygoid
TMJ, retromandibular
area, tongue
Restriction of mandibular
movements, contralateral
deviation of mandible
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Negative characteristics
No radiographic evidenceabsence of radiographic or
biochemical evidence in the TMJ.
No tendernesslack of tenderness in TMJ area, on
palpation via the external auditory meatus.
Management
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TMJ Disorders
Psychotherapy
Stress impasse stagesthe stress impasse stages in the
TMJ syndrome are characterized by three distinct steps
based on the evolution and progression of the disease.
Stress impasse Iconflict from personality fixation,
usually in adolescents, chronic symptoms develop
(bruxism, clenching, grinding).
Stress impasse IIonset of acute symptoms (pain, jaw
clicking).
Stress impasse IIIsevere symptoms resulting in TMJ
damage.
Treatment planthe treatment plan includes a three stage
programme, which will include basic relaxation
exercises, sleep preparation and containment strategies
for worry, grief and guilt.
Physical medication
Hot packsthe one of moist heat is advantageous. Heat
should be applied directly to the trigger zones. Temperature changes can alter the amount of vasodilation
substance held within the tissue spaces. The patient
should be instructed to place hot fomentation over a
particular area for not less than 10 minutes, preceding
the therapeutic exercises. Woolen cloth soaked in boiling
water is usually used.
Massageit provides relief from muscle spasm and also
improves the local circulation, by reducing the local
biogenic amines.
Diathermy and ultrasoundthis is a more effective method
for the treatment of myospasm of deeper muscles. It
produces heat and thus improves the local circulation.
Electrical stimulation (TENS)tetanizing and sinusoidal
current is used in this therapy. It is another effective
way to break acute painful muscle spasms. Electrodes
are placed over the most painful areas and then
tetanizing current is turned on gradually, until good
contraction of the affected muscle has been obtained.
Current should not exceed the tolerance level. The current
is left for 120 minutes. Then with the electrode remaining
in the same position, the tetanizing current is switched
off and sinusoidal current is gradually applied, till good
contraction is obtained.
Oral myofunctional therapy is a program to re-educate the
muscles of the mouth and face to work in a balanced
relationship. It includes breaking of a habit (Lip biting,
tongue thrusting), proper feeding of infant and proper
balancing of environmental forces. The appliances used
are activator, bionator, Frnkels appliance and oral
screen.
Applied kinesiology
What is itdental Kinesiology is the study of motion
and function of the jaws, oral musculature, the
accompanying neurological, vascular and other support
system network and the impact these muscle functions
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Suggested Reading
1. Anil Ghom. Benign tumor of jaw (non-odontogenic), in textbook
of oral medicine. Jaypee Brothers publication 2004; 530-60.
2. Bell WE. Clinical diagnosis of pain dysfunction syndrome. JADA
1969;79:154-60.
3. Berger SS, Stewart RE. Mandibular hypoplasia secondary to
perinatal trauma. A report of case. J Oral Surg 1977;35:147-53.
4. Blackwood H. Arthritis of the mandibular joint. Br Dent J 1963;
115:317-24.
5. Blackwood HJJ. Arthritis of the mandibular joint. Br Dent J
1963;115:317-24.
6. Bluick MF, et al. Diagnosis and treatment of internal derangements
of the TMJ. Dent Clin North Am 1983; Jul,27(3):561-72.
7. Bruce RA, Hayward JR. Condylar hyperplasia and mandibular
asymmetry. J Oral Surg 1968;26:281-90.
8. Bruce RA. Condylar hyperplasia and mandibular asymmetry
A Review. J Oral Surg 1968;26:281-90.
9. Cacioppi J, et al. Condyle destruction concomitant with advance
gout and rheumatoid arthritis. Report of case. Oral Surg, Oral
Med, Oral Patho 1968;25:919.
10. Cacoppi JT, et al. Condyle destruction concomitant with advanced
gout and rheumatoid arthritis: report of a case. Oral Surg, Oral
Med, Oral Pathol 1968;25:919-21.
11. Cowan DF, Ferguson MM. Bifid mandibular condyle.
Dentomaxillofacial Radiol 1997;26:70-3.
12. Cruin RJ. Incidence of TMJ symptom in male patients with
rheumatoid arthritis. JADA 1970;81:129-33.
13. De Bont LG, Dijkgraaf LC, Stegenga B. Epidemiology and natural
progression of articular temporomandibular joint. Oral Surg,
Oral Med, Oral Patho 1997;83:72.
14. De Leeuw R, Boering G, Stegenga B, Bont LG. TMJ articular disc
position and configuration 30 years after intial diagnosis of
internal derangement. J Oral Maxillofac Surg 1995;53:234-41.
15. Dijkgraaf LC, Spikervet FK, de Bont LG. Arthroscopic finding in
osteoarthritic temporomandibular joint. J Oral Maxillofac Surg
1999;57:1270-80.
16. Dolwick MF. Diagnosis and treatment of Internal derangement
of the TMJ. DCNA July 1983;27(3):561-72.
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TMJ Disorders
42. Larheim TA, et al. TMJ involvement and dental occlusion in a
group of adults with rheumatoid arthritis. Acta Odontol Scand
1983;Oct:41(5):301-9.
43. Larheim TA, Westesson PL. Temporomandibular joint in
maxillofacial imaging. Springer 2005;143-77.
44. Leighty SM, et al. Septic arthritis of the TMJ. A review of the
literature and report of two cases in children. Int J Oral Maxillofac
Surg 1993;22:292.
45. Loh FC, Yeo IF. Bifid mandibular condyle. Oral Surg, Oral Med,
Oral Pathol 1990;69:24-7.
46. Loiselle RJ. Symposium on TMJ disorders. JADA 1969;79:145-6.
47. Loury JL. Psoriatic arthritis involving TMJ. J Oral Surg Mar
1975;33 (3):206-8.
48. Lupton DE. Symposium on TMJ disorders; psychological aspect
of TMJ disorders. JADA 1969;79:131-6.
49. Lustmann J, Zelster R. Synovial chondromatosis, a review of
literature and case report. Int J Oral Maxillofac Surg 1989;18:90.
50. Mayne JG, et al. Arthritis of TMJ. JADA July 1969;79:123-30.
51. Mcloughlin PM, et al. Hyperplasia of the mandibular coronoid
process. An analysis of 31 cases and a review of the literature. J
Oral Maxillofac Surg 1995;53:250.
52. McNeil C (Chairman AdHoc Committee 1982, Paper presented
at the meeting of American Academy of Cranio-mandibular
Disorders Chicago). Cranio-mandibular disordersThe state of
the art part-2: Accepted diagnostic and Treatment modalities. J
Prosthetic Dent 1983;49:393-7.
53. McNeill C, et al. Temporomandibular disorders, diagnosis,
management, education and research. JADA 1990;120:253.
54. Merril RG. Habitual Subluxation and recurrent dislocation in a
patient with Parkinsons disease. J Oral Surg July1968;26:473-7.
55. Mikhail M. History and etiology of MPD syndrome. J Prosthetic
Dent 1980;44:438-43.
56. Miles DA, Kaugars BS, Dis MV, Lovas GL. Disorders of
temporomandibular joint: radiologic/pathologic correlations, WB
Saunders, 1991;261-92.
57. Miller GA. TMJ ankylosis-Review of literature and Report of two
cases of bilateral involvement. J Oral Surg. Oct 1975;33(10):
792-810.
58. Miyamoto H, Sakashita H, et al. Synovial chondromatosis of the
temporomandibular joint. Br J Oral Maxillofac Surg 2000;38:
205-8.
59. Mizukawa JH, et al. Metastatic breast adenocarcinoma of the
mandibular condyle-Report of case. J Oral Surg 1978;36(6):44851.
60. Morgan DH, et al. Disease of the temporomandibular apparatusA multidisciplinary approach (2nd edn), CV Mosby and
Company, 1982.
61. Musgrove BT. Dislocation of the mandibular condyle into middle
cranial fossa. Br J Oral and Maxillofacial Surg 1979;17:17.
62. Musgrove BT. Dislocation of the mandibular condyle into the
middle cranial fossa. Brit J Oral and Maxillofacial Surgery 1986;
24(1):7-26.
63. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology,
(2nd edn), Saunders Elsevier, 2004.
64. Ogus H. Regenerative Disease of TMJ in young persons. Br J Oral
Surg 1979;17(1):17-26.
65. Palton DW. Recurrent subluxation of TMJ in psychiatric illness.
Brit Dent J 1988:153(4):141-4.
66. Perry HT. Symposium on TMJ disorders, Orthodontic viewpoint.
JADA 1967;79:137-41.
67. Rasmussen OC. TMJ Arthopathy, clinical, radiologic and
therapeutic aspects with emphasis on diagnosis: Int J Oral Surg
1983;12(6):365-97.
68. Richter KJ. Chondrosarcoma of TMJ: report of a case. J Oral Surg
1974;32(10):771-81.
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26
Parotid Gland
Locationit comes from the word paraaround and
oticear. It is like an inverted flattened pyramid. It is the
largest of the salivary glands weighing about 15 grams
each. It lies between the mastoid process and vertical
ramus of the mandible. The bulk of the parotid gland is
situated in the retromandibular fossa (Fig. 26-1).
Shapeit is wedge shaped, with the broad edge of the
wedge lying subcutaneously and the apex lying deep
between the parotid fascias. It is divided into superficial
and deep lobes by the facial nerve and its branches. It
forms an irregular lobulated yellowish mass, lying below
the external acoustic meatus, between the mandible and
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Sublingual Gland
Locationit lies above the mylohyoid and below the
mucosa of the floor of mouth. It is medial to the
sublingual fossa of the mandible, on either side of the
symphysis menti and lateral to genioglossus muscle. It
has about 15 ducts which open directly into the floor of
mouth.
Bartholins ductthe duct of sublingual gland is called
as Bartholins duct. They are eight to twenty in number.
Some of the smaller sublingual ducts open into the
sublingual fold, in the floor of the mouth, on either side
of lingual frenum. Some open into the submandibular
duct and others unite to form the principle sublingual
duct which opens in the floor.
Blood supplyit is supplied by sublingual and
submental arteries.
Nerve supplyit is supplied by lingual and chorda
tympani nerve.
Lymphatic drainageit passes to the submandibular
lymph nodes.
Submandibular Gland
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Saliva
Composition of Saliva
Source of salivasaliva is secreted by salivary glands:
viz the parotid, submandibular and sublingual glands.
These glands produce approximately 1.5 liters of saliva
daily: 70% is from the submandibular glands, 25% is
from the parotid glands and 5% is from the sublingual
glands. Minor salivary glands located on the palate,
buccal mucosa and tongue also produce modest amounts
of saliva.
Normal stimulated flow of salivathe normal stimulated
flow for different ages can be calculated with following
equation:
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Collection Technique
Parotid Collector
Compositionit was developed by Lashley in 1916. It
makes possible the collection of parotid fluid uncontaminated by the oral content. It is composed of two
concentric circles and is made of either plastic or metal.
Techniquethe center circle is designed to fit over the
opening of Stensens duct and is connected to a
graduated collecting tube. The outer concentric circle is
attached to a rubber bulb, which exhausts air from the
outer circle, when collector is held in place and draws
the cheek surrounding the opening of Stensens duct
into it.
Disadvantagedue to different anatomy, it cannot be
used in submandibular and sublingual gland.
Segregator
Compositionit is developed by Schneyer which allows
the collection of submandibular and sublingual gland.
It is made up of plastic or metal. It must be constructed
for each individual on the stone model. In it, preformed
basic plastic collector is utilized.
Techniquethis plastic is covered with rubber base
impression material and placed on the floor of mouth
beneath the tongue. In 5 minutes, impression can be
removed. A recess is then made in the impression, over
the opening of Whartons duct and plastic collecting
tube is attached. The collector stays in position when
the patient places his tongue against the lingual surface
of the lower incisors.
Advantageit may be sorted and reused for the
individual patient. It collects saliva from sublingual and
submandibular ducts.
Function of Saliva
Digestive functionit participates in digestion by
providing fluid environment for solubilization of food
and taste substance, through action of enzyme amylase
and lipase. It helps in formation of food bolus, which is
readily chewed.
Lubricatingit keeps the oral tissues moist and facilitates
swallowing and speaking. Mucus glycoproteins provide
lubricant for the movement of oral tissues against each
other and protection from chemical and thermal insults.
Protection of teethit helps to protect the teeth from dental
caries by means of, both, cleansing and buffering action
of saliva. It also controls the calcium and phosphate
concentration in the saliva and around the teeth.
Protection from injuryit dilutes hot or irritant substance
and thus prevents injury to mucus membrane.
Maintenance of mucus membrane integritythe salivary
mucin possesses rheological properties which include
low solubility, high viscosity, elasticity and
adhesiveness which enable them to concentrate on the
oral mucosal surface. They provide an effective barrier
against desiccation and environmental insult. Salivary
mucin binds water effectively and hence serves as
natural water proofing and helps to maintain these
tissues in a hydrated state. The glycosylated mucins of
saliva are resistant to proteolysis. This maintains the
integrity of mucus membrane by neutralizing the
bacterial and PMN proteases.
Antibacterial propertiesseveral salivary substances are
capable of inhibiting the growth of microorganisms. They
are glycoproteins, antibacterial protein, i.e. lysozome,
immunoglobulin IgA, IgG, IgM and lactoferrin.
Debridment and lavagethe physical flow of saliva,
augmented by muscular activity of lips and tongue,
effectively removes a large number of potentially harmful
bacteria from the teeth and mucosal surface.
Anti-carcinogenic activitymucins limit the penetration
of variety of potential irritants and toxins in foods,
beverages as well as potentially hazardous agents from
tobacco smoke and other sources.
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Submandibular Glands
Location of swellingsubmandibular salivary gland
enlargement is characterized by medial and inferior
extension, the later resulting in discontinuity if the tissue
contours at the inferior border of mandible.
External palpationexternal palpation should start with
the finger extending towards the midline and the thumb
on the body of the mandible. Pressure is exerted, both,
superiorly and laterally and the finger is gradually
moved beneath the inferior border of the mandible.
Palpationthe patient should be advised to relax the
tongue during palpation. Enlarged lymph nodes, except
those involved with malignancy, will invariably move
laterally with the examining finger, while the submandibular salivary gland will remain stationary.
Bimanual palpationafter this, bimanual palpation
should be performed; the examiner placing the 2nd
finger of one hand into the floor of the mouth beneath
the tongue, the patient resting his teeth on the examiners
fingers, while the fingers of the other hand are placed as
previously described, that is on the skin beneath and
medial to the body of the mandible. While pressure is
exerted inferiorly intraorally by the finger, the other hand
moves superiorly and laterally so that all organs come
between the examiners two hands.
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Functional disorders
Sialorrhea
Xerostomia
Obstructive disorders
Sialolithiasis
Mucus plug
Stricture and stenosis
Foreign bodies
Extra-ductal causes
Classification
Developmental disorders
Aberrancy
Aplasia and hypoplasia
Hyperplasia
Atresia
Accessory ducts
Diverticuli
Congenital fistula
Cyst
Mucocele
Ranula
Asymptomatic enlargement
Sialosis
Allergic
Associated with malnutrition and alcoholism
Infection
Viral infection
Bacterial infection
Mycotic infection
Autoimmune disorders
Sjgrens syndrome
Mikuliczs disease
Uveoparotid fever
Recurrent non-specific parotitis
Developmental Disorders of
Salivary Gland
Aberrancy
It is defined as the situation in which the salivary gland
tissue develops at a site where it is not normally found. It is
also called as ectopic salivary gland.
Ectopic salivary tissue can develop anywhere within
the territory of the first and second branchial arches, in the
lateral neck, pharynx or middle ear.
Clinical Features
Sitetrue aberrant salivary glands are most frequently
reported in the cervical region, near the parotid gland or
body of the mandible. The salivary gland tissue in the
mandible is found posterior to the first molar and often
has a small communication with a major salivary gland.
Developmental lingual salivary gland depressionthe
aberrancy of the salivary gland tissue represents only
an extreme example of the condition known as the
developmental lingual mandibular salivary gland
depression. It is the developmental inclusion of the
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Fig. 26-5: Hypoplasia of the unilateral parotid gland (Plain CT). Size of
the left parotid gland (yellow arrow) is remarkably smaller compared with
normal size of the right parotid gland (red arrow) (Courtesy M Shimizu).
Diagnosis
Clinical Features
Management
Causes
Radiological Features
CT featuresit is sometimes observed that unilateral
gland is missing (Fig. 26-5) or is very small compared to
the contralateral side with congenital or posterior
reasons. As they are mostly asymptomatic, the condition
is mostly diagnosed by chance.
Causes
Hormonal disordersendocrine disorders and menopause.
Metabolic disordersgout, diabetes mellitus.
AutoimmuneSjgrens syndrome, Waldenstrom
macroglobulinemia.
Syndromeaglossia-adactylia syndrome, Heerfordts
syndrome and Feltys syndrome.
Miscellaneoushepatic disease, starvation, alcoholism,
inflammation, benign lympho-epithelial lesion,
adiposity, hyperthermia, oligomenorrhea and certain
drugs.
Clinical Features
Prevalenceit is more common in minor salivary glands
of the palate.
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Radiological Features
CT featuresComputed tomography will diagnose this
condition.
Congenital Fistula
Patients with branchial cleft anomalies usually present
with unilateral, painless swelling in the region of parotid.
Rarely, they are bilateral. They form sinus tracts either in
the crease behind the pinna or in front of tragus. They
discharge saliva intermittently. Abscess formation, due to
secondary infection, may occur. Complete surgical excision
of the sinus tract is essential. The dissection is often very
extensive and full dissection of facial nerve may be
required.
Diagnosis
Clinical diagnosisit is not specific.
Radiological featurescomputed tomography will
diagnose this condition.
Management
Excision for microscopic examinationas it cannot be
differentiated from minor salivary gland tumors, it
becomes essential to excise it for microscopic
examination.
Atresia
It is the congenital occlusion or absence of one or two major
salivary gland ducts. Usually the submandibular duct in
the floor of the mouth fails to cannulate during embryological development. The newborn infant presents, within
2 or 3 days of life, with submandibular swelling on the
affected side due to the presence of a retention cyst. It may
produce a relatively severe xerostomia.
Accessory Duct
An accessory parotid lobe is the most common
developmental anomaly. It occurs in as many as 20% of
subjects. Its position is constant, arising from the horizontal
component of the parotid duct as it crosses the masseter
muscle. Its importance lies in the fact that any of the diseases
that can affect the salivary glands, may involve the
accessory lobe and lead to diagnostic confusion, as the
possibility is not considered. This is because the symptoms
and signs are not within the normal anatomical territory of
the parotid. Presence of additional duct in some salivary
glands has been reported.
Diverticuli
They are small pouches or out pocketing of the ductal
system of one of the major salivary glands. Their presence
leads to recurrent episodes of acute parotitis.
Clinical Features
Incidence and sexit is rare. Males are affected more
commonly than females.
Siteit is located in the posterior body of the mandible.
Sublingual gland bony defectin some cases cortical defect
can also occur in anterior region. These defects are related
to sublingual gland.
Symptomsit is asymptomatic and only diagnosed on
radiographical examination.
Signsometime a notch or depression can be palpable
on clinical examination in the posterior area.
Radiographic Features
Siteit is found below the mandibular canal and above
the inferior border of mandible, just anterior to the angle
of jaw and below and just posterior to third or second
molar (Fig. 26-6).
Size and shaperound or ovoid radiolucency that will
vary in size from 1 to 3 cm in diameter. It is occasionally
bilateral.
Bordersit is well defined by dense radiopaque border
that is the result of the rays passing tangentially through
the relatively thick wall of depression.
Sublingual bony defectin some instances, round or ovoid
radiolucency may occur in the anterior segment of the
mandible, generally appearing as a rather poorly
circumscribed lesion, somewhere between the first
premolar and central incisor area. This may be caused
by impingement of sublingual gland.
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Fig. 26-6: Stafnes bone cyst presented as radiolucency below the
mandibular canal and surrounded by well corticated border (Courtesy
Dr Tapasya Karamore).
Diagnosis
Clinical diagnosisit is not possible or suspect this
disease clinically.
Radiological diagnosisround radiolucency located
below the mandibular canal in molar area will diagnose
this condition.
Differential Diagnosis
Radicularit is associated with carious tooth and
radiolucency is attached to the root of teeth.
Residualpre-extraction radiograph shows tooth with
evidence of deep caries.
Management
No treatment is necessary as the patient is asymptomatic.
Clinical Features
Droolingthe salivary flow is more in infancy and
childhood, but the drooling observed in infants is related
to inadequate swallowing rather than excessive
production. Drooling or sialorrhea can be a devastating
problem for the affected child or adult.
Symptomsthe problem may range from mild embarrassment and discomfort to emotional and physical
impairment. The involved person may require numerous
clothings and/or bib changes per day.
Signshe or she may develop cheek scarring, lip
chapping or infection from constant exposure to saliva.
The soiling of clothes, carpets, furniture, books and
people, often results in social rejection, employment
difficulties and stigmatization.
Management
Sialorrhea (Ptyalism)
An increased salivary secretion is termed as sialorrhea or
ptyalism.
Mechanisms
The secretory innervations of the salivary glands are
primarily under the control of the parasympathetic nervous
system. Stimulation of the parasympathetic system causes
profuse secretion of watery saliva. Some persons are unable
to swallow their saliva fast enough to prevent drooling.
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Xerostomia
It is the subjective clinical condition of less than normal
amount of saliva. It is dryness of mouth, which is a clinical
manifestation of salivary gland dysfunction.
Etiology
Radiation inducedionizing radiation to head and neck
region for the treatment of cancer results in pronounced
Clinical Features
Effect of xerostomia on oral functionspatient may notice
increased thirst, increased uptake of fluid especially
while eating. There is also frequent use of means like
chewing gums and consumption of sour candy. Patient
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Management
Stimulation of salivary production
Local stimulationchewing of gums, mints, paraffin and
citric acid containing lozenges and rinses. Disadvantages of it are:
Effects are short lived.
Frequent application can be inconvenient.
Citric acid may irritate oral mucosa.
Continuous use may contribute to demineralization.
Systemic stimulation
Bromhexineit is a mucolytic and mucokinetic agent,
capable of inducing thin copious bronchial secretions.
Doseadults (8 mg TDS), children 1-5 years (4 mg
BD) and children 5-10 years (4 mg TDS).
Anethole trithione (ANTT)it is a directly acting
cholinergic agonist which acts by neurostimulation.
Dose 1 to 2 tabs (25 mg) TDS.
Pilocarpinepilocarpine is a cholinergic parasympathomimetic agent with a broad range of pharmacologic effects. It increases the secretion by exocrine
glands and can affect the sweat, salivary, lacrimal,
gastric, pancreatic, intestinal glands and mucosal
cells of the respiratory tract. The usual dose is 5 mg,
TDS. It produces short duration of (3 hours) increased
salivary flow, without the accompanying side effects.
It should not be used in patients suffering from asthma.
Symptomatic treatment
Salivary substitutethere are number of salivary
substitute available for the treatment of xerostomia. Most
commonly contain carboxymethylcellulose or
hydroxyethylcellulose as lubricants and variety of
artificial sweeteners, preservative and chloride or
fluoride salts. Disadvantages are:
Their regular use is inconvenient to the patient.
Most of them are more viscous than the natural
saliva.
They are expensive.
They fail to provide antimicrobial and other protective
functions of natural saliva.
Composition of artificial saliva
Carboxymethylcellulose10 gm/l.
Sorbitol30 gm/l.
Potassium chloride1.2 gm/l.
Sodium chloride0.843 gm/l.
Magnesium chloride0.051 gm/l.
Calcium chloride0.146 gm/l.
Dipotassium hydrogen phosphate0.342 gm/l.
Oral hygiene productpatient should use oral hygiene
product which include lactoperoxidase, lysozyme, and
lactoferrin.
Discontinuous of drugdrug which is causing xerostomia
should be discontinued.
Suggestions to the patient having xerostomia
Sweet and tart foodtry very sweet or tart foods and
beverages such as lemonade; these foods may help to
produce more saliva. (Do not try this in sensitive teeth or
sore throat.)
Sucking of sugar free candysuck on sugar-free hard
candy (avoiding those with citric acid), popsicles or
chew sugar-free gum. These can help produce more
saliva.
Sucking ice cubestry sucking ice cubes or ice lollies.
Home-made lollies can be easily made by freezing fresh
juice in ice-cube trays or in special lolly containers with
sticks, which can be bought from many kitchenware
shops.
Dont take following thingavoid chewable vitamin C
and acidic, sugared lozenges. Avoid dry foods such
as cookies, toast and crackers, or soften them with
liquids before eating. Avoid chocolates, peanut butter
and pastry: they stick to the roof of mouth. Avoid over
salty foods.
Soft and liquid fooduse soft and liquid foods, which
may be easier to swallow.
Drink frequentlyhave a sip of water every few minutes
to help in swallowing and talking more easily. Carry a
small water bottle for frequent sips during the day.
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Obstructive Disorders
Clinical Features
Sialolithiasis
It is the formation of calcific concretions within the
parenchyma or ductal system of the major or minor salivary
glands. It is also called as salivary gland stone or salivary
gland calculus. These are stones within major and minor
salivary glands. These are the most common calcifications
found in soft tissues of oro-orbital region.
Composition
Calculusthe calculus consists of laminated layers of
organic material, covered with concentric shells of
calcified material.
Crystalline structurethe crystalline structure is chiefly
hydroxyapatite and contains octacalcium phosphate.
Chemical compositionthe chemical composition is
principally calcium phosphate and carbon with traces
of magnesium, potassium, chloride and ammonium.
Etiopathogenesis
Neurohumoral mechanisma neurohumoral condition,
leading to salivary stagnation, results in a nidus and
matrix formation.
Metabolic mechanismin the presence of coexisting
inflammation, a metabolic mechanism favors
precipitation of salivary salts into the matrix.
Prevalence
Submandibular (83%) calculi are more commonly seen than
the parotid (10%) or sublingual (7%) calculi, due to
following factors.
Anatomic factors
The length and irregular course of Whartons duct.
The submandibular gland and ductal system lies in
a dependent position.
The greater size and position of the orifice.
The orifice is much smaller than duct lumen.
Physiochemical factors
High mucin content of saliva.
Great degree of alkalinity with high percentage of
organic matter.
Greater concentration of calcium and phosphate
salts.
Low content of carbon dioxide.
Richness in phosphatase enzyme.
Types
Ductal sialolithsit is located in the duct of gland.
Glandular sialoliths.
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Radiographic Features
Fig. 26-7: Well defined radiopacity seen at the angle of mandible due
to salivary stone (Courtesy Enzio Rovigutti)
Diagnosis
Palpationpalpation is an indispensable tool in the
diagnosis of sialoliths. Palpation of the suspected gland
frequently reveals it to be larger or firmer than the normal
gland of the opposite side. Digital manipulation will
produce a flow of saliva through the duct orifice and
will allow visual inspection of the salivary fluid. During
examination, the soft tissues overlying the duct should
be manually stretched. Often, the physical distortion
caused by the presence of calculus will become apparent.
In addition yellowish color of the calcific deposits may
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Management
Manual manipulationin case of small stone, gentle
massage of the gland should be done. It will help to
move the stone toward the duct orifice. Sialogogues, moist
heat and increased fluid intake will also promote the
passage of stone.
Stone in the submandibular ductif the stone is palpated
near the orifice of the duct it can be removed by an
incision made directly over it through the mucus
membrane of the mouth.
Stone in the submandibular glandin this case, excision
of gland is advised.
Antibioticsif acute infection is present, then antibiotics
should be given.
Salivary gland endoscopythis is newer method which
is useful in removal of sialoliths.
Lithotripsythis is fragmentation of stone in the gland.
Nowadays, extracorporeal shock wave lithotripsy has
been successful in many patients.
Mucus Plugs
These are incompletely mineralized sialoliths. Clinical
symptoms and signs are same as that of stones. The diagnosis
of mucus plug is based upon clinical history, radiography
and sialograms. If sialograms confirm the intraductal
obstructive disease secondary to non-mineralized intraductal object, the diagnosis of mucus plug can be made.
Types
Papillary obstructionit may be either acute ulcerative
obstruction or chronic fibrotic stenosis. Acute ulcerative
obstruction is usually caused by acute trauma to the
papilla and is treated conservatively with saline rinses
and salivary gland massage. The ulcer generally heals
without scarring and the symptoms will subside in such
cases. In chronic fibrotic papillary obstruction irritations
to papilla has been recurrent and scarring exists.
Duct obstructionit may be due to a variety of factors. In
cases of ductal obstruction secondary to acute trauma
treatment is directed towards providing the duct
patency until the edema is resolved. When the ductal
obstruction occurs secondary to irritation or scar
contracture, sialograms are helpful in localizing the
status of gland. If the gland is healthy, progressive and
frequent dilatation of involved duct with lacrimal probes
is generally successful in relieving the symptoms and
signs. If this does not prove beneficial, ductoplasty is
indicated.
Foreign Bodies
Rarely, foreign bodies become lodged within Whartons
duct and less commonly in Stensens duct. Toothbrush
bristles, toothpicks, spikes of wheat, fish bone, portions of
fingernail have been reported within the salivary gland
duct and act as causes of obstructive and/or inflammatory
disease of the salivary gland.
Extraductal Causes
Muscle pressure, tumors, enlarged lymph nodes and
denture flanges associated with the primary salivary duct
can cause obstructive signs and symptoms.
Parotid Fistula
It may arise from parotid gland or duct. It may be internal,
when it opens inside the mouth and external, when it opens
to the exterior.
Causes
Etiology
Irritationirritation from prosthetic appliances,
maloccluded or malpositioned teeth.
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Clinical Features
Symptomsthe main complaint is opening in the cheek
with discharge.
Signsdischarge come out only during meals.
Adjacent skinthere may be excoriation of the
neighborhood skin.
Sialograms
Diagnosis
Clinical diagnosisdischarged from Stensens duct after
trauma or surgery.
Radiological diagnosisit will exactly diagnose the
parotid fistula.
Management
Reconstruction of the ductit is done by surgical approach.
Etiopathogenesis
Traumait is caused by laceration of a minor salivary
gland duct by trauma resulting in extravasation of mucus
into the connective tissue. There is accumulation of
mucus in the connective tissue and with the continuous
pooling of saliva a clearly demarcated cavity develops
which has no epithelial lining.
Clinical Features
Age and sexmucus extravasation cysts occur in
younger patients. The reason for occurrence in young
people as they are more prone to trauma that induce
mucin spillage. It is equal in both sexes.
Sitethey are very common and occur most frequently
on the inner aspect of lower lip (Fig. 26-10); but may also
occur on the palate, cheek, tongue and floor of mouth.
The lesion may lie fairly deep in the tissues or may be
exceptionally superficial.
Symptomspatient may complain of painless swelling
which is frequently recurrent. The swelling may suddenly develop at meal time and may drain simultaneously at intervals.
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Clinical Features
Age and sexit is usually fun in children and young
adults with no sex predilection.
Sitethe typical position is on the floor of the mouth
(Fig. 26-13), below the tongue and on the side of frenum.
They are usually unilateral.
Fig. 26-12: Dome-shaped swelling of mucocele (Courtesy Dr Parate).
Diagnosis
Clinical diagnosisdome shaped soft swelling on lower
lip which is lateral to midline is typical features of
mucocele.
Laboratory diagnosisin biopsy, it shows vacuolated
macrophages which are sometimes called as muciphage.
Differential Diagnosis
Vascular lesion and superficial non-keratin cystaspiration
should be done.
Early Mucoepidermoid tumor and adenocarcinoma
induration is present.
Management
Surgical excisioncomplete excision of the mucocele
should be done under local anesthesia. To avoid
recurrence, adjacent minor salivary gland should also
be removed which are feeding the lesion.
Cryosurgerysurgery with cryoprobe is also helpful in
managing the mucocele.
Ranula
It is derived from Latin word Rana tigerina, i.e. frog belly.
The term ranula is used for the mucoceles occurring in the
floor of the mouth, in association with ducts of submandibular or sublingual glands.
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Radiological Features
CT featuresOn CT, the lesion is observed as a
homogeneous, water density mass with clear boundary
(Fig. 26-15A)
MRI featureson MR images, the lesion shows low signal
intensity on T1 weighted images; very high signal
intensity on T2 weighted images. On sonograms, the
plunging ranulas are observed as a well-delineated, but
not round, anechoic mass (Fig. 26-15B).
Diagnosis
Clinical diagnosisblue shaped swelling in floor of mouth
in lateral position will go in favor of ranula.
Radiological diagnosisMRI and CT scan will
demonstrate lesion.
B
Figs 26-15A and B: Simple ranula. (A) T1 weighted MR image shows
lower signal intensity than that of muscles in the left sublingual region;
(B) T2 weighted MR image of the same case. Note the remarkably high
signal intensity of the lesion (Courtesy M Shimzu).
Management
Surgical excisionthey are best treated by surgical
excision including a portion of the surrounding tissues.
Partial excision with marsupializationthe major part of
the cyst wall together with its overlying mucus
membrane is excised.
Differential Diagnosis
Etiopathogenesis
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Diagnosis
Radiological Features
Sialographyon sialography, leafless tree appearance
is seen (Fig. 26-16). This appearance is caused by
compression of finer duct by hypertrophic aciner cells.
Management
Surgical excisionit is treated by conservative surgical
excision.
Antibioticsin some cases of multiple retention cyst,
antibiotics like erythromycin and chlorhexidine mouth
is helpful in relieving the pain of the patient.
Sialogoguesthis is helpful in stimulating salivary flow
and thereby preventing an accumulation of mucin.
Etiopathogenesis
Systemic diseasethe condition is found in association
with systemic diseases especially cirrhosis, diabetes,
ovarian and thyroid insufficiency, alcoholism, general
malnutrition, anorexia nervosa, and malnutrition.
Neurogenic medicationneurogenic medication like
antihypertensive drugs, psychotropic drugs and
sympathomimetic drugs can cause sialosis.
Mechanismabove disease may result in dysregulation
of the autonomic innervations of the salivary acini
causing an aberrant intercellular secretory cycle.
Clinical Features
Age and sex distributionit more commonly affects the
females. As such there is no age predilection.
Diagnosis
Clinical diagnosisbilateral non-inflammatory enlargement of parotid gland gives one clue to the diagnosis.
Radiological diagnosisleafless tree appearance seen in
this disease.
Laboratory diagnosisa characteristic alteration in the
chemical constituents of saliva is a distinguishing feature
of sialosis. Significant elevation of salivary potassium
and concomitant decrease in salivary sodium is observed.
Management
Control of underlying causethis is most important
management for sialosis.
Partial parotidectomyit can be performed if swelling
becomes cosmetic concern.
Allergic Sialadenitis
In some cases, it may not appear as a true hypersensitivity
reaction but rather as a toxic or idiosyncratic reaction to
drugs that cause decreased salivary flow, resulting in
secondary infection.
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Etiopathogenesis
Transmission
Saliva and urineit usually spreads from human
reservoir, by airborne infection of infected saliva and
possibly urine.
Clinical Features
Clinical Features
Appearancethe clinical appearance of allergic sialadenitis varies, but in most of the cases, there is bilateral
parotid gland enlargement following the administration
of the drug.
Symptomsthe enlargement may be painful and is
usually associated with conjunctivitis and skin rashes.
Diagnosis
Clinical diagnosisenlargement of gland with skin
rashes and conjunctivitis.
Management
It is a self-limiting disease and needs no treatment. But
in some cases, secondary bacterial infection may develop
and need treatment.
Viral Infection
Complications
Mumps
It is also called as epidemic parotitis. It is an acute contagious
viral infection, characterized chiefly by unilateral or
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Diagnosis
Clinical diagnosisthe presence of parotitis and
accompanying systemic signs of viral infections.
Laboratory diagnosissalivary amylase level is increased.
A paramyxovirus may be isolated from saliva for as long
as 6 days before and up to 99 days after the appearance
of salivary gland swelling.
Management
Vaccinationprevention with live attenuated vaccine is
the best method of controlling the disease. Vaccine
should be given in 12 to 15 months of life. It should be
repeated at the age of 4 to 5 years.
Symptomatic treatmentsymptomatic treatment is given
to control pain and swelling. Mainly non-aspirin
analgesic and antipyretic should be given.
Restbedrest is recommended to minimize the chances
of orchitis.
Diet restrictionpatient should avoid sour foods and
drinks to decrease salivary gland discomfort.
Etiology
Microorganismsit is most commonly caused by
penicillin resistant Staphylococcus aureus or streptococci
viridians.
Host factorit may be caused due to decreased host
resistance, decreased salivary secretion and decreased
bactericidal effect of saliva.
Predisposing factorsit can occur in conditions such as
dehydration, malnutrition, cancer and surgical
infections.
Surgical procedureit is common when major surgical
procedure is carried out in patient with poor oral hygiene.
Oral hygienepoor oral hygiene is an important
contributory factor.
Drugsdrugs like anti-Parkinsons, diuretics and
antihistaminic have been reported to be a contributory
factor for acute bacterial sialadenitis.
Clinical Features
Agemost of the cases occur in adults but neonates and
childhood form of the disease may occur.
Siteunilateral involvement of parotid gland is common.
Prodromal symptomsit begins with the elevation of body
temperature and sudden onset of pain at the angle of the
jaw which is intense when the extensive infection is
contained within the confines of the parotid capsule.
Symptomsthe localized symptoms are accompanied
by fever, leukocytosis and other generalized signs and
symptoms of acute bacterial infection.
Signsparotid gland is tender, enlarged and the
overlying skin is warm and red. The swelling usually
causes elevation of the ear lobule (Fig. 26-17) and the
overlying skin is characteristically warm and red.
Bacterial Infection
Bacterial infection of salivary gland may be recurrent and
generally develops owing to spread of microorganisms from
the oral flora along the excretory duct.
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Radiological Features
Sonographythe affected gland shows swelling,
increased vascularity, however, echo level is not
decreased.
CT featureswhen the glands are involved in cellulitis,
swelling of the glands and obscuration of the glands
contour can be observed. On enhanced CT, the affected
glands are seen with a higher CT values compared with
the normal side because of the increased vascularity (Figs
26-18A and B).
Diagnosis
Clinical diagnosistender parotid gland with elevation
of ear lobule with purulent material seen from Stensens
duct.
Radiological diagnosissonography and computed
tomography will diagnose this condition.
B
Figs 26-18A and B: Sonograms of acute sialadenitis of the
submandibular gland scanned perpendicular to the mandibular plane
(left side: cranial, right side: caudal). (A) The left submandibular gland
shows swelling, however, normal echo level. The black lines inside the
gland are not dilated ducts, they are blood vessels; (B) The gland
shows increased vascularity (Courtesy Dr M Shimizu).
Management
Oral hygienemeticulous oral hygiene should be
practiced. Oral hygiene should be maintained by
debridement and irrigation.
Dietsoft diet should be given as chewing is painful.
Antibioticsit is treated aggressively with antibiotics.
Even death can result in debilitated patients. Specimen
of purulent material should be immediately sent to
laboratory for sensitivity and culture. Treatment usually
starts with high dose of parenteral antibiotics active
against penicillin resistant Staphylococcus.
Electrolyte balancethe patient must be adequately
hydrated and the electrolyte balance should be properly
maintained with intravenous fluids.
Stimulation of salivasalivation should be stimulated to
facilitate drainage by sucking the sour hard candy.
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Etiology
Ductal obstructionit results due to recurrent or persistent
ductal obstruction.
Other causescongenital stenosis, Sjgrens syndrome,
or previous viral infection or allergy.
Clinical Features
Agethe childhood form commonly begins between the
ages of 3 and 5 years and is usually unilateral.
Symptomsthe pain is usually minimal and antibiotic
therapy resolves the infection within a week.
Appearanceit appears as a unilateral swelling at the
angle of the jaw in a patient with the history of similar
occurrence (Fig. 26-19).
Signssalivary flow is accompanied by flecks of
purulent material. After several recurrences, fibrosis of
the glandular parenchyma occurs, which leads to
decreased salivary flow.
Diagnosis
Clinical diagnosisminimum pain in parotid gland area
with purulent material seen from duct of gland.
Radiological diagnosisdilation and multiple ectasia
seen on the radiograph.
Management
Radiation therapyit is used extensively to cause fibrosis
of salivary gland, but there are then increase incidences
of head and neck tumors.
Surgical removaltotal removal of parotid gland in cases
of intractable cases. But is risk of facial nerve palsy.
Antibiotics injectionintraductal injection of erythromycin or tetracycline. In it, cannulate the duct and anesthetize the area with an infusion of lidocaine directly in the
duct system, which is followed by infusion of antibiotics
into the duct at a concentration of 15 mg/ml.
Ligation of Stensens ductligation of Stensens duct is a
relatively simple procedure and can lead to fibrosis.
Pathogenesis
Radiological Finding
Clinical Features
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Radiographic Features
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosissialectasis with sausage link
appearance with absence with terminal branches will
diagnose this condition.
Management
There is no specific treatment for this disease. In some cases
removal of gland is recommended.
Autoimmune Disorders
Sjgrens Syndrome
It is a chronic inflammatory disease that predominately
affects salivary, lacrimal and other exocrine glands. It was
first described by Henrik Sjgren in 1933. It predominately
affects middle aged and elderly women.
Types
Primary Sjgrens syndromeit is also called as sicca
syndrome and it consists of dry eyes (xerophthalmia)
and dry mouth (xerostomia).
Secondary Sjgrens syndromeit consists of dry eyes, dry
mouth and collagen disorders usually rheumatoid
arthritis or systemic lupus erythematous.
Clinical Features
Age and sex distributionit is more commonly seen in
middle age adults. It is most commonly found in females
with 90% of cases are reported in them.
Eyesthe effect on eye is called as keratoconjunctivitis
sicca (dry). The patient usually complains of dry eyes or
continuous irritation in the eyes. Severe lacrimal gland
involvement may lead to corneal ulceration as well as
conjunctivitis.
Connective tissue disordersin patients with secondary
Sjgrens syndrome, rheumatoid arthritis is typically
long standing and clinically obvious feature. Patients
may have small joint and ulnar deviation of fingers and
rheumatoid nodules.
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Oral Manifestation
Symptomsxerostomia is a major complaint in most of
the patients. But many patients do not complain of dry
mouth, but rather of an unpleasant taste, difficulty in
eating dry food, soreness or difficulty in controlling
dentures.
SignsPus may be emitted from the duct. Angular
stomatitis and denture stomatitis also occur.
Enlargementdry mouth may be accompanied by
unilateral or bilateral enlargement of parotid gland,
which occurs in about one-third of the patients and may
be intermittent. Enlargement of submandibular gland
may also occur.
Salivaclinically, the mouth may appear moist in early
stages of Sjgrens syndrome but later, there may be lack
of the usual pooling of saliva in the floor of the mouth
and frothy saliva may form along the lines of contact
with oral soft tissue.
Mucosain advanced cases, the mucosa is glazed, dry
and tends to form fine wrinkles. Soreness and redness
of mucosa is usually the result of candidial infection.
Speechin some patients, there may be clicking quality
of their speech, caused by sticking of the tongue to the
palate.
Tonguethe tongue typically develops a characteristic
lobulated, usually red surface with partial or complete
depapillation. There is also decrease in number of taste
buds, which leads to an abnormal and impaired sense
of taste.
Dental cariesdental caries is severe and gross
accumulation of plaque may be obvious.
Periodontal diseaseperiodontal disease can also occur.
Acute bacterial sialadenitisSjgrens syndrome is the
most common underlying cause of acute bacterial
sialadenitis in ambulated patients. Such infections are
usually either staphylococcal or pneumoccocal and
usually cause swelling of the salivary gland. The
overlying skin is red, tender and shiny.
Lymph nodesthe regional lymph nodes may be enlarged
and tender.
Radiological Features
Sialographyif the salivary flow rate is equivocal,
sialography can be used to detect the damage. The most
typical finding in Sjgrens syndrome is that of
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Diagnosis
Clinical diagnosisxerostomia, keratoconjunctivitis sicca
with parotid enlargement may aid in diagnosis of
Sjgrens syndrome
Sialographysnowstorm and branchless fruit laden tree
appearance.
San Diego criteria for diagnosis of Sjgrens syndrome.
Ocular drynessSchirmers
test less than 8 mm wetting
per 5 minute, positive rose
Bengal staining of cornea
Dry mouthdecreases
parotid flow Lashley cups
method
Systemic autoimmunity
elevated Rh factors, elevated
antinuclear antibody and
presence of anti-SS and
anti-SS-B antibodies
Laboratory Investigations
Rose Bengal staining testkeratoconjunctivitis sicca is
characterized by corneal keratotic lesion, which stains
pink when rose Bengal dye is used.
Schirmer testthe reduced lacrimal flow rate is measured
by this test. A strip of filter paper is placed in between
the eye and the eyelid to determine the degree of tears
which should be measured in millimeter. When the flow
is reduced to less than 5 mm in a 5 minute sample, patient
should be considered positive for Sjgrens syndrome.
Sialometrysalivary flow rate estimation is a sensitive
indicator of salivary gland function. Parotid glands make
the major contribution to total salivary flow and are the
most consistently affected glands in patients with
Sjgrens syndrome. Stimulated flow rate in symptomatic primary and secondary Sjgrens syndrome is
usually below 0.5 to 1.0 ml/minute (normal 1 to 1.5 ml/
minute).
Sialochemistryparotid saliva in Sjgrens syndrome
contains twice as much total lipid and has elevated
content of phospholipids and glycolipids than the
normal saliva. The sodium chloride and phospholipids
levels are higher in saliva of Sjgrens syndrome patient.
Immunologica routine autoantibody profile can usually
be carried out with the particular aim of detecting
rheumatoid and antinuclear factors.
Hematological investigationsit is necessary, particularly
to exclude anemia. ESR or plasma viscosity, leucopenia
occasionally may also be found.
Microbiological investigationsa swab from oral mucosa
should be taken to confirm candidiasis, if there is
soreness and erythema. Examination of pus is also
Management
Ocular lubricantkeratoconjunctivitis is treated by
instillation of ocular lubricants, such as artificial tears
coating methylcellulose and xerostomia is treated by
saliva substitutes.
Oral hygiene maintenancescrupulous oral hygiene and
frequent fluoride application is indicated to reduce these
problems.
Salivary stimulantbromhexine, pilocarpine and
cevimeline can be used to stimulate salivary flow.
Surgerysurgery for enlargement of salivary gland is
only recommended when the enlargement is casing
discomfort to the patient.
Clinical Features
Age and sexit occurs more commonly in women in
middle and later life.
Siteit is manifested as a unilateral or bilateral enlargement of parotid and/or submandibular gland.
Prodromal symptomsthe onset of the lesion is some
times associated with fever, upper respiratory tract
infection, oral infection, tooth extraction or some local
inflammatory disorders.
Symptomsin some cases, there is mild local discomfort,
occasional pain and xerostomia.
Signsthere is often diffuse, poorly outlined enlargement
of salivary gland rather than formation of a discrete tumor
nodule. The enlargement varies in size but generally
few centimeters in diameter. There is history of
alternating increases and decreases in the size of mass,
from time to time.
Durationthe duration of the tumor mass may be only a
few months or many years.
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Management
Surgical excisionsurgical removal of involved gland
should be carried out. Prognosis is good.
Uveoparotid Fever
It is a form of sarcoidosis and it is also called as Heerfordts
syndrome.
It consists of a triad of
Uveitisinflammation of uveal tract of the eye.
Parotid swellingfirm, painless and bilateral enlargement of parotid gland.
Facial palsy
Etiology
Infectiontuberculosis was earlier thought to be the
causative agent.
Hereditaryhereditary factors also play an important
role in this syndrome.
Autoimmuneautoimmune mechanism of the body can
also be responsible.
Clinical Features
Ageit usually occurs in 3rd and 4th decades of life.
Prodromal symptomsprodromal symptoms lasting from
a few days to several weeks are the usual initial signs of
the disease and patient complains of fever, malaise,
weakness, nausea and night sweat.
Appearanceit appears as a bilateral, firm, painless
parotid swelling. The parotid swelling lasts from several
months to several years.
Involvement of other glandsubmandibular, sublingual
and lacrimal gland swelling may develop independently
or during the course of the parotid swelling.
Sarcodial lesionsarcodial lesion may also be found in
the oral cavity.
Uveitisit is an inflammation of the uveal tract, is a
feature of this disease. Although ocular symptoms are
usually bilateral, they become more apparent before the
appearances of parotid swelling.
Nerve involvementthe most common nerve involved is
facial nerve. there is unilateral or bilateral seventh nerve
paralysis. The neurological signs may precede, follow
or appear simultaneously with parotid swelling. There
Radiographic Features
The sialographic picture merely shows the severity and
duration of the disease process within the particular
gland.
Diagnosis
Clinical diagnosisparotid swelling with facial palsy
and uveitis will diagnose this syndrome.
Laboratory diagnosisit will reveal a characteristic
sarcoid nodule.
Management
Corticosteroidsit is largely asymptomatic as it may
undergo spontaneous remission. Corticosteroid can be
used in cases of acute exacerbation.
Classification
See Tables 26-1 and 26-2.
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Adenoma
Pleomorphic adenoma
Myoepithelioma
Basal cell adenoma
Warthins tumor
Oncocytoma
Canalicular adenoma
Sebaceous adenoma
Ductal papilloma
Inverted ductal papilloma
Intraductal papilloma
Sialadenoma papilliferum
Cystadenoma
Papillary cystadenoma
Mucinous cystadenoma
Monomorphic adenoma
Adenolymphoma (Warthins tumor)
Oxyphilic adenoma (oncocytoma)
Other types
Basal cell adenoma
Canalicular adenoma
Mucoepidermoid tumor
Acinic cell tumor
Carcinoma
Acinic cell carcinoma
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Polymorphous low grade adenocarcinoma
Epithelial myoepithelial carcinoma
Basal cell adenocarcinoma
Sebaceous carcinoma
Papillary cystadenocarcinoma
Mucinous adenocarcinoma
Oncocytic carcinoma
Salivary duct carcinoma
Adenocarcinoma
Malignant myoepithelioma
Carcinoma in pleomorphic adenoma (Malignant pleomorphic
adenoma)
Squamous cell carcinoma
Small cell carcinoma
Undifferentiated carcinoma
Other carcinomas
Non-epithelial tumors
Malignant lymphoma
Secondary tumors
Unclassified tumors
Tumor like lesions
Sialadenosis
Oncocytosis
Necrotizing sialometaplasia
Benign lymphoepithelial lesions
Salivary gland cyst
Chronic sclerosing sialadenitis of submandibular gland
Cystic lymphoid hyperplasia in AIDS
Firm tumor
Soft tumor
Pleomorphic adenoma
Adenoid cystic carcinoma
Mucoepidermoid tumor of
high grade
Carcinoma in pleomorphic
adenoma
Acinic cell carcinoma
Oncocytoma
Well differentiated
Mucoepidermoid tumor
Papillary cyst adenoma
Mucus producing
adenocarcinoma
Warthins tumor
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Benign Tumors
Pleomorphic Adenoma
Pathogenesis
Myoepithelial cellsmyoepithelial cells are responsible
for morphologic diversity of tumor including production
of fibrous, mucinous, chondroid and osseous structures.
Differentiation of ductal reserve cellsintercalated duct
reserve cells can differentiate into ductal and myoepithelial cells and the later can then undergo mesenchymal
metaplasia since they inherently have smooth muscle
like properties.
Neoplastic altered epithelial cellsa neoplastically altered
epithelial cell with potential for multidirectional
differentiation may be responsible for pleomorphic
adenoma.
Clinical Features
Sex and agewomen to men ratio is 6:4. It is common in
4th to 6th decades but also seen in young adults and
children
Siteparotid 90% and intraoral palatal gland on lip. In
parotid involvement, superficial portion is most
commonly affected (Fig. 26-23).
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Fig. 26-26: Ball in hand appearance seen on sialography in
pleomorphic adenoma (Courtesy M Shimizu).
Diagnosis
Clinical diagnosissmooth surface enlargement in the
parotid region will suspect pleomorphic adenoma.
Sialographyball in hand appearance seen (Fig. 26-26).
CT diagnosisthis will also help to know exact extension
of location (Fig. 26-27).
Laboratory diagnosisbiopsy shows cuboidal cells
arranged in tubes or duct-like structures, which begin to
resemble the normal ductal epithelium. Duct-like spaces
contains eosinophilic coagulum.
Management
Surgical excision.
Parotid glandtumor and the involved lobe of gland
is removed.
Submaxillary glandremoval of the gland and tumor
in continuity.
Intraoral lesionextracapsular incision.
Hard palateexcised with overlying mucosa.
Lip, soft palateenucleation or extracapsular excision.
Recurrence raterecurrence rate is 5 to 30% due to
hypocellularity, incomplete resection and encapsulation.
Monomorphic Adenoma
Monomorphic adenoma is divided into three groups by
WHO, i.e. adenolymphoma (Warthins tumor), Oxyphilic
adenoma (oncocytoma) and other histologic patterns like
basal cell adenoma and canalicular adenoma. But
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Clinical Features
Age and sexit is more common in females. Older age
group, usually over 60 years of age are affected.
Siteit occurs primarily in major salivary glands
particularly in the parotid gland and intraorally, upper
lip.
Symptomsthe tumor is usually painless and is characterized by slow growth.
Membranous basal cell adenomathis type of variant of
basal cell adenoma occurs in association with appendage
tumors like dermal cylindroma and trichoepitheliomas.
Diagnosis
Clinical diagnosisit is difficult to make clinical
diagnosis.
Laboratory diagnosisbiopsy shows fairly well defined
connective tissue capsule. The cells are isomorphic and
baseloid with round to oval nuclei.
Management
Warthins Tumor
It is also called as adenolymphoma and primary cystadenoma
lymphomatosum. This tumor was first described by Albrecht
and Arzt but it usually bears the name of Warthin in the
recognition of the pathologist who first described it in USA
in 1929.
Development
Heterotrophic salivary gland tissuetumor arises from
salivary gland tissue entrapped with para-parotid or
intra-parotid lymph nodes during embryogenesis.
Delayed hypersensitivity diseaseit is most likely a delayed
hypersensitivity disease, the lymphocytes being an
immune reaction to the salivary ducts which undergo
oncocytic change.
Secretory immune responseHsu has suggested that it is
an exaggerated secretory immune response.
Other factorsother factors like smoking and EpsteinBarr virus have also been responsible for Warthin tumor.
Clinical Features
Management
Surgical excisionit is treated by surgical excision and
recurrence is seldom seen.
Canalicular Adenoma
It occurs exclusively in minor salivary gland.
Clinical Features
Age and sexit is common in patient over the age of 60
years with no sex predilection.
Siteit originates primarily in the intraoral accessory
glands. It occurs in upper lips followed by palate, buccal
mucosa and lower lip.
Symptomsit presents as a slowly growing, well
circumscribed, firm nodule.
Signsit is firm and fluctuant to palpation.
Diagnosis
Radiological Features
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Management
Superficial parotidectomyit is done as tumor is usually
located in superficial part of the parotid gland.
Oncocytoma
Clinical Features
contour. It contains cystic parts, which are seen on CT,
MR images (Fig. 26-29) and sonograms.
Sonographyon sonograms, this tumor is observed as a
very clearly delineated mass with multiple cystic areas.
On Doppler mode, relatively abundant vascularization
is observed.
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Clinical Features
Management
Surgical excisionsurgical excision of tumor should be
carried out. Facial nerve should be preserved.
Myoepithelioma
It is an uncommon salivary gland tumor. It occurs in adults
and has equal sex distribution. Parotid gland is most
commonly involved and the palate is the most frequent
intraoral site of occurrence. The clinical features are same
as pleomorphic adenoma.
The tumor is composed of spindle shaped or
plasmacytoid cells or combination of the two cell types.
These cells may be set in myxomatous background, which
may vary from scanty to copious. It is managed by surgical
excision.
Ductus Papillomas
These are the group of tumor characterized microscopically
by papillomatous pattern.
Diagnosis
Clinical diagnosisit is difficult to make. But small
swelling in relation with minor salivary gland, one
should suspect ductal papilloma.
Laboratory diagnosison biopsy, it shows multiple
exophytic papillary projection which is covered by
stratified squamous epithelium.
Management
Surgical excisionit is best treated by conservative
surgical excision.
Malignant Tumors
Peripheral Mucoepidermoid Carcinoma
Types
Simple or intraductal papillomaappears as submucosal
swelling.
Inverted ductal papillomais present most commonly on
lip.
Sialadenoma papilliferumis seen most commonly on
palate (Fig. 26-31).
Clinical Features
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Fig. 26-33: Mucoepidermoid tumor occurring on buccal mucosa
(Courtesy Dr Soni).
B
Figs 26-32A and B: Mucoepidermoid carcinoma of parotid gland.
(A) Extraoral view, (B) Intraoral view (Courtesy Dr Parate).
Diagnosis
Clinical diagnosisit is difficult to make clinical
diagnosis of mucoepidermoid carcinoma.
Management
Subtotal parotidectomyearly stage tumor is managed
by subtotal parotidectomy and facial nerve preservation.
Total removaladvanced cases need total removal of the
parotid gland.
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Origin
Entrapment of retromolar mucus glandit may originate
from entrapment of retromolar mucus glands within the
mandible, which subsequently undergo neoplastic
transformation.
Embryonic remnants of submaxillary glandit may also
form from developmentally retained embryonic remnants
of the submaxillary gland within the mandible and
neoplastic transformation of the mucus secreting cells
commonly found in the epithelial lining of dentigerous
cyst.
Clinical Features
Age and sex distributionit is most commonly seen in
middle age individual. It is more common in females
than males.
Siteit occurs in mandible in premolar-molar area. It
does not extend anteriorly beyond the premolar region.
Symptomspatient complains of painless swelling.
There may be paresthesia of inferior alveolar nerve.
Signswelling may cause facial asymmetry. Tenderness
is present. Regional lymph nodes are enlarged.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosissoap bubble and honeycomb
appearance may be seen.
Differential Diagnosis
Ameloblastomaradiologically, it is difficult to differentiate. Diagnosis should be confirmed by histopathological investigation.
Odontogenic myxomathere is history of missing tooth.
Central giant cell granulomait frequently crosses the
midline.
Management
Surgical excisionit is treated by surgical excision of
tumor.
Neck dissectionneck dissection should be carried out
in case of metastatic.
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Clinical Features
Radiological Features
AppearanceCT scan will demonstrate destructive lesion
(Fig. 26-37).
Diagnosis
Clinical diagnosisnot possible.
Laboratory diagnosisbiopsy shows thin capsule, which
composed of cells of varying degrees of differentiation.
Well differentiated cells bear remarkable resemblance to
normal acinar cells, whereas less differentiated cells
resemble embryonic ducts and immature acinar cells.
Management
Lobectomysuperficial lobe of the parotid gland should
be excised, is the treatment of choice. Recurrence rate
varies from 8 to 59%.
Clinical Features
Ageit occurs in the 5th and 6th decade of life.
Sitemost common glands involved are the parotid, submaxillary and the accessory glands in palate and tongue.
Symptomsthe most common initial symptom is
presence of mass followed by local pain, facial nerve
paralysis in case of parotid tumor and tenderness.
Signssome of the lesions exhibit surface ulceration.
Other findings include nasal obstruction, proptosis,
Fig. 26-37: This tumor shows bone destruction and absorption of the
dental root. Some fine calcification can also be seen in the
tumor(Courtesy Dr Shimizu).
Diagnosis
Clinical diagnosisnot possible.
Laboratory diagnosisbiopsy shows basal cells arranged
in anastomosing cords or may contain a mucoid material
producing the typical cribriform honeycomb or Swiss
cheese pattern. The stromal connective tissue becomes
hyalinized and surrounds the tumor cells, forming a
structural pattern of cylinder from which the lesion
originally derived the name cylindroma.
Management
Surgical excisionsurgical excision is the treatment of
choice. Recurrence rate is about 60 to 92%. Long-term
follow up is hence essential.
Adjunct radiotherapysurgery should be accompanied
by radiation therapy.
Adenocarcinoma
It is a malignant epithelial tumor showing tubules or
papillary glandular formation. All adenocarcinoma are
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Fig. 26-38: Enhanced CT shows round, slightly enhanced mass with
bone invasion in the lingual side of the left retro-molar region. Bone
invasion suggests malignant nature of this tumor
Management
Clinical Features
Agethe tumor occurs from 2nd to 9th decades, but most
frequently in 5th and 6th decade. The average age of
patients with malignant pleomorphic adenoma is about
ten years older than the patients with benign form of the
disease.
Symptomspain is more frequently a feature of malignant, than the benign pleomorphic adenoma
Sizethe tumors are usually larger than benign ones.
Signsthere is often fixation of the tumor to underlying
structures as well as to overlying skin or mucosa.
Epidermoid Carcinoma
It is also called as squamous cell carcinoma of salivary glands.
It is thought to be ductal in origin, since duct may undergo
squamous metaplasia with ease. It exhibits infiltrative
properties and early metastasis. It recurs readily. It is not a
common lesion and arises more frequently in the major
salivary gland. The combined use of surgery and
radiotherapy is more beneficial.
Undifferentiated Carcinoma
Radiological Features
Metastatic Carcinoma
Diagnosis
Clinical diagnosisnot possible.
Laboratory diagnosisbiopsy shows malignant component. There is presence of nuclear hyperchromatism and
pleomorphism, increased or abnormal mitosis and
destruction of normal tissues.
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Diagnosis
Necrotizing Sialometaplasia
Clinical Features
Age and sexit is more common in males than females.
Occurs in 4th and 5th decade.
Sitemost of the cases occur in palate, although cases
of lip or retromolar pad also have been reported.
Onsetthere may be early mild swelling which appears
as non-ulcerated swelling (Fig. 26-40).
Differential Diagnosis
Traumaticshort duration and history.
Aphthous ulcershort duration, painful and heals in
2 to 3 weeks.
Squamous cell carcinomarare on palate, older age and
biopsy.
Syphilispainless indurated edema, painless lymph
node swelling and serology.
Non-Hodgkins lymphomabiopsy.
Management
Self limitingit is a self-limiting condition. It does not
require any treatment. The healing occurs in six to twelve
weeks via secondary intention.
Debridementdebridement and saline rinses may aid in
the healing process.
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Suggested Reading
1. Abbey LM. Solitary intraductal papilloma of the minor salivary
glands. Oral Surg, Oral Med, Oral Pathol 1975;40:135-40.
2. Aguirre JM, Echebarria MA, et al. Warthin tumor: a new
hypothesis concerning its development. Oral Surg, Oral Med,
Oral Pathol, Oral Radiol Endod 1998;85:60-3.
3. Apruzzese D, Longoni S. Stafnes cyst in an anterior location. J
Oral Maxillofac Surg 1999;57:333-8.
4. Ariji E, Fujiwara N, Tabata O, et al. Stafnes bone cavity: a
classification based on outline and content determined by
computed tomography. Oral Surg, Oral Med, Oral Pathol, 1993;
76:375-80.
5. Atkinson JC, Fox PC. Sjgrens syndrome: Oral and dental
considerations. JADA 1993;124:74-86.
6. Atkinson JC, Travis WD, Pilemer SR, et al. Major salivary gland
function in primary Sjgrens syndrome and its relationship to
clinical features. J Rheumatol l990;17:319-22.
7. Auclair PL, Goode RK, Ellis GL. Mucoepidermoid carcinoma of
intraoral salivary gland. Cancer 1992;69:2021-30.
8. Avery J K. Oral development and histology, 1st edition, BC Decker
Inc, Philadelphia, 1988.
9. Brannon RB, Fowler CB, Hartman KS. Necrotizing sialometaplasia: clinicopathologic study of sixty nine cases and review of
literature. Oral Surg, Oral Med, Oral Pathol 1991;72:317-25.
10. Brookstone MS, Huvos AG. Central salivary gland tumor of the
maxilla and mandible: a clinicopathological study of 11 cases
with an analysis of literature. J Oral Maxillofac Surg 1992;50:22936.
11. Chau MNY, Radden BG. A clinicopathological study of 53
intraoral pleomorphic adenoma. Int J Oral Maxillofac Surg 1989;
18:158-62.
12. Correl RW, Jensen JL, Rhyne RR. Lingual cortical mandibular
defect: a radiographic incidence study. Oral Surg, Oral Med,
Oral Pathol 1980;50:287-91.
13. Daley TD, Gardner DG, Smout MS. Canalicular adenoma. Oral
Surg, Oral Med, Oral Pathol 1984;57:181-8.
14. Damm DD, White DK, et al. Benign solid oncocytoma of intraoral
minor salivary glands. Oral Surg, Oral Med, Oral Pathol 1989;
67:84-6.
15. Daniels TE. Sjgrens syndrome: Clinical spectrum and current
diagnostic controversies. Adv Dent Res l996;10:3-8.
16. de Visscher JGAM, van der Wal KGH, de Vogel PL. The plunging
ranula: pathogenesis, diagnosis and management. J Craniomaxillofac Surg 1989;17:182-5.
17. Ellis GL, Auclair PL, Gnepp DR. Surgical Pathology of the Salivary
Glands. Major Problems in Pathology Vol 25. Philadelphia, USA:
WB Saunders, 1991.
18. Epstein JB, Scully C. The role of saliva in oral health and the cases
and effect of xerostomia. J Can Dent Assoc 1992;58:217-21.
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Disorders of Maxillary
Sinus
Introduction
Paranasal sinuses are the air filled spaces present with
some bone around the nasal cavities. The sinuses are
frontal, maxillary, sphenoidal and ethmoidal. Because of
the close proximity of the maxillary teeth with the maxillary
sinuses, these are the most important paranasal sinuses in
dental point of view. They are the largest air filled sinuses
surrounding the nose.
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Developmental Disorders
Crouzon syndromeearly synostosis of the sutures
produce hypoplasia of the maxillae and therefore the
maxillary sinus, together with the high arched palate.
Treacher Collins syndromeMandibulofacial dysostosis
is associated with grossly and symmetrically underdeveloped maxillary sinuses and malar bones.
Binder syndromemaxillonasal dysplasia (Binder
syndrome) involves hypoplasia of the middle third of the
face. There is maxillary retrognathism, smaller maxillary
length and frontal and maxillary sinus hypoplasia.
Inflammatory Disorders
They are caused by chemical irritation, introduction of
foreign body, facial trauma, etc.
Mucositis
It is the name given when there is thickened mucous
membrane of maxillary sinus. Normally, mucous membrane of maxillary sinus is about 1 mm in thickness. When
the lining mucosa becomes inflamed from either infection
or an allergic process, it may increase in thickness by about
10 to 15 times. This inflammation is called as mucositis.
Maxillary Sinusitis
Causes
Inflammatory diseasedental inflammatory lesion such
as periodontal disease or periapical disease may cause
localized mucositis.
Clinical Features
It is usually asymptomatic and it is discovered on routine
radiograph.
Radiological Features
Appearanceimage is detected on a radiograph as a band,
noticeable more radiopaque than the air filled sinus and
paralleling the bony wall of the sinus.
Sizemucosal thickening can vary from a few millimeters
to a thick, hypertrophic, redundant mucosa (Fig. 27-3).
Diagnosis
Clinical diagnosisnot possible to make clinical
diagnosis.
Radiological diagnosisparallel radiopaque band seen
in the wall of sinus will diagnose this lesion.
Management
Removal of causeit will disappear after removing the
cause.
Etiology
Dental causes
Periapical infection from the teethit may follow dental
infection particularly from upper molar and premolar
teeth. The anatomic proximity of the roots of the
maxillary bicuspids and molar teeth to the floor of the
sinus leads to potential infection of the sinus by direct
extension of an apical abscess.
Oroantral fistulathe accidental opening in the floor of
the maxillary sinus during dental extraction is called as
oroantral opening.
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Clinical Features
Acute maxillary sinusitis
Symptomsthe main symptom is severe pain which is
constant and localized. Pain may be felt in the area of
eyeball, cheek and frontal region. Pain may be
exacerbated by stooping or lowering the head. Pain is
Subacute
SymptomsIt is devoid of symptoms associated with
acute congestion such as pain and generalized toxemia.
Dischargedischarge is usually purulent and associated
with a nasal voice and stuffiness.
Sorenesssoreness of throat is common feature.
Disturbed sleeppatient can not sleep well due to cough
that irritates the patient constantly.
Chronic
Symptomsgeneral symptoms of chronic sinusitis
include sense of tiredness, low grade fever and feeling
of being unwell. Stuffy sensation over the affected side
of the face.
Other featuresthere is nasal obstruction, nasal
discharge and headache are the related symptoms.
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Radiographic Features
Diagnosis
Management
Removal of the cause of dental infectiontreatment should
be directed to drain the periapical abscess from the root
canal or by extracting the teeth.
Antibioticmost commonly used antibiotic is doxycycline hydrochloride. Doxycycline is given in the dose
of 100 mg daily. Penicillin is also the drug of choice as it
is effective against most of the anaerobic microorganisms.
In some cases, amoxicillin or clotrimazole can be given.
Analgesic and anti-inflammatory drugsthese drug are
used to control pain and inflammation. Most commonly
used are Ibuprofen or Nimesulide.
Nasal decongestantEphedrine nasal drops (0.5%) are
most commonly used and give relief for several hours.
Xylometazoline (0.1%) is the alternative drugs to
Ephedrine but it can lead to more rebound effect.
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Cysts
Cysts are classified into dental and nondental.
Nondental Cyst
Nondental cysts of maxillary sinus are as follows.
Pathogenesis
Inflammatory exudatesevere inflammation around
the ducts of mucus glands of the antral lining may
alter their integrity. When the patient sneezes, mucus
can be expelled into soft tissue through the wall of such
injured duct. Once the pathway for extraglandular
accumulation of mucus has been established, the process
may continue until a cyst has developed. Infection may
result from odontogenic source or it may cause due to
allergy.
Mechanical factorsbecause of frequent location of the
lesion at the sharp angle between the floor and frontal
or lateral aspect of the sinus cavity close to the alveolar
process mechanical factors might be involved in the
Clinical Features
Age and sexthe great majority of cases were found in
patients in the age group of 21-30 years. Males are more
commonly affected than females in the ratio of 2:1.
Sitesmost commonly involved sites are the antral floor
and the lateral wall of maxillary sinus.
Symptomsthere may be localized dull pain in the antral
region, or fullness and numbness of the cheek. If it is
completely filled sinus, it will prolapse through the
ostium and cause obstruction and postnasal drip.
There may be pain in the teeth and face over or near the
sinus. There may be stuffiness, fullness, headache,
symptoms of cold, and numbness of upper lip.
Signssometimes, antral swelling may also occur.
There is copious discharge of yellow fluid from the
nostrils. Retention of pseudocyst may enlarge and fill
the sinus cavity completely, it frequently rupture as a
result of abrupt pressure change caused by sneezing or
blowing the nose. Expanding cyst will cause herniation
through the ostium into the nasal cavity where it
subsequently ruptures.
Radiological Features
Radiodensityit is homogenous mass that is more
radiopaque than the surrounding sinus cavity.
AppearanceIt appears as a soft tissue mass rather than
a calcified area so that medial and lateral landmarks
can generally be visualized through the lesion.
SiteIt is found projecting from the floor of the sinus,
although some may form on the lateral walls.
Shapethe cyst appears as a spherical, ovoid or dome
shaped radiopacity (Fig. 27-6).
Marginsit has a smooth and uniform outline. The
smooth curved borders are well defined but not well
corticated.
Basethey may have a narrow or broad base.
Sizethey vary in size from minute to very large and
may occasionally occupy the entire maxillary sinus.
Image may be of a fingertip to that of a completely filled
sinus making it opaque.
Bonethere is no resorption of adjacent bone and of
particular importance is the persistence of thin
radiopaque line of the antral cortex.
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Management
Removal of foci of infectionthe adjacent tooth should be
treated for any source of infection.
Caldwell-Luc operationlarge cysts should be removed
through Caldwell-Luc operation.
Sinus Mucocele
It is an expanding destructive lesion that begins with the
development of mucus retention cyst in a blocked ostium.
If mucocele becomes infected, it is called as pyocele or
mucopyocele.
Etiopathogenesis
Fig. 27-6: Dome shaped radiolucency seen in left
maxillary sinus suggestive of antral pseudocyst.
Diagnosis
Clinical diagnosisdull pain in antral area, discharge of
yellow fluid from nostril should suspect this cyst.
Radiological diagnosisovoid and dome shaped
radiopacity projecting from the floor will diagnose this
condition.
Laboratory diagnosisbiopsy shows infiltration of
chronic inflammatory cells in connective tissue wall of
the cyst. Cystic fluid is thick, tenacious, white translucent and sterile.
Differential Diagnosis
Inflammatory lesions of the sinusin inflammatory
lesions, patient may complain of pain which is absent
in case of cyst.
Apical radicular cysttooth is not vital.
Odontogenic cystmucus retention cyst is dome shaped
and does not have thin marginal line representing the
hyperostotic borders characterized by odontogenic cyst.
Odontogenic cysts are more rounded and tear shaped
and most are not so homogenous, as mucus retention
cyst. Lamina dura is not intact in odontogenic cysts.
Antral polypthey are more opaque, more heterogeneous
and multiple commonly associated with thickened
mucosa.
Surgical ciliated cystmore rounded and more
radiolucent.
Clinical Features
Sitethere is predilection for ethmoid and frontal
sinuses due to the relative difficulty as a cyst has
protruding through the longer and narrower nasofrontal
duct and infundibulum into the nasal cavity, in contrast
to the shorter and larger ostium in case of maxillary and
sphenoidal sinuses.
Symptomsit may exert pressure on the superior
alveolar nerve in the resorbing sinus wall and cause
radiating pain. Sensation of fullness in the cheek may
be accompanied swelling over the anteroinferior aspect
of the antrum, the area where the wall is thinnest. If the
cyst expands inferiorly, it may cause loosening of the
posterior teeth in that area. If it expands medially, lateral
wall of the nasal cavity is deformed and nasal airway is
obstructed.
Signsif expands towards the orbit, it may cause diplopia
and proptosis (protrusion of the globe of the eye).
Radiographic Features
Siteabout 90% of the cases are in ethmoidal and frontal
sinuses and are rare in maxillary and sphenoid sinuses.
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Diagnosis
Clinical diagnosissymptoms of sinus mucocele are
severe and consist of radiating pain, diplopia and
obstruction of nasal airway.
Radiological diagnosisopacification of sinus with
erosion of septa. Displacement of teeth can also occur.
Clinical Features
Age and sex distributionthe great majority of the patients
are in the fourth and fifth decades and their age ranges
from 21 to 72 years. There is a preponderance of males to
females (2:1).
Symptomspain, discomfort or swelling in the cheek or
face or intraorally in the palate or alveolus is a common
complaint.
Signpus may be discharged.
Radiological Features
Sitewell defined radiolucency closely related to the
maxillary sinus.
Marginsurrounding bone sclerosis is evident in at
least a part of the bony margin. There is pneumatization
and relatively well defined unilocular radiolucent
margins showing marked osteosclerotic changes.
Pressure effectoccasionally, cyst appears to encroach
on the sinus itself but lack of communication between
the two has been demonstrated by injecting the sinus
with a radio-opaque material. As the lesion enlarges,
sinus walls become thinned and eventually perforate
and may resemble a malignant neoplasm. Resorption of
maxillary alveolar processes also occurs.
Differential Diagnosis
Malignancyany suggestion of a lesion associated with
occluded ostium should be mucocele.
Management
Surgicalsurgical removal by the Caldwell-Luc
operation is traditional method for management of sinus
mucocele.
Endoscopic middle meatal antrostomynowadays, this
treatment module gives good results.
Pathogenesis
Trapping of epithelium in wound closurethey are derived
from the epithelial lining of the maxillary sinus which
is trapped in the wound during closure of the CaldwellLuc incision and subsequently begins to proliferate.
Sinus lining will separate from the sinus and epithelium
lined cavity is formed in which mucin is secreted. This
type of cyst is originated after difficult extraction in
which sinus lining is damaged.
Diagnosis
Clinical diagnosishistory of trauma or operation
followed by pain and discomfort in the sinus region.
Radiological featurescontrast study will help to
diagnose this cyst. Well defined radiolucency close to
sinus will give clue to diagnose the case.
Laboratory diagnosiscysts are lined by pseudo-stratified
columnar epithelium with squamous metaplasia in
chronically inflamed cases. Combination of ciliated,
cuboidal and squamous epithelium with varying
numbers of mucus cells may be seen.
Management
Enucleationenucleation through an approach appropriate to the site is the treatment of choice. Recurrence
may occur if the wall is very thin and there is perforation
of the bone making enucleation difficult.
Dental Cyst
These are described in detail in Chapter 13: Cysts of Jaw.
Radicularthose that develop in the maxilla may extend
into the maxillary sinus. They may cause elevation of
the floor of the sinus resulting in a halo appearance.
Large cysts may obliterate the sinus and make
differentiation of this form from sinusitis is difficult.
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Radiological Features
Appearanceit appear as homogenous soft masses with
smooth, outwardly convex borders. Single or multiple
lesions may be present. If polyp occurs in the roof of the
maxillary sinus in a patient with a history of trauma, the
plain film examination may simulate a blow out fracture.
Destruction of walls of sinusPolyps may cause
destruction or displacement of bone. They can displace
or destroy medial or lateral wall.
CT featureshave mucoid attenuation with mucosal
enhancement seen at the polyps surface. It appears as
smooth homogenous mass.
MRI featurespolyps will have low to intermediate T1weighted and high T 2-weighted signal intensities.
Mucosa adjacent to polyps will enhance as compared
(Fig. 27-8) to polyps.
Benign Tumor
Antral Polyp
The thickened mucosa of chronically inflamed sinus
frequently form irregular folds called as polyps. Polypoid
atrophy of mucosa may develop into an isolated area or
number of areas throughout the sinus.
Clinical Features
Ageit usually occurs in young persons.
Sitemaxillary sinus is more involved as compared to
other sinus. In maxillary sinus they may arise from any
part of the sinus wall and occasionally pass through
the ostium to appear in the nose as antrochoanal polyps.
Symptomspatients present with nasal obstruction,
pain is very mild on pressure as mass present inside the
nose.
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Diagnosis
Clinical diagnosissaint tried with pain and pressure
inside the nasal cavity may give clue to the diagnosis.
Radiological diagnosisCT and MRI will diagnose the
polyp as homogenous radiopaque mass in the sinus
(Fig. 27-9).
Management
Excisionsurgical excision of tumor should be carried out.
Management
Excisionsimple excision is close with endoscopic
surgery or Caldwell-Luc operation.
Antral Papilloma
It is a rare tumor of respiratory epithelium that occurs in
the nasal cavity and the paranasal sinuses.
Osteoma
It is most common mesenchymal neoplasm in the paranasal
sinus.
Clinical Features
Radiographic Features
Radiological Features
Diagnosis
Diagnosis
Clinical Features
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Management
Excisionthis tumor should be surgically removed.
Ameloblastoma
It is most common extrinsic tumor affecting the maxillary
sinus. It may cause loosening of teeth, nasal obstruction
and painless facial deformity. Sinus cavity is invaded at
an early stage. There is radiographic appearance equivalent
to soft tissue density. Antral cavity is expanded and filled
with soft tissue mass. Bony wall is eroded.
Malignant Tumor
Squamous Cell Carcinoma
It originates from metaplastic epithelium of the sinus
mucous membrane lining. It is the most common primary
tumor of paranasal sinuses comprising 80 to 90% of cancers
in this site.
Etiology
IdiopathicMost cases of squamous cell carcinoma of
maxillary sinus are without any cause.
Sinusitisrespiratory epithelium is known to undergo
squamous metaplasia in the presence of infection and
chronic sinusitis can be predisposing factor for antral
carcinoma.
Snuff and smokethe use of indigenous snuff and the
smoky atmosphere may be causal factor for carcinoma
of paranasal sinus.
Occupational hazardsit is more common in boot and
shoe and nickel worker. Adenocarcinoma of the nasal
passage is an occupational hazard for furniture workers.
Clinical Features
Age and sexmean age of occurrence is 60 years. Males
are commonly affected more than females in the ratio of
2:1.
Symptomsthere is facial pain, swelling, nasal obstruction. Patient also complains unilateral nasal stiffness.
When the second division of trigeminal nerve is involved,
there is intense pain or paresthesia of midface occurs.
Signsthere is ulceration or mass seen on the hard palate
(Fig. 27-11).
Lymph nodeslymphadenopathy is always present in
carcinoma of maxillary sinus.
Medial wall involvementmedial wall involvement leads
to nasal obstruction, discharge, bleeding and pain.
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Radiographic Features
Small early lesion
Shape and radiodensitynon-specific well defined round
soft tissue opacity within the antrum (Fig. 27-15).
Antral wallvariable destruction of the bony antral wall.
Loss of fine linear outline of the lateral wall is a
particularly sensitive sign of bone destruction.
Large well established lesion
Pressure effectdestructive outline of the sinus destroying bone and causing irregular bony radiolucency with
Diagnosis
Clinical and radiological diagnosisulceration in palate
with radiopacity in maxillary antrum may suggest
maxillary antrum malignancy.
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Management
Cytotoxic drugslocal intra-arterial infusion of cytotoxic
drugs may be helpful for pain control.
Radiotherapyit is the main mode of treatment. A course
of high voltage radiotherapy or gamma rays are given.
Surgeryif radiotherapy cannot control the disease upto
the expectation, excision of the maxilla should be
performed.
Reconstructionafter surgery, sophisticated prosthesis
should be constructed.
Foreign Bodies
Root fragment and teethdisplaced root fragments or teeth
may present in the sinus.
Excess root canal fillingexcess root canal filling material
forced through the apex of an upper posterior tooth
during endodontic treatment.
Oroantral communicationforeign material pushed
into the antrum through an existing oroantral communication.
Metallic objectmetallic object such as pellets, bullets
and fragments of shells or bombs.
Radiological detectionthe presence, position and
often the nature of the foreign body can be seen by using
the radiograph (Fig. 27-18). When roots are present in
the socket, it usually reveals root canal but in some
cases, there is only root tip present with no root canal
seen. If you want to determine it is in the socket or in the
sinus then you have to look for the lamina dura and
periodontal ligament. If lamina dura and periodontal
ligament is present then the root is in the socket.
Sinus Contusion
Metastatic Carcinoma of the Maxillary Sinus
It is rare site for the secondary tumor deposits. The
most common site for the primary disease is kidney followed
by the breast in females and the testicle (seminoma) in
males.
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3
Fig. 27-19: Blow-out fracture showing edema below the eye.
Blow-out Fracture
Causeblow-out fracture results from sudden increase
in intraorbital pressure due to blow to the eye. The
pressure of blow forces the inferior orbital content (fat
and muscle) through the fracture.
Symptomsdiplopia (double vision) when victim looks
upward (caused by entrapment of inferior rectus) and
enophthalmos (backwardly depressed eyelid) following
reduction of edema (Fig. 27-19) and fat atrophy.
Radiological featuresopacification of sinus with or
without a fluid level. Soft tissue mass in upper portion
of sinus and image of depressed bone fragment (orbital
floor in sinus) (Fig. 27-20). It will produce a tear-drop
shaped opacity in the upper part of the antrum, the
hanging drop appearance caused by herniation of the
Isolated Fracture
It involves single wall, which are identified on the
radiograph by a bright line. Anterolateral wall of the
maxillary sinus is the most common site. Sometimes fracture
of the floor of the maxillary sinus occurs into which roots
of the posterior teeth are projecting which occurs during
tooth extraction.
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Fractured Tuberosity
693
Oroantral Fistula
Clinical Features
Causes
Extraction of teethteeth which is having periapical
infection. Inappropriate or incorrect use of elevators
during root or tooth removal may lead to oroantral fistula.
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Radiographic Features
Break in continuity of maxillary sinusradiograph will
show break in continuity of maxillary sinus. In some
cases there is disalignment of a small portion of the
cortical layer of bone.
Features of sinusitisthere are also characteristic features
of acute or chronic sinusitis due to ingress of bacteria.
Second view should be taken by tilting the head to know
locationevidence of displaced root or tooth and second
view of the antrum with the head in a different position
may be required to ascertain the exact location of the
displaced object.
Silver probe examinationconfirmation of presence of
fistula can be done by introducing silver probe into the
orifice, followed by taking the radiograph.
Diagnosis
Clinical diagnosisall extracted upper posterior teeth
should be examined, not only to ensure they are intact
but also for indication of a sinus contamination. If the
root is covered with a thin plate of bone or adherent
sinus mucosa a communication may be present.
Air blow techniquethe patient should be asked to blow
air into the pinched nose with the mouth open. This
forces the air into the sinus via ostium. If an oroantral
opening is present, bubbles appear in the extraction
socket.
Probing of sinusGentle probing of the socket with a
blunt instrument, such as ball ended periodontal probe
or small amalgam plugger will confirm the bone defect
without perforating an intact lining.
Radiological diagnosisCT will be able to confirm the
diagnosis of oroantral fistula (Fig. 27-23).
Management
Drug therapyantibiotic therapy for 1 week. Most commonly given antibiotics is amoxicillin. Decongestants
are given for 1 week.
Drainageto promote drainage, the oroantral fistula can
be enlarged by excising a margin of surrounding
mucosa, by cauterizing any granulation tissue and
polyps protruding from the sinus with electrocoagulation or simply by cautious application of a chemical
agent such as trichloroacetic acid. The patient is provided
with a syringe and blunted wide bore needle or a plastic
irrigating tube, to wash out the sinus with warm salt
water three or four times daily. In some cases, antral
lavage and antrostomy is done to help drainage.
Prevention from dislodging clotif opening is small, great
care is to be exercised such as avoidance of use of
irrigation, vigorous mouth washing and frequent lusty
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Etiology
Endogenous nidusendogenous nidus is usually root tip
or may be simply fragment of soft tissue, bone, blood or
mucus.
Exogenous nidusexogenous nidus are consisting of
snuff or paper.
Clinical Features
Age and sexit can occur at any age in either sex.
Symptomsit is usually asymptomatic. But if they continue to grow the patient may complaint of bloodstained
nasal discharge, nasal obstruction or facial pain.
Radiographic Features
Calcification
Antroliths
These are calcified masses found in the maxillary sinus. It
is defined as a complete or partial calcific encrustation of
an antral foreign body, either endogenous or exogenous
which serves as nidus. There is calcification of masses of
stagnant mucus in site of previous inflammation, root
fragments or bone chips or foreign body.
B
Figs 27-24A and B: Antroliths seen as round shaped radiopacity in
the maxillary sinus (Courtesy Dr Ashok L).
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Diagnosis
Clinical diagnosisit is not possible to make confirmed
clinical diagnosis.
Radiological diagnosisround shaped radiopaque
structure in the sinus will give clue to the diagnosis.
Differential Diagnosis
Management
Removal of antroliths can be done if it is symptomatic.
Suggested Reading
1. Adekeye EO, Ord RA. Giant frontal sinus mucocele. Report of
two cases. T. Maxillofac Surg 1984;12(4):184-7.
2. Allard RHB, van der Kwast WAM, van der Wall I. Mucosal
antral cyst: review of the literature and report of radiographic
survey. Oral Surg, Oral Med, Oral Pathol 1981;51:2-9.
3. Aygyn N, Ozuner O, Zinreich SJ. Staging system for sinusitis.
Otolaryngol. Clin North Am 2005;38(3).
4. Ballenger JJ. Diseases of the Nose, Throat, Ear, Head and Neck.
14th ed. 1991, Lea and Febiger, Philadelphia.
5. Bavsley RE, Thunthy KH, Weir JC. Maxillary sinus mucocele
report of an unusual case. Oral Surg Oral Med Oral Pathol 1984;
58(4):499-505.
6. Blitzer A, Lawson W. Fungal infection of nose and paranasal
sinuses. Part i. Otolaryngol Clin North Am 1993;26:114-6.
7. Bowerman JE. The maxillary antrolith. J Laryngol Otol 1969;83:
873-82.
8. Breiman A, Sadowsky D, Friedman J. MucosmycosisDiscussion
and a report of case involving the maxillary sinus. Oral Surg Oral
Med Oral Path 1981;52(4):375-8.
9. Brook I. Aerobic and Anaerobic bacterial flora of normal maxillary
sinuses and sinusitis. Laryngoscope 1981;91:372-6.
10. Brook I. Bacteriologic features of chronic sinusitis in children.
JAMA 1981;246:967-9.
11. Cohen MA, Packota GV, Hall MJ, Steinberg J. Large asymptomatic
antrolith of the maxillary sinus. Report of a case. Oral Surg, Oral
Med, Oral Pathol 1991;71:1557.
12. Cummings LW, Fredrickson JM, Harker LA, Krausing LT, Schuller
PE. Otolaryngology head and neck surgery. II ed. Vol. I. 1993,
Mosby Philadelphia.
13. Daghistani K, Jamal T, Zaher S. Allergic aspargillus sinusitis
with proptosis. J Laryngol Otol 1992;106:799-803.
14. Dhingra PL. Diseases of Ear, Nose and Throat. IIIrd ed. 2005.
Churchill, BI Livingstone.
15. Donald C. Lanza, Kennedy WD. Current concepts in the surgical
management of frontal sinus diseases. Otolaryngol Clin North
Am 2001.
16. Esser WJ. Calculus formation in the maxillary sinus. Oral Surg,
Oral Med, Oral Pathol 1965;19:755.
17. Evans J. Maxillary antrolith: a case report. Br J Oral Surg
1975;13:737.
18. Evans OF. Sinusitis of the maxillary antrum. N Engl J Med 1975;
293:735-9.
19. Evans OF. Sinusitis of the maxillary antrum. N Engl J Med 1976;
293:735-8.
20. Forman AG, Baker I. Mucus cyst of the sphenoid sinus.
Dentomaxillofac Radiol 1990;19(4):178-80.
21. Frederick J, Braude AL. Anaerobic infection of the paranasal
sinuses. N Engl J Med 1974;200:135-9.
22. Freguson BJ. Fungus balls of the paranasal sinuses. Otolaryngol
Clin North Am 2000;33(2):389-98.
23. Gardner DG. Pseudocyst and retention cysts of the maxillary
sinus. Oral Surg, Oral Med, Oral Pathol 1984;58:561-7.
24. Gardner PG. Cullane PJ. Mucoceles of the maxillary sinus. Oral
Surg Oral Med Oral Path 1986;62(5):538-43.
25. Ghom Anil. Textbook oral radiology: Elsevier publication, New
Delhi: 2008.
26. Giri SP, Reddy EK, et al. Management of advanced squamous
cell carcinoma of the maxillary antrum. Cancer 1992;69:657-61.
27. Hav-El G. Management of the paranasal sinus mucocele. J Oral
maxillofacial Surg 2001;59(2): 246-7.
28. Hyams V. Papillomas of the nasal cavity and paranasal sinuses.
A clinicopathologic study of 315 cases. Ann Otol Rhinol Laryngol
1971;80:192-206.
29. Kaneshiro S, Nakajima T, et al. Postoperative maxillary cyst: a
report of 7 cases. J Oral Surg 1981;39:191-8.
30. Karma P. Bacteria in chronic maxillary sinusitis. Arch Otolaryngol
1979;105:386.
31. Kurihara K, Saiki T, Takeda K, Kobayashi J. Epitheloid
heman-gioma of the maxillary sinus. A case report of J Oral
Maxillofac Surg 1995;53(10):1221-3.
32. MacArthur CJ, Lindbeck E, Jones Dt. Paranasal phycomycosis in
the immunocompetent host. Otolaryngol. Head Neck Surg 1992;
107:460-2.
33. Moran PR, Morrison WV. Complications of frontal and ethmoid
sinusitis. Laryngoscope 1980;90:661-6.
34. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology
(2nd edn), 2004: Saunders Elsevier.
35. Ogata Y, Okinaka Y, Takahashi M. Antroliths associated with
Aspergillosis of maxillary sinus: a report of case. J Oral Maxillofac
Surg 1997;55:1339-41.
36. Ruoppi P, Seppa J, Pukkila M, Nuutinen J. Isolated sphenoid
sinus disease report of 39 cases. Arch Otolaryngol Head Neck
Surg 2000;126(6):777-81.
37. Ruprecht A, Batniji S, el-Neweishi E. Mucous retention cyst of
the maxillary sinus. Oral Surg Oral Med Oral Path 1986;62(6):
728-37.
38. Sadoff RS, Rubin MM. Bilateral antral mucocele a report of a
case. J oral Maxillofacial Surg 1991;49(2):193-6.
39. Som P, Curtin H. Chronic inflammatory sinonasal diseases
including fungal infections. The role of imaging. Radiol Clin North
Am 1993;31:33-44.
40. Som PM, Curtin HP, Head and Imaging, (4th edn). Vol. I, 2003.
Mosby, Philadelphia.
41. Van Dis ML, Miles DA. Disorders of maxillary sinus. Dent Clin
North Am 1994;38(1):155-66.
42. Wald E. Acute maxillary sinuits in children. N Engl J med 1981;
304:749-53.
43. Weissman J, Tabor E, Curtin H. Sphenochoanal polyps evaluation
with CT and MR imaging. Radiology 1991;178:145-8.
44. Whaites E. Essentials of Dental Radiography and Radiology (2nd
edn), Churchill Livingstone, Philadelphia, 1998.
45. White SS, Pharoah MJ. Oral Radiology. Principles and
Interpretation (5th edn). Mosby. A. Hartcourt Health Sciences
Company, St.Louis, Missouri, 2003.
46. Zinreich S, Kennedy D, Malat J. Fungal sinusitis, diagnosis with
CT and MR imaging. Radiology 1988;169:439-44.
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Traumatic Injuries of
Oral Cavity
Clinical Features
Sitecommon sites are anterior and lateral border of
tongue (Fig. 28-1), floor of mouth, posterior palate, buccal
mucosa and mucosal surface of lip.
Symptomsmild to considerable pain and it regresses
after the cause is removed.
Signsit may blanch when digital pressure is used.
Sizesize of red zone corresponds closely to size of
traumatic agent.
Marginsmargins may or may not sharply define.
Management
Removal of irritantmechanical irritant is identified and
should be removed.
Diagnosis
Clinical Features
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Clinical Features
Symptomspatient complains of pain and bubbling
sensation while palpating the tissue and often difficulty
in breathing.
Appearanceit is manifested as unilateral swelling of the
tissues of face and/or neck which occurs very rapidly.
Crepitusit can be felt while auscultating the swelling.
Mediastinal involvementspread to mediastinum will
result in dysphonia, dysphagia or dyspnea.
Hammans crunchcardiac auscultation reveals crepitus
synchronous with the heart beat in case of mediastinum
involvement.
Pneumoparotidit occurs when air enters parotid duct.
It appears as unilateral enlargement of the parotid.
Milking of parotid duct produce frothy air filled saliva.
Diagnosis
Clinical diagnosishistory and presence of crepitus on
palpation are two important diagnostic indicators for
cervicofacial emphysema.
Fig. 28-3: Macular lesion seen on upper lip due to blunt trauma.
Diagnosis
Clinical diagnosismacular lesion with history of blunt
trauma.
Management
Management
Antibiotics therapyusually broad spectrum antibiotics
are prescribed for dental related cervicofacial
emphysema. It usually resolves in 2 to 5 days of time.
Management of pneumoparotidthese are treated with
antibiotics, massage, hydration, sialogogues and warm
compress.
Factitious Injury
Cervicofacial Emphysema
It is a swelling occurs due to introduction of gas or air in
the interstices of the connective tissue. In orofacial region,
forced air may spread to mediastinal and retropharyngeal
area.
Etiology
Dental procedureit follows variety of oral and dental
procedures like tooth extraction, blowing of compressed
air into the root canal during endodontic treatment or
into a periodontal pocket, blowing of air from high speed
air rotor machine.
Fractureit can also follow mid facial fractures.
Surgical procedureit can occur spontaneously as a result
of patients breathing actions following some type of
surgical procedure with the break in tissue permitting
air to enter the connective tissue space. In some cases,
while surgical operation, compressed air may be forced
in small intraoral laceration.
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Fig. 28-4: Factitious injury seen on the neck of patient to get relief
from the pain.
Classification
Ellis and Daveys classification
Class Isimple fracture of the crown involving enamel.
Class IIextensive fracture of the crown, with
considerable amount of dentin involved but no pulp
exposure.
Class IIIextensive fracture of the crown with
considerable amount of dentin involved with pulp
exposure.
Class IVtraumatized tooth becomes nonvital (with or
without loss of crown structure).
Class Vtooth lost due to trauma.
Class VIfracture of root with or without loss of crown
structure.
Class VIIdisplacement of the tooth without crown or
root fracture.
Class VIIIfracture of crown and mass.
Class IXfracture of deciduous teeth.
Classification by Andreessen
This classification is based on a system adopted by WHO
in its application of the international classification of
disease to dentistry and stomatology.
Injuries to the hard dental tissues and pulp
Crown infractionan incomplete fracture of the
enamel without loss of the tooth substance.
Uncomplicated crown fractureit is restricted to enamel
or involves enamel and dentin, but does not expose
the pulp.
Complicated crown fracturea fracture involving
enamel and dentin and exposing the pulp.
Complicated crown root fracturea fracture involving
enamel, dentin and cementum and exposing pulp.
Root fracturea fracture involving dentin, cementum
and the pulp.
Injuries to the periodontal tissue
Concussionan injury to the tooth supporting structures without abnormal loosening or displacement
of the tooth, but with marked reaction to percussion.
Subluxationan injury to the tooth supporting
structure with abnormal loosening but without
displacement of tooth.
Intrusive luxation (central dislocation)displacement
of the tooth into alveolar bone. This injury is
accompanied by comminution or fracture of the
alveolar socket.
Extrusive luxation (peripheral dislocation)partial
displacement of the tooth out of its socket.
Lateral luxationdisplacement of the tooth in a
direction other than axially. This is accompanied by
comminution or fracture of the alveolar crest.
Extra-articulation (complete avulsion)complete
displacement of the tooth out of its socket.
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Radiographic Features
PDL space wideningwidening of periodontal ligament
space in the apical portion.
Reduce pulp canal sizereduction in the size of the pulp
canal after a year following the trauma.
Management
Conservativeadjustment of opposing teeth should be
done to avoid pain.
Luxation
It is the dislocation or disarticulation of teeth which are
abnormally mobile and are displaced. There may be
complete or partial necrosis of the pulp.
Types
Subluxationit denotes abnormal loosening of teeth
without frank dislocation.
Intrusive luxationdisplacement of teeth into the alveolar
bone.
Extrusive luxationpartial displacement of teeth out of
the socket.
Lateral luxationmovement other than axial displacement.
Clinical Features
Siteteeth commonly involved are maxillary incisors
in both dentitions.
Symptomsteeth are abnormally mobile. Pain is also
present.
Signsbleeding from the gingival crevice indicating
periodontal damage. Tooth is extremely sensitive to
percussion and masticatory force. Clinical crown may
appear shortened in case of intrusive luxation.
Sequelae of luxationthere may be external root
resorption, ankylosis of tooth, obliteration of root canals,
pulp necrosis and marginal bone loss.
Concussion
Radiographic Features
Clinical Features
Management
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Figs 28-5A and B: Missing tooth from the arch in Figure A and sample
tooth is kept in saline solution in Figure B ( Courtesy Dr Shetty).
Management
Avulsion
It is complete displacement of tooth from its alveolus.
Clinical Features
Ageencountered in a relatively younger age
Sitemaxillary central incisors are commonly affected.
Teeth may be missing from the arch (Fig. 28-5A).
Associated signsfracture of the alveolar wall and lip
injuries are frequently seen.
Radiographic Features
Socket without toothpresence of dental socket without
correspondent tooth. Tooth may be located in the adjacent
soft tissue.
Noticeable lamina duraif recent wound is seen, lamina
dura will be noticeable.
Socket sclerosissocket sclerosis occurs.
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Bruxism
The word bruxism is taken from the Greek word brychein:
gnashing of teeth. Although the term bruxism is not
generally known to lay people, it is shorter and more
convenient than teeth clenching or grinding. Bruxism can
perhaps be best defined as the involuntary, unconscious
and excessive grinding, tapping, or clenching of teeth.
When it occurs during sleep, it may be best called as sleep
or nocturnal bruxism. A few people, on the other hand, brux
while they are awake, in which case the condition may be
called wakeful or diurnal bruxism.
All forms of bruxism entail forceful contact between the
biting surfaces of the upper and lower teeth. It is also called
as night grinding or bruxomania. It is a habitual grinding
of the teeth, either during sleep or as an unconscious habit
during waking hours. It is the term used both for clenching
habit during which pressure is exerted on the teeth and
periodontium by the actual grinding or clamping of the
teeth and, also to repeated tapping of the teeth.
Clinical Features
Symptomsin grinding and tapping, this is contact
which involves movements of the lower jaw and unpleasant sounds which can often awaken housemates.
Clenching (or clamping) on the other hand, involves
inaudible, sustained, forceful teeth contact unaccompanied by mandibular movements. Long-term bruxers
sometimes experience jaw tenderness, jaw pain, fatigue
of facial muscles, headaches, neckaches, earaches and
hearing loss.
Teethchronic bruxism may lead to sensitive, wornout, decayed, fractured, loose or missing teeth. Grinding
or clenching breaks down the enamel; sometimes in
long-term bruxers, the teeth height is reduced to stumps
(Fig. 28-6). Instead of a white enamel cover, one often
sees the more yellowish and softer dentin. The posterior
teeth of some chronic bruxers often loose their cusps
and natural contours, appearing instead flat, as if they
had been worked over with a file or sandpaper. When
anterior teeth are affected, their biting surfaces are
damaged.
Etiology
Localmild occlusal disturbances, unconscious attempt
by the patient to establish a greater number of teeth in
contact or to counteract a local irritating situation.
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Fig. 28-7: Severe destruction tooth seen in bruxism patient.
Management
Psychotherapythe belief that bruxism is traceable to
stress and other emotional and psychological factors
give rise to a variety of psychotherapeutic approaches.
For instance, listening to progressive relaxation or
autosuggestion tapes just before going to sleep may foster
calmness and self-confidence.
Wakeful EMG Feedbackanother psychological approach
to stress reduction resorts to instrumentation. During
bruxing, the relevant muscles are active and this
increased activity or tension can in turn be measured
with an electromyograph (EMG: electroelectric; myo
muscle; graphrecord). During treatment sessions at
home or the laboratory, the patient sits or reclines
comfortably. One or more pairs of recording electrodes
are then attached to the surface of the skin in close contact
to appropriate muscles (e.g. masseter muscles). These
electrodes transmit information about the level of muscle
activity to a computer monitor. The patient is instructed
to consciously lower that level below a threshold line
(also visible on the screen). Gradually, by becoming alert
to the presence of muscle tension, patients may develop
techniques for reducing that tension and hence, bruxism.
ExerciseQuinn suggested isokinetic and stretching
exercises of the mandible. Such exercises may or may
not help alleviate bruxism, but perhaps may be used to
complement other approaches. However, but it seems
unlikely that they could ever be used as the sole
therapeutic approach. Evidences that this approach is
effective and non-existent.
Drugsboth, the stress and brain malfunction etiological
theories give at times, rise to the use of anti-anxiety
agents, muscle relaxant and other drugs. Most
authorities, however, feels that at best, drugs in use now
are of limited value in the treatment of great majority of
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B
Figs 28-9A and B: Uncomplicated fracture of crown of teeth
(Courtesy Dr Shetty).
Types
Enamel infraction or crackfracture that involves only
enamel without loss of enamel substance.
Uncomplicated fracturefracture involving enamel or
enamel and dentin with loss of tooth substance without
pulpal involvement.
Complicated fracturefracture that extends through
enamel, dentin and pulp with loss of tooth substance.
Radiographic Features
Appearanceit will show size and position of pulp
chamber, location and extent of exposure and stage of
root development.
Management
Clinical Features
Cracksit can be seen in indirect light (directing the beam
along the long axis of tooth).
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B
Figs 28-10A and B: Complicated crown fracture of
upper central incisor (Courtesy Dr Shetty).
Radiographic Features
Appearanceif the X ray beam is projected parallel with
the plane of the root, sharp radiolucent line between the
fragments can be seen (Fig. 28-12B) . If the X-ray beam is
not parallel, it will look as poorly defined gray shadow.
Fracture linefracture line may be transverse or oblique.
Obliteration of pulp chambercalcification and obliteration of pulp chamber can be seen in due course of time.
Fig. 28-11: Crown fracture involving the enamel and dentin.
Differential Diagnosis
Soft tissue imageit extends beyond tooth margin.
Management
Fracture in middle or apical third of rootteeth mainly
restored to their proper position and securely immobilized.
Fracture at coronal/cervical areaextraction is indicated.
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It is also called as Cracked tooth syndrome. It runs lengthwise from crown towards apex of tooth.
Causes
Clinical Features
Clinical Features
Crown/Root Fracture
Radiographic Features
Appearanceif central X-ray lies in the plane of the
fracture, it may be visible as a radiolucent line.
PDL thickeningafter bacterial invasion, radiograph
will show thickening of periodontal ligament space or a
diffuse radiolucent lesion.
Management
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Radiological Features
Loss of PDL spaceit may be visible on the radiograph as
loss of the normal thin radiolucent line representing the
periodontal ligament.
Sclerosisthere may be mild sclerosis and apparent
blending of the bone with the tooth root.
Management
It has good prognosis and as such no treatment is
required.
Fig. 28-14: Root perforation seen in the central incisor (Courtesy Dr Soni).
Tooth Ankylosis
Ankylosis between tooth and bone is an uncommon
phenomenon in the deciduous dentition and even more
rare in permanent teeth.
Causes
Partial root resorptionit occurs when partial root
resorption is followed by repair; with either cementum
or bone that unite the tooth root with alveolar bone.
Occlusal traumaankylosis can occur after traumatic
injury particularly due to occlusal trauma.
Following root canal therapyit may follow root canal
therapy, if the apical periodontal ligament is irritated or
seriously damaged.
Clinical Features
Symptomsit seldom manifests any clinical symptoms
unless there is concomitant pulp infection.
Dull muffled soundif the extensive area of the root
surface is involved, the tooth gives a dull muffled sound
on percussion rather than the normal sharp sound.
Difficulty in extractionthere is considerable difficulty
while doing extraction of the teeth, sometimes
necessitating surgical removal.
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Dentoalveolar Fractures
These are defined as those in which avulsion, subluxation
or fracture of teeth occur in relation with fracture of the
alveolus. Anterior alveolar fractures are most common.
Labial plate is more prone to fracture than palatal plate.
Fracture line is most often horizontal.
Clinical Features
Sitealveolar process of maxilla is more commonly
fractured than that of mandible. The most common sites
are the upper incisor and cuspid regions and region of
tuberosity.
Lipthere is full thickness wound of the lower lip or
ragged laceration on its inner aspect caused by impaction
against the lower anterior teeth. There may be local
bruising and portions of teeth or foreign bodies may get
lodged in soft tissue of lip.
Gingivathere may be laceration of gingiva and
deformity of alveolus.
Teeththere may be fracture of crown and root portion
of teeth. Teeth in fractured fragment will have
recognizable dual sound when percussed.
Occlusionmarked malocclusion along with displacement and mobility.
Alveolar fracturea complete alveolar fragment may be
displaced into the soft tissue of the floor of mouth and
can be covered by mucosa. There may be gross
comminution of alveolus occurs.
Maxillary tuberosity fracturethe detached bone may
include the floor of maxillary sinus (Fig. 28-15); which
is indicated by discharge from the nose on the involved
side. Ecchymosis of buccal vestibule can also occur.
Cracked pot noiseimpacted alveolar fracture may be
virtually immobile. Sometimes crepitations can be
detected on palpation and a cracked pot noise is detected
when the teeth within the alveolar fracture are purcussed.
Radiological Features
Radiologically, fracture line is seen above the apices of
root of teeth.
Management
Fracture of maxillary tuberosityif the tuberosity is
completely detached from the periosteum, it should be
carefully dissected out and the resulting soft tissue defect
are sutured to prevent any residual opening into the
maxillary sinus.
Extensive fracture of alveolus with teeth attachedsplinting
of teeth and anchoring to teeth elsewhere in the upper
jaw.
Mandibular Fractures
Fracture of mandible occurs more frequently than any other
fracture of the facial skeleton. It is more common than
middle third fracture. The most common facial fractures
are mandible (61%), followed by maxilla (46%), the zygoma
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Classification
According to type of fracture:
Simpleit includes closed linear fracture of the
condyle, coronoid, ramus and edentulous body of the
mandible. Greenstick fracture occurring in children
is also included in it.
Compoundfracture of tooth bearing portions of the
mandible are nearly always compound into the mouth
via the periodontal membrane and some severe
injuries are compound through the overlying skin.
Comminuteddirect violence to mandible from
penetrating sharp objects and missiles are usually
compound and may be further complicated by bone
and soft tissue loss.
Pathologicalwhen fractures result from minimum
trauma to mandible which is already weakened by
pathological conditions like osteomyelitis, neoplasm
and generalized skeletal diseases.
According to site of fracture:
Dentoalveolar
Condyle
Coronoid
Ramus
Angle
Body (molar and premolar)
Parasymphysis
Symphysis
According to cause of fracture:
Direct violencefracture occurs at the site of trauma.
Indirect violencefracture occurs away from the site
of trauma.
Excessive muscular contractionoccasionally, fractures
of coronoid process occur because of sudden reflex
contracture of temporalis muscle.
According to treatment plan
Unilateralit is more frequently caused by direct
violence.
Bilateralit occurs due to combination of direct and
indirect violence.
Multipleit is also associated with direct and indirect
violence. Most common fracture of this type is
Guardsman fracture when soldier faints on parade
at midpoint of chin causing fracture of symphysis
and both the condyle.
Comminutedit is usually seen in war missile injury
(Fig. 28-17).
Fry and colleagues classified, in descriptive manner, the
different directions of the fracture:
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premature dental contact. Lateral mandibular movements may be inhibited by bilateral condylar fractures
and fracture of ramus with bone displacement.
Change in facial contour and mandibular arch formfacial
asymmetry should alert clinician to the possibility of
mandibular fracture. A retruded chin can be caused by
bilateral parasymphyseal fracture. The appearance of
an elongated face may be the result of bilateral subcondylar, angle, or body fracture, allowing the anterior
mandible to be displaced downward. If there is a
deviation from the normal U-shaped curve of the
mandible, fracture should be suspected.
Lacerations, hematoma and ecchymosistrauma significant
enough to cause loss of skin or mucosal continuity or
subcutaneous-submucosal bleeding certainly can result
from trauma to the underlying mandible. Lacerations
should be carefully inspected before closure. The
direction and type of fracture may be visualized directly
through the laceration. In rare cases of animal bites there
may be the loss of soft as well as hard tissue. The
diagnostic sign of ecchymosis or hematoma in the floor
of the mouth indicates mandibular body or symphyseal
fracture.
Radiographic Features
Technique requiredfollowing types of radiographs are
helpful in the diagnosis of mandibular fractures, i.e.
panoramic (Figs 28-21 and 28-23) radiograph, lateral
oblique radiograph, posteroanterior radiograph, occlusal
view, periapical view, reverse Townes view, CT scan.
Margin of fracturethe margins of the fractures usually
appear as sharply defined radiolucent lines of separation
that are confined to the structure of the mandible.
Occasionally the margins of the fracture overlap each
other, resulting in the area of increased radiopacity at
the fractured site.
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Differential Diagnosis
Soft tissue shadow of space between tongue and soft palate
in lateral radiograph of normal mandible, it is possible
to see the gray shadow of tongue which has curved upper
and posterior borders. Immediately behind lies the soft
palate, which presents a shape somewhat similar to an
inverted triangle. In many radiographs, there is a dark
line situated between these two shadows which is
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Management
B
Figs 28-25A and B: 3D CT image of mandibular fracture at symphysis
region (Courtesy Dr Amit Parate, Lecturer, GDCH, Nagpur, India)
Preliminary management
Examinationthe first aid required consists of careful
examination of mouth and removal of all fragments of
teeth, broken filling and dentures.
Airwayif there is danger of falling tongue back, then
dorsum of the tongue should be sutured.
Hemorrhageobvious bleeding point such as facial
vessels should be secured with artery forceps and
temporary dressing should be applied.
Soft tissue lacerationsoft tissue wound should be sutured
within 24 hours of injury.
Antibioticsbenzyl penicillin should be administered
IM injection or 1 mega unit every 6 hours for first 2 to 3
days and oral penicillin should be continued for further
one week. In recent, oral metronidazole 400-800 mg BD
is given to all patients with mandibular fracture.
Planned management
Reductionreduction of fracture means the restoration
of functional alignment of bone fragments.
Immobilization of fractured bonethe fracture site must be
immobilized to allow bone healing to occur.
Immobilization can be done with intermaxillary fixation
and bone plating.
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Postoperative Care
Sitting positionpatient with fracture of mandible finds
it more comfortable if they are in sitting position with
chin forward, provided that there is no contraindication
to this posture such as fracture of vertebra.
Drugsmorphine and its derivative are contraindicated
in patients with maxillofacial injuries as these drugs
depress the respiratory center and cough reflex. Prophylactic antibiotics should be administered to control the
infection. Maintenance of good oral hygiene is essential
for prevention of infection.
Coronoid Fracture
It is rare. It usually results from the reflex contracture of the
powerful anterior fibers of temporalis muscle. During
operation on large cyst of ramus, coronoid may get fracture
(Fig. 28-28).
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Le Fort II
It is also called as Pyramidal or Subzygomatic fracture. There
is a pyramidal appearance of fracture in PA skull view
(Fig. 28-30).
This fracture runs from the thin middle area of the Nasal
Bones down to either side crossing the frontal processes
of maxilla into the medial wall of each orbit.
Within each orbit, the fracture line crosses the lacrimal
bone behind the lacrimal sac before turning forward to
cross the infraorbital margin slightly medial to or
through the infraorbital foramen.
The #(fracture line) now extends downwards and
backwards across the lateral wall of the antrum below
zygomatico-maxillary suture and divides the pterygoid
laminae about halfway up. Separation of block from the
base of skull is completed via the nasal septum and may
involve the floor of the anterior cranial fossa.
Le Fort III
It is also called as High transverse or Suprazygomatic fracture.
It completely separates the middle third of the facial
skeleton from the cranium (Fig. 28-31).
The fracture line runs from near the frontonasal suture
transversely, parallel with the base of the skull and
involves the full depth of the ethmoid bone, including
the cribriform plate.
Within the orbit, the fracture line passes below the optic
foramen into the posterior limit of the inferior orbital
fissure.
Clinical Features
Le Fort I
Locationit may be unilateral or bilateral.
Symptomsin recent injury, there may be slight swelling
of upper lip. Some fractures are so mobile that the
patient has to keep the mouth slightly open to
accommodate the increased vertical dimension of bite.
Paresthesia presents over the distribution of infra-orbital
nerve and pain over nose and face.
Signsecchymosis is present in the buccal sulcus
beneath the zygomatic arch. Occlusion is disturbed and
variable amount of mobility may be found in the tooth
bearing segment of maxilla. If the fracture line is at high
level, the fragment will include the pterygoid muscle
attachment. It will pull the fragment posteriorly and
depress its posterior margin. Due to this, posterior
maxillary teeth will force the mandible open resulting
in open bite, retruded chin and long face.
Cracked pot soundin impacted type of fracture, there may
be damage to cusps of individual teeth caused by impaction of the mandibular teeth against them. Percussion of
upper teeth results in a distinctive Cracked pot sound.
Flattening of facein some cases, there is flattening of
middle of the face and epistaxis.
Palpationmanipulation will reveal mobile maxilla and
crepitation.
Le Fort II
Moon face appearancethere is massive edema that cause
marked swelling of the middle third of face giving rise to
moon face appearance.
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Radiographic Features
Le Fort Iit is identified on PA, lateral skull and Waters
projection (Fig. 28-33). Both the maxillary sinuses are
cloudy and may show air filled level. Lateral view shows
slight posterior displacement of fragment.
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Management
Le Fort ILow levelintermaxillary fixation. High level
intermaxillary fixation and cranio-maxillary fixation.
Le Fort IIreduction followed by intermaxillary fixation.
Open reduction and inter-osseous wiring of infraorbital
rims. Antibiotics should be given to the patient.
Le Fort IIIcontrol hemorrhage and maintain airway.
Surgery should be delayed until edema subsides.
External immobilization should be done.
Classification
Class IFracture of zygomatic bone with minimum or
no displacement.
Clinical Features
Signflattening of the cheek, swelling of the cheek,
periorbital hematoma, subconjunctival hemorrhage (Fig.
28-36) and limitations of ocular movements, diplopia,
ecchymosis and tenderness intraorally over zygomatic
buttress, enophthalmos.
Symptomslowering of pupil level, tenderness over
orbital rim and frontozygomatic suture, epistaxis.
Limitations of mandibular movements. Anesthesia of
cheek, temple, upper teeth and gingiva. Possible gagging
of back teeth on injured side.
Othersstep deformity of infraorbital margin. Separation
of frontozygomatic suture.
Radiological Features
Traditional facial radiographs like submentovertex view
offers excellent resolution of the zygomatic arches (Fig.
28-37).
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Fig. 28-38: Waters view showing the fractured zygoma.
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Management
Greenstick Fracture
It occurs in young people. Rare in maxilla and mandible.
Radiologically, there is sharp angulation present at the
site of fracture. There may be one or more linear dark streaks
running some distance along the length of the bones from
each side of the angulation. Small spicules of bone may be
seen standing away from the surface, which had been
stripped away at the time of fracture.
Nasoethmoidal Injuries
An area behind which lies the interorbital space, which is
situated between the medial walls of orbits (Fig. 28-42).
Fractures in this region are invariably comminuted.
Fig. 28-41: Postoperative radiograph of the
patient of zygomatic fracture.
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Clinical Features
It includes frontal bone depression, nasal deformity,
traumatic telecanthus, CSF fluid rhinorrhea, diplopia, and
hemorrhage from anterior or posterior branches of
ethmoidal artery.
Management
Closed reductionthe use of transnasal wires and
compression plates is often unsatisfactory.
Open reductionrealignment of bony fragments under
direct vision especially at early stages gives better results.
Repair of bony skeletonNasal bridge re-attached to
frontal bone. All bone fragments must be preserved,
aligned and either directly wired or plated with micro
plates.
Complications of Healing
In Fracture
Non-unionit results when callus of osteogenic tissue,
over each of the two fragments, fails to meet and fuse or
when endosteal formation of bone is inadequate. It can
occur due to infection of the fracture site, inadequate
immobilization and unsatisfactory apposition of bone.
Radiograph shows rounding off and sclerosis of the
bone ends, a condition known as eburnation. It is
common in elderly patients.
Fibrous unionit occurs as a result of lack of immobilization of the damaged bone. The fractured ends united
In Extraction
Dry Socket
It is also called as Alveolitis sicca dolorosa , Alveolagia or
Postoperative osteitis. It is basically focal osteomyelitis in
which blood clot has disintegrated or is lost. It is called as
dry socket as after the clot is lost, the socket gives dry
appearance because of exposed bone.
Etiology
Difficult extractiondifficult or traumatic extraction,
usually removal of impacted mandibular 3rd molars.
Dislodgement of clotdislodgment and disintegration of
the clot and subsequent infection of the bone.
Clinical Features
Duration of occurrenceit is the most common
complication in healing of extraction wound. It arises
within the first few days after extraction.
Symptomsit is extremely painful and odor is foul, but
with no suppuration.
Signsexposed bone is necrotic and sequestration of
fragments is common.
Healinghealing of such infected wounds is extremely
slow.
Prevention
Experiment by placing sulfanilamidesulfathiazole cones
placed in fresh tooth socket of dog can prevent the
occurrence of dry socket but it will cause retarded blood
clot formation and even cause some breakdown of clot
and remarkable delay in epithelialization.
Oxidase celluloseinserted for hemostatic purpose,
produces retardation of healing similar to that of
combined sulfonamide.
Sulfathiazole in 60% glycerin base reduces the frequency
of occurrence of dry socket.
Aureomycincauses significant reduction in
decomposition of blood clot. There is decreased incidence
of postoperative pain and swelling after one week.
Tetracycline hydrochlorideif tablet is placed in extraction
sockets, it helps in reduction of dry socket to 0.78%.
Trypsindigests necrotic tissue and debris and restrains
bacterial growth.
Antiseptic mouth rinsesuse phenolated antiseptic
mouth-rinses prior to extraction.
Little traumaone should try to cause a little trauma to
tissue as possible. So that it helps in normal healing.
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Management
Packing materialinsertion of packing material
containing an obtundent.
Zinc oxide and eugenol packidoform gauze with zinc
oxide and eugenol.
In Wound
Fibrous Healing of a Wound
It is an uncommon complication following a difficult,
complicated or surgical extraction of tooth. It occurs most
frequently when tooth extraction is accompanied by loss of
both, lingual and labial cortical plates of bone with
accompanied loss of periosteum.
It is usually asymptomatic and discovered only on
radiological examination. Radiologically, it appears as a
well circumscribed radiolucent area at the site of extraction
wound.
Excision of the lesion for the purpose of establishing the
diagnosis and to produce normal healing with subsequent
bony repair.
Suggested Reading
1. Al,-Khateen TL, EL-Marsafi. The relationship between the indication for the surgical removal of impacted third molar and the
incidence of alveolar osteitis. J Oral Maxillofac Surg 1991;49:1415.
2. Andreasen JO. Traumatic injuries to the teeth (2nd edn), 1981.
3. Catellani JE. A review of factors contributing to dry socket through
enhanced fibrinolysis. J Oral Surg 1989;37:42-6.
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Definition
Clinical Features
Classification of Calcification
Dystrophic calcification
General dystrophic calcification of the oral regions
Calcified lymph nodes
Dystrophic calcification in the tonsil
Cysticercosis
Calcified carotid artery
Idiopathic calcification
Sialoliths
Phleboliths
Metastatic calcification
Ossification of the stylohyoid ligament
Osteoma cutis
Myositis ossificans.
Radiographic Features
Sitethe common sites are long standing and
chronically inflamed cyst.
Appearanceappear as fine grains of radiopacities which
are sparse and diffuse (Fig. 29-1).
Dystrophic Calcification
General Dystrophic Calcification of the
Oral Region
When calcium salt precipitate into primary site of chronic
inflammatory dead and dying tissue, it is called as
dystrophic calcification. It is associated with high local
concentration of phosphatase, as in normal bone calcification and with anoxic conditions within the devitalized
tissue.
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Causes
Tuberculosis lymphadenitistuberculous lymphadenitis
is probably a disease in which calcified lymph nodes
occur.
Other diseasesactinomycosis, histoplasmosis, catscratch fever and other chronic inflammatory diseases
may also present calcified lymph nodes.
Clinical Features
Sitenodes involved are submandibular or cervical
chain.
Symptomsit is usually asymptomatic.
Numberit may be single or multiple or sometimes chain
of nodes.
Size and shapethey are hard, round or oblong masses.
Outline is well contoured and well defined.
Fixity to underlying tissuethey are mobile during
palpation.
Radiographic Features
Siteit is most commonly seen behind or below the angle
of the mandible (Fig. 29-2A). In some cases, it is seen in
more inferior location when cervical lymph nodes are
involved (Fig. 29-2B). In rare cases, calcified node is
found posterior to the ramus.
Radiodensityit is opaque and well defined. In some
cases radiodensity is variable showing both opaque and
radiolucent appearance.
Appearanceit may have laminated appearance.
Radiopacity often exhibits a patchy pattern with a
reticular arrangement of radiolucent lines or gaps.
Mass of coral appearancesometimes, irregular heterogeneous opaque masses are seen which appear to resemble
a mass of coral.
Marginswell defined and usually irregular, occasionally having a lobulated appearance similar to outer
shape of cauliflower.
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis.
B
Figs 29-2A and B: Calcified lymph nodes, cervical lymph nodes that
is cauliflower shaped and chainlike (Courtesy Dr Enzio Rovigatti).
Differential Diagnosis
Sialolithsit is painful and has a smooth outline whereas
calcified lymph nodes are usually irregular and sometimes lobulated.
Phlebolithsthey are smaller and have concentric
radiopaque and radiolucent rings.
Management
Surgical removallarge calcified lymph nodes should
be surgically removed.
Tonsillolithiasis
It is dystrophic calcification in the tonsil. It is also called as
Tonsillar calculi, Tonsil concretions, and Tonsilloliths. The
mechanism is similar to that of calcified lymph nodes. It
occurs due to recurrent inflammation of tonsil.
Clinical Features
Age and sex distributionit is common in older age groups
between 20 to 68 years of age. Women are more
commonly affected.
Locationit can be unilateral or bilateral.
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Radiographic Features
Siteit is seen in middle portion of the mandibular ramus
in the region where the image of the dorsal surface of
tongue crosses the ramus.
Appearanceit can produce speckled appearances of
multiple radiopaque superimposed bilaterally on the
images of the mandibular rami in a panoramic
radiograph.
Sizeit may reach the size of 0.5 cm to 14.5 cm.
Marginsmultiple small ill defined radiopacities are
seen.
Internal structureit appears more radiopaque than the
cancellous bone and same as cortical bone (Fig. 29-3).
Management
Enucleationlarger calcifications with associated
symptoms are removed surgically.
Cysticercosis
When eggs or gravid proglottids from Taenia sodium (pork
tapeworm) are ingested by human, their covering is digested
in stomach and larval form (Cysticercus cellulosae) of the
parasite is hatched. Larvae penetrate the mucosa, enter the
blood vessels and lymphatics and are distributed in the
tissue all over the body. After the larva die, the larval spaces
are replaced with fibrous connective tissue, which may
become calcified.
Clinical Features
Mild casesthey are completely asymptomatic.
Severe casesthere is mild to severe GIT upset with
epigastric pain, severe nausea and vomiting.
Nervous systemconvulsion, irritability and loss of
consciousness.
Sizepalpable firm mass upto 1 cm in diameter.
Oral findingmultiple small nodules may be felt in the
region of masseter and suprahyoid muscles and in
buccal mucosa or lip.
Radiographic Features
Sitethe muscle of mastication and facial expression,
the suprahyoid muscle and the postcervical musculature.
Marginsthe margins are well defined.
Shapethe shape is elongated, elliptical or ovoid.
Internal structureit is homogenous and radiopaque.
Diagnosis
Fig. 29-3: Tonsillitis is present (red arrow) on CT scan
(Courtesy RS Kamikawa).
Diagnosis
Clinical diagnosisrecurrent tonsillitis is common
features
Radiological diagnosisspeckled appearance with
multiple radiopaque image on ramus area.
Differential Diagnosis
Salivary stoneit is not multiple as compared to
cysticerci.
Differential Diagnosis
Radiopaque lesion in mandibular ramusin it right angle
view such as PA skull or open Townes view may show
that calcification lies to the medial aspect of the ramus.
Management
Medical managementmedical management by the
physician.
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Causes
Clinical Features
Usually no clinical sign or symptoms develop.
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis.
Radiological diagnosiscalcified deposit seen on walls
of artery.
Radiographic Features
Sitecalcification with the carotid artery are located in
the soft tissue below the angle of the mandible and
between the hyoid bone and the image of the cervical
spine (Figs 29-4A and B).
Marginscalcific deposits on wall of artery will outline
the image of the artery.
Differential Diagnosis
Other calcific depositsusually, the linear nature of the
calcified arterial wall indicates the nature of this
condition.
Management
This disease requires no treatment. Only special care
should be taken for stroke.
Idiopathic Calcification
The deposition of calcium in normal tissue despite normal
serum calcium and phosphate level is referred to as
Idiopathic calcification.
Sialoliths
It is described in Chapter 26: Salivary Gland Disorders.
Phleboliths
These are thought to be formed in older thrombi in veins or
hemangiomas with slow blood flow. The thrombus
organizes into granulation tissue and occasionally
mineralizes with the deposition of calcium phosphate and
calcium carbonate.
Clinical Features
B
Figs 29-4A and B: OPG showing calcification in the carotid artery
(Courtesy Dr Fbio de Lima Cravo).
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Clinical Features
Palpationthere is hard pointed structure over the tonsil.
Symptomsvague pain on swallowing, turning the head
and opening the mouth. Patient may describe earache,
headache, dizziness or transient syncope which is
caused by elongated styloid process impinging on
glossopharyngeal nerve.
Signsthere may be visible swelling on the region of the
angle of mandible (Fig. 29-6A).
Stylohyoid syndromeclinical finding without the history
of neck trauma constitutes Stylohyoid syndrome.
Diagnosis
Clinical diagnosisswelling swollen tissue over the vein
may suspect the disease.
Radiological diagnosisround shaped radiopacity with
radiolucent center will give clue to the diagnosis.
Differential Diagnosis
Sialolithssialoliths occur single as compared to
phleboliths which is usually multiple.
Management
Radiographic Features
Metastatic Calcification
In this, calcium salts are precipitated in previous
undamaged tissue. This precipitation is due to an excess of
blood calcium and occurs particularly in such diseases as
hyperthyroidism which depletes the bone calcium and
causes a high level of blood calcium. The deposits of calcium
occur in the kidney, lungs, gastric mucosa and media of
blood vessels.
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Diagnosis
Osteoma Cutis
Clinical Features
Management
Radiographic Features
Sitemost commonly appears in the cheek and lip
regions. Image can be superimposed over a tooth root or
alveolar process.
Margins and shapesmoothly outlined radiopaque
washer-shaped image.
Sizethey are very small, although size can range from
0.1 to 5 cm.
Internal structureit may be homogenous radiopaque or
may have a radiolucent center that represent normal
fatty marrow.
Diagnosis
Clinical diagnosisThere are areas of dense viable bone
in the dermis or subcutaneous tissue.
Radiological diagnosiswasher shaped image seen on
the periapical radiograph (Figs 29-7B and C).
Differential Diagnosis
Fig. 29-6C: Elongated styloid process with nodular
mineralization pattern (Courtesy RS Kamikawa).
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Etiology
Traumait is caused by acute or chronic trauma or heavy
muscular strains caused by certain occupation or sports.
Traumatization of the periosteum of an adjacent bone
with the displacement of osteoblasts into the muscle and
subsequent formation of bone.
Periosteal implantsactivation of periosteal implants
already present in muscle by trauma or hemorrhage.
Metaplasiametaplasia of the pluripotential intermuscular connective tissue into the bone. Metaplasia of
fibrocartilage.
Pathogenesis
Injury hemorrhage into the muscle or associated tendon
or fascia the hemorrhage organized and undergoes
scarring during healing process cartilage is formed
calcification of cartilage ossification of cartilage.
Clinical Features
C
Figs 29-7B and C: Multiple miliary osteoma cutis. Patient with history
of large quantity of acne for a long period of time. Periapical radiographs
showing evidence of ossifications in the soft tissues of the cheek
(Courtesy RS Kamikawa).
Management
Surgical removalosteomas are occasionally removed
for cosmetic reasons.
Myositis Ossificans
It is a condition in which fibrous tissue and heterotopic
bone form within the interstitial tissue or muscle, as well
as in associated tendons and ligaments. Secondary
destruction and atrophy of the muscle occurs, as this fibrous
tissue and bone interdigitate and separate the muscle fibers.
Types
Localized myositis ossificans or traumatic myositis
ossificans.
Progressive myositis ossificans or generalized myositis
ossificans.
Age and sexit can occur at any age, sex and more often
in young persons.
Sitethe most commonly involved muscles are the
masseter and sternocleidomastoid but in some cases,
lateral pterygoid muscle can be involved.
Symptomssite of trauma remains swollen, tender and
painful much longer than expected. In some cases, there
is a mild discomfort associated with a progressive
limitation of motion.
Signsthe overlying skin may be red and inflamed.
Intramuscular mass is palpated at 2 to 3 weeks. The lesion
may appear fixed or it may be freely movable on palpation.
Oral Manifestations
Siteit involves the muscles of face particularly masseter
and temporal following single traumatic injury.
Symptomssome difficulty in opening of the mouth.
Radiographic Features
Siteradiolucent band can be seen between the area of
ossification and adjacent bone and heterotopic bone may
lie along the long axis of the muscle.
Internal structurefaintly homogenous opacity. Delicate
lacy or feathery internal structure of increased radiodensity develop indicating bone has formed (Fig. 29-8).
Sometimes it is accompanied by circumscribed cortical
periphery.
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Clinical Features
Diagnosis
Clinical diagnosispalpable intramuscular mass with
swelling area of trauma may give clue to the diagnosis.
Radiological diagnosispseudotrabeculae and more
radiopaque margin is present.
Laboratory diagnosisbiopsy shows degeneration of
muscle and connective tissue hyperplasia to chondrification and ossification. The trabecular pattern is
often extremely bizarre with the cartilage and
myxomatous tissue present which may resemble callus
formation.
Differential Diagnosis
Ossification of stylohyoid ligament, dystrophic calcification
in areas of necrosis, pathological calcification and
phlebitisthe form and location of myositis ossificans
are enough make the differential diagnosis.
Radiographic Features
Appearancethere is evidence of dense osseous
replacement of the greater part or whole of the muscle.
Internal structuredensities of heterotrophic bone vary
widely. The bone that is laid down in the muscle does
not show structure of normal bone but it is rather
structureless mass of variable density.
Linear striae of increase densitycoarse linear striae of
increased density represent new bone formation in some
cases; the streaks follow the long axis of the particular
muscle involved. In early stages calcified deposits are
granular and fragmentary.
Marginslesion have smooth or irregular margins, lying
in close relationship with the bone.
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Diagnosis
Clinical diagnosisPetrified man appearance with
gradual limitation of movement of the body.
Radiological diagnosisbone in muscle show structureless mass of variable density.
Laboratory diagnosisthe muscle in this disease is
gradually replaced by connective tissue which undergoes osteoid formation and subsequently ossification.
In some cases, cartilage formation may become evident.
Differential Diagnosis
Rheumatoid arthritisin initial stage, it is difficult but as
disease progress specific anomalies confirms the
diagnosis.
Calcinosisthe deposits of amorphous calcium salts
frequently resorb, but in progressive myositis ossificans
the bone never disappear.
Management
No effective treatment exists. Nodules that are
traumatized and then ulcerated frequently should be
excised.
Suggested Reading
1. Appleton SS, Kimbrough RE, Engstrom HIM. Rhinolithiasis: a
review. Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod
1988;65:693-8.
2. Basler RS, Watters JH, Taylor WB. Calcifying acne lesions. Int J
Dermatol 1977;16(9):755-8.
3. Beder E, Ozgursoy OB, Karatayli Ozgursoy S. Current diagnosis
and transoral surgical treatment of Eagles syndrome. J Oral
Maxillofac Surg 2005;63(12):1742-5.
4. Boulman N, Slobodin G, Rozenbaum M, Rosner I. Calcinosis in
rheumatic diseases. Semin Arthritis Rheum 2005;34:805-12.
5. Boylan PA. Rhinolith. Oral Surg, Oral Med, Oral Pathol, Oral
Radiol Endod 1973;36:290.
6. Carter LC. Discrimination between calcified triticeous cartilage
and calcified carotid atheroma on panoramic radiography. Oral
Surg, Oral Med, Oral Pathol, Oral Radiol Endod 2000;90(1):10810.
7. Conlin PA, Jimenez-Quintero LP, Rapini, RP. Osteomas of the
skin revisited. A clinicopathologic review of 74 cases. The American
Journal of Dermatopathology 2002;24(6):479-83.
8. Cooper MM, Steinberg JJ, et al. Tonsillar calculi: report of a case
and review of the literature. Oral Surg, Oral Med, Oral Pathol
1983;55:239-43.
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30
Bacterial Infections
Introduction
Etiology
Syphilis
It is also called as lues. The incidence of syphilis is
decreased after introduction of penicillin in late 1940s.
Patient infected with Treponema pallidum and HIV may
exhibit a malignant form of syphilis with slow development
of standard serological response to syphilis. The tertiary
manifestations lead to considerable morbidity and
mortality.
Classification
Acquired syphiliscontacted primarily as venereal
disease due to sexual intercourse with infected partner.
Primaryit is evident clinically 3 to 90 days after the
exposure.
Secondaryit is discovered 4 to 10 weeks after primary
stage.
Tertiarythis stage develop after the latent phase.
Quaternary syphilisthe atypical malignant progression of tertiary neurosyphilis in immunocompromised HIV individuals is referred as
quaternary syphilis.
Latent phasethis appear after secondary stage and
in this stage, there is no sign and symptoms are
present. Serological test is positive in this stage.
Congenitalthis is secondary to fetal infection.
Early syphilisprimary syphilis, secondary syphilis and
the early latent phase of the disease are grouped as early
syphilis. Early syphilis may last up to two years and is
infectious.
Late syphiliswhile late latent and tertiary are grouped
as late syphilis. Late syphilis is locally destructive and
non-infectious.
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Primary Syphilis
Clinical features
Incubation periodlesion develop at the site of inoculation
approximately 3 to 90 days after the inoculation.
Siteit occurs most frequently on penis in males and
vulva or cervix in females. Recently, occurrence on
extragenital sites have increased as a result of increase
in orogenital sex and increased contact among the
infected homosexuals. Extragenital sites of involvement
include fingers, perianal region, nipples, lips, tonsils
and intraoral structures such as tongue and palate.
Chancreit is slightly raised, ulcerated, non-tender, nonbleeding, firm plaque which is usually round, indurated
and with rolled raised edges.
Sizeit varies in size from 5 mm to several centimeters.
Symptomsit is painless, unless superinfected. It
disappears without therapy after 10 days.
Lymph nodesregional lymph nodes become firm
enlarged, rubbery in consistency and non-tender.
Oral manifestations
Siteoral lesions of primary syphilis are rare and occur
at the site of entry of treponema. Chancre has been
described on lips, oral mucosa, lateral surface of tongue,
soft palate, tonsillar area, pharyngeal area and gingiva.
Transmissiontransmission can occur during kissing
as a consequence of sexual practice among homosexual
and heterosexuals, or by contact with objects such as
mouth piece of musical instruments and medical or
dental instruments.
Appearanceit has narrow copper colored, slightly
raised borders with reddish brown base in center.
Symptomsintraoral chancres are slightly painful due
to secondary infection and are covered with grayish
white film.
Sizeit measures from 0.5 to 2 cm in diameter.
Signsoccasionally, it retains white sloughy material.
In some cases, there is proliferation that resembles
pyogenic granuloma.
Tonsilsprimary involvement of tonsils is manifested
by considerable edema, redness, ulcerated and eroded
lesion.
Lymph nodesregional lymphadenopathy occurs.
Extraoral lip chancreextraoral lip chancre may have
more typical brown crusted appearance which may be
multiple. Lower lip involved more frequently (Fig. 30-1).
Healingoral chancre heals spontaneously in 3 to 8
weeks leaving small scars.
Secondary Syphilis
Clinical features
Spreadorganisms proliferate and spread by the way of
bloodstream to produce lesions elsewhere.
Fig. 30-1: Chancre present on the lower lip in male patient which
has got slightly raised border (Courtesy Dr Jitu Sachdeo).
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Tertiary Syphilis
Clinical features
Incubation periodit may occur at any age from the third
year upto the patients life.
Formsin tertiary syphilis, 1/3rd develop benign or
gummatous form, 1/3rd cardiovascular form and
1/3rd neurosyphilis, i.e. general paresis and tabes
dorsalis.
Gummagumma is due to a chronic destructive
granulomatous process which occurs anywhere in the
body. Gumma is the result of hypersensitivity reaction
between hyperergic host and treponema. Single cerebral
gumma may produce symptoms suggestive of brain
tumor
Typesthere are two types of gumma, i.e. central and
cortical.
Appearancethe characteristic gumma appear as
chronic granulomatous localized lesion, which
ulcerates. It is nodular in appearance.
Signspunched out ulcer with vertical walls and dull
red granulomatous base is the typical clinical feature
of ulcerative gummatous lesion.
Cutaneous lesionscutaneous lesions heal slowly and
leave behind tissue paper-like scars.
Neurosyphilisit occurs due to obliteration of small
vessel artery involving vasa vasorum of aorta and other
large vessels of the central nervous system (neurosyphilis). Neurosyphilis is manifested as tabes dorsalis
and general paresis. Tabes dorsalis is the syphilitic
involvement of dorsal column of spinal cord and dorsal
root ganglion. General paresis is syphilitic involvement
of cerebral tissue.
Tabes dorsalis
Symptomspatient looses the positional sense of his
lower extremities and walks with a slapping step.
Burning and pricking sensation of the extremities,
paresthesia, or actual anesthesia of the part may
accompany the characteristic gait.
Positive Rombergs signperson is unable to stand
erect unaided with his eyes closed.
Tabetic crisesshort, shooting, knife-like pains may
be experienced in the abdominal region called tabetic
crises, which results from involvement of the dorsal
root ganglion.
Charcots jointtrophic changes consist of deep
perforating ulcers and painless destruction of larger
joints.
General paresis
Argyll Robertson pupilpupils that react to accommodation but not to light.
Symptomsincreased irritability, fatigue, mental
sluggishness and carelessness in personal habits.
Signsloss of fine muscular coordination is indicated
by inability to enunciate clearly or to perform delicate
tasks with the hands.
Spinal cord involvementinvolvement of spinal cord
is late manifestation characterized by paresthesia,
burning and prickling sensation in the extremities.
Patient may get unrealistic ideas of wealth or ability.
Cardiovascular syphilisit occurs in 10% cases of late
syphilis. Involvement of CVS in tertiary syphilis affects
aorta and aortic valve and 80% of deaths occur due to it.
There is medial necrosis and destruction of elastic tissue
occurs in the wall of large blood vessels. Dilatation and
aneurysm occurs.
Tertiary syphilis in HIV patienta recent feature has been
an apparent alteration in the behavior of syphilis in HIV
positive patients. Natural history of syphilis may be
altered in HIV positive patients and this group is at high
risk for the development of tertiary syphilis. Genital
ulcerations due to syphilitic infection allows a portal of
entry for the viral particles and may lead to greater risk
of infections in these patients.
Oral manifestations
Sitegumma can occur anywhere in the jaw but are
more frequently on palate, mandible, and tongue.
Gumma
Appearancegumma may manifest as solitary, deep,
punched out mucosal ulcer.
Symptomsbreathing and swallowing difficulty may
be encountered by the patient.
Progressit usually starts as small, pale, raised,
nodular mass in the midline of the palate which
ulcerates and rapidly progresses to the zone of
necrosis.
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Syphilitic Periostitis
It is the most common manifestation of congenital syphilis
and may also be seen in secondary stage of acquired
syphilis. The lesion may develop very late in the disease
process and is characterized by periosteal reaction, which
may either be limited and circumscribed or extensive.
Siteit involves mandible more commonly and it
appears as a single layer or several layers of new bone,
more or less parallel with the margins of jaw. The
calvarium is one of the usual sites of involvement in this
manifestation of syphilis.
Network of latticea rare manifestation of syphilitic
periostitis is new bone arranged with trabeculae forming
a loose type of pattern which is best described as a gross
caricature of a network of lattice. There is often a dark
line between the new bone and jaw and between the
layers of new bone.
Syphilitic osteitisthere are small superficial areas of rarefaction, in the underlying bone, due to syphilitic osteitis.
Congenital Syphilis
It is infection of fetus established by the passage of
spirochetes from mother, through the placenta.
Transplacental infection after 18-week gestation is related
to development of immune complement rather than any
toxic effect on organism.
Congenital syphilis has got three diagnostic features
called as Hutchinsons triad which includes hypoplasia of
permanent incisors and 1st permanent molars, eight nerve
deafness and interstitial keratitis.
Clinical features
Early manifestationsit is manifested within the first 2
years of life (neonatal congenital syphilis) as rhinitis and
chronic nasal discharge with maculopapular eruptions,
other than mucocutaneous lesion and loss of weight. The
lesions can be seen in spleen, kidney, bones and CNS.
Bullae, vesicle and superficial desquamation with cracking and scaling of reddened soles and palms, petechiae,
mucus patches and condyloma latum also occurs.
Late manifestationsafter 2 years, interstitial keratitis
(opacification of corneal surface with resultant loss of
vision), vascularization of cornea, 8th nerve deafness,
arthropathy, signs of congenital neurosyphilis, gummatous destruction of palate and nasal septum develop.
There are also saber shins or anterior tibial bowing.
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Non-venereal Treponematoses
Endemic syphilis is also called as bejel which is caused
by spirillar form of Treponema palladium, yaws which is
caused by Treponema pertenue and pinta which is caused by
Treponema carateum are most non-venereal treponematoses
which occur in children and causes destructive skin and
bone diseases. These diseases run a milder course
compared to venereal treponematoses.
Endemic Syphilis
It is also called as bejel and most commonly occurs in
childhood.
Transmission
Direct transferdirect transfer is through lesion to skin
contact.
Indirect transferindirect transfer is through the common
use of drinking, bowls, or possibly by flies.
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Clinical features
Agethe disease is primarily seen in children, although
adult cases are often reported.
Early stagethe early stage disease is characterized by
the appearance of mucus patches in the oronasopharyngeal region, angular stomatitis, skin rashes,
pigmentary changes and tenderness of the long bones
and regional lymphadenopathy.
Oral patchesoral mucus patches are shallow, relatively
painless lesions, initially seen as white which soon
become erosive. The lesions are usually found on the
lips, tongue and other intraoral surface.
Skin lesionskin lesions may be papular, papillomatous,
macular, papulosquamous, annular or circinate.
Sabre tibiaosteoperiostitis usually involving long bones
is the most common manifestation which may cause
nocturnal pains in the legs. Long standing osteitis and
periostitis may eventually lead to forward bowing of
tibia known as sabre tibia.
Late stageit is seen where early endemic syphilis
remains untreated for 6-9 months or even longer as an
alteration in about 1/3rd of the patients or as tertiary
state of the disease. Late lesions are mainly of gummatous
type, involving skin, mucous membrane and bone. Skin
lesions are usually extensive, chronic, destructive,
scarring and with depigmentation. Gummatous
destruction of nasal septum is common.
Rhinopharyngitis mutilansdestruction of the lips, soft
palate and nasopharynx can occur leading to gross
deformity of the face.
Diagnosis
Clinical diagnosisRhinopharyngitis mutilans with
sabre tibia will give clue to the diagnosis.
Management
Penicillinit is the drug of choice and where penicillin
is contraindicated; drugs such as tetracycline and
erythromycin can be given.
Surgical correctionsurgical correction of the defects of
face should be carried out for aesthetic purpose.
Pinta
It is almost exclusively confined to the Western hemisphere.
The mode of transmission is either by direct or indirect
contact.
Clinical features
Incubation periodthe incubation period is usually
2-3 weeks, after which the disease is clinically
manifested. Infection is seen in young adults of 15-30
years of age.
Subcutaneous lesionthe basic lesion of pinta is a solely
developing subcutaneous granulomatous lesion.
Yaws
It is also called as framboesia or buba. It is caused by
Treponema pertenue, which is pathogenic for monkeys,
rabbits and hamsters. It is transmitted either by direct
contact with the exudates of the early infectious lesion or
indirectly by contaminated utensils.
Clinical features
Primary stagethe incubation period is between 9 to 90
days. The initial lesion, a papule, appears at the site of
entry of the Treponema. It occurs usually through an
abraded or lacerated site. The lesion may ulcerate and
infection can spread via bloodstream. Regional lymph
nodes are usually palpable. Children with only primary
lesion may complain of pain.
Secondary stageusually 1 to 3 months after the
appearance of the papular primary lesion, infection
spreads and a painless papilloma or frambesial granuloma appears. Lesions in the secondary stage are usually
found in warm and moist sites such as axilla, groin and
the skin around the natural orifices, including the mouth.
They may be multiple and condylomatous in appearance.
Partially, healed skin lesions often have an annular or
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sexual intercourse, they penetrate through the intercellular spaces of the epithelium and reach the
subepithelial connective tissue.
Inflammatory reactionwithin 2 to 3 days of infection, an
intense inflammatory reaction occurs resulting in
characteristic mucopurulent discharge through urethral
lumen.
Chronic stagea chronic stage may be reached, if
untreated and spread is either by direct extension
through lymphatics or hematogenous route.
Oral manifestation
Lipsduring secondary stage, mucosal surface of lips
may involve due to direct extension of the lesion present
at the mucocutaneous junction.
Goundousecondary changes of the nasal processes of
maxillary bone have been reported during the secondary
and tertiary stages of the disease. These result in
thickening of the face on either side of the bridge of the
nose, gives rise to a characteristic facial appearance
called goundou.
Gangosa or saddle nose defectin some cases, the lesion
starting either on the soft palate, uvula or hard palate,
eventually invades and destroys soft and bony parts of
nose which is called as Gangosa thereby causing
saddle nose defect.
Diagnosis
Clinical diagnosissaddle nose defect with sabre tibia
goundou shape appearance gives clue to diagnosis.
Management
Penicillinit is the drug of choice.
Gonorrhea
It is primarily an infection of the genitourinary tract mucosa.
It is caused by gram ve intrabacillary located diplococcus
Neisseria gonorrhoeae. It is an oval, paired, gram-negative
microorganism.
Local infection may occur at extra-genital site (Rectal
and pharyngeal gonorrhea). Rectal mucosa is affected in
30% to 50% of women with urogenital gonorrhea.
Uncomplicated local infection at other extra-genital sites is
rare in adults.
Early sexual awakening, prostitution and varied
sexuality are believed to be responsible for the increase
incidence of gonorrhea.
Pathogenesis
Penetration of gonococcionce the gonococci are directly
deposited on the genitourinary tract mucosa during
Clinical Features
Oral Manifestations
Pharyngeal gonorrheaPharyngeal gonorrhea is a term
used for patients in whom neisseria gonorrhea is isolated
from nasopharynx. It is higher in pregnant women,
sexually active homosexuals and heterosexuals
practicing oral sex. History of fellatio is more associated
with pharyngeal gonorrhea. Patient also noticed sore
throat and evidence of pharyngitis.
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Management
Antibioticssingle dose of the broad-spectrum
cephalosporin antibiotic ceftriaxone 125 to 250 IM plus
doxycycline 100 mg orally, twice a day for 7 days. In
case of patient allergic to above drug, sepectinomycin
2 gm IM plus doxycycline. In some cases, orally or
intramuscular administered fluorinated Quinolones
may be helpful.
Prophylactic treatmentprophylactic ophthalmic
erythromycin should be given to prevent gonococcal
ophthalmia neonatorum.
Recurrencewithout adequate treatment, disease
will recur.
Clinical Features
Symptomssudden onset of sore throat, fever,
dysphagia.
Signsredness of oropharynx and tonsils (Fig. 30-2),
palatal petechiae and yellowish tonsillar exudate.
Lymph nodesthere is cervical lymphadenopathy.
Systemic featuresheadache, anorexia, abdominal pain
and vomiting can also occur.
Radiographic Features
Radiologically, the joint reveals no abnormalities. Rarely,
perforation through the tympanic plate may occur.
Diagnosis
Clinical diagnosispurulent urethral discharge with
pharyngitis with TMJ involvement can give clue to
diagnosis.
Differential Diagnosis
Primary syphilitic lesionpainless indurated edema,
painless lymph node swelling, causative agent in lesion.
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Management
Antibioticspenicillin and cephalosporin should be
given. Erythromycin should be used in patient who is
sensitive to penicillin.
Analgesicanalgesic should be given to control pain and
inflammation.
Warm saline gargleit is also effective treatment in case
of tonsillitis.
Pathogenesis
Multiplication of bacteriaafter entry in the body the bacilli
reach the lymphatic and bloodstream and are taken up
by Schwann cells in peripheral nervous system, where
they start multiplying. If the host cell mediated immunity
is adequate, bacilli are destroyed and there is no disease.
In the host, immunity is unstable and suboptimal, there
will be some restricted multiplication of bacilli and lesion
will develop.
Effect of immunitythe variable status of host cell
mediated immunity is reflected in the different clinical
types of leprosy. When there is relatively good immunity
but not enough to eliminate the infection, a localized
type of disease called as tuberculoid type, is seen. When
the host cell immunity is deficient a generalized form of
the disease lepromatous leprosy develops.
Borderline varietyin between these two polar varieties
of the disease, there is a wide spectrum of manifestations,
categorized as borderline leprosy.
Clinical Manifestations
Tuberculoid type or paucibacillary type
Incubation periodincubation period of 2 to 5 years during
which patient passes through silent or latent period.
Sexmales are affected more commonly than females
with ratio of 3:1.
Skinlesions are hypopigmented, erythematous and flat
or raised cutaneous lesions. Nerve involvement with
loss of different types of sensation is also manifested.
Early tuberculoid leprosyit is manifested by hypopigmented macules which are sharply demarcated and
hyperesthetic.
Intermediate tuberculoid lesionlater, the lesions are larger
with elevated and circinate margin. There is peripheral
spread (Fig. 30-3) and central healing. At the end of this
stage, the symptoms are those of irritation of nerve
ending in the skin, persistent or recurrent paresthesia
and numbness localized to certain area with no accompanying visible alteration in the corresponding skin
lesion.
Types
Tuberculoid leprosyit develops in patient with high
immune reaction. It is localized. It is a benign form of
leprosy involving the skin, nerves and regional lymph
node.
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Diagnosis
Ziehl-Neelsen stainskin smears should be examined
as a routine with Ziehl-Neelsen stain. The percentage
of solid bacilli in a smear is known as morphological
index.
Biopsyskin, mucosal and nerve biopsy for histopathological examination are helpful in doubtful cases.
Lepromin testlepromin test is non-specific test to
determine the hypersensitivity reaction and is useful in
determining the immunological status of patient for
classification of leprosy.
Differential Diagnosis
Gummatous lesion of syphilisVDRL test should be
performed.
Ulcerative proliferative lesion of coccidioidomycosis and
sporotrichosisperipheral nerve involvement is common
in leprosy.
Management
Paucibacillary leprosyit is treated with 6 month regimen
of rifampin and dapsone. Patient allergic to rifampin
are treated with clofazimine, ofloxacin and minocycline.
Multibacillary leprosythis is treated with 24 months
therapy of rifampin, dapsone and clofazimine.
Reconstructive surgeryreconstructive and plastic
surgery is essential for deformities of the hand and face
VaccineBCG vaccines provide some protection against
non-lepromatous leprosy.
Social developmentenvironmental changes with social
and economic development are useful.
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Tuberculosis
Types
Pathogenesis
Clinical Features
Agethey are relatively uncommon and seen in middle
and older age groups, as cleansing action of saliva and
its antibacterial properties, in general also provide
protection against tubercle bacilli.
Symptomspatient may suffer episodes of fever and
chills, easy fatigability and malaise. There may be
gradual loss of weight accompanied by persistent cough
with or without hemoptysis. Local symptoms depend
upon the tissue or organs involved.
Signstubercular lymphadenitis may progress to acute
abscess or remain as granulomatous lesion (Fig. 30-8).
In any case, swelling of neck is present which is tender,
painful and often show inflammation of the overlying
skin. When abscess forms, it perforates and discharges
pus.
Etiology
Causative organismthe first member identified as
tuberculous bacillus and designate as Mycobacterium
tuberculosis. Other microorganisms associated are
Mycobacterium bovis, Mycobacterium kanasasi,
Mycobacterium xenopi and Mycobacterium malmoense. The
organism is anaerobic, non-motile, non-sporing, rod
shaped and is stained with special Ziell-Neelsen stain.
Constitutional factorit is more common in low income
group, unhygienic living conditions, malnutrition and
overcrowding.
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Oral Manifestations
Sitetongue is most commonly affected followed by
palate, lips, buccal mucosa and gingiva.
Primary oral lesionit develops when bacteria is directly
inoculated in the oral tissue of a person who has not
acquired immunity to the disease. It involves gingiva,
tooth extraction socket and buccal fold.
Secondary oral lesioninfection is carried by hematogenous route or through break in the tissue surface, is
deposited in the submucosa, subsequently proliferates
and ulcerates the overlying mucosa. It occurs more
frequently in cases of extra-pulmonary tuberculosis.
Tubercular ulcerthe lesion may be preceded by an
opalescent vesicle or nodule, a result of caseation
necrosis. It breaks down into an ulcer which is usually
superficial or deep and painful. Margin of the ulcer are
undermined with minimum induration. It tends to be
increased slowly in size. Mucosa surrounding the ulcer
is inflamed and edematous. Base of ulcer is yellowish
and granular.
Sentinel tubercletiny, single and multiple nodules called
sentinel tubercle may also be seen surrounding the
ulcer.
Mucocutaneous junctionat the mucocutaneous junction,
tubercular ulcers are usually extremely shallow with
granulating base. Crusting and oozing is seen when the
lesion involves adjacent cutaneous surface. They are
usually painful.
Nodular formthe nodular form of tuberculosis presents
as single or multiple nodules of variable sizes, which
initially may appear as semitransparent lesion of
pinhead size. They are gray in size and of variable
consistency.
Radiographic Features
General
Early changesthe chest radiograph in patient with
secondary tuberculosis may show fibronodular changes
most often in upper lobe. There is also cavity formation
and volume loss. The earliest changes usually are ill
defined opacity or opacities situated in the upper lobes.
Advanced casesin more advanced cases, opacities are
larger and more widespread and may be bilateral. An
area of translucency within the opacities indicates
cavitations.
Displacement of tracheatrachea and mediastinal
structures are displaced towards the side of the lesion.
Oral
It may be described as a localized or diffused with wide
variation in size.
Locationmandibles show greater predisposition than
maxilla.
Localized lesionthe localized lesion is of rarefying
osteitis, while diffuse one is the nature of osteomyelitis.
Diffuse lesionin diffuse type of tuberculosis of bone,
scattered area of bone destruction separated by portions
of bone having normal or near normal appearance are
seen.
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Diagnosis
Dental Considerations
Evaluation of patientDental personnels are at constant
risk of contacting the disease while treating the patient
of tuberculosis. It is known that smallest droplet of
contaminated saliva from the patient may be sufficient
source of contagion, particularly if they are inhaled by
previously uninfected or non-immunized individual.
Patient with past history of tuberculosis should be
evaluated by the physician to ensure the course of the
treatment and follow up.
Delayed dental treatmentif the culture is positive, dental
treatment should not be performed unless there is
emergency. In emergency dental treatment special
precautions should be taken.
Protection of doctorsto avoid aerosolization use of
rubber dam and minimum use of ultrasonic scalers
and high speed handpieces should be done. The
operating air should be vented to the outside, i.e. not
recirculated.
Differential Diagnosis
Syphilisprimary lesion is harder and spirochetes are
found.
Traumatic ulcershort duration and history of trauma.
Sarcoidosistuberculin test negative, the granuloma of
sarcoidosis are of non-necrotizing type.
Lupus erythematosushistology, causative agent test
negative, skin changes.
Leukemiaimmature WBCs, prolonged bleeding and
clotting time.
Management
Chemotherapyshort term chemotherapy, isoniazid (5
mg/kg with maximum of 300 mg daily or 15 mg/kg two
to three times weekly) and rifampicin (10 gm/kg),
ethambutol (25 gm/kg daily for not more than 2 months).
Other drugsother drugs which can be used are
streptomycin, para-aminosalicylic acid, pyrazinamide,
thiacetazone, ethionamide and cycloserine.
Surgerysurgery is rarely performed nowadays, as most
patients respond well to medication. When indicated, it
is usually for a persisting pulmonary cavity with acidfast positive sputum despite 6 months of chemotherapy.
The usual type of surgery done is segmental resection of
lung or a complete lobectomy.
Actinomycosis
It is a chronic granulomatous suppurative and fibrous type
of disease caused by anaerobic, gram +ve, non-acid fast
bacteria. Most common are Actinomycoes israelii, A.
nasalundi, A. viscosus and A. odontolyticus. The organism is
considered to be transitional form between bacteria and
fungi. The term Actinomyces was given by Harz to refer the
ray-like appearance of the organism in the granule.
Classification
Cervicofacialit involve facial and cervical region.
Abdominalit is serious form and involves abdomen.
Pulmonaryin this, there is pleural invasion resulting
in empyema.
Cutaneousthere is subcutaneous swelling in this form.
Centralhere, the infection is from the tooth or its
membrane and is accompanied by radiographic
changes.
Peripheralthe peripheral types originate in the soft
tissues and do not involve bone.
Predisposing Factors
Traumathe breach in the continuity of mucosa caused
either by trauma or surgery, if the prerequisite for
majority of actinomycosis infections.
Local factorscervicofacial actinomycosis infections are
endogenous in origin and occur when dental plaque,
calculus or gingival debris contaminate the relatively
deep wounds around the mouth. Presence of carious
teeth may act as predisposing factors for actinomycosis.
Otherssecondary bacterial invasion and hypersensitivity reaction may act as predisposing factors for
actinomycosis.
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Abdominal form
Abdominal actinomyces is extremely serious form of the
disease.
Precipitating factorstrauma, due to surgery or other
causes such as fish bone or chicken bone injury, usually
precedes the onset of the disease.
Symptomsgeneralized symptoms of fever, chills,
vomiting, develop followed by symptoms of involvement
of organs, such as liver and spleen.
Signthere is palpable abdominal mass. Intestinal
manifestations develop later.
Pulmonary form
Symptomsit produces findings such as fever and chills,
accompanied by a productive cough and pleural pain.
Oral Manifestations
Causeorganism may enter the tissue through oral
mucous membrane and may either remain localized in
the adjacent soft tissue or spread to involve salivary
glands, bone or skin of face and neck.
Signsit produces swelling and induration of tissue. It
may develop into one or more abscesses, which tend to
discharge upon the skin surface liberating pus, which
contains typical sulfur granules. There may be nonhealing tooth socket, exuberant granulation tissue and
periosteal thickening of alveolus. Skin overlying abscess
is purple red and indurate or fluctuant.
Sinusit is common for sinus, through which the
abscess has drained, to heal but due to chronicity,
new abscesses are formed and perforate through skin
surface.
Facethere is disfigurement of face. Infection may
involve maxilla and mandible.
Periapical granulomathere is formation of periapical
granuloma.
Tongueon the tongue, the lesion is a painful nodule
which eventually ulcerates. Untreated cases may reach
to the point where the tongue may become fixed.
Actinomycosis osteomyelitisit can occur in patient with
periodontal infection, nonvital teeth.
Radiographic Features
Appearanceit may appear as an area of bone destruction, which resembles a dental cyst, with a well defined
area of radiolucency with cortical lining of dense bone.
Lamina duralamina dura is deficient at the apex of
tooth.
Rarefying osteitisscattered area of bone destruction,
separated from one another by normal or sclerosed bone,
is another manifestation.
Tooth featuresthe persistence radiolucency of tooth
socket with an increased density of adjacent bone may
be the first sign of disease.
Diagnosis
Clinical dagnosissulphur granules with development
of fistula and sinus with fever give clue to diagnosis.
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Noma
Diagnosis
Management
Predisposing Factors
Povertyit occur in persons who are undernourished.
Debilitated diseasedebilitated infections such as
diphtheria, dysentery, measles, pneumonia, scarlet fever,
syphilis, measles, tuberculosis and blood dyscrasias.
Injuryexcessive mechanical injury is also predisposing
factors.
Poor oral hygienethis may lead to growth of the bacteria
causing increased susceptibility for the infection.
AIDSas it is immunological disorders, it can lead to
Noma.
Othersmiscellaneous factors such as leukemia, sickle
cell trait, stress and chemotherapeutic agents can cause
noma.
Clinical Features
Ageit is seen chiefly in children, but can be found in
adults in certain conditions like in malnourished states.
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Oral Manifestations
Scarlet Fever
Predominately occurs in children during winter months,
caused by infection with group-A streptococci of beta
hemolytic type that elaborate erythrogenic toxins.
Clinical Features
Incubation periodincubation period is 1 to 7 days.
Symptomspatient exhibits severe pharyngitis and
tonsillitis, chills, fever and vomiting.
Signsthroat becomes highly erythematous and
exudation is common. There may be enlargement and
tenderness of regional lymph nodes.
Skin rashcharacteristic diffuse, bright scarlet to dusky
red skin rash which appear on the second or third day
of the illness (Fig. 30-11). This rash is also called as
sunburn with goose pimples. Rash is more intense in areas
of pressure and skin fold. There is a transverse red streak
which is called as Pastias line. After 3 to 4 days, the
rash fades. This rash is due to toxic injury to the vascular
endothelium which produces dilation of the small blood
vessels and consequent hyperemia.
Complications
Hypersensitivity reactionlocalized or generalized
bacterial dissemination or hypersensitivity reaction to
the bacterial toxins.
Systemic complicationperitonsillar abscess, rhinitis,
sinusitis, otitis media, mastoiditis, meningitis, pneumonia, glomerulonephritis, rheumatic fever and arthritis.
Oral complicationit includes cancrum oris, ulceration
with perforation of palate, osteomyelitis and involvement
of the temporomandibular joint.
Diagnosis
Clinical diagnosiswhite strawberry and red raspberry
tongue are typical of scarlet fever.
Differential Diagnosis
Pernicious anemiatongue in pernicious anemia is not
as red as in scarlet fever.
Atrophic glossitis in vitamin deficiencyswab culture of
oropharynx disclose the presence of hemolytic
streptococci and antistreptolysin -O titer is elevated.
Management
Antibioticspenicillin is the drug of choice, since group
A streptococci are generally highly sensitive to this antibiotic. The species are also sensitive to other antibiotics
like erythromycin, tetracycline and chloramphenicol.
Diphtheria
Fig. 30-11: Rash of scarlet fever seen on the skin of the hand
(Courtesy Dr Pincha).
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Pathogenesis
Diagnosis
Clinical diagnosisbull neck, sore throat with edematous
larynx will give clue to diagnosis.
Prevention
The disease may be prevented by prophylactic active
immunization with diphtheria toxoid.
Differential Diagnosis
Herpes simplex infectionsmall blisters, small shallow
ulceration and history of prodromal symptoms. No patch
on soft palate.
Hand-foot-mouth diseasenausea, diarrhea, fever and
vesiculoulcerative lesion occur simultaneously in the
oral cavity and on hand and feet. No patch is seen.
Clinical Features
Management
Oral Manifestations
Diphtheritic membraneformation of patchy diphtheritic
membrane which begins on tonsils and enlarges,
becoming confluent over the surface. It is thick and
grayish in color.
Clinical Features
Ageit occur at any age, but predominant in children
and young adults. It is thought to arise after traumatic
break in skin due to scratch or bite of household cat.
Incubation periodthe incubation time of the disease
ranges from 3-14 days.
Symptomsin early stage, low grade fever, headache,
chills, nausea, malaise or even abdominal pain may
occur.
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Types
Cutaneous
Ophthalmic
Pleuropulmonary
Oral
Abdominal
Clinical Features
Incubation periodincubation period is up to seven days.
Symptomspatient complaint of sudden headache,
nausea, bony pain, profuse sweating, vomiting, chills
and fever.
Suppurative ulcera single cut or sore on the skin
develops into a suppurative ulcer.
Lymph nodeslymphatic vessels become swollen and
painful and the lymph nodes are remarkably enlarged.
Eyesthe eyes also become involved with conjunctivitis
developing through localization of disease in the
conjunctival sac.
Complicationstularemic pneumonia and pleuritis are
complications of this disease.
Oral Manifestations
Diagnostic Criteria
Out of the following four, three should be positive for the
diagnosis of cat scratch disease:
Contact with cat with presence of scratch. Dermal and
ocular lesion should be present.
Negative results for other cause of lymphadenopathy.
Characteristic histopathological finding of staining of
pleomorphic bacilli.
Positive cat scratch disease skin test (no longer widely
used).
Management
Self limitingthe disease has a benign course and it is
self limiting.
Symptomatic treatmentsymptomatic treatment is given
in the form of analgesic.
Antibioticserythromycin is first choice of antibiotics.
Another antibiotic which can be given is Doxycycline.
Node aspiration and drainageaspiration of the nodes
should be done with needle tunneled laterally in the
node.
Tularemia
It is also called as Rabbit fever. It is caused by gram negative
bacillus Francisella tularensis. It is contacted through infected
rabbits, muskrats, ground squirrels and other wild germ,
particularly of rodent family.
Diagnosis
Clinical diagnosissevere pain with ulcer with systemic
symptom of headache, fever may give clue to the
diagnosis.
Serologyan agglutination test is used to demonstrate a
rising titer of antibody in the serum of patients of F.
tularensis.
Skin testingintradermal injection of an extract of F.
tularensis gives a positive delayed hypersensitivity
reaction in 1st or 2nd week of illness.
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Management
Antibioticsantibiotics of choice are streptomycin and
tetracycline, either alone or in combination.
Tetanus
It is also called as lock jaw. It is a disease of nervous system
characterized by intense activity of motor neurons and
resulting in severe muscle spasm.
Pathogenesis
Transmission
Injuryit can enter the body through the most trivial
injury.
Intravenous drug userit is often reported amongst
intravenous drug users.
Contaminationit is transmitted through contaminated
soil, dust or wood splinters.
Tetanus neonatoruminfection of the cut surface of
umbilical cord or circumcision wound, due to use of
unclean instruments or dressing, may result in tetanus
of the newborn which is called as tetanus neonatorum.
Types
Local tetanusmuscle spasm at the site of entry is known
as local tetanus.
Generalized formthis type of tetanus involve many
system of the body.
Cephalic formthis type of tetanus occurs in association
with facial palsy.
Neonatal formthis occurs in infant and route of
transmission is from mother.
Chronic formthe cause of it is due to the persistence of
focus of infection and fibrosis from inadequately
controlled spasms.
Clinical Features
Age and sexit is more common in young males during
their accident prone years.
Oral Manifestation
Rigidity of muscle of masticationthis is usually first
manifestation of tetanus.
Risus sardonicusrigidity of facial muscles may occur,
producing the typical risus sardonicus. In this, corners
of mouth are drawn back with protruded lip, wrinkling
of forehead not possible.
Symptomspatient complaint of difficulty in chewing,
swallowing and inability to insert denture.
Lock jawas spasm of muscle of mastication increase
jaw is locked and mouth cannot be open.
Diagnosis
Clinical diagnosislock jaw with risus sardonicus and
opisthotonus will give clue to the diagnosis.
Management
Antitoxinneutralizing the toxin is achieved by administered of human tetanus immunoglobulin. Specific
therapy includes immediate intravenous injection of
immune serum containing 20,000 IU of antitoxin.
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Granuloma Inguinale
It is also called as granuloma venereum and donovanosis.
It is found in inguinal and anogenital region and is caused
by Calymmatobacterium granulomatis a gram negative
bacillus with prominent polar granules. It is chronic slowly
progressing, mildly contagious disease.
Clinical Features
Rhinoscleroma
It is unusual chronic infection caused by bacillus Klebsiella
rhinoscleromatis and it is common in Europe and central
and South America.
Clinical Features
Age and sexboth sexes are equally affected. Common
between the ages of 20 to 40 years.
Siteusually found in upper respiratory tract, often
originating from nose, but involvement of lacrimal
glands, orbit, skin, paranasal sinus and intracranial
invasion have been described.
Rhinitis stagein this stage, there is nasal obstruction,
nasal deformity and epistaxis. There is also swelling of
upper lip and sore throat.
Infiltrative stageit is characterized by nasal obstruction,
due to the presence of exuberant granulation tissue.
Hoarseness results due to laryngeal involvement.
Anesthesia of soft palate is common in this stage.
Nodular stagethe proliferation of nasal masses may
produce configuration known as Hebra nose. Posterior
extension of the lesion may produce laryngeal and
tracheal obstruction of varying degrees. Complications
include scleromatous infiltration of eustachian tube and
unilateral scleroma of maxillary sinus.
Oral Manifestations
Siteit is common on lip, soft palate, and tonsil.
Appearancethey appear as proliferative granulomatous
lesion of lip, soft palate and tonsil.
Symptomsthere is anesthesia of soft palate, impaired
taste, upper lip and uvula enlargement.
Diagnosis
Clinical diagnosishebra nose with rhinitis and
enlargement of lip, and anesthesia of soft palate will
give clue to the diagnosis.
Management
Antibioticsit should be given to control infection.
Oral Manifestations
Causeoral lesion appears to be the most common extragenital form of granuloma inguinale. Oral lesions occur
either as a result of autoinoculation through infected
fingers or through oral coitus.
Siteit is most commonly found on lips, buccal mucosa
or palate or they may diffusely involve the mucosal
surface
Liplesions of lip are characterized by extensive
superficial ulceration with well defined elevated,
granulomatous margins.
Multiple sinuslong standing lesion is associated with
multiple extraoral sinuses.
Typesmay be of three types, i.e. ulcerative, exuberant
and cicatricial.
Ulcerativeit is painful, extensive with punched out
appearance. It has got smooth red base with tendency
of bleeding from the lesion.
Exuberantit appears as proliferative granular mass.
The surface of the lesion is rough due to projection. It
has got sharp border and lesion are multiple. The
mucous membrane is inflamed and edematous.
Cicatricialfibrous scar formation may become
extensive in nature.
Diagnosis
Clinical diagnosisulcerative lesion in the oral cavity
which can be multiple and exuberant in variety, will
give clue to the diagnosis.
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Management
Diagnosis
Lymphogranuloma Venereum
It is a venereal disease caused by one of the three strains of
Chlamydia trachomatis.
Management
Antibiotic therapyit consists of macrolides, tetracycline,
and fluoroquinolones.
Surgical managementsurgical treatment of bubos and
secondary scarring.
Clinical Features
Myiasis
Predisposing Factors
Poor oral hygieneit has been associated with poor oral
hygiene, such as in mouth-breathers, thumb-suckers.
Mentally retarded personit is common in mentally
retarded persons.
Cerebral palsy and hemiplegiathis person cannot
maintain normal lip closure or normal level of oral
care.
Pathogenesis
Oral Manifestations
Causesresults due to orogenital contact or antiinoculation.
Sitetongue is the most common site.
Appearancelesion consists of small, slightly painful
superficial ulceration with non-indurated borders
which appear on lip.
Signsin long standing infection, there is zone of
cicatrical refraction, dark red area with loss of superficial
epithelium, or opaque lichenoid grayish papules.
Tongue enlargementtongue may become enlarged
with areas of scarring and grooves on its dorsal
surface.
Associated symptoms and signsdysphagia, red soft palate
and small red granulomatous lesions accompanied by
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Clinical Features
Cutaneous myiasisit is characterized by papular or
migratory lesions.
Symptomspapular lesions are itchy and occasionally
painful.
Open lesionsopen lesion may produce serious
discharge and larvae may be detected through the
opening (Fig. 30-12).
Migratory lesionsmigratory lesions are superficial, red
tunnel-like lesions, which form creeping eruptions.
4
A
Oral Manifestation
Diagnosis
Clinical diagnosisit is easy to make clinical diagnosing
by observing larvae in the lesion.
Management
Irrigationirrigation of the tissue with hydrogen
peroxide will come larvae out the lesion (Fig. 30-14).
Treating the defect with ether, mercuric chloride, or
turpentine oil, this irritates the parasites forcing them to
Fig. 30-14: Larvae seen in the plate which are removed after patient
given hydrogen peroxide (Courtesy Dr Bhaskar Patle).
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Suggested Reading
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31
Viral Infections
Definition
Viruses have been defined as submicroscopic entities which
reproduce within the specific living cells. Virus may
contain either ribonucleic acid (RNA) or deoxyribonucleic
acid (DNA).
Classification
RNA Virus
Orthomyxovirus
Influenza
Paramyxovirus
Measles (rubeola)
Mumps
Rhabdovirus
Rabies
Hemorrhagic fever
Arenavirus
Lymphocytic choriomeningitis
Lassa fever
Calicivirus
Coronavirus
Upper respiratory infection
Bunyavirus
Picornavirus
Poliomyelitis
Coxsackie diseases
Common cold
Foot and mouth disease
Encephalomyocarditis
Reovirus
Togavirus
Rubella
Yellow fever
St. Louis encephalitis
Retrovirus
DNA Virus
Herpes virus
Herpes simplex I (herpes stomatitis and herpes labialis)
or HHV 1
Herpes simplex II (genital lesion) or HHV 2
Herpes zoster (chicken pox and shingles) or HHV 3
Epstein-Barr virus (EBV) (infectious mononucleosis,
hepatitis, oral hairy leukoplakia and nasopharyngeal
carcinoma) or HHV 4
Cytomegalovirus (infectious mononucleosis, hepatitis)
or HHV 5
Human herpes virus 6 (roseola infantum, otitis media,
encephalitis) or
Human herpes virus -7 (roseola infantum)
Human herpes virus -8 (infectious mononucleosis,
febrile exanthema, Kaposis sarcoma)
Simian herpes virus B (mucocutaneous lesions, encephalitis)
Pox virus
Small pox
Molluscum contagiosum
Adenovirus
Pharyngoconjunctival fever
Epidemic keratoconjunctivitis
Parvovirus
Iridovirus
Papovavirus
Human warts or papillomas
Tumorigenic virus in animals
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Epidemiology
Types
Herpetic genitalisit is caused by HSV-II and is common
in uterine cervix, vagina, vulva and penis. Lesions are
more likely to occur on well keratinized areas such as
shaft of penis but may progress, more or less rapidly,
into superficial erosions that are very painful when
touched or contaminated with urine. Urethra may be
involved and extremely painful dysuria may develop,
especially in women. Regional lymphadenopathy, fever,
malaise and anorexia may develop.
Genital herpes in HIV patientsthe lesion of genital herpes
in immunocompromised patients and HIV infected
patients are larger, deeper and are likely to persist and
release of virus for periods as long as 30 days. Antibodies
to the virus develop 4 to 6 weeks after primary infection.
Herpetic meningoencephalitisthis is serious form characterized by sudden fever and symptoms of increased
intracranial pressure. Paralysis of various muscle groups
with convulsion and even death may occur.
Herpetic conjunctivitisswelling and congestion of
palpebral conjunctiva, keratitis and corneal ulceration.
Recurrent lesions can lead to serious corneal scarring,
which may produce blindness.
Herpetic eczema (Kaposi varicelliform eruption)it is
epidermal form of herpetic infections superimposed
Transmission
Close contactit occurs during close personal contact, in
which exchange of saliva or other secretion happened.
Newborn infectionprimary infection of newborn is
believed to be caused by vaginal secretions during birth,
which results in viremia and disseminated infection of
brain, liver, adrenals and lungs.
Socioeconomic statusincidence varies according to
socioeconomic group. Person who is having lower
economic status will have earlier exposure.
Clinical Features
Ageit develops in both, children and young adults. It
can be seen in high school and college students where it
is transmitted by kissing and sexual contact.
Incubation periodincubation period is 5 to 7 days.
Prodormal symptomsprodormal symptoms precede
local lesion by 1 to 2 days and it includes fever, headache,
malaise, nausea, vomiting and within a few days, mouth
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Fig. 31-1: Showing skin lesion of herpes infection
(Courtesy Dr Sanjay Pincha).
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A
Fig. 31-5: Acute marginal gingivitis present in the case of herpes
simplex infection (Courtesy Dr Chole).
B
Figs 31-6A and B: Primary infection occurring in adult patient.
(A) Ulcer seen with acute marginal gingivitis and (B) Large ulcer seen
on the tongue.
Types
Precipitating Factors
Clinical Features
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Fig. 31-9: Recurrent intraoral, herpes infection seen on the tongue
(Courtesy Dr Amit Parate).
Diagnosis
Historynegative past history of recurrent herpes
labialis and a positive history of close contact with a
patient with primary or recurrent herpes is helpful in
making the diagnosis.
Typical clinical featurespatient is easily diagnosed as
having primary herpetic gingivostomatitis; if he/she
presents with typical clinical features of generalized
symptoms followed by eruption of oral vesicles and acute
marginal gingivitis and does not have history of
recurrent herpes.
HSV isolationisolation and neutralization of virus in
tissue culture is most positive method of identification.
Rabbit kidney and human amnion are sensitive to HSV.
Antibody titerantibodies to HSV appear in a week and
react peak in 3 weeks.
Differential Diagnosis
Hand-foot and mouth diseasein this case, lesion are not
clustered and gingiva is not affected. Lesions can also
be seen on feet and hand.
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Management
Primary herpes simplex infection
Symptomatic
Pain control measurestopical anesthetics like 2%
lidocaine, 0.1% diclonine hydrochloride, 0.5% benzocaine
hydrochloride are used. Solution of diphenylhydramine
hydrochloride (Benadryl) 5 mg mixed with equal amount
of milk of magnesia can also reduce the pain. In some cases
systemic administration of analgesics is also given.
Topical anti-infective agentsit is given to prevent
secondary infection. Agents used are 0.2% chlorhexidine
gluconate, tetracycline mouth wash and elixir or
diphenylhydramine.
Supportive carefluid is given to maintain proper
hydration and electrolyte balance. Antipyretics can also
be given to control the fever.
Good oral hygieneoral hygiene should be properly
maintained to avoid any secondary infection.
Specific
Acyclovirit inhibits DNA replication in HSV infected
cells reducing the duration of illness but with few side
effects. The optimum oral dosage of acyclovir is 1,000 to
1600 mg daily, for 7 to 10 days. It should be ideally given
in a dose of 15 mg/kg five times a day.
Valacyclovirit is prodrug of acyclovir and it has far
better biocompatibility as compared to acyclovir. It
should be used in combination with famciclovir.
Forms
Chickenpox (Varicella)it is primary infection with zoster
virus.
Shingles (herpes zoster) or zonait is recurrent infection
with zoster virus. It increases with age and occurs in
immunocompromised patient. It can be seen in AIDS
patient.
Postherpetic neuralgiait is neuropathic disease resulting
from peripheral and central nervous injury by zoster
virus.
James Ramsay Hunt syndromeit is zoster infection of
geniculate ganglion.
Chickenpox
It is also called as varicella. It is an acute viral disease
occurring in children and most commonly in winter and
spring months.
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Management
Pain controlpatient should be managed with all pain
control method which is described in herpes simplex
infection. Aspirin is contraindicated as it can lead to
Reyes syndrome.
Control of prurituswarm baths with soap or baking
soda, application of calamine lotion should be done. As
VZV is having lipid envelope, it can destroy by soap
and detergent. Systemic diphenhydramine is also given
to control pruritus.
Antiviral drugacyclovir should be used in a dose of
800 mg five times daily. It will reduce the severity of
lesion. Another antiviral agents use are valacyclovir
(1000 mg TDS) and famciclovir (500 mg TDS) for 7 days
should be given.
Varicella zoster immune globulinthis is given in case of
immunocompromised patient. This will help to reduce
severity of clinical manifestation.
Local antisepticat the first sign of secondary infection,
a local antiseptic should be applied to the skin. If the
bacterial infection progresses, appropriate antibiotics
should be prescribed.
Prevention by vaccinationlive attenuated VZV vaccine
should be given in children at 12 and 18 months of age.
It should usually combined with MMR (measles, mumps
and rubella).
Herpes Zoster
Fig. 31-10: Dewdrop like vesicle formation seen on the
abdomen of the patient (Courtesy Dr Pincha).
Oral Manifestation
Sitesmall blister-like lesions occasionally involve the
oral mucosa chiefly buccal mucosa, tongue, gingiva,
palate as well as the mucosa of pharynx.
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Predisposing Factors
Traumain some cases, trauma in the distribution of
trigeminal nerve can lead to herpes zoster infection.
Malignancydevelopment of malignancy or tumor in
the region of dorsal root ganglion can also cause herpes
zoster.
RadiationLocal X-ray radiation can also be predisposing factors.
Immunosuppressive therapythis will lead to reactivation
of virus and development of lesion.
Clinical Features
Oral Manifestations
Fig. 31-12: Intact vesicle seen showing dermatome involvement
(Courtesy Dr Pincha).
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Diagnosis
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Herpes zoster
Severe pain
Moderate pain
No skin lesions
No recurrence
Recurrent appearance
Differential Diagnosis
Recurrent herpes simplex infectiondescribed in Table
31-1.
Herpanginaacute infection, palatal vault is affected.
Etiopathogenesis
Peripheral injuryzoster virus injures the peripheral
nerve by demyelination, wallerian degeneration and
sclerosis.
Central injurythere is also atrophy of dorsal horn cells
in the spinal cord.
Infectionlow grade persistent infection of trigeminal
ganglion also cause postherpetic neuralgia.
Clinical Features
Management
Antiviral drugsacyclovir 800 mg five times daily which
is associated with significantly accelerated healing
within 48 hours of the onset of rash.
Symptomatic treatmentantipyretic medication with antipruritics diphenhydramine can be administered to
decrease itching.
Prevention of postherpetic neuralgiaintralesional steroids
and local anesthetic can be used to decrease healing
time and to prevent postherpetic neuralgia. But this
comes with many side effects and there are some
conflicting reports about the efficiency of steroid in
control of postherpetic neuralgia.
Capsaicintopical capsaicin 0.025% four times a day
has been suggested for temporary relief of neuralgia
following herpes zoster infection. Capsaicin is derived
from red peppers The mechanism of action apparently
involves the depletion of substance P in the peripheral
sensory neurons causing the skin less sensitive. After
treatment patient should wash hand after use and avoid
contact with mucosal surface.
Tetracycline rinsemouth rinsing with tetracycline, three
to five times daily, may reduce the pain.
Postherpetic Neuralgia
This is complication of zoster infection.
Management
Preventionuse of live attenuated Varicella zoster vaccine
after age of 60 years will reduce the incidence of postherpetic neuralgia. To control postherpetic neuralgia,
antiviral drug should be given in early course of disease.
Topical therapyuse of topical agents like lidocaine
(anesthetics), capsaicin (an extract of hot chili peppers
that depletes the neurotransmitter substance P) should
be used.
Drug therapythe use of TCA (tricyclic antidepressant)
like Amitriptyline, nortriptyline, doxepin and desipramine have been used to minimize painful sequelae of
this infection. The patient who cannot tolerate TCA due
to cardiovascular side effect, the other drug gabapentin
and pregabalin should be given. Carbamazepine or
phenytoin can also be given to minimize the pain.
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Oral Manifestations
Onsetoral lesions precede 2 to 3 days before cutaneous
rash and are pathognomonic of this disease.
Sitethe most common site is on buccal mucosa.
Kopliks spotsintraoral lesions are called as Kopliks
spots and occur in 97% of cases (Fig. 31-20). They are
small, irregularly shaped flecks which appear as bluish
white specks surrounded by bright red margins. They
are described as grains of salt on red background.
Other featuresthere is generalized inflammation,
congestion, swelling and focal ulceration of gingiva,
palate, and throat may occur.
Mumps
It is described in Chapter 26: Salivary Gland Disorders.
Measles
It is also called as Rubeola or morbilli. It is an acute
contagious dermatotropic viral infection, primarily affecting
children and occurs many times in epidemic form.
Diagnosis
Transmission
Droplet infectionspread of disease occurs by direct
contact with a person or by droplet infection, the portal
of entry being the respiratory tract.
Clinical Features
Incubation periodincubation period is 8 to 10 days.
Prodromal symptomsonset of fever, malaise, cough and
coryza (running nose).
Eye lesionthere is conjunctivitis, photophobia,
lacrimation occurs.
Skin lesionskin eruption begins on face, in the hair
line and behind the ear and spread to neck, chest, back
and extremities. They appears as tiny red macules or
papules which enlarge and coalesce to form blotchy
discolored irregular lesions, which blanch on pressure.
Skin lesions fade away in 4 to 5 days with fine
desquamation.
Complicationit is the disease which lowers general body
resistance and for this, it often leads to complications.
Complications include bronchial asthma, encephalitis,
otitis media, noma, and Hodgkins lymphoma.
Differential Diagnosis
Small poxhigh fever, monoform exanthema.
Chickenpoxtypical exanthema that follows the
intraoral lesion. The diagnosis can be established
microscopically (blister swab) and virologically.
Management
Vaccinationbest treatment for the measles is
vaccination. The widely used vaccine is MMR. One
injection of live, attenuated measles virus should be
given subcutaneously in children over one year. Second
dose of vaccine is given in 12 to 15 months.
Passive immunizationhuman immunoglobulin given
intramuscularly is recommended for the prevention and
attenuation of measles, particularly for contact under
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Transmission
Droplet infectionit is transmitted through droplet infection in individual who is living in close living condition.
In uteroinfants with congenital infection may be
present. It may result in birth defect. Infant born with
rubella is called as congenital rubella syndrome (CRS).
Clinical Features
Incubation periodincubation time is 14 to 21 days.
Prodromal symptomsit includes fever, headache,
malaise, anorexia, conjunctivitis, coryza, cough and
pharyngitis.
Lymphadenopathyit is seen in suboccipital, postauricular, and cervical chains.
Complicationit includes arthritis, encephalitis and
thrombocytopenia.
Rashthe exanthematous rash seen on face and neck. It
is discrete pink macule and it fades as it spreads.
Congenital rubella syndromeit results in deafness, heart
disease and cataracts.
Oral Manifestation
Forschheimers signsmall, discrete, dark red papules
seen on soft palate.
Petechiaepetechiae can also be seen on the palate.
Diagnosis
Clinical diagnosisit is very difficult to establish
clinical diagnosis as clinical presentation is mild and
subclinical.
Laboratoryserological analysis should be carried out
to establish diagnosis.
Management
Vaccinationthis has dramatic results after vaccine was
released in 1969.
Human rubella immunoglobulinit is administered to
have passive immunity. If it is given within days after
the exposure, it will decrease the severity of infection.
Coxsackievirus Infection
They are RNA retroviruses and are named after town in
upper New York where they were first discovered. They
are divided into 2 groups:
Type A24 types
Type B6 types
These viruses can cause hepatitis, meningitis, myocarditis, pericarditis and respiratory disease. Three clinical
types of infection are important and discuss below. These
diseases occur more frequently from June to October
(summer and early fall).
Transmission
Fecal oral routeit is major path of transmission. Frequent
hand washing will diminish the spread of this virus.
Salivavirus can spread through saliva during acute
condition.
Predisposing factorsovercrowding, poor oral hygiene
may aid to infection.
Herpangina
It is also called as aphthous pharyngitis, vesicular
pharyngitis. A4 causes majority of the cases. A4 to A10 and
A16 to A22 have also been implicated.
Clinical Features
Agemajority affected are young children aged 3 to 10
years.
Incubation periodincubation period is of 2 to 10 days.
Siteit occur on posterior pharynx, tonsil, faucial pillars
and soft palate.
Prodromal symptomsinitially, generalized symptoms
of fever, chills, headache, anorexia, prostration,
abdominal pain and sometimes vomiting. Sore throat,
dysphagia and occasionally, sore mouth can occur.
Ulcerationlesion starts as punctate macule which
evolves into papules and vesicles (Fig. 31-21). Within
24 to 48 hours, vesicles get ruptured forming small 1 to
2 mm ulcers.
Base and marginsulcers show a gray base and inflamed
periphery.
Healingthey generally heal without treatment in 1
week.
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Diagnosis
Clinical diagnosisoral lesion in association with skin
lesion will aid to diagnosis.
Differential Diagnosis
Diagnosis
Clinical diagnosislesions are seen posterior part of oral
mucosa.
Differential Diagnosis
Primary herpes simplex infectionherpangina occur in
epidemic, and HSV does not. Clinical manifestations of
herpangina are generally milder than HSV infection.
Lesions of herpangina occur in pharynx and posterior
portions of oral mucosa and in case of herpes simplex
infection, it occur in anterior part of oral cavity.
Herpangina does not cause generalized acute, marginal
gingivitis which is typical feature of herpes simplex
infection.
Herpes zosterin this, segmental distribution of vesicle
is seen which is absent in case of herpangina.
Hand-Foot-and-Mouth Disease
It is caused by A16, A5, A7, A9, A10, B2 and B5.
Clinical Features
Ageit primarily affects children between the age of 6
months and 5 years.
Symptomsthere is anorexia, low grade fever, diarrhea,
nausea and vomiting.
Appearanceit is characterized by appearance of maculopapular, exanthematous and vesicular lesions of skin,
particularly involving the hands, feet, legs, arms and
occasionally buttocks.
Oral Manifestations
Sitesthe most common sites for oral lesions are hard
palate, tongue and buccal mucosa.
Symptomsa sore mouth with refusal to eat is one of the
most common findings in this disease.
Clinical Features
Agethe disease affects predominantly children and
young adults, occasionally older adults can also be
affected.
Sitethe lesion appears on uvula, soft palate, anterior
pillars and posterior oropharynx.
Incubation periodit has got 5 days incubation period
and course may run for 4 to 14 days, with local oral
lesions resolving within 6 to 10 days.
Symptomsthe chief complain is of sore throat, 41o C
temperature, mild headache, anorexia and loss of apetite.
Appearanceit consists of raised, discrete, and whitish
to yellowish solid papules of 3 to 6 mm in diameter,
surrounded by narrow well defined zone of erythema.
Signslesion is non-vascular, non-ulcerated, tender,
superficial and bilateral.
Diagnosis
Clinical diagnosiswhitish nodule with sore throat can
lead to diagnosis.
Management
Symptomatic treatmentno specific treatment is
necessary since the disease is self limiting and generally
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regresses within one to two weeks. Symptomatic treatment directed towards giving anti-pyretic and topical
anesthetics.
Nutritional supplementas eating and swallowing is
difficult, patient should be given proper hydration.
Infectious Mononucleosis
Clinical Features
Incubation periodit varies from 10 to 40 days.
Agedisease occurs chiefly in children and young adult
in 4 to 15 age groups.
Symptomsthe patient usually complaint of sore throat
accompanied by fever usually 101F to 103F and
extreme fatigability. Occasionally, there is a complaint
of headache, photophobia, nausea, vomiting, diarrhea
and presence of erythematous macular rash (Morbilliform skin rash).
Signsphysical examination reveals enlarged palatine
tonsils with copious amount of cheesy yellow exudate
filling tonsillar crypt. Patient may also be having
splenomegaly and hepatomegaly.
Lymphadenopathyenlargement of the superficial lymph
nodes, particularly the posterior cervical are common
manifestations. Lymph nodes are slightly tender on
palpation.
Chronic fatigue syndromethis is controversial whether
this is associated with EBV infection. In this, patient
noticed chronic fatigue, fever, pharyngitis, myalgia,
headache, arthralgia, paresthesia, depression and
cognitive defect.
Complicationsairway obstruction, splenic rupture,
progressive neurological involvement and hemolytic
anemia.
Hematological findingthere is an increase in white
blood cell count.
Oral Manifestations
Sitelesion present on soft palate, labial and buccal
mucosa.
Petechiaeit can be seen on soft palate (Fig. 31-22). They
are transient.
Ulcerative gingivitis, periodontitis and stomatitisulcerative gingivitis, periodontitis and stomatitis may be present
and the lesion normality persisting for 3 to 11 days.
Tonsilsintraorally, the most prominent sign is
enlargement and inflammation of the tonsils along with
sore throat and difficulty in swallowing. Quite commonly
the tonsils are covered by a white or grayish pseudomembrane.
Bleeding1/3rd of the patients with hemorrhagic
tendency exhibit oronasopharyngeal bleeding,
including bleeding from gingiva.
Diagnosis
Clinical diagnosismorbilliform skin rash with enlarged
palatine tonsil with fever can aid in diagnosis.
Laboratory diagnosisthere is positive Paul Bunnel (test
for detecting EBV antibody) and mono spot test.
Management
Symptomaticthe oral lesion of infectious mononucleosis is treated symptomatically. A topical anesthetic
may be used in painful ulcers and hydrogen peroxide
rinses aid in ameliorating the fusospirochetal gingivitis.
Patient should be given antipyretic and antiinflammatory therapy to control fever and pain.
Antiviral drugsganciclovir and Alfa interferon inhibit
the replication of Epstein Barr virus in vitro. Alpha
interferon reduces EBV replication and shedding in
organ transplant patient.
Corticosteroidcorticosteroids are indicated only in the
presence of complications like airway obstruction,
progressive neurological involvement, hemolytic anemia.
Normaly corticosteroid should be avoided.
Precautionpatient should avoid sports as it may lead
to splenic rupture.
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Transmission
In utero transmissioninfants can acquire it in utero from
placenta, during delivery. Infant can also acquire
infection through breastfeeding.
Sexual transmissiontransmission can also occur
through exchange of body fluid like saliva, during sexual
activity.
Blood transfusion and organ transplantationblood and
transplanted tissues are also potential means of
transmission of virus to susceptible individuals.
Clinical Features
Management
Oral Manifestations
Salivary gland involvementthis can occur in immunocompetent patient. Patient usually present with acute
sialadenitis which can involve major and minor salivary
gland. Affected gland is painful. Patient may suffer from
xerostomia.
Mucosal ulcerationoral ulcer occur in patient with CMV
disease. It is more commonly seen in AIDS patient.
Gingival infection and hyperplasiapatient may suffer
from gingivitis and gingival hyperplasia (Fig. 31-23).
Dental significancesusceptible dental personnel may
acquire CMV infection in the absence of barrier protection.
Diagnosis
Clinical diagnosisCMV produces deep, penetrating oral
ulcerations on the lips, tongue, pharynx, or any mucosal
site.
Condyloma Acuminatum
It is also called as genital wart, venereal wart or verruca
acuminata. It is caused by human papillomavirus (HPV). It
can be transmitted from mother to infant, at birth and
resulting syndrome is called as juvenile onset respiratory
papillomatosis.
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Clinical Features
Clinical Features
Oral Manifestations
Diagnosis
Clinical diagnosissessile pink pedunculated growth
with history of oral sex is important in clinical diagnosis.
Laboratory diagnosisvirus isolation can be done by
staining of viral antigen DNA by hybridization restriction, endonuclease analysis and polymerase chain
reaction.
Differential Diagnosis
Focal epithelial hyperplasiain it, fine granular surface
texture and plaque-like shape of enlargement while in
case of condyloma, there is cauliflower appearance.
Fig. 31-24: Common wart seen on finger (Courtesy Dr Pincha).
Management
Surgicalgenital warts are treated by excision, electroor cryosurgery, CO2 laser therapy.
Application of chemical agentsapplication of chemical
agents such as podophyllin, cantharidin and 5-fluorouracil can be given.
Immunomodulating agentsimmunomodulating agent
such as interferon can also be used in case of condyloma
acuminatum.
Diagnosis
Clinical diagnosiskeratin horn with pedunculated surface pebbly lesion on hand will diagnose this condition.
Laboratory diagnosisthere is proliferation of hyperkeratotic stratified squamous epithelium which are
arranged in finger-like projection. There is also cupping
effect.
Management
Cryotherapyliquid nitrogen cryotherapy is the
treatment of choice in this condition. Cryotherapy will
induce subepithelial blister which lifts the infected
epithelium from the connective tissue allowing it to
slough away.
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Transmission
Skin contactit occurs due to intimate skin contact.
Sexual contactthere is marked increase at the time of
onset of sexual activity.
Predisposing factorspoverty, overcrowding and poor
hygiene are predisposing factors for transmission of
virus.
Clinical Features
Incubation periodincubation period is 14 to 50 days.
Ageit is more common in children and young adults.
Sitesit is more common on skin of inner thigh, lower
abdomen or external genitals. Some cases may be seen
on lips, tongue and buccal mucosa.
Appearanceit manifests as multiple or isolated discrete
elevated nodules, or sometimes papules, with depressed
centers, which may be keratinized and are normal or
pink in color.
Adjacent areaadjacent area is surrounded by the zone
of erythema.
Shape and sizethese lesions are hemisphere in shape,
usually about 5 mm in diameter.
Numbermultiple lesions sometimes numbering 100
can also occur.
Healingit is self limiting and regresses spontaneously
within 1 to 2 months.
Diagnosis
Clinical diagnosisdiscrete nodule with depressed
center is typical of this disease.
Laboratory diagnosisit shows large eosinophilic intracytoplasmic inclusion bodies known as HendersonPaterson inclusion or simply Molluscum bodies,
measuring approximately 25 microns in diameter in the
biopsy.
Management
Surgical therapyit includes curettage, followed by local
cautery, cryotherapy.
Topical therapytopical application of caustic acid and
irritants such as phenol, TCA, podophyllin and
cantharidin.
Smallpox
It is also called as variola. On December 9, 1979, the
WHO global commission for the certification of smallpox
declared that smallpox eradication has been achieved
throughout the world. Thus, there has been for the first
time in history that a disease was totally eliminated from
this planet.
Previously this disease manifested as occurrence of high
fever, nausea, vomiting, chills and headache. The patient
is extremely ill and may become comatose during this
period. Orally there is ulceration of oral mucosa and
pharynx is common. Multiple vesicles appear and rupture
to form ulcers of non-specific nature.
Immunization is essential in the early period of life.
Chikungunya
Chikungunya is a relatively rare form of viral fever caused
by an alpha virus that is spread by mosquito bites from the
Aedes Aegypti mosquito, though recent search by the
Pasteur Institute in Paris claims the virus has suffered a
mutation that enables it to be transmitted by Aedes
Albopictus (Tiger mosquito). Chikungunya is closely related
to Onyongnyong virus.
The disease was first described by Marion Robinson
and W.H.R. Lumbsden in 1955, following an outbreak on
the Makonde Plateau, along the border between Tanganyika
and Mozambique, in 1952.
Chikungunya is not considered to be fatal. However, in
2005-2006, 200 deaths have been associated with this
disease on Reunion Island and a widespread outbreak in
southern India. Tamilnadu reported the largest no. of
cases as of July 2006, specifically in Madurai and
Tirunelveli.
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Clinical Features
Management
There is not any treatment available for this disease.
Only symptomatic treatment in the form of analgesics
can be given.
Suggested Reading
1. Barrett AP, Katelaris CH, et al. Zoster sine herpete of trigeminal
nerve. Oral Surg, Oral Med, Oral Pathol 1993;75:173-5.
2. Brightman VI, Guggenheimar IG. Herpetic paronchyaprimary
herpes infection of finger. J AM Dent Assoc 1970;80:112-5.
3. Buchner A. Hand Foot and mouth disease. Oral Surg, Oral Med,
Oral Pathol 1976;41:333-7.
4. Chauvin PJ, Ajar AH. Acute herpetic ginginvostomatitis in adults,
a review of 13 cases including diagnosis and management. J Can
Dent Assoc 2002;68:247-51.
5. Cohen SG, Greenberg MS. Chronic oral herpes simplex virus
infection in immunocompromised patients. Oral Surg, Oral Med,
Oral Pathol 1985;59:465-71.
6. Courant P, Sobkov T. Oral manifestation of infectious mononucleosis. J Periodontal 1979;40:279-83.
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Fungal Infections
Introduction
Nowadays as patient is receiving broad spectrum
antibiotics, radiation, cytotoxic and immunosuppressive
drugs, there is increases incidence of fungal disease in the
society. Many of the fungal disease are not diagnosed due
to lack of diagnostic facility. Fungi belongs to plant kingdom
which are non-photosynthetic due to absence of chlorophyll. Pathogenic fungi exists in three forms like yeasts,
yeast like and filamentous organism.
Histoplasmosis
It is also called as Darlings disease. It is caused by
Histoplasma capsulatum, a dimorphic fungus that grows in
the yeast form in infected tissue. Infection results from
inhalation of dust contaminated with dropping, particularly from infected birds.
Types
Acute primary histoplasmosis
Progressive disseminated histoplasmosis
Chronic cavitary histoplasmosis.
Clinical Features
Acute primary histoplasmosisprimary infection is mild,
manifesting as self limited pulmonary disease that heals
to leave fibrosis and calcification. There is chronic low
grade fever, malaise, headache and productive cough.
There may be pleuritic pain. Chest radiograph may
Oral Manifestations
Sitesit is seen on buccal mucosa, gingiva, tongue, palate
or lip. Oral lesions are common in the progressive
disseminated form.
Symptomspatient may complain of sore throat, painful
chewing, hoarseness, difficulty in swallowing.
Appearanceoral lesions are nodular, ulcerative or
vegetative. If left untreated, it will progress to form firm
papule or nodules which ulcerate and slowly enlarge. It
resembles malignancy.
Base and surfaceulcerated area covered by nonspecific
gray membrane (Fig. 32-1) and is indurated.
Diagnosis
Clinical diagnosishepatomegaly, splenomegaly, with
oral ulcerative lesion will give clue to the diagnosis.
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Oral Manifestation
Siteit involves mucosa and jaw bones.
Signsmandibular and maxillary involvement is
usually presented as bony resorption, resulting in
loosening of teeth.
Diagnosis
Management
Amphotericin Bamphotericin B is the drug of choice
and lesion may require surgical intervention.
Differential Diagnosis
Blastomycosis
Management
Supportive treatmentpatient should be given analgesic
and antipyretics to control pain and fever.
Ketoconazoleit should be given for 6 months in nonimmunosuppressed patient.
Itraconazolethis agent is more effective and less toxic
than ketoconazole.
Amphotericin Bintravenous amphotericin B should be
given in chronic and severe form.
African Histoplasmosis
It is caused by fungus Histoplasma duboisii that is larger
than Histoplasma capsulatum. The disease, because of its
clinically distinct form and geographical distribution is
called as African histoplasmosis.
The disease exists in two forms, i.e. localized and
disseminated.
Clinical Features
Localized formit is confined to the skin, lymph nodes
or localized bony areas. Bones when involved, may show
cyst-like lesions.
Types
Primary pulmonary blastomycosis
Cutaneous blastomycosis
Disseminated or systemic blastomycosis.
Clinical Features
Primary pulmonary blastomycosis
Age and sexit is more common in men than women
and typically occurs in middle age.
Symptomsit follows a chronic course with malaise, high
grade fever and mild cough. If untreated, shortness of
breath, weight loss and blood tinged sputum are
encountered. In some cases, it may precipitate adult
respiratory distress syndrome.
Cutaneous Blastomycosis
Sitesinfection of skin, mucosa and bone may also occur,
resulting from metastatic spread of organism through
lymphatic system.
Appearanceskin and mucosal lesion starts as subcutaneous nodule and progresses to well circumscribed
indurated ulcer.
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Oral Manifestations
Symptomsoropharyngeal pain is present.
Signsenlargement of cervical lymph nodes occurs.
Appearancenon-specific, painless verrucous ulcer with
indurated borders is present. It is often mistaken for
squamous cell carcinoma (Fig. 32-2). Some lesions are
hard nodules and appear as sessile, granulomatous
appearing plaque.
Differential Diagnosis
Squamous cell carcinomapresent for weeks or months,
palpation shows induration, most common in older
patient.
Tuberculosisundermined flabby borders, usually
painless, sputum examination, Mantoux test.
Histoplasmosisculture and biopsy should be done.
Mucormycosisbiopsy.
Cryptococcosisorganism culture should be done.
Management
Itraconazoleit is generally recommended for the patient
of chronic blastomycosis.
Amphotericin Bit is usually given in chronic case of
blastomycosis. Intravenous amphotericin B for 8 to 10
weeks causes resolution of the disease. In case of acute
blastomycosis, it does not require any treatment.
Mucormycosis
It is also called as phycomycosis, zygomycosis. It is caused
by saprobic organism of class Zygomycetes. It is more
common in patients with decreased resistance, due to
diseases like diabetes, tuberculosis, renal failure, leukemia,
cirrhosis and in severe burn cases. It begins with inhalation
of fungus by susceptible individual.
Types
Radiographic Features
Periosteal reactionradiograph may show periostitis and
sub-periosteal new bone formation. Osteoblastic reaction
is usually present in the later stages of disease.
Chest radiographchest radiograph show concomitant
pulmonary involvement in most of the cases.
Diagnosis
Clinical diagnosisthe index of suspicion is increased
when chronic, painless, oral ulcer appears in an agri-
Clinical Features
Locationsinfection usually arise in lateral wall of
nose and maxillary sinus; may rapidly spread by
arterial invasion to involve the orbit, palate, maxillary
alveolus and ultimately the cavernous sinus and
brain through hematogenous spread and may cause
death.
Symptomsptosis, proptosis, nasal obstruction, fever,
swelling of cheek and paresthesia of face can occur.
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Oral Manifestations
RadiologicalfindingCTscanwillhelpfulinthediagnosis.
Laboratory diagnosisorganism appear as nonseptate
hyphae with branching at obtuse angles.
Differential Diagnosis
Squamous cell carcinomaindurated, longer history,
resistance to therapy, firm borders, older patient, biopsy.
Necrotizing sialometaplasiarare, limited to hard and soft
palate, usually painless.
Aphthous ulcershort duration, painful, heals in one to
three weeks.
Management
Fig. 32-3: Mucormycosis showing deep ulceration of the palate
(Courtesy Dr Ashok L).
Radiographic Features
Appearanceparanasal sinus may reveal mucoperiosteal thickening of the involved sinus. With disease
progression, there is increased nodularity and soft tissue
thickening, usually mimics a tumor on radiographical
examination.
CT scan featuresCT scan is most helpful for detecting
the degree of bone destruction and for evaluating disease
extension into the orbit and brain (Fig. 32-4).
Diagnosis
Clinical diagnosisthe nose involvement with destruction of palate, neurological finding may give clue to the
diagnosis.
Cryptococcosis
It is also called as torulosis. It is a chronic fungal infection
caused by Cryptococcus neoformans and Cryptococcus
bacillispora. The causative organism is gram positive,
budding, yeast-like cell with an extremely thick, gelatinous
capsule, measuring 5 to 20 microns in diameter. Infection
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Clinical Features
Agethere is slight predilection for middle aged males.
Sitethe infection usually occurs in lungs.
Symptomsit may be asymptomatic and in some cases,
patient may complain of cough with mucoid expectoration. Occasionally, pleuritic pain and hemoptysis can
also occur.
Skin lesionthe skin lesion appears as multiple brown
papules which ultimately ulcerate, the clinical picture
is nonspecific.
Neurological featuresmeningoencephalic lesions produce a variety of neurologic signs and symptoms,
generally associated with increased intracranial
pressure.
Coin lesionthe radiograph of chest shows infiltrates
and occasionally coin lesion.
Diagnosisthe organisms can be cultured on Sabourauds glucose agar.
Oral Manifestations
Locationslesion of hard palate, soft palate, gingiva,
extraction socket, tongue and tonsillar pillar are common.
Appearancethey appear as simple non-specific, single
or multiple ulcers. They are nodular and granulomatous,
which may ulcerate during the course of disease.
Types
Primary non-disseminated coccidioidomycosis.
Progressive disseminated coccidioidomycosis.
Clinical Features
Age and sexit is common in all age groups and
predominantly seen in males.
Primary pulmonary coccidioidomycosisthe patient
generally develops manifestations suggestive of respiratory disease such as cough, pleural pain, headache
and anorexia. Patient may also complain of low grade
fever and joint pain.
Primary cutaneous coccidioidomycosisskin lesions are
also present, like erythema nodosum or erythema
multiforme. Primary lesions, when they occur, are associated with regional lymphadenopathy. Granulomatous,
verrucous or necrotic ulcers exuding thick pus are seen
on involved skin surface.
Progressive disseminated coccidioidomycosisthe disease
usually runs rapid course and the dissemination
extends from the lungs to various viscera, bones, joints,
skin and central nervous system, where meningitis is
the most frequent cause of death.
Diagnosis
Clinical diagnosisthe brown skin lesion with neurological features and non-specific ulcer seen in oral cavity.
Laboratory diagnosisgram positive yeast-like cell with
gelatinous capsule.
Management
Ketoconazolemild to moderate cases can be treated with
ketoconazole for 6 to 12 weeks.
Amphotericin Bthe severe form requires amphotericinB, intravenously for up to 10 weeks.
Combination therapycombination therapy of amphotericin B and flucytosine is used in many cases to treat
the disease. Another combination of fluconazole and
itraconazole is also useful in Cryptococcosis infection.
Oral Manifestations
Appearancethe lesions of oral mucosa and skin are
proliferative, granulomatous and ulcerated lesions that
are non-specific in their clinical appearance.
Healingthese lesions tend to heal by hyalinization and
scar formation.
Lytic lesionlytic lesions of jaw may develop.
Diagnosis
Clinical diagnosissymptoms suggestive of respiratory
disease, granulomatous and ulcerated oral lesion may
give clue to the diagnosis.
Laboratory diagnosisbiopsy shows mononuclear cell,
lymphocytes, and plasma cells with foci of coagulation
necrosis.
Coccidioidomycosis
It is also called as valley fever, desert fever or coccidiodal
granuloma. The disease appears to be transmitted to man
and animals by inhalation of dust contaminated by the
Management
Amphotericin Bit has been found to be an effective
chemotherapeutic agent for the disease. It is given in
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Paracoccidioidomycosis
It is also called as South American blastomycosis, Lutz
disease. It is caused by Paracoccidioides brasiliensis. It is more
commonly seen in farmers.
Oral Manifestations
Appearancethey are similar to candidiasis or thrush
(Fig. 32-5), being white, velvety, patch like covering of
the oral mucosa, isolated or diffuse in distribution.
Tonsillar lesiontonsillar lesions are common in
association with oral lesions.
Clinical Features
Geographic locationthis is more commonly seen in South
America.
Age and sex distributionit is exclusively found in males
as compared to females. It is more common in middle
age group.
Signspatient usually present with signs of pulmonary
infection. In some cases, adrenal involvement also occur
resulting in hypoadrenocorticism.
Oral Manifestation
Sitecommonly affected site are alveolar mucosa,
gingiva, and palate. Lips can also be affected.
Appearanceoral lesion appear as mulberry-like
ulceration.
Fig. 32-5: Geotrichosis presenting as candidiasis
type lesion on oral cavity.
Diagnosis
Clinical diagnosissigns of pulmonary infection, with
mulberry-like ulceration.
Laboratory diagnosissize of this organism is larger than
North American form.
Management
Sulfonamidethis can be used to treat mild to moderate
infection.
Amphotericin Bthis is used in severe cases. It should be
used intravenously.
Itraconazole and ketoconazolethis can also be used in
some cases when the condition is not life threatening.
Diagnosis
Clinical diagnosislung involvement with candidal type
lesion in debilitated patient.
Laboratory diagnosisthe organism is small, rectangular
shaped; spores measuring approximately 4 to 8 microns,
often with rounded ends. The tissue reaction is nonspecific and of acute inflammatory type.
Management
Antifungal therapyit includes topical and systemic
application of nystatin and amphotericin B.
Geotrichosis
Sporotrichosis
Clinical Features
Causes
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Rhinosporidiosis
Clinical Features
Clinical Features
Locationit is more common on oropharynx, nasopharynx, larynx, skin, eyes and genital mucosa.
Symptomsinitial symptoms include nasal irritation,
accompanied by mucoid discharge.
Skin lesionthe skin lesion appears as small verrucae or
warts, which ultimately become pedunculated.
Signsposteriorly, these polypoid masses may extend
into the pharynx. The lesions are soft, friable and highly
vascular.
Genital lesionsgenital lesion resembles condyolomas.
Oral Manifestations
Locationnon-specific ulceration of the oral, nasal and
pharyngeal mucosa.
Appearancelong standing lesions become granulomatous, vegetative or papillomatous.
Symptomspain is present and the cervical lymph nodes
are always enlarged.
Radiographic Features
Incidenceit rarely involves the bone, it resembles to
those which occur in tuberculosis.
Appearancein the mandible, there is large destructive
lesion in the molar region and ramus. It has a loculated
cystic appearance, which causes marked expansion of
the inferior aspect of the jaw.
Periosteal reactionin long bones, sporotrichosis may
produce some periosteal new bone, but this reaction is
confined to jaws of children.
Diagnosis
Clinical diagnosislymph nodes enlargement with non
specific ulceration of oral cavity will give clue to the
diagnosis.
Radiological diagnosisperiosteal reaction with expansion of inferior portion of jaw.
Laboratory diagnosisthe fungus is small, ovoid
branching organism with septate hyphae showing
budding form. It is only 3 to 5 microns in diameter and
can be cultured on Sabourauds glucose agar medium.
The tissue reaction is a granulomatous.
Management
Potassium iodideit includes oral administration of
potassium iodide in suitable doses.
Oral Manifestations
Sitesthe soft palate appears to be the most frequent site
of oral involvement.
Appearanceit is accompanied by a mucoid discharge
and appears as soft, reddish pink, polypoid growth of
tumor like nature which spreads to the pharynx and
larynx. The lesions are vascular and bleed readily.
Diagnosis
Clinical diagnosispedunculated wart with nasal
polypoid mass, with intraoral soft reddish pink growth
on soft palate.
Laboratory diagnosisthe organisms appear as
sporangia containing large number of round or ovoid
endospores with size of 5 to 7 microns in diameter.
Management
Surgicalsurgical removal of the growths and application of cautery is the treatment recommended for
rhinosporidiosis.
Aspergillosis
It is a fungal infection caused either by sensitization to
parasitic colonization, or tissue invasion by species of
genus Aspergillus. It is second to candidiasis, as an
opportunistic infection, in immunocompromised patients.
It is more commonly seen in diabetes mellitus patients.
Clinical Features
Sitesthe respiratory tract, external auditory canal,
nasopharynx, cornea, gastrointestinal tract and
occasionally the skin may be the primary sites of
infection.
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Oral Manifestation
Sitesit is seen on palate and tongue. Soft palate
involvement seems to be more common in upper
respiratory tract involvement.
Palatal lesiona lesion on the palate is manifested as a
painful ulcer, surrounded by a ring of black necrotic tissue.
Gingival ulcerationthis is also a common feature of
aspergillosis infection in oral cavity. The color of
ulceration may be gray or violaceous hue.
Antrolithsthis is also reported from patient suffering
from aspergillosis.
Disseminated infectionoropharyngeal aspergillosis, in
patients with hematological malignancies, presents as
yellowish-black ulceration of soft palate and posterior
part of tongue. These patients complain of intense local
pain, oral bleeding and dysphagia.
Diagnosis
Clinical diagnosisgray color ulceration in oral cavity
accompanied by nasal infection, chest pain may give
clue to the diagnosis.
Laboratory diagnosisorganism can be seen on biopsy.
Management
Amphotericin Bit is the treatment of choice. It can be
given intravenously.
Surgical debridementdisseminated aspergillosis in
immunocompromised patients should be treated on an
individual basis surgical debridement.
Itraconazoleitraconazole can be given local debridement of the lesion.
Protozoal Infection
Types
Visceral leishmaniasisit is also called as Kalaazar. It is
caused by Leishmania donovani.
Cutaneous leishmaniasisit is caused by Leishmania
braziliensis.
Clinical Features
Visceral leishmaniasis
Incubation periodincubation period is 2 weeks to 2
years.
Symptomsonset may be insidious with a low grade
fever or it may be abrupt with sweating and high
intermittent fever. Cough and diarrhea can also develop.
Signsthe spleen becomes enlarged, often massively. If
not treated, patient will become anemic and wasted.
Mucocutaneous leishmaniasis
Incubation periodis 1 week to 1 month.
Ageit is usually seen in young men.
Historythere is past history of superficial ulcer of skin,
caused by bite of an infected sandfly, which heals with
depressed scar.
Nosenasal mucosa becomes congested and ulcerates.
Later, all the soft tissues of nose may be destroyed.
Oral Manifestation
Visceral leishmaniasis
Pigmentation of facethere may be increased pigmentation of face.
Gingival findingthere may be spontaneous bleeding,
edematous gingiva and loose teeth.
Mucocutaneous leishmaniasis
Incidencemucosal lesion usually occurs 1-2 years after
skin lesion.
Sitelips, soft palate and larynx may be involved.
Appearancethe mucosal lesions are long standing,
destructive, granulating ulcers which in many instance
cause severe mutilation of structure involved.
Lymph nodesregional lymphadenopathy is common.
Diagnosis
Clinical diagnosisface pigmentation with edematous
gingiva will suspect the disease.
Laboratory diagnosisorganisms can be isolated from the
lesion.
Leishmaniasis
Management
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Trichinosis
It is caused by Trichinella spiralis, which is small, spiral,
thread-like organism. Human infection occurs as a result
of eating parasitized food, usually pork, which has not
been completely cooked.
Clinical Features
Sitesstriated muscle, masseter, neck muscle and
diaphragm.
Symptomsthere is fever, facial and periorbital edema,
muscle pain and eosinophilia.
Oral Manifestations
Sitetongue is the most common site involved. It also
occurs in muscles attached to mandible, in mandibular
alveolar process and in gingival tissues.
Symptomsthere is trismus, muscular cramps of the
facial muscle, jaw and tongue. There is also monotony
of speech.
Signsthere may be petechiae of buccal mucosa, palate
and floor of mouth. There is also bleeding from gingiva,
lips and nose.
Diagnosis
Clinical diagnosistrismus, monotonous speech with
petechiae of buccal mucosa or palate may give clue to
the diagnosis.
Management
There is no specific treatment for trichinosis and in severe
cases, prognosis is poor.
Suggested Reading
1. Bradsher RW. Histoplasmosis and blastomycosis. Clin Infect
Dis 1996;22(suppl):102-11.
2. Brightman VI, Guggenheimar IG. Herpetic paronchya- primary
herpes infection of finger. J AM Dent Assoc 1970;80:112-5.
3. Damante JH, Flury RN. Oral and rhinoorbital Mucormycosis: a
case report. J Oral Maxillofac Surg 1998;56:267-71.
4. Economopoulou P, Laskaris G, Ferekidis E, et al. Rhino cerebral
Mucormycosis with severe oral lesion: a case report. J Oral
Maxillofac Surg 1995;53:215-7.
5. Einstein HE, Johnson RH. Coccidioidomycosis new aspect of
epidemiology and therapy. Clin Infect Dis 1993;16:349-56.
6. Falworth MS, Herlod J. Aspergillosis of the paranasal sinus: a
case report and radiographic review. Oral Surg, Oral Med, Oral
Pathol 1996;81:255-60.
7. Greenberg, Glick, Ship. Burkets Oral Medicine (11th edn), BC
Decker Inc, Hamilton, 2008.
8. Jones AC et al. Mucormycosis of the oral cavity. Oral Surg, Oral
Med, Oral Path 1993;75(4):455-60.
9. Jones AC, Bentsen TY, Freedman PD. Mucormycosis of the oral
cavity. Oral Surg, Oral Med, Oral Pathol 1989;68:624-7.
10. Jones AC, Bentsen TY, Freedman PD. Mucormycosis of the oral
cavity. Oral Surg, Oral Med, Oral Pathol 1993;75:455-60.
11. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology
(2nd edn), Saunders Elsevier, 2004.
12. Oda D, et al. Oral histoplasmosis as a presenting disease in
AIDS. Oral Surg, Oral Med, Oral Path 1990;70:631-6.
13. Ogata Y, Okinaka Y, Takahashi M. Antroliths associated with
aspergillosis of maxillary sinus: a report of case. J Oral Maxillofac
Surg 1997;55:1339-41.
14. Paes De Almeida O, Jorge J, Scully C, et al. Oral Manifestation of
Paracoccidioidomycosis (south American blastomycosis). Oral
Surg, Oral Med, Oral Pathol 1991;72:430-5.
15. Rose HD, Gingrass DJ. Localized oral blastomycosis mimicking
actinomycosis. Oral Surg, Oral Med, Oral Pathol 1982;54:12-4.
16. Samaranayake LP. Oral mycoses in HIV infection. Oral Surg,
Oral Med, Oral Pathol 1992;73:171-80.
17. Schmidt-Westhausen A, Grunewald T et al. Oral cryptococcosis
in patient with AIDS: a case report. Oral Dis 1975;1:77-9.
18. Scully C, Cawson RA. Medical problems in dentistry (5th edn),
Churchill Livingstone: an imprint of Elsevier, 2005.
19. Scully C, Paes De Almeida O. Orofacial manifestation of the
systemic mycoses. J Oral Pathol Med 1992;21:289-94.
20. Sposto MR, Mendes Glannini MJ, Moraes RA et al. Paracoccidioidomycosis manifesting as oral lesion: Clinical, cytological
and serological investigation. J Oral Pathol Med 1994; 23:85-7.
21. Sugata T, Myoken Y, et al. Invasive oral aspergillosis in immunocompromised patient with leukemia. J Oral Maxillofac Surg 1994;
52:383-6.
22. Young LL et al. Oral Manifestation of histoplasmosis. Oral Surg,
Oral Med, Oral Path 1972;33:191-204.
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4
Specific System
Disorders
Airway
Opening the airway and restoration of breathing constitutes
the basic steps in life support. Any type of head support on
the dental chair should be removed because such support
flex the neck and thus making airway maintenance more
difficult.
Head tiltthis procedure is accomplished by placing
the rescuers hand on the victims forehead and
applying a firm, backward pressure with the palm.
Head tilt chin lift (Figs 33.1 A and B)in this, the fingers,
of one hand are placed under the body- symphysis region
of the mandible to lift the tip of the mandible up, bringing
the chin forward. As the tongue is attached to the
mandible, it is thereby pulled forward and off from the
posterior pharyngeal wall.
Head tilt, neck liftin this, one hand of the rescuer is
placed beneath the victims neck to lift and support it.
Foreign material in airwayif there is evidence of foreign
matter in the airway, then check for airway patency.
Partial airway obstruction produces noise and complete
airway obstruction produces silence. If foreign body is
suspected, the patient must be rolled on one side with
lowering its head below the level of heart. Rescuer
should place two fingers in the patients mouth and
remove anything in the entire oral cavity.
Breathing
You have to position your cheek close to victims nose and
mouth, look towards victims chest; then look, listen and feel
for breathing (5-10 second) (Fig. 33-2). Exhaled air ventilation
can be give by mouth to mouth or mouth to nose.
Mouth to mouthif not breathing, pinch victims nose
close and give 2 full breaths into victims mouth. This is
done by taking a deep inspiration and exhaling in the
patients mouth and then patient is allowed to exhale
passively. This procedure is continued at the rate of
12-14/min.
Mouth to nosewhen it is impossible to breathe into
patients mouth and if the rescuer if unable to adequately
seal the mouth, the above technique is followed. In this
technique, the rescuer keeps the head tilted backwards,
with one hand on the forehead and other hand lifts
victims mandible, sealing the lips. Taking a deep breath,
rescuer seals his lips around the victims nose and blows
in, until he feels and visualize the expansion of victims
lungs.
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Fig. 33-3: Abdominal thrust should be given to patient if
patient is not able to breathe.
Circulation
Carotid pulse checkingyou have to check for carotid
pulse for 5-10 seconds, at side of victims neck
Rescue breathingif there is a pulse but victim is not
breathing, give rescue breathing at the rate of 1 breath
every 5 second or 12 breaths per minute
Technique to give compression to chest (Fig. 33-4)place
heel of one hand on lower part of victims sternum; with
B
Figs 33-1A and B: Head tilt chins lift method to
maintain the airway of the patient.
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Cardiovascular Disease
Symptoms
Signs
Anemiapallor of skin and mucous membrane
Obesitysuch patients are more likely to have cardiac
disease.
Peripheral cyanosisit occurs due to impairment of
circulation, as in vasoconstriction, low cardiac output
or stress.
Central cyanosisit occurs due to improper oxygen
saturation of blood or due to right to left shunt.
Clubbingit is seen in congenital heart disease and in
advanced cases of infective endocarditis (Fig. 33-5).
Temperatureskin may be cold in cardiac failure and
syncope.
Arterial pulsechanges in the pulse pattern are noted in
arrhythmias, reduced cardiac output, pulmonary
embolism and aortic stenosis.
Consideration of Prophylaxis in
Cardiovascular Disease
Heart disease in which prophylaxis recommendedthe
disease in which prophylaxis recommended are
prosthetic cardiac valve including bioprosthetic and
homograft valve, previous bacterial endocarditis,
surgically constructed systemic pulmonary shunt,
rheumatic and other acquired valvular dysfunction, even
after valve surgery, cardiomyopathy, mitral valves
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Angina Pectoris
It is hypoxia of the cardiac muscles, resulting from an
imbalance between the oxygen consumption and oxygen
supply of the cardiac muscles. It is the name given to
paroxysm of pain. If anginal pain persists for more than
half an hour, myocardial infarction or some acute
abdominal condition should be considered.
Etiology
Coronary artery diseaseit is commonly associated with
coronary artery disease and coronary artery spasm
associated with atherosclerosis.
Oxygen carrying capacity of bloodlimited oxygen
carrying capacity of blood and excessive oxygen demand.
Predisposing factorsstress, physical or emotional or use
of tobacco may predispose to an attack. Stress cause
release of catecholamine and tachycardia.
Types
Stableit occurs with known physical effort and is
relieved at rest and on administration of nitrates. It also
gets aggravated by cold weather, smoking, emotional
upset, high altitude, sexual excitement and straining at
stools.
Nocturnalangina appears in the middle of the night
due to left ventricular failure, which may be precipitate
by dreams, causing release of catecholamine.
Clinical Features
Age and sexit is most common in age range from 45 to
65 years and male to female ratio is 4:1.
Symptomsthere is substernal pain radiating to both
arms and ulnar border of the left arm, jaw, teeth, occipital
region or epigastrium. The nature of pain is of crushing
type. Pain is of short duration, lasting for 3 to 5 minutes.
Pressure or discomfort in the substernal region. Patient
may feel as if heavy weight has been placed on his chest.
There may be breathlessness or fatigue, due to low
cardiac output.
Relieving of pain after cessation of exertionin most of the
cases, the pain is relieved by cessation of exertion. For
this reason and because of intense pain, the person
commonly maintains a fixed position during the attack.
Signsvariation in pulse rate with generalized facial or
circumoral pallor with cold perspiration may be
exhibited.
Diagnosis
Clinical diagnosisa typical history of angina itself could
give the diagnosis, even in absence of any other
abnormalities on investigation or examination. Though
physical examination in angina is often normal, certain
clues to the presence of IHD may be present like gallop
rhythm (third heart sound), left ventricular enlargement,
thickened blood vessels and absent pulse, systolic
murmur of mitral regurgitation or papillary muscle
dysfunction.
Diagnostic tests
ECGin 50% of patients resting ECG may be normal.
Stress testingwith bicycle ergometer using standard
protocols, or treadmill.
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Clinical Features
Myocardial Infarction
Management
Nitroglycerine tabletif the patient experiences an
anginal attack in the dental chair, nitroglycerine tablet
or sublingual spray (amyl nitrite) should be immediately
applied under the tongue. Dose should be 0.5 mg of
glycerine tri-nitrate or 5 mg of isosorbide dinitrate.
Prophylactic drugsin a known case of angina pectoris
relatively short acting antianginal drugs such as
sublingual isosorbide dinitrate tablet is recommended
prophylactically, before initiating the dental therapy or
a particularly stressful phase of dental therapy.
Dental Considerations
Difference between anginal pain and pain of dental origin
the pain is usually referred to jaws and teeth, resembling
a toothache and causing patient to seek dental attentions.
Due to overlapping of the fifth cranial nerve, cardiac
pain may be transmitted to jaws and interpreted as dental
pain. Anginal jaw pain is characterized by its severity,
its onset associated with exertion and its disappearance
with rest. These characters differentiate it from the usual
pain of dental origin.
Anginal attacks in dental chairacute anginal attacks may
occur as a result of stress associated with dental services,
i.e. extraction. If a patient is known to be angina pectoris
patient, short acting antianginal drug such as sublingual
isosorbide dinitrate is given prophylactically in addition
to any long acting nitrate drugs before initiating dental
therapy.
Deferring the procedure which require general anesthesia or
conscious sedationany dental procedure which require
general anesthesia or conscious sedation should defer
for 3 months duration after recent anginal attacks.
Diagnosis
Historythe characteristic history of chest pain and pain
radiating to other areas, as described for angina may be
the only guide. Patient who presents the history must be
carefully evaluated because in early disease history may
be the only positive finding.
Clinical symptomsclinical symptoms of collapse, severe
unremitting chest pain, changes in heart rate, hypotension will give clue to diagnosis.
ECG changesthe electrocardiogram shows changes
characteristic of or compatible with acute myocardial
infarction in only 80% of the cases and therefore cannot
be used, always, to exclude the presence of myocardial
infarction. Also shows the earliest change in ST segment
elevation with the onset of pain.
Nonspecific testpolymorphonuclear leucocytosis with
high ESR may be seen in the first week, due to tissue
necrosis.
Serum enzymesthere may be elevation in certain
enzymes like CPK, SGOT, LDH and AST in the blood.
Radionuclide technique provides accurate information
about myocardial infarction. In these, gammas emitting
radionuclide are used in making cardiac scintigrams.
Normally, perfuse myocardium is labeled by these
radionuclide and abnormally perfuse myocardium is
not labeled, producing the cold spot on scintigrams.
Positron emission tomography is also very useful nowadays.
Management
Cardiopulmonary resuscitationin case of cardiopulmonary arrest, cardiopulmonary resuscitation should
be immediately begun.
Prophylactic lidocainein patients with life threatening
acute arrhythmias, usually premature ventricular
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Dental Consideration
Premedicationthese patients require special management because they may have decreased ability to
withstand stressful conditions. Patients, for whom
dental treatment is particularly stressful, should be premedicated before treatment. Oral benzodiazepam are
helpful in 5 mg doses. It should be given in a waiting
room 45 minute before the procedure.
Patient on anticoagulant therapycareful history taking
is a must in such patients. Patients on long-term
anticoagulant therapy should be given instructions with
regard to bleeding, if surgical procedures like dental
extraction are carried out. Anticoagulant dosage should
be decreased by the cardiologist before any surgery.
Sudden withdrawal of anticoagulant drugs may result
in thrombosis or embolism.
Timing of dental treatmentafter acute myocardial
infraction all dental procedure should be deferred for
3 weeks and after that simple emergency dental treatment
can be carried out but with the opinion from physician.
B
Figs 33-6A and B: (A) Hand deformity in rheumatoid arthritis
(B) same hand in palmar view (Courtesy Dr Milind Chandurkar).
Diagnosis
Rheumatic Heart Disease and Fever
It is an inflammatory complication that may follow group
of streptococcal infection; manifested by one or more of the
following arthritis, carditis, and chorea. Rheumatic fever
usually comes on 1 to 3 weeks after the streptococcal
infection.
Clinical Features
Ageit is usually a disease of childhood occurring most
often between the ages of 6 to 16 years with peak of 8 years.
Symptomschorea (involuntary movement), the
symptoms of acute carditis. The child often complains
of sore throat and has a temperature of 38 to 39C.
Minor criteria
Fever
Arthralgia
Previous rheumatic fever or
rheumatic heart disease
Elevated ESR and positive
C-reactive protein
Protein raised
Carditis
Polyarthritis
Chorea
Subcutaneous nodule
Erythema marginatum
Characteristic ECG change
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Management
Restbed rest and sedation during acute episode.
Salicylatessalicylates are almost specific for the pain
of rheumatic fever.
Prophylaxiscontinued prophylaxis against a beta
hemolytic streptococcal infection is indicated and given
in the form of a monthly injection of 1.2 million units of
benzathine penicillin G or in 200,000 units of oral
penicillin, given twice daily or 1 g of sulfadiazine, given
orally, once a day. Such prophylactic therapy is
discontinued after 20 to 39 years of age.
Dental Considerations
Following are suggestions for prophylactic procedures, for
reduction of postextraction bacteremia and the possible
development of subacute bacterial endocarditis Historyproper history taking about evidence of
rheumatic fever, MV prolapse. If there is history of
rheumatic fever, administer prophylactic antibiotic
therapy before dental procedure.
Antibacterial mouth rinsemake the patient rinse with
antibacterial mouthwash, such as chlorhexidine
immediately before the treatment to help reduce the
number of microorganisms.
Atraumatic procedurekeep dental procedure atraumatic
as best possible.
Refer to physicianif a febrile illness develops within
3 months of the dental procedure, refer the patient to
physician.
Hypertension
Hypertension is the most common and significant medical
condition encountered in dental practice. Normal blood
pressure is 120/80 mm Hg.
Clinical Features
Symptomspatient may complaint of occipital headache,
dizziness, nausea, vomiting, malaise, and shortness of
breath and nose bleed. In some cases chest pain occurs.
In a milder form, there is extensive intraoperative
bleeding.
Signsblood pressure above 160 /100 mm Hg. There is
cardiac enlargement and narrowing of retinal arterioles
also occurs. Hypertensive patients may lead to hemorrhage, myocardial infarction, cardiac decompression
and renal failure.
Odontalgiaodontalgia is observed in hypertensive
patients, which occurs due to hyperemia of dental pulp
or congestion of this tissue resulting from increase blood
pressure.
Drug side effectmany patients in dental office may be
reported with gingival enlargement which occurs due
to nifedipine (calcium channels blocker) use in
hypertensive patients. Antihypertensive medication like
thiazides, methyldopa, propranolol, etc. can cause
lichenoid reaction in the oral cavity. ACE (angiotensin
converting enzyme) inhibitors can cause taste
impairment, burning sensation of mouth called as
scalded mouth syndrome. Xerostomia can also occur due
to many antihypertensive drugs.
Hypertensive crisishypertensive crisis is a sudden rise
of arterial blood pressure to a very high level (160/100
or 250/150 mm Hg) with clinical and pathological
manifestations. Such patients can pose problems
involving heart, brain and kidney.
Stages
Stage I (mild) hypertensiona diastolic pressure of 90-99
mm Hg and systolic pressure of 140-160 mm Hg.
Stage II (moderate) hypertensiondiastolic pressure of 100
to 109 mm Hg and systolic pressure 160-170 mm Hg.
Stage III (severe) hypertensionit has diastolic pressure
110-119 mm Hg and systolic pressure of 170-190 mm Hg.
Stage IV (very severe) hypertensionit is also called as
malignant hypertension. It has diastolic pressure more than
120 mm Hg and systolic pressure of 190 mm Hg.
Types
Primary or essential or idiopathic hypertensionit occurs
due to hereditary or environmental cause. Environmental
cause includes high sodium intake, excessive alcohol
consumption, physical inactivity, smoking and stress.
Dental Significance
Treatment planningan elevated blood pressure in a
dental patient requires careful consideration in treatment
planning, premedication, selection of an anesthetic and
determining the duration and extent of operative
procedure.
Risk of medical emergenciesundetected hypertension
increases the risk of experiencing cardiovascular
conditions such as angina, myocardial infarction and
cerebrovascular accident while undergoing dental care.
Effects of antihypertensive drugsoral health care can be
affected by the known side effects of antihypertensive
drugs and their interaction with other medications.
Care of general healththe dentist can perform a valuable
patient service by identifying undetected hypertension.
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Pathogenesis
Organism responsibleit is usually caused by oral
microorganism like alpha hemolytic streptococci,
enterococci, pneumococci, staphylococci and group A
streptococci.
Damaged blood flowin normal patients blood becomes
sterile after this transient phase. In patients with
damaged heart valves, initially there is formation of a
sterile platelet fibrin clot or thrombus on the damaged
heart surface. It acts as nidus for bacterial proliferation,
subsequently leading to infective endocarditis.
Oral bacteremiadental procedure can lead to release of
bacteria into the blood circulation. The most common
type of organism responsible for this oral bacteremia is
streptococci viridians which are abundantly found in
the mouth. It occurs in person who is having poor oral
hygiene and undergoing extraction.
Consequence of infective endocarditisinfective endocarditis will lead to proliferation of bacteria on the
damaged heart surface can lead to impaired valvular
function, congestive heart failure, abscess of
myocardium due to production of pus and release of
infectious emboli which can get lodged in organs such
as brain, kidney and spleen.
Predisposing Factors
Heart diseaseit has marked predisposition for persons
with rheumatic or congenital, cardiac or vascular defect,
bicuspid aortic valve, leutic aortic valvular disease,
idiopathic hypertrophic subaortic stenosis and mitral
valve prolapse.
Surgical correctionrecent surgical correction of
congenital valvular defect within 6 months.
Hypertrophic cardiomyopathyit can also occur in
hypertrophic cardiomyopathy.
Surgical traumasurgical trauma and dental extraction
are commonly related chronologically, to the onset of
clinical symptoms.
Clinical Features
Ageit can occur at any age, but most common in middle
age group.
Progressafter formation of vegetative lesion (thrombi),
they serve as foci of the intermittent dissemination of
microorganisms throughout the body. These vegetative
lesions are friable and small pieces may break off and
form septic emboli.
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Diagnosis
Management
Antibiotics therapyintensive antibiotic therapy, usually
20,000,000 units of penicillin in combination with
gentamicin for 2 weeks should be given.
Removal of infected valveearly removal of infected valve
should be done with sterile replacement.
Dental Considerations
Oral cavity, a source of infectionorganisms responsible
for subacute bacterial endocarditis were disseminated
commonly through bloodstream, following dental
extraction. It was demonstrated that gingival sulcus was
an important site from which the bacteria gained
entrance into the bloodstream. Actual cauterization of
gingival crevice before extraction markedly reduces the
percentage of transient bacteremia. Even in the absence
of direct dental procedure, bacteremia can be produced
secondary to foci of infection in the oral cavity.
Prophylactic measureevery known prophylactic
measure should be taken to preclude the possibility of
transient bacteremia occurring in patients with known
vascular lesions.
Prevention
Proper history should be takenask the patient about
history of rheumatic fever, heart disease with valvular
involvement or heart murmur.
Prophylactic antibiotics therapyif the heart disease to
endocarditis is known to be present, administer the
prophylactic antibiotic therapy before the dental
treatment.
Physician consultationif questionable positive history
of heart disease is obtained, you have to consult the
patients physician. All patients who are at risk of
developing endocarditis, subsequent to dental treatment,
Classification
Low output cardiac failurethere is a primary lesion in
heart which decreases the contractibility of the heart
and causes diminished cardiac output.
High output cardiac failurethere is primarily no lesion
in the heart, but due to extra cardiac condition, there is
increased work load on the heart which causes cardiac
failure with increased cardiac output.
Causes
Low output failureit is caused by myocardial lesions
like ischemic heart disease, rheumatoid heart disease,
cardiomyopathy, valvular endocarditis, congenital heart
disease and vascular lesions like hypertension and
aneurysm of aorta.
High output failurethyrotoxicosis, anemia, hypoproteinemia, beriberi, AV Fistula and cirrhosis of liver can
cause congestive cardiac failure.
Clinical Features
Symptomsthere is increased breathlessness following
moderate exertion, chronic productive cough associated
with blood tinged sputum. Patient also complains of
wheezing, anorexia, bronchospasm, and dyspnea.
Signspitting edema of lower extremities, hepatic
enlargement, and generalized edema. Congestion of the
large veins of neck and raised jugular venous pressure.
There is also cyanosis of lips, tongue and oral mucosa
with ankle edema.
Diagnosis
Clinical diagnosisbreathlessness, generalized edema
and raised jugular venous pressure will give clue to
diagnosis.
Management
Bed restcomplete bed rest is required.
Digoxinit should be the first line therapy for heart failure.
Diureticin cardiac failure, there is always sodium and
water retention, hence diuretics are given.
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Dental Considerations
Heart attack in dental officethe dentist should watch for
early signs of congestive cardiac failure like cyanosis of
lips, tongue. If the patient develops acute pulmonary
edema in the dental office, patient should be made
comfortable in sitting position or semisitting position
and administered 100% O2. Injection frusemide and
aminophylline should be given. Physician should be
immediately called for.
Clinical Features
Symptomsthey are variable. Some children manifest
breathlessness, inability to thrive, growth retardation
and central cyanosis.
Persistent ductus arteriosusit is failure of closure of
ductus arteriosus which plays role in fetal life as most of
the blood passes through ductus arteriosus into the
aorta. It results in recirculation of blood through the
lungs, leading to increased workload on the heart. It
occurs commonly in women. Affected individuals may
suffer from growth retardation, dyspnea, cyanosis and
cardiac failure. Surgical correction is possible in some
cases.
Atrial septal defectit results in shunting of blood from
left atrium and then to the right ventricle and pulmonary
arteries, leading to progressive enlargement of the right
side of the heart and the pulmonary artery with its
branches. Females are affected more than males. There
is dyspnea, cardiac failure and arrhythmias. It is treated
by surgical closure.
Ventricular septal defectit is usually asymptomatic.
Pulmonary stenosisit occurs either alone or along with
atrial septal defect or ventricular septal defect. Larger
pulmonary stenosis results in dyspnea, fatigue or
syncope.
Oral Manifestations
Bluish red discolorationgeneral bluish red discoloration
of oral mucosa with severe marginal gingivitis and
bleeding.
Diagnosis
Clinical diagnosisgeneralized bluish discoloration of
oral muscle with symptoms of atrial septal defect and
persistent ductus arteriosus.
Management
Antibiotics prophylaxisantibiotics cover is needed for
operative procedure.
Cardiac surgerythis should be done to correct congenital
anomalies.
Dental Considerations
Adequate analgesiaadequate analgesia should be given
to the patient during oral surgical operation. General
anesthesia should be avoided.
Conscious sedationconscious sedation with nitrous
oxide should be given with approval of physician.
Avoid using gingival retraction cord containing epinephrinegingival retraction cord containing epinephrine
should be avoided.
Cardiac Transplantation
These patients are on immunotherapy for life. Too little
therapy will result in rejection of episode, while too much
runs the risk of both infection and neoplasm. Opportunistic
infections like fungal, protozoal and viral infection are
common in these patients.
Dental treatment after transplantation should be
carefully planned in view of the patients lower immune
status with particular attention to WBC count and Hb
concentration. Before performing any treatment, the dentist
should take consent of the patients physician and consider
antibiotic prophylaxis. As many of these patients are on
long-term steroid therapy, steroid supplements should be
given.
Prophylactic antibiotic dose and its indications:
Amoxicillin3 gm orally, 1 hr before the procedure.
1.5 gm 6 hours after the initial dose.
Patients with allergy to penicillinErythromycin ethyl
succinate 800 mg, Erythromycin stearate 1 gm orally,
2 hours before the procedure. Clindamycin 300 mg
1 hour before the procedure and 150 mg, 6 hours after
the initial dose.
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Coarctation of Aorta
It is a developmental anomaly characterized by marked
diminution in the caliber of aortic arch, just distal to where
the left subclavian artery arise.
Patient suffers from secondary hypertension and
cerebral aneurysm with hemorrhage.
Intraorally there is marked enlargement of mandibular
arteries and branches leading to individual teeth. Arterial
hemorrhage will occur following tooth extraction. Pulp of
all the four maxillary incisors were markedly enlarged and
funnel shaped, occupying great portion of crown and roots.
Respiratory Disorders
Bronchial Asthma
Asthma is a common disease estimated to affect 4 to 5%
population. It is initially a spontaneously, reversible,
spasmodic contraction of the smooth muscles of bronchi
resulting in bronchiolar narrowing. As the attack
progresses, resistance to airflow may be further exacerbated
by mucosal edema and inflammatory infiltrate of mucosa.
Types
Extrinsic asthmait is developed by allergic factors. It is
also called as allergic asthma. Patient, who is having
asthma of allergic origin, often has positive family
history of disease and positive atopic history including
hay fever, rose fever and eczema.
Intrinsic asthmait is precipitated by nonallergic factors.
It is also called as non-allergic asthma, idiopathic asthma
and infective asthma.
Mixed asthmait is combination of allergic and nonallergic asthma.
Status asthmaticusit is persistent exacerbation of
asthma.
Predisposing Factors
Extrinsic asthma
Airborne allergenhouse dust, feathers, animal dander,
furniture stuffing, fungal spores and a wide variety of
plant pollens.
Allergenic foodit includes cows milk, eggs, fish,
chocolate, shellfish and tomatoes.
Allergic drugit includes penicillin, vaccines and aspirin.
Intrinsic asthma
Infectionsrespiratory infections, usually viral, are well
known initiating factor in the asthmatic patient.
Exercisesome patients have acute asthmatic attack after
prolonged exercise.
Clinical Features
Ageit is more common in children, especially boys. It
can also occur in older individuals.
Symptomspatients notice a sensation of fullness in the
chest. Predominately, symptoms of acute attack are
wheezing, coughing and labored breathing. There is also
sneezing and gasping sounds are heard while
attempting to breath.
Attack terminationtermination of attack is usually
heralded by a period of intense coughing with expectoration of thick, tenacious mucous plug which is followed
by sensation of relief.
Signswith severe attack, the patient is extremely
anxious and agitated. Heart rate is increased to 130 per
minute. Cyanosis of mucous membrane of lips may be
visible along with perspiration and flushing of face and
upper torso in severe attack. Patient is more comfortable
if allowed to sit or stand upright with the back upright
and the chest, shoulder and head fixed.
Extrinsic asthmabronchospasm usually develop within
minutes after exposure to allergens. These attacks
usually become less frequent and less severe during
middle and late adolescence and may disappear entirely.
Intrinsic asthmaattack of intrinsic asthma is usually
more fulminant and severe than those of allergic asthma.
The long-term prognosis is poorer and the patient
eventually exhibits clinical signs and symptoms in
interval between acute episodes.
Status asthmaticusin it, acute asthmatic attack persists
in spite of drug therapy. Bronchospasm may continue
for hours or even days without remission. Patient more
commonly exhibits extreme fatigue, dehydration, severe
hypoxia, cyanosis, peripheral vascular shock and drug
intoxication from intensive therapy. Chronic partial
airway obstruction may lead to death from respiratory
acidosis.
Diagnosis
Clinical diagnosisdiagnosis of bronchial asthma is
based on the symptoms, pulmonary function test and
physical finding of expiratory wheezes during the acute
attack.
Laboratory diagnosisthere is raised total IgE and specific
IgE antibody concentration.
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Dental Considerations
Avoid inhalation anestheticspatient using betaadrenergic inhaler should be reminded to bring the
inhaler with them to dental office; the dentist should
avoid inhalation anesthetics or analgesic in asthmatic
patient because of the possibility of stimulating an acute
asthmatic attack.
Dental workif attacks are seasonal, routine dental work
can be performed during the time when frequency of
attack is lowest. Patients on steroids may require
additional steroid to avoid serious reaction to stress of
dental procedure.
Attacks in dental chairin case of acute attack occurring
on dental chair, following measures should be taken:
Terminate the procedureterminate the dental therapy
and position the patient in any comfortable position.
Administration of bronchodilators0.5 ml, 1:1000
adrenalines can be injected subcutaneously or
intramuscularly. If attack is prolonged, steroids are
indicated
Aerosol spraythe onset of aerosol drug is rapid and
relief of symptoms occurs within seconds.
Administer oxygenit may be administered by full face
mask, nasalhood or nasal cannula.
Types
Chronic bronchitisit refers to inflammation of bronchi.
It is defined as a condition in which there is mucus
producing cough present, for at least 3 months of the
year, for more than 2 consecutive years.
Emphysemait is dilatation of air spaces distal to
terminal bronchioles with destruction of alveoli reducing
alveolar surface area for respiratory exchange.
Causes
Smokingthe most common cause of COPD is smoking.
Environmental dustthe other factors are chronic
recurrent infection, air pollution and occupational
inhalants.
Deficiency of antiproteolytic enzymedeficiency of antiproteolytic enzyme alpha 1-antitrypsin is a rare cause
of emphysema.
Clinical Features
Early morning coughpatient shows early morning
mucoid cough which becomes purulent during
exacerbation.
Pink panter or pink pufferthis is present in emphysema
in hyperventilation, occurs to maintain normal blood
gases. This will cause vasodilatation and patient will
be pink due to CO2 retention.
Cutaneous vasculitisin some cases of emphysema
cutaneous vasculitis may be present (Fig. 33-7).
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Diagnosis
Clinical diagnosiscutaneous vasculitis with pink panter
with blue bloated appearance will aid in diagnosis.
Management
Stoppage of habitpatient should ask to quit the habit of
smoking.
Bronchodilatorbronchodilators are particularly
effective in relieving bronchospasm. Bronchodilators
used are ipratropium bromide, oxitropium, and
theophylline.
Antibioticsantibiotic therapy should be initiated with
earliest sign of chest infection. Antibiotics used are
amoxicillin, trimethoprim, or tetracycline.
Oxygen therapyoxygen is useful both, intermittently
on a chronic basis and continuously with an acute
exacerbation of disease.
Renal Disorder
Renal Failure
Dental Considerations
Upright positionpatient should be treated in upright
position. If patient is flat there are chances of
breathlessness.
Avoid using rubber damthe patients tolerance to partial
airway obstructing devices such as rubber dam is less
so use of rubber dam should be avoided.
Short treatment timemucus producing cough, wheezing,
and dyspnea in these patients prevent long treatment
sessions. This should be taken into consideration while
planning the dental therapy.
Inhalation analgesicinhalation analgesic should be
given only when it is necessary and in conjunction with
anesthesiologist.
Drug interactionas patient is taking theophylline, many
drugs like epinephrine, erythromycin, clindamycin, etc.
should be given cautiously.
Avoid giving general anesthesiapatient should be
avoided giving general anesthesia unless it is very
necessary.
Etiology
Glomerulonephritisit represents a heterogeneous
group of disease of varying etiologies that produce
irreversible impairment of function. The attack of
glomerulonephritis is either streptococcal or nonstreptococcal. Chronic glomerulonephritis has usually
very slowly, but steadily progressive course, leading to
renal failure or uremia in few years to as many as 30
years.
Pyelonephritisit refers to the effect of bacterial infection
in kidney, with E. coli being the cause of infection. Any
obstruction of urinary tract can predispose to active
pyelonephritis and also can occur due to generalized
sepsis in patients with bacterial endocarditis or with
staphylococcal infection. Clinically, there is sudden rise
of body temperature, shaking chills, aching pain in one
or both costovertebral areas or flanks and symptoms of
bladder inflammation.
Hemolytic uremic conditionthis condition is caused by
E. coli.
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Diagnosis
Clinical diagnosisvariety of clinical symptoms occur
in it with oral manifestation.
Radiological diagnosispulpal narrowing with loss of
lamina dura can be seen.
Management
Clinical Features
Gastrointestinalnausea, vomiting, anorexia, parotitis,
gastritis and gastrointestinal bleeding.
Neuromuscularheadache, myoclonic jerks, peripheral
neuropathy, paralysis, seizures and asterixis.
Hematological and immunologicalnormocytic and
normochromic anemia, coagulation defects, increased
susceptibility to infections, decreased erythropoietin
production and lymphocytopenia.
Endocrine and metabolicrenal osteodystrophy,
secondary hyperparathyroidism, impaired growth and
development, loss of libido and sexual function and
amenorrhea.
Cardiovasculararterial hypertension, congestive heart
failure, cardiomyopathy, pericarditis and arrhythmias.
Dermatologicalpallor, hyperpigmentation, ecchymosis,
uremic frost, pruritus, reddish brown distal nail beds.
Oral Manifestations
Incidencein the study of renal patients, 90% were found
to have oral manifestations.
Ammonic taste and smellpatients complain of ammonic
taste and smell, particularly in the morning. It is caused
by the high concentration of urea in saliva and its
breakdown to ammonia.
Xerostomiathe patients may complain of xerostomia
which is caused by direct involvement of salivary gland,
chemical inflammation, dehydration and mouth
breathing.
Erythemopultaceous formthe acute rise in BUN level may
result in uremic stomatitis, which appears as
erythemopultaceous form, characterized by red mucosa
covered with a thick exudate and a pseudomembrane.
Ulcerative formin some cases, stomatitis may be in
ulcerative form which appears as frank ulceration with
red and pultaceous coat.
Low caries activitylow caries activity despite of high
sugar intake; poor oral hygiene due to increased salivary
urea nitrogen.
Enamel hypoplasiait is frequently seen in patients where
renal disease is started at young age.
Otherthere is pulpal narrowing and calcification,
severe tooth erosion and loss of lamina dura can also be
seen.
Dental Consideration
Many patients who are receiving dialysis have
conditions of oral neglect.
Dialysisif time and patients conditions permit,
dialysis should be part of the preoperative preparation.
Dialysis will return the state of hydration, serum
electrolyte, urea nitrogen and creatinine toward normal
and will reduce the need for dialysis in the immediate
postoperative period.
Control of bleedingas bleeding is common problems in
renal failure patient, hemostatis should be done with
the help of desmopressin, cryoprecipitate and
conjugated estrogens.
Position of patient in dental treatmentblood flow through
the arm should not be impeded by requiring the patient
to assume a cramped position or using that arm to
measure blood pressure. Patient should avoid sitting
for long periods of time with leg dependent. If dental
treatment is long, then patient should be allowed to walk
for few minutes every hour.
Infective endocarditisthe presence of an access site
increases the susceptibility to infective endocarditis.
Antibiotic prophylaxis is required for control of infective
endocarditis. Start with broad spectrum antibiotic, e.g.
amoxicillin 3 g, 1 hr before treatment and 500 mg every
8 hours for 1-2 days.
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Renal Osteodystrophy
It occurs due to defect in hydroxylation of 25-HCC to 1, 25DHCC a process that normally occurs in kidney.
Hypocalcemia occurs due to impaired calcium absorption
and hyperphosphatemia, due to reduction in renal
phosphorous excretion. Hypocalcemia results in secondary
hyperparathyroidism with increased level of serum
parathyroid hormone. Systemic acidosis is also associated
with these conditions. There are symptoms of chronic renal
failure.
Clinical Features
Myopathymuscle cramps are more common; restless
leg syndrome, where patients legs jump at night.
Neuropathysensory neuropathy may cause paresthesia. Motor neuropathy may present as foot drop.
Autonomic neuropathy may cause delayed gastric
emptying, diarrhea and postural hypotension.
Endocrine functionthere may be hyperporlactinemia
and hyperparathyroidism. Amenorrhea is common in
females. There is also loss of libido and sexual functions.
Growth retardation occurs in children and bone fractures
occur frequently.
CVS effectshypertension results in 80% of patients. This
is due to sodium retention and increased secretion of
renin, angiotensin-I and aldosterone. Atherosclerosis is
common.
Acidosisthere is also acidosis; cellular and humoral
immunity are impaired.
Bonein adults, gradual softening and bowing of bone
occurs.
Radiographic Features
Radiodensitygeneralized loss of bone density and
thinning of bony cortex.
Lamina duraloss of lamina dura.
Angle of mandiblethickness of cortex of mandibular
angle is reduced.
Medullary spacesincrease in medullary space at the
expense of trabeculae. Other bones may show areas of
sclerosis.
Diagnosis
Clinical diagnosismyopathy, neuropathy can give clue
to diagnosis.
Radiological diagnosisgeneralized loss of bone density
with thinning of bony cortex will aid in diagnosis.
Management
Vitamin Dplasma Ca++ and K+ are kept as near as
normal.
Vitamin Dhypocalcemia is corrected by giving
hydroxylated synthetic analogues of vitamin D.
Phosphate binding agentshyperphosphatemia is
controlled by dietary restriction of foods with high
phosphate content (like milk, cheese, eggs) and the use
of phosphate binding drugs.
Uremia
It is a clinical condition caused by the retention of urinary
constituents in the blood. The characteristic symptoms are
headache, itching, nausea, convulsions, and eventually
coma. Patients breath may have urinous odor.
There is unpleasant taste and dryness of mouth. There
is erythematous, pseudomembranous type of uremic
stomatitis. If pseudomembrane is removed, it will expose
dry, red, swollen mucosa. The oral bleeding tendency, often
observed in patients with uremia, is due to uremic
thrombopathy. Patient has an increased disposition to
develop oral candidiasis.
Kidney Transplantation
In order to prolong life in patients with end stage renal
failure, renal transplantation is done. It involves surgical
removal of kidney from living first degree relative such as
sibling, parent, child or a recently expired source. Kidney
transplant patient usually receives a continuous regimen
of immunosuppressive medication to ensure graft survival.
Clinical Features
Majority of clinical manifestation occur secondary to
immunosuppressive drugs.
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Oral Manifestations
Oral mucosapale mucosa with diminished color
demarcation between attached gingiva and alveolar
mucosa.
Salivary glandenlarged salivary glands and decreased
salivary flow resulting in xerostomia.
Odor and tasteodor of urea on breath and metallic taste.
Teethenamel hypoplasia, dark brown stain on crowns,
dental malocclusion, and low caries rate.
Gingivaincrease in calculus formation, low grade
gingival inflammation and bleeding from gingiva and
mouth.
Candidiasiscandidal infection can occur on tongue.
Otherpetechiae, ecchymosis, erosive glossitis, burning
and tenderness with dryness of mucosa. Dehiscence of
wounds also occurs.
Radiological Features
Demineralization of bonethere is demineralization of
bone with loss of bony trabeculation.
Ground glass appearancesometimes, ground glass
appearance can be seen.
Other findingloss of lamina dura, socket sclerosis is
other radiological findings.
Diagnosis
Diagnosis can be made by history.
Types
Dental Considerations
Elimination of source of infectionOral infection in
transplant patients has been reported as frequently as
pneumonia or urinary tract infection. Prompt diagnosis
of the site and cause of infection in immunosuppressed
patient should be on high priority. Identification of pathogens should be performed with culture, sensitivity,
smear, aspiration technique or biopsy. The successful
management of transplant patient begins before
transplantation, with the preoperative elimination of
potential sources of infection.
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Phases of Hepatitis
Prodromal phaseis of 1-2 weeks; symptoms like
anorexia, nausea, malaise and fever occur.
Icteric phase(6-8 weeks) anorexia, nausea, vomiting and
pain in the right upper quadrant of abdomen. Hepatomegaly and splenomegaly may also be seen.
Convalescent (recovery) phasesymptoms disappear, but
abnormal liver function values may persist.
Clinical Features
Incubation periodin this, most cases resolve completely
within 4 months after onset of symptoms but, some end
in fulminating disease and others progress to chronic
hepatitis.
Symptomssystemic complains include malaise,
arthralgia, morbilliform skin rash, anorexia, vomiting
and myalgia. Patient has high grade fever with
tenderness and enlargement of liver. Patient also
complains of upper respiratory tract infection, distaste
for cigarette, fever and enlargement of liver.
Signsjaundice, darkening of urine, splenomegaly and
whitish stools occurs.
Oral manifestationicterus of the oral mucosa, which is
seen on the palate and in the sublingual region.
Laboratory Findings
Plasma bilirubin levelplasma bilirubin level excess of 3
mg/dl.
SGPT SGOT levelSGPT, SGOT levels increase 10 times
in hepatitis.
Management
General treatment:
Symptomatic treatment like bed rest and prevention
by isolation of blood, saliva contaminated objects; use
of gloves and apron and sterilized instruments are
must.
Nutritiona high calorie diet should be given. It is
usually given in morning because many patients
experience nausea in evening.
Drugsthere is no specific drug useful for it. But
interferon and ribavirin have been tried, with some
success in chronic hepatitis.
Preventionthe patient should avoid salivary
transmission to others by avoiding kissing, spitting
and sharing food, cigarettes, utensils and sexual
contact.
Hepatitis Ait is self limiting and resolves with in one
month mortality is very low. Treatment is usually
symptomatic.
Hepatitis Bchronic hepatitis B infection can be treated
with lamivudine or interferon. Treatment is needed for
1 to 3 years.
Hepatitis Cchronic hepatitis C is treated by combination
of ribavirin, interferon alpha or pegylated interferon.
Hepatitis Ddrug treatment with alpha interferon is
effective.
Hepatitis Galpha interferon is also effective against
hepatitis G.
Prevention
Hepatitis Apeople who are known to have contact with
a patient, such that they may have ingested minute
amounts of fecal material or have been injected with as
little as 0.0004 ml of infected blood, should be given
prophylactic gamma globulin injections.
Hepatitis Ba vaccine has been prepared from the
plasma of asymptomatic carriers of hepatitis B. It is
composed of non-infectious hepatitis B surface antigen
particles. It is recommended in all high-risk groups.
Hepatitis Cthere is no vaccine available for this
hepatitis. Preventing measure like not sharing
personal item with bloodstain, not sharing needle in
drug user, avoid having tattoo without strict health
precaution.
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Dental Considerations
Risk to dental professionalhepatitis B, C and other types
can be transmitted to the dentist by blood contaminated
needles or instrument stick from an infected patient in
acute phase of disease.
Clotting factors assessmentif surgery is necessary, obtain
preoperative prothrombin time and bleeding time, as in
liver diseases deficiency of clotting factor may be present.
Universal infection precautiondental personnel may act
as a source of infection to patient. Dentists who are
carriers of HBV and who do not practice universal
infection control precautions can transmit the infection
to patient. At the same time it is required to avoid infection from patient to be transmitted to dental personnel.
Strict aseptic procedurestrict aseptic procedureuse of
masks, gloves for all persons is a must.
Minimize aerosol productionminimize aerosol
production by using a slow speed handpiece and using
air syringe.
Diagnosis
Types
Ulcerative colitisit is an inflammatory disease that is
confined to the mucosa and submucosa of colon.
Crohns diseaseit is an inflammatory disease involving
the entire wall of a portion of small gut.
Clinical Features
Management
Oral Manifestations
Dental Considerations
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Causes
Hemolysisthere is increased destruction of red blood
cells with excessive pigment production.
Gilberts syndromeit is a common form of congenital
hyperbilirubinemia.
Transport diseaseinability of the liver to transport
bilirubin into the bile.
Othersjaundice can occur due to primary biliary
cirrhosis, cystic fibrosis and traumatic biliary strictures.
Clinical Features
Urineincreased urobilinogen excretion causes the urine
to turn dark.
Anemiapallor occurs due to anemia and thus can be
noticed on nails.
Splenomegalyit occurs due to excessive reticuloendothelial activity.
Otherspruritus, abdominal pain and pale stools can
also occur in jaundice.
Icterusyellowish discoloration of sclera of eye is also
present. This yellow discoloration is caused by
hypercarotenemia (Fig. 33-9).
Oral Manifestations
Icterus of oral mucosait can be seen on palate and in the
sublingual area.
Spontaneous bleedingin cases of severe jaundice patient
may present with spontaneous bleeding in the oral
cavity or severe bleeding following oral surgical or
periodontal operation.
Jaundice
It is a symptom rather than a disease, resulting from excess
of bilirubin in circulation. Jaundice can be recognized by
color of skin, oral mucous membrane and sclera of the eyes.
There is yellowish discoloration of skin, muscle membrane
and sclera of eyes due to increased level of bilirubin and
deposition of bile pigment tissues. Jaundice appears when
serum concentration exceeds 2 to 3 mg /dl.
Diagnosis
Clinical diagnosisicterus and yellow discoloration of
skin can easily be noted
Laboratory diagnosisserum bilirubin level is increased
Types
Hemolytic jaundiceresults from an excessive hemolysis
or destruction of erythrocytes produced by an inherited
abnormality in the cells, some acute diseases and
certain drugs or poisonous agent or acquired immune
disease.
Obstructive jaundicecaused by gallstone and external
pressure on biliary passage, associated with infection
or neoplastic lesions.
Hepatocellular jaundiceit can be caused by diseases such
as hepatitis and alcoholic and postnecrotic cirrhosis.
Fig. 33.9: Icterus seen in eyes of patient who is suffering from jaundice.
Note also yellowish discoloration of facial skin (Courtesy Dr Milind
Chandurkar).
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Clinical Features
Diseases of Esophagus
Plummer-Vinson syndromeIt is characterized by an
esophageal web with resulting dysphagia, particularly
in the upper segment of esophagus, as well as by atrophic
changes in the mucous membrane of mouth and by a
hypochromic microcytic anemia.
Dysphagiait is difficulty in swallowing which may
result from mechanical obstruction in the esophagus or
from disorders of the nervous system that prevent the
coordinated reflex contraction of the appropriate
muscles.
Esophageal ulcerit can be associated with tetracycline
therapy. It occurs more often after dry swallow of tablet
or capsule, especially at bedtime. The patient complaints
of severe retrosternal burning pain.
Dental considerationdue to unique position in treating
in the oral cavity, dentist may be the first to detect this
condition and should promptly refer it to physician for
early diagnosis and prompt treatment. Special precautions should be taken while treating these diseases,
to avoid aspirations secondary to dental procedures.
Patients who have been prescribed tetracycline should
be warned to swallow the capsule or tablet with adequate
amount of liquid.
Peptic Ulceration
Ulceration of the mucosa of gastrointestinal tract caused
by the action of protein-digesting pepsin on mucosa is one
of the most common disease affecting GIT and one of the
most common disease to afflict man.
Oral Manifestations
Sitevascular formation is more commonly seen at the
inner surface of the labial commissure and is more
common in males than females.
Vascular malformationit is rarely manifested in the oral
cavity but in certain cases, vascular formations of lip are
also found in peptic ulcer. The vascular formations are
of three types:
Microcherryit is small, sharply circumscribed, red
dot type of lesion.
Glomerulia conglomeration of tortuous, thin walled
vessels 1-2 mm or more in size.
Venous lakesdilated submucosal vein resembling a
miniature varix.
Complicationmassive bleeding, obstruction, perforation
and intractability to medical treatment.
Diagnosis
Clinical diagnosiscoffee ground vomitus with vascular
malformation of lip may give clue to diagnosis.
Management
Predisposing Factors
Acid productionthe normal stimuli for acid secretion
include the thought, sight, smell or taste of food, which
is mediated by the anterior hypothalamus, acts by vagal
stimulation directly on the mucosa of stomach to cause
acid production.
Hypoglycemia and mental stresshypoglycemia and
mental stress also act by the same mechanism to increase
stomach acid production.
Gastrin productionpresence of food in the antrum of
stomach wall, by the mechanism of distention, cause
increased production of the hormone gastrin, which acts
directly on the acid producing cells of stomach.
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Dental Considerations
Etiology
Neuromuscular Disorders
Auriculotemporal Syndrome
It is also called as Freys syndrome or gustatory sweating. It is
characterized by flushing and sweating of facial skin along
the region of distribution of auriculotemporal nerve. It is
an unusual phenomenon which arises as a result of damage
to the auriculotemporal nerve.
Clinical Features
Age and sexthere is no age and sex predilection.
Symptomsthe patient exhibits preauricular flushing
and sweating of the involved side of face, following
ingestion of food or visual stimulation by food. Patient
may sometimes feel pain while eating. The severity of
sweating is increased by tart food. Profuse sweating may
be evoked by parenteral administration of pilocarpine
or eliminated by the administration of atropine. Local
skin temperature can increase up to 2 C.
Crocodile tearsin it patient exhibits profuse lacrimation
when food is eaten particularly hot and spicy food.
Cutaneous hyperesthesiapresence of cutaneous
hyperaesthesia in front and above the ear, the area
supplied by the auriculotemporal nerve.
Diagnosis
Pathogenesis
Auriculotemporal nerveit gives sensory supply to the
preauricular and temporal region, carries parasympathetic fibers to parotid gland.
Scar formationafter damage to nerve scar formation
occur around the nerve.
Re-established innervationsthe fibers regenerate, become
misdirected and become connected with sympathetic
nerve fibers of sweat gland and blood vessels of the facial
skin.
Sweating and vasodilationparasympathetic fibers
would therefore induce salivation; inadvertently
stimulate the preauricular-dermal sweat gland and
arterioles, causing vasodilation.
Management
Nerve dissectionintracranial division of auriculo
temporal nerve has been reported to be successful.
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Bells Palsy
It is also called as 7th nerve paralysis or idiopathic facial
paralysis.
Pathogenesis
Normal coursethe cortical tract communicating with
the motor nucleus ambiguous of facial nerve crosses over
to get innervated into the lower face musculature. Upper
face fibers are ipsilateral proximal to the nucleus.
Lower face palsya cortical lesion will cause contralateral
lower face palsy.
Total hemifacial palsylesions of brainstem, main trunk
or peripheral fibers will result in total hemifacial
paralysis.
Clinical Features
Age and sexwomen are more commonly affected than
men and usually, it occurs in the middle age group. It
arises more frequently in spring and fall, than at any
other time of the year.
Onsetit begins abruptly as paralysis of the facial
musculature, usually unilaterally.
Prodromal symptomsin some cases, it is preceded by
pain on the side of the face which is ultimately involved,
particularly within the ear, temple, and mastoid area or
at the angle of the jaw.
Symptomsspeech and eating is difficult and
occasionally, taste sensation on the anterior portion of
tongue is lost or altered. Food is retained in the upper
and lower buccal and labial folds due to weakness of
buccinator.
Eyeon the affected side, eye cannot be closed and
wrinkles are absent on that side. There is watering of
eye, which leads to infection.
Facial featureswhen the patient smiles, the paralysis
becomes obvious since the corner of the mouth does not
rise nor does the skin of the forehead wrinkles or the
eyebrows raise (Fig. 33-10).
Etiology
Coldit usually occurs after exposure to cold. But many
workers believe that it is a chance finding.
Traumait may be a causative factor as Bells palsy
occurs after extraction of teeth and after injection of local
anesthesia. Extraction and injection may cause damage
to the nerve and subsequent paralysis.
Surgical proceduresurgical procedures such as removal
of parotid gland tumor in which the facial nerve is
sectioned can also cause facial paralysis.
Ischemiait may caused by ischemia of the nerve near
the stylomastoid foramen, resulting in edema of the
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Diagnosis
Clinical diagnosisslurred speech, mask like face,
drooling of salvia can diagnose this condition.
Management
Vasodilatorthe use of vasodilator drug like histamine
has been proved beneficial in some cases.
Surgical decompression and anastamosis of nervesurgical
anastamosis of nerves has been carried out, especially
with facial and hypoglossal nerve; thus can restore
partial function.
Nicotinic acidadministration of physiologic flushing
dose of nicotinic acid.
Othersystemic steroids or ACTH injection have been
successful in treating Bells palsy.
Types
Diagnosis
Etiopathogenesis
Clinical Features
Progressive muscular atrophy
Age and sexit usually occurs in childhood. It shows a
strong hereditary pattern, affects males more frequently
than females.
Symptomsthe initial symptoms usually consist of
difficulty in walking with leg pain and paresthesia.
Management
Antiglutamate agentsantiglutamate agent riluzole
shows some improvement in this disease. As such there
is no specific treatment for this disease and it is usually
fatal.
Multiple Sclerosis
It is also called as disseminated sclerosis. This disease affects
central nervous system. It is autoimmune disease.
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Diagnosis
Management
Drug treatmentbeta interferon, mitoxantrone, and
glatiramer can be effective in this patient. Medication to
reduce muscle fatigue can also be used.
Physical and occupational therapythis can be use to
patient up to certain extent.
Clinical Features
Age and sexit occurs chiefly in younger age group with
an onset of symptoms between the ages of 20 and 40
years. There is slight female predilection with familial
occurrences.
Symptomsfatigability, weakness and stiffness of the
extremities with ataxia or gait difficulty, involving one or
both legs. Superficial or deep paresthesia. Personality
and mood deviation towards friendliness and
cheerfulness.
Signsvariety of ocular disturbances including visual
impairment as a manifestation of retrobulbar neuritis,
nystagmus and diplopia.
Staccato speechstaccato (a series of short, detached
sound or words) type of speech.
Charcots triadit consist of intentional tremors,
nystagmus, dysarthria and scanning speech.
Oral Manifestations
Jaw weaknessfacial and jaw weakness occur in some
patients.
Reduced mouth openingthis may occur due to stiffness
and weakness of muscle (Fig. 33-11).
Trigeminal neuralgiathis occurs in multiple sclerosis
patients and it usually bilateral.
Facial palsythis can also be present in the multiple
sclerosis.
Cerebral Palsy
The term cerebral palsy refers to a group of disorders with
motor manifestations due to nonprogressive brain damage,
occurring before or after birth.
Causes
Anoxia and ischemiaanoxia and ischemia during labor
can cause cerebral palsy.
Congenital infectioncongenital infection like toxoplasmosis, rubella, cytomegalovirus disease, herpes
simplex, syphilis and influenza can also cause cerebral
palsy.
Clinical Features
Formscerebral palsy can be manifested in spastic,
dyskinetic, ataxic or a combination, affecting one or four
limbs.
Spastic formlegs are commonly involved. Speaking
problems with dysarthria, chewing and swallowing
difficulty. Sometime, there are seizures associated with
mental retardation.
Dyskinetic formit is characterized by athetotic purposeless movement, involving both agonist and antagonist
muscles, which is increased by voluntary activity. Head
movement and facial grimacing are characteristic.
Lead pipe type movementthis occur due to excessive
muscle tone.
Oral Manifestations
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Diagnosis
Clinical diagnosislead pipe type of movement with
hemiplegia will lead to the diagnosis. There is also delay
in development of motor skill.
Management
Epilepsy
It is a disorder, which results due to a sudden discharge by
cerebral neurons, resulting in convulsive movements. It can
cause sensory and motor abnormalities as well as loss of
consciousness. Convulsions can also be seen with high
grade fever, brain tumor, head injury, hypoglycemia,
hypocalcemia, and drug toxicity.
Types
Grand malit is most common type of seizure which
can occur alone or with other types of seizure.
Petit malit is the second most common type and it occur
without aura and with little or no clonic or tonic
movements.
Psychomotorthe seizures are preceded by an aura,
which is often a hallucination or a felling of dj vu.
Jacksonianin it, attack begins in one part and spreads
gradually.
Simple partial seizureit originates from one localized
area of the brain and does not feature loss of
consciousness.
Complex partial seizureit is same as psychomotor, with
impairment of consciousness.
Status epilepticusit is the period of recurrent seizure
attacks, without recovery between each attack.
Clinical Features
Grand malit begins in childhood. There is warning
followed by loss of consciousness.
Aura phasea grand mal seizure begins with aura in
which patient experiences epigastric discomfort, an
emotion or hallucination of hearing, vision or smell.
Tonic phasethe aura is followed, in seconds to
minute, by unconsciousness, cry, and tonic muscle
spasms. There is also breathlessness due to spasm of
respiratory muscles and the patient becomes cyanotic.
Diagnosis
Clinical diagnosistonic muscle spasm, convulsive jerky
movement with headache and confusion will diagnose
this condition.
Management
Immediate care of seizuresyou should move person away
from danger like fire, water, machinery and furniture.
After convulsion ceases it turns into recovery position,
i.e. semiprone position. Do not insert anything in the
mouth as tongue biting occurs at the start of seizure, so
it cannot be prevented. If convulsion continues for more
than 5 minutes or recur without person regains
coconscious, summon urgent medical attention. Give
intravenous anticonvulsants, i.e. diazepam, if
convulsion continues or repeated. Airway should be kept
patent during the epileptic fits.
Anticonvulsive drug therapythe drug of choice for grand
mal, psychomotor and Jacksonian seizure is phenytoin
(Dilantin), often in combination with phenobarbital.
Patient resistant to it are given primidone. Drug of choice
for petit mal is ethosuximide because of few side effects
associated with it. Other drugs used are trimethadione,
paramethadione and acetazolamide.
Dental Considerations
Gingival enlargementpatients taking anticonvulsant
drug such as phenytoin, develop gingival hyperplasia
which may exacerbate due to local inflammatory factors.
You should also look for level of drug in the gingival
tissues and the effect of drug on gingival mast cells.
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Parkinsons Disease
It is a major cause of chronic disability in patients over
50 years of age.
Causes
Depletion of neurotransmitterit is caused by depletion
of neurotransmitters, dopamine and norepinephrine in
the basal ganglion.
Other diseasesome are caused by encephalitis, trauma,
carbon monoxide intoxication, atherosclerosis, metal
poisoning and brain tumor.
Clinical Features
Triadthe triad is rigidity, tremor and bradykinesia
(slowness in the initiation of movements).
Onsetthe onset is insidious. Mild stiffness of muscle of
the extremities and tremor of hand are early signs.
Pill-rolling movementthe typical hand tremors are called
as pill-rolling movements and are caused by movement
of thumb and fingers rubbing against one another.
Gaitwalking becomes more difficult and patients
develop a slow shuffling gait in a stooped position
because of the inability to stand straight.
Speechspeech becomes slow owing to lack of muscle
control (dysarthria) and as the disease progresses there
is a decrease in all voluntary movements and increase
in tremor.
Oral Manifestations
Appearance of facerigidity of facial muscle is common.
The loss of flexibility gives the patient an expressionless
or masklike face.
Droolingthe muscle rigidity also causes difficulty in
swallowing, resulting in drooling.
Tremorstremor of tongue and mandible are also
common, making speech and eating difficult for the
patient and dental procedures difficult for the dentist.
Complication of Levodopa therapydue to Levodopa
therapy, patient exhibits purposeless chewing, grinding
and sucking movements that are quite bizarre. The
patient may thrust or shake his tongue and chew or
suck vigorously when there is nothing in mouth.
Diagnosis
Clinical diagnosistriad of tremor, rigidity and bradykinesia can be seen.
Management
Levodopalevodopa can cause dramatic reversal of
symptoms of Parkinsons disease.
Anticholinergic drugsmild form of Parkinsons disease
can be managed by anticholinergic drugs such as
trihexyphenidyl, like benzotropine or ethopropazine.
Propranololpropranolol an adrenergic antagonist may
be used to reduce tremors.
Bromcriptinebromcriptine is one of the newer drugs
which are an agonist at the dopamine receptors.
Dental Considerations
Pretreatment sedationanxiety will increase both, tremor
and degree of muscle rigidity. Pretreatment sedation with
diazepam is often recommended, as it will reduce
anxiety.
Precaution while changing posturewhen the dental
treatment has finished, the patient should be warned to
take care while changing from a supine to standing
position, since levodopa has a significant orthostatic
hypotensive effect.
Orofacial Dyskinesia
It is caused by extrapyramidal disorders, complication of
phenothiazine therapy and dentures in gross malocclusion.
It is more commonly occurs above 60 years.
It is characterized by severe involuntary, dystonic
movements of the facial, oral and cervical musculature.
Irregular and involuntary movements such as lip-smacking
and lip-licking, protrusion of lips -as in pouting, protrusion
of tongue and mandible with uncoordinated movements
are mostly observed.
Correction of the denture occlusion may be effective
therapy. Anti-Parkinsonism drugs therapy can be effective
in some of the cases.
Granulomatous Disorders
Wegeners Granulomatosis
It is a disease of unknown etiology which basically involves
the vascular, renal and respiratory systems. It is a
granulomatous involvement of blood vessels resulting in
necrosis of tissue. It is generally thought that the disease is
aberrant hypersensitivity reaction to an unknown antigen.
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Types (Clinical)
Generalized or classic Wegeners granulomatosisit involve
upper respiratory tract, pulmonary and renal lesions.
Localized or limited Wegeners granulomatosisit affects
oral and nasal cavity and the lungs.
Superficial Wegeners granulomatosisit exhibits lesion
of skin and mucosa.
Clinical Features
Oral Manifestations
Onsetthe disease usually starts with tumor like
vegetations in mouth and nose (Fig. 33-12). Then
inflammatory process starts in the interdental papilla,
spreading rapidly in to the periodontium.
Ulcerationulceration can occur on any surface.
Ulceration is usually perforating in nature.
Radiological Features
Alveolar bonethere are often signs of alveolar bone loss.
Diagnosis
Clinical diagnosistypical strawberry gingivitis with
necrotic ulceration in the oral cavity.
Laboratory diagnosiscytoplasmic localization is present
with Wegeners granulomatosis. Histopathologically
chronic inflammatory cells and multinucleated giant
cells are found.
Differential Diagnosis
Agranulocytosis, leukemia, lymphomadiagnosis by blood
picture, possibly histology.
Management
Cotrimoxazoleit is combination of trimethoprim and
sulfamethoxazole. It has proved to be effective as an adjuvant or sole therapy in both localized and generalized
forms.
Corticosteroidsregimen of cyclophosphamide 12 mg/
kg body weight/day with prednisolone 1 mg/kg body
weight have been utilized to obtain complete remission.
Othersother treatment modalities includes cyclosporine, intravenous pooled immunoglobulin, and local
irradiation.
Sarcoidosis
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Diagnosis
Clinical diagnosissalivary gland involvement with
lymph nodes involvement with non-specific ulcer in the
oral cavity, aids in clinical diagnosis.
Kveim-Siltzbach testis an intracutaneous test for the
diagnosis of sarcoidosisKveim-Siltzbach test is
positive in some cases. In this test, intradermal injection
of a saline suspension of known human sarcoid tissue
used as an antigen is given to a patient suspected to
have sarcoidosis. One month after the injection, any
palpable nodule is excised and examined histologically
for evidence of a sarcoid reaction, or epithelial tubercle.
Laboratory diagnosisthere is increased serum angiotensin converting level. Histopathologically asteroid
bodies and Schumanns bodies are found.
Oral Manifestations
Management
Corticosteroidasymptomatic patient requires no treatment as the lesion may resolve in 2 years of duration. In
patient with symptoms corticosteroids can be given.
Refractory (does not respond to treatment) sarcoidosisin
this case methotrexate, azathioprine, chlorambucil and
cyclophosphamide is used.
Radiological Features
Etiology
Clinical Features
Ageit is more commonly seen in adults.
Sitecommonly involved sites are nose, palate, face and
pharynx.
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Management
Corticosteroidscorticosteroid therapy has proven
beneficial in some cases.
Radiation therapyradiation therapy of 5000 rad
appears to be a treatment modality, in which remission
of over 15 years is reported.
Clinical Features
Age and sexmajority of the patient are males, but
females are also commonly affected. It is commonly
found in children and infants.
Sitethere is widespread infection from infancy; usually
affecting lymph nodes, lung, liver, spleen, bone and skin.
Skin lesionskin lesions occur on face, leading to tissue
necrosis and granuloma formation.
Signsabscess, septicemia, pneumonia, pericarditis,
meningitis and osteomyelitis are common features.
Oral Manifestations
Diagnosis
Clinical diagnosedestructive lesion in the midline of
palate will diagnose this condition.
Laboratory diagnosisbiopsy shows extensive necrosis
with infiltration of some inflammatory cells and
formation of occasional new capillaries.
Diagnosis
Differential Diagnosis
Management
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Collagen Disorders
Scleroderma
It is also called as systemic sclerosis, or Hidebound disease. It
is rare collagen disorder, which is characterized by
hardening and tightening of the skin that can manifest as
either localized or systemic form. It is a disease which
involves connective tissue, blood vessels and lead to
fibrosis. It is also called as progressive systemic sclerosis.
Name is derived from sclerohard dermaskin.
Types
Systemic or progressive systemic sclerosisit is diffuse and
involves both skin and internal organ.
Localized formit involve the underlying muscle and
bone along with skin and subcutaneous tissue. It is of
two types:
Morpheait is circumscribed form and is
characterized by local changes limited to skin
Linearit affects face, scalp and frontoparietal region.
Etiology
An endocrine dysfunctionin some cases of endocrine
dysfunction mainly thyroid and parathyroid
disturbances can cause scleroderma.
Vascular diseasebasically an endarteritis obliterans,
resulting in decreased vascular supply.
Nervous disordersince skin lesion often follows the
distribution of nerves, nervous disorder may be causative
factor.
Toxic or infectious agentsshock or pneumonia,
influenza, diphtheria and exanthematous disease.
Allergic reactionan antigen-antibody type of reaction
is observed in scleroderma.
Environmental factorssuch as exposure to silica dust,
vinyl chloride, benzene and tryptophan.
Clinical Features
Progressive systemic sclerosis
Age and sexit generally begins in childhood or young
adult and greatest incidence is between 30 and 50 years
of age. Females are more commonly affected with a ratio
of 3:1.
Siteit usually begins on face, hand or trunk.
Oral Manifestations
Sitethe tongue, soft palate, lips and larynx are
commonly involved.
Appearancethese are characterized by mild edema,
which is followed by atrophy and induration of mucosal
and muscular tissue.
Mask like faciesinvolvement of facial skin results in
characteristic smooth, taut and masklike facies.
Mouse faciesnasal alae may become atrophied resulting
in pinched appearance to the nose resulting in mouse
species.
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Radiographic Features
Periodontal ligamentextreme widening of the
periodontal ligament, two to four times the normal
thickness, which is more prominent around posterior
teeth with intact lamina dura. The periodontal changes
are the direct result of changes within the membrane
due to the underlying disease.
Marginsborders of the lesions are smooth and sharply
defined.
Bone resorptionbone resorption occur usually at the
angle of mandible. It is bilateral and symmetrical.
Condylar involvementpartial or complete resorption of
condyle and coronoid process of the mandible, as a result
of abnormal muscle pull or pressure from soft tissues is
reported.
Management
D-penicillaminea drug has shown promise in the
management by decreasing both, the skin thickening
and organ involvement by interference with crosslinking of collagen and immunosuppression.
Extracorporeal photochemotherapyit is beneficial in skin
lesion.
Other therapyother therapy like angiotensin converting
enzyme inhibitor and calcium channel blocking agents
may control hypertension in the patient.
Dental managementthe mouth opening may be increased
by use of stretching exercises. Effective treatment of it is
to use an increasing number of tongue blades between
posterior teeth. If this is insufficient, bilateral removal of
commissure may be necessary. Patient with extensive
resorption of the angle of mandible is at risk of fracture
and should therefore avoid trauma.
Kawasaki Disease
Kawasaki disease, or mucocutaneous lymph node syndrome, is a vasculitis that affects medium and large arteries
with a corresponding cutaneous lymph node syndrome.
Clinical Features
Ageit most commonly occurs in children between
3 months and 12 years of age.
Symptomspatients present acutely with edema,
erythema of the hands and feet, fever and rash. The
associated temperature must exceed 38.5C (101.3F) for
5 days to meet diagnostic criteria.
Signsbilateral congestion of ocular conjunctiva,
indurative edema, erythema of palms, soles and
membranous desquamation of fingers and toes. There is
also polymorphous exanthema of torso without vesicles
or crusts.
Lymphadenopathyacute nonpurulent swelling of
cervical lymph nodes.
Cardiac sequelaecardiac sequelae to the vasculitis may
result in aneurysm and myocardial infarction.
Myocarditis commonly occurs within a week after the
fever. Within 2-3 weeks, the previously edematous palms
and soles peel and slough.
Diagnosis
Clinical diagnosisclaw like finger, ulceration in finger,
Raynauds phenomenon, shiny skin, tobacco pouch
mouth are typical features of this disease.
Oral Manifestations
Strawberry tonguestrawberry like reddening and
swelling of tongue papillae and diffuse reddening of
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Diagnosis
Clinical diagnosisfor diagnosis, 4 of the 5 following
criteria must also be met: (1) peripheral extremity edema,
erythema, or desquamation; (2) polymorphous exanthem; (3) bilateral conjunctival injection; (4) erythema
and strawberry tongue in the oral cavity; and (5) acute
cervical adenopathy.
Laboratory diagnosisthere is proteinuria, leukocytosis,
increased sedimentation rate and positive C-reactive
protein.
Fig. 33-14: Superficial red macule seen over the skin in case of
Pityriasis rosea ( Courtesy Dr Pincha).
Oral Manifestations
Skin Disorders
Pityriasis Rosea
Diagnosis
Management
Intravenous gammaglobulinit is the most effective
treatment in case of Kawasakis disease.
Other drugsaspirin or systemic steroids can also be
given in some cases.
Clinical Features
Age and sexit is more common in spring and autumn
and it involves young adults chiefly, with no sex
predilection.
Symptomsthe lesion often manifests mild headache
and low grade fever and cervical lymphadenopathy.
Primary lesionsthe generalized outbreak is frequently
preceded by the appearance of a primary lesion or
herald spot seven to ten days previously.
Appearanceit is characterized by the appearance of
superficial, light red macules or papules, generalized
over most of the skin surface (Fig. 33-14).
Sizethe spot is bright-red and larger (3 to 4 cm in
diameter) than the multiple eruptions which follow its
appearance.
Shapethe individual exanthematous lesion is
commonly ovoid, with long axis parallel to the natural
lines of cleavage of skin and are covered by a thin silvery
scales.
Management
It requires no treatment since the disease is self limiting
and generally undergoes rapid spontaneous regression.
Incontinentia Pigmenti
It is also called as Bloch-Sulzberger syndrome. It is transmitted
as sex-linked dominant trait.
Clinical Features
Age and sexit appears shortly after birth and exclusively
seen in females.
Appearanceit is characterized by the appearance of
erythematous and vesiculobullous lesions on the trunk
and extremities which frequently disappear and
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Clinical Staging
Vesicular stagevesiculobullous lesion seen in trunk and
limbs. Resolution within 4 months.
Verrucous stageverrucous cutaneous plaques develop.
Resolution by 6 months.
Hyperpigmentation stagebrown skin lesion with
swirling (twisting) pattern.
Atrophy and depigmentation stageatrophy and
depigmentation of skin can occur (Fig. 33-15).
Oral Manifestations
Siteboth the deciduous and permanent dentitions may
be affected.
Teeththere is delayed tooth eruption, peg and cone
shaped crowns, congenitally missing teeth, malformed
teeth and additional cusps.
Diagnosis
Clinical diagnosisdepigmentated or vesicular lesion
on trunk with cone shaped crown may suspect this
disease.
Laboratory diagnosisbiopsy shows intraepithelial
clefts filled with eosinophils. It may show melanin
containing macrophages.
Management
Dental managementdental defects can be corrected with
the assistance of orthodontics and prosthetic dentistry.
Acanthosis Nigricans
It is acquired dermatological disorders characterized by
velvety brownish discoloration of the skin.
Types
Benignit may be present at birth or occur later in
childhood; appears to be genetic in origin inherited as a
dominant characteristic.
Malignantit is associated with internal malignancy
like adenocarcinoma of stomach and occurs in older
age group.
Pseudoacanthosis nigricansit is most common and is
associated with endocrinopathy.
Clinical Features
Sitethe most common areas involved are axilla, palms
and soles and face and neck.
Appearanceskin lesions are symmetric with mild
hyperpigmentation and mild papillary hypertrophy of
only small patchy areas. In some cases, it is heavily
pigmented, aggressively verrucous lesion involving
much of the skin.
Symptomsthe verrucous lesions are often pigmented
and generalized pruritis is also a common finding.
Oral Manifestations
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Diagnosis
Clinical diagnosisbrownish alteration of skin velvety
white appearance of buccal mucosa may be diagnostic
features of scleroderma.
Laboratory diagnosisthere is marked acanthosis,
coupled with peculiar parakeratosis.
Diagnosis
Management
Management
Ehlers-Danlos Syndrome
Tuberous Sclerosis
It is also called as Epiloia-Bourneville syndrome. It is inherited
as autosomal dominant trait.
Clinical Features
Clinical Features
Hyperelasticitythere is hyperelasticity of skin, hyperextensibility of the joints and fragility of skin and blood
vessels, resulting in excessive bruising as well as
defective healing of skin wounds.
Rupture of large arteriesrupture of large arteries as well
as of intestine often occurs, producing a life threatening
situation.
Rubber manin some patients, skin extensibility is
pronounced, so that he can stretch the skin significantly.
It is called as rubber man.
Signshypertelorism, a wide nasal bridge, epicanthic
folds, protruding ears and frontal bossing are often
present.
Subcutaneous nodulesfreely movable subcutaneous
nodules are frequently found, which represent fibrosed
lobules of fat.
Papyraceous scarringthe scarring of skin following
wound healing in these patients is unusual, as the scars
tend to spread rather than contract in time. It resembles
crumpled cigarette paper.
Oral Manifestations
Oral mucosaoral mucosa is of normal color but is
excessively fragile and bruises easily.
Gingivathe gingival tissue appears fragile and bleeds
after toothbrushing.
Gorlin signit is positive in this patient. Patient can
touch its nose with the tip of tongue.
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Oral Manifestations
Enamel defectthere is developmental pitting defect on
facial aspect of permanent dentition.
Fibrous papuleit can also be present in this syndrome.
These are most commonly occur in anterior gingival
mucosa. In some cases diffuse gingival enlargement can
also occur.
Diagnosis
Management
Anticonvulsant agentsthese are given to manage seizure.
Maintenance of oral hygieneas phenytoin is given in
these cases, maintenance of oral hygiene is very important.
Seborrheic Keratosis
It is skin lesion which is characterized by benign
proliferation of epidermal basal cells.
Management
Cryotherapycryotherapy with liquid nitrogen is used
to remove the lesion.
Sebaceous Hyperplasia
It is localized proliferation of sebaceous gland of skin.
Clinical Features
Ageit is common in older age group and seen in fourth
decade of life.
Siteit is seen most commonly on facial skin in the region
of cheeks and forehead.
Symptomsit is usually painless.
Signsit is soft, nontender with yellow and white discoloration. There is small central depression which
represents area where duct of sebaceous gland terminated.
Compression testafter compression of lesion sebum
(thick yellow product) is expressed from sebaceous
gland.
Diagnosis
Clinical diagnosiscompression test showing sebum
from the lesion.
Laboratory diagnosisbiopsy shows collection of
enlarged sebaceous gland around the centrally located
sebaceous ducts.
Management
Clinical Features
Ageit is common in older age group and seen in fourth
decade of life.
Siteit is seen on face, trunk, and extremities.
Appearancethese are multiple, small tan to brown
macule which enlarge gradually. They appear as stuck
onto the skin.
Surfacesurface of lesion is fissured, pitted and
verrucous.
Sizesize is less than 2 cm in diameter.
Dermatosis papulosa nigrait is seen in black people and
is characterized by multiple, small dark brown papule
scattered in zygomatic and periorbital region.
Leser-Trelat signsudden appearance of seborrheic
keratosis with pruritis has been associated with internal
malignancy. This is called as Laser-Trelat sign.
Diagnosis
Clinical diagnosissmall brown papular lesion seen on
face and trunk will diagnose this condition.
Laboratory diagnosisthere is exophytic proliferation of
basilar epithelial cells with surface keratinization,
acanthosis and papillomatosis.
Actinic Lentigo
Lesion which occurs due to ultraviolet light damage to skin.
It is also called as lentigo solaris, solar lentigo, age spot, liver
spot and senile lentigo.
Clinical Features
Ageit is common in older age group, in the age group
of 40 to 70 years.
Siteit is common on dorsal surface of hand, face and
arms. Commonly seen in white people.
Appearanceit is multiple with individual lesion appear
as uniformly pigmented brown to tan macule with well
demarcated and irregular border.
Sizesize is less than 5 mm.
Diagnosis
Clinical diagnosisbrown to tan pigmented macule on
face may give clue to diagnosis
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Management
Topical retinoic acidthis can reduce the color intensity
of lesion.
LaserQ shaped ruby laser can be use for the treatment
of this lesion.
Melasma
It is symmetric hyperpigmentation of sun exposed skin,
face and neck. This is usually associated with pregnancy
so it is also called as mask of pregnancy.
Clinical Features
Ageit is seen in adult women.
Siteit is seen in midface, forehead, upper lip, and chin.
Appearanceit is bilateral, light to dark brown cutaneous
macule. Pigmentation may darken with time.
Sizesize range from few millimeter to 2 cm in diameter.
Diagnosis
Clinical diagnosisskin cancer in young individual will
give strong clue to diagnosis of Xeroderma pigmentosum.
Laboratory diagnosisbiopsy shows features of cutaneous
malignancies.
Management
Topical chemotherapeutic agentstopical chemotherapeutic agents 5-fluorouracil is used to treat actinic
keratosis.
Genetic counselingit should be done before marriage.
Preventionpatient is ask to avoid sun exposure, wear
protective clothing
Muscle Disorders
Muscular Dystrophy
It is genetically determined disease characterized by
degeneration of muscle leading to progressive weakness.
Diagnosis
Types
Xeroderma Pigmentosum
Clinical Features
Management
Clinical Features
Ageit occurs in early age group.
Symptomsthere is increased tendency to sunburn.
Patient also notices freckled pigmentation and patchy
depigmentation of skin. Patient also notices neurological
manifestation like below normal intelligence.
Actinic keratosisit is evident in early age group. These
lesions will change into basal cell carcinoma or
squamous cell carcinoma.
Oral featuressquamous cell carcinoma develops on
lower lip and tongue.
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Oral Manifestations
Locationthe muscles of mastication, facial ocular,
laryngeal and the pharyngeal muscles are usually
involved, only in the late course of disease.
Teethdue to lack of muscle tension, teeth cannot be
kept properly aligned in the arch.
Tapir-lipsthe lips develop a characteristic looseness
and protrusion, which have been described as tapirlips. The patient is unable to whistle or smile.
Open bite and diastemathere may be severe open bite
and development of diastema.
Temporomandibular jointlocking and clicking of the jaw.
Diagnosis
Clinical diagnosisthere is muscular weakness,
waddling gait, tapir-lip will give clue to diagnosis.
Laboratory diagnosisthere is gradual disappearance of
muscle fibers, as the disease progresses no fibers may be
recognized. Serum creatinine phosphokinase levels are
elevated in all males.
Diagnosis
Types
Management
Management
There is no treatment for this disease. Physical therapy
may help prolong the use of specific muscle group.
Myotonias
Hemifacial Spasm
It is a disease characterized by a repeated, rapid, painless,
irregular, nonrhythmic, uncontrollable, unilateral contraction of the facial muscles. It may occur due to compression
of the facial nerve, in the facial canal, adjacent to the
stylomastoid foramen.
Clinical Features
Clinical Features
Locationatrophy of the muscles is seen usually in the
hands and forearms. It can be seen in muscles of face,
jaws, neck and levator of eyelids.
Symptomsthere is associated weakness of the muscles.
Muscular contraction induces a severe, painless
muscular spasm, and an actually delay in relaxation.
Facial musclealteration in the facial muscles, which
consist of ptosis of the eyelids and atrophy of the masseter
and sternocleidomastoid muscles.
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Management
Decompression of the nervedecompression of the nerve
in its canal has offered relief in some cases. Prognosis is
good, remission and recurrence may occur over a period
of years.
Paramyotonia
It is a nonprogressive myotonia, inherited as an autosomal
dominant characteristic that is not associated with
muscular wasting. Characteristically, the cramping attacks
are precipitated on exposure to cold.
Clinical Features
Symptomsit is manifested by cramping, stiffness and
weakness of the muscles of the face and neck, fingers
and hands, upon exposure to cold. Muscles cramping
may disappear within an hour; the weakness may
persist for several days.
Mask-like appearancethe eyelids are closed and the face
assumes a mask-like appearance.
Tonguethe tongue may exhibit a similar cramping after
drinking cold liquids and the speech becomes blurred.
In many cases, myotonia of the tongue may be induced
by percussion.
Diagnosis
Clinical diagnosismasklike appearance seen in face.
Muscle cramping will disappear within hour after
exposure to cold.
Management
There is no specific treatment for it, but the prognosis is
excellent with frequent improvement during adult life.
Myasthenia Gravis
It is an autoimmune chronic disease characterized by
progressive weakness of the skeletal muscles, particularly
those innervated by the cranial nerves. It is characterized
by easy fatigability of the striated muscles secondary to
disorders at the neuromuscular junction. It affects acetylcholine receptors of muscle fibers resulting in fatigability
of skeletal muscle.
Etiology
Defective neuromuscular transmissionthere is a defect in
the neuromuscular transmission, which occurs due to
Clinical Features
Age and sexit occurs in adults in the middle age group
with a predilection for women.
Symptomsthere is rapidly developing weakness in
voluntary muscles, following even minute activities.
Patient may suffer from diplopia (double vision) and
ptosis (drooling eyelids) and extraocular muscular
paresis (an inability to focus the eyes) and dysarthria
(slurring of word).
Sorrowful appearance of facethere is dropping of the face,
leads to sorrowful appearance of the patient.
Signsthe neck muscles may be so weak that the head
can not be held up without support.
Progresspatients become exhausted, looses weight
becomes further weakened and may eventually become
bedridden. Death frequently occurs from respiratory
failure.
Oral Manifestations
Symptomsthe patients chief complains may be
difficulty in mastication, deglutition and dropping of
the jaw. Speech is often slow and slurred and
disturbance in taste sensation occurs. Dysphagia and
regurgitation of food are common.
Tonguethere may be weakness of the tongue and
palatal muscles. Protrusive movements of the tongue
may become weak leading, at times to posterior collapse
of the organ with airway obstruction.
Diagnosis
Clinical diagnosisptosis, diplopia, dysphagia, sorrowful appearance of face.
Laboratory diagnosiselevated serum AChr (acetylcholine) level. Biopsy shows focal collection of small
lymphocytes or lymphorrhages around small blood
vessels in the interstitial tissue of the affected muscles.
Management
Anticholinesterasespyridostigmine, edrophonium, and
neostigmine, administered intra-muscularly improve the
strength of the affected muscles few minutes.
Corticosteroidsthese can be use in combination with
cholinesterase inhibitors.
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Radiographic Features
Dermatomyositis
It is also called as polymyositis. It is an acute or a chronic
disease of unknown etiology and is characterized by
gradual onset with vague and indefinite prodromata,
followed by edema, dermatitis, myositis and sometimes
neuritis and mucositis.
Clinical Features
Age and sexit may occur in patients of any age ranging
from very young children to elderly, but majority occurs
in the 5th decade of life. There is no sex predilection.
Onsetit begins with erythematous skin eruptions,
edema, tenderness, swelling and weakness of the proximal muscles of limbs. Fever may be associated with it.
Progressthe weakness of muscle is progressive and
characteristically spreads to face, neck, larynx, pharynx
and heart.
Skinthe skin becomes the seat of violaceous erythema
and edema with a predilection for the eyelids, malar
area and dorsa of hands. The typical skin lesions include
heliotrope (liac-colored) changes around the face and
fingers.
Signsthe edema which gives the skin a puffy
consistency including the face, leaves a reticulated
telangiectatic erythema when it subsides.
Calcinosis cutisthe skin lesions frequently calcify and
form calcium carbonate nodules with a foreign body
reaction which is known as calcinosis cutis.
Calcinosis universalisthe term calcinosis universalis is
applied when these calcified masses are found
generalized throughout the soft tissues.
Prognosismuscle involvement may become severe
enough to confine the patient to bed or cause death
owing to failure of respiratory muscle.
Oral Manifestations
Diffuse stomatitis and pharyngitisthe oral lesions consist
of diffuse stomatitis and pharyngitis and are extremely
common.
Symptomsinvolvement of the muscles of jaw, tongue and
pharynx may pose problems in eating and phonation.
Oral mucosathe oral mucosa may show dark red or
bluish erythema.
Tonguein the early stages, tongue is swollen and later
becomes harder and gradually it becomes atrophic. The
tongue may become rigid owing to severe calcinosis.
Pulp calcificationthere is severe calcification and obliteration of pulp chambers of deciduous and permanent
teeth.
Diagnosis
Clinical diagnosisheliotrope lesion with dark red oral
mucosa, calcinosis cutis will give clue to the diagnosis.
Radiological diagnosispulp calcification and
obliteration is present.
Laboratory diagnosisthe muscle fibers in dermatomyositis exhibit widespread degeneration and hyalinization.
Many fibers show vacuolization, granulation and
fragmentation with phagocytosis of disintegrating fibers.
There is also mild anemia or leukocytosis. In addition,
creatinuria is a constant finding as well as elevated levels
of serum transaminase and aldolase.
Management
Corticosteroidscorticosteroid should be given but its
effectiveness is doubted.
Immunological Disorders
Primary Immune Deficiency
These are hereditary abnormalities characterized by an
inborn defect of the immune system. These diseases may
involve the B-cell system, T-cell system or a defect in both.
Types
Sex linked agammaglobulinemia- it is caused by a defect
in B-cell function with the T-cell function remaining
intact. Due to this, these patients slack the ability to
synthesize all classes of antibodies including the
secretory immunoglobulin, making them more
susceptible to bacterial infection. The symptoms begin
at 6 months of age.
Primary adult immunoglobulin deficiencyit is characterized by an abnormality of the B-cell or humoral
antibody system that does not become clinically
apparent until adulthood. Usually one or two Ig classes
are deficient. The selective deficiency accounts for the
relatively asymptomatic nature of the disease throughout
childhood.
Thymic hypoplasiait consists of DiGeorges syndrome
and Nezelofs syndrome. These patients have normal
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Clinical Features
Sex-linked agammaglobulinemiapatients experience
severe recurrent bacterial infections of lungs, meninges,
skin and sinuses. There is hypoplasia of lymph nodes,
adenoid and tonsils. There is increased incidence of
rheumatoid arthritis, dermatomyositis, lymphoma and
leukemia.
Primary adults immunoglobulin deficiencythe most
common symptoms include recurrent gram-positive
bacterial infections of upper and lower respiratory tracts.
Thymic hypoplasiathere is increased susceptibility to
infections with virus and fungi. Infection with Candida
albicans is especially prominent.
Severe combine immunodeficiencysymptoms begin in first
few week of life and include bacterial, viral and fungal
infections. Localized and systemic candidiasis is
common. The patient dies of overwhelming infections
during the first year of life, unless a histocompatible
relative is found for a bone marrow transplant.
Immunodeficiency with ataxia telangiectasiatelangiectasia of the skin and eyes becomes apparent at about
3 years of age. The lesion becomes more extensive with
age and mainly occurs on conjunctiva, ears and malar
eminences. These are also associated with Gonadal
dysgenesis and increased incidence of malignancies of
lymphoreticular system.
Oral Manifestations
Infectionin T-cell deficiency, there may be chronic oral
candidiasis and herpes simplex infection. In B-cell
deficiency, there are recurrent bacterial infections and
chronic maxillary sinusitis.
Diagnosis
Clinical diagnosisincrease susceptibility to infection
and severe recurrent infection will suspect immune
deficiency.
Management
Control of local infectionminimize the chances of local
infection or septicemia and oral candidiasis, treated with
antifungal therapy, prior to dental treatment.
Concentrated human gamma globulinpatient with
symptomatic B-cell abnormalities are usually given
continuous therapy with concentrated human gamma
globulin. When oral surgery is necessary, an extra dose
of gamma globulin should be administrated the day
before surgery.
Blood replacement therapypatients with B cell deficiency
resulting in the absence of particular immunoglobulin
may experience severe transfusion reaction when
receiving blood from a patient who has normal
immunoglobulin levels. The immunoglobulin acts as a
foreign protein and causes an allergic response. For
these reasons, patient with selective IgA deficiency must
be given IgA depleted blood in blood replacement
therapy.
Miscellaneous Conditions
Drug Allergy
Allergy or hypersensitivity is an unwanted response of the
body to the complete dose of drug.
Mechanism
Formation of antibodya patient previously exposed to a
drug or other antigen has antibody, primarily IgE, fixed
to basophils and mast cells.
Releasing of active mediatorswhen the antigen in the
form of a drug, food or airborne substance is reintroduced
into the body it will react with the fixed antibody, bind
complement and open the mast cells releasing active
mediators such as histamine and slow reactive
substance of anaphylaxis.
Vasodilation and increases capillary permeabilitythese
substances cause vasodilation and increased capillary
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Clinical Features
Localized anaphylaxis
Urticariawhen it involves the superficial blood vessels,
urticaria (hives). It begins with pruritus in the area of
release of histamine and other active substances.
Skinwheals (welts) then appear on the skin as an area
of localized edema on an erythematous base.
Edemathere is also macular papular or nodular rash
with edema of skin and subcutaneous tissue.
Angioneurotic edema
Causesit can be caused by contact with an allergen or
can be idiopathic. A recurrent form is inherited as an
autosomal dominant trait. There is deficiency of an
alpha-2 globulin, which normally acts as an inhibitor of
the first component of complement and kallikrein.
LocationsAngioneurotic edema of lips, tongue, eyelids,
larynx and bronchi may occur.
Appearancein angioneurotic edema, when deeper
blood vessels in the subcutaneous tissue are affected, a
large diffuse area of subcutaneous swelling is produced
under the normal overlying skin.
Respirationit is temporarily disfiguring, but not serious,
unless the posterior portion of the tongue or larynx
compromise respiration.
Serum sickness
Causesit frequently occurs after administration of
foreign serum, which before antibiotics, was given for
the treatment of infectious disease. It occurs from tetanus
antitoxin, rabies antiserum and drugs that combine with
body proteins to form allergens.
Mechanismin it, antibodies form immune complexes
in blood vessels with administrated antigens. The
complexes fix complement, which attract the leukocytes
to the area causing direct tissue injury.
Symptomsmajor symptoms consist of fever, swelling,
lymphadenopathy, joint and muscle pain and rash.
Signsless common manifestation include peripheral
neuritis, kidney disease and myocardial ischemia.
Generalized anaphylaxis
Mechanismit is an allergic emergency with no time to
call consultants. It is reaction of IgE antibodies with an
allergen, causing the release of histamine, bradykinin
and SRS-A (slow reacting substance of anaphylaxis).
These chemical mediators cause contraction of smooth
Management
Cutaneous rashesoral administration or injection of
chlorpheniramine, intramuscularly.
Angioneurotic edemathe patients respiratory distress
should be treated immediately with 0.5 ml epinephrine,
1:1000 subcutaneously or 0.2 ml injected slowly
intravenously. When immediate danger is passed, then
50 mg of diphenhydramine hydrochloride should be
given 4 times daily, until the swelling is diminished.
Severe symptomsinjection hydrocortisone sodium
succinate or injection epinephrine.
Serum sicknessIt is self-limiting with spontaneous
recovery within 1 to 3 weeks. Other treatment is symptomatic with aspirin, for arthralgia and antihistamines,
for skin rashes.
Anaphylactic reaction with sudden cardiovascular and
respiratory collapse can be treated by following method: Make the patient to lie down in supine position.
Patent airway is to be maintained.
Administer 100% O2.
Injection epinephrine 1.1000 IM. It should be given if
the blood pressure falls below 60 mm of Hg.
For bronchospasm, slowly inject aminophylline 250
mg IV over a period of 10 minutes. Too rapid
administration can lead to fatal cardiac arrhythmias.
Start IV infusion stat.
Monitor pulse, blood pressure and respiration.
Hydrocortisone 100 mg IV.
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Syncope
It is also called as simple faint, swoon, psychogenic syncope,
and vasodepressor syncope. It is a transient loss of
consciousness due to cerebral anoxia.
Causes
Young and poor health personit is commonly seen in
younger individuals and people having poor health.
Precipitating factorsthe other factors are anxiety, fear,
and sight of blood, pain, exhaustion, fasting and hot
environment. These emotional stresses induce release
of increased amount of catecholamine.
Cerebral anoxiathe chief cause is cerebral anoxia or
anemia. A blood loss of one liter will cause fainting.
Clinical Features
Presyncopevictim falls gently to the floor, regains
consciousness almost immediately or within a short
period of time, appears to recover completely.
Early signs and symptomsthe patient complains for
warmth in the neck and face. He bathes in beads of cold
sweat. He also complains of nausea and feeling vague.
Blood pressure at this time is at baseline or slightly lower
than baseline. There is also rapid heart rate. Face is pale
or has ashen gray skin tone.
Late signs and symptomsas the process continues
papillary dilation, yawning, hyperpnea, coldness in
hand and feet, hypotension, bradycardia, visual
disturbances, dizziness and loss of consciousness occur.
Syncopewith loss of consciousness, breathing may
become irregular, jerky and gasping. The pupils of eye
dilate and patient has deathlike appearance. Convulsive
movements or muscular twitching of hands, legs or
facial muscle. Blood pressure is low and pulse rate is
also decrease.
Post syncopewith proper positioning, recovery usually
appears rapidly. Patient exhibits pallor, nausea,
weakness and sweating, which may persist for few
minutes to few hours.
Shock
If the primary shock or syncope is not tackled and allowed
to persist, the secondary or true shock appears. Shock
can be hemorrhagic, hypovolemic, septic, anaphylactic
shock.
Clinical Features
Management
Supine positionwhen there are signs of fainting he/
she should be made to lie down in supine position with
legs raised to improve venous return to the heart (Fig.
33-17). In case of patient being on the dental chair the
back of the chair should be immediately lowered so that
the head of the patient is at a lower level than the feet.
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Management
Suggested Reading
1. Academy report. Periodontal management of patients with
cardiovascular disease. J Periodontal 2002;73:954-68.
2. Alexandridis C, White SC. Periodontal ligament changes in patients
with progressive systemic sclerosis. Oral Surg 1984; 58:113-8.
3. Allen CM, et al. Wegeners granulomatosis: report of three cases
with oral lesions. J Oral Maxillofac Surg 1991;49:294-8.
4. Auluck A, Pai K. Progressive hemifacial atrophy with morphea of
cheek. JIAOMR 2006;18(3):172-5.
5. Bader JD, Bonito AJ, Shugars DA. A systemic review of
cardiovascular effects of epinephrine on hypertensive dental patient.
Oral Surg, Oral Med, Oral Pathol, Oral Radiol 2002; 93:647-53.
6. Bali RK, Chhabra N, Zarina. Freys syndrome as a sequelae of
superficial parotidectomy JIAOMR 2006;18(3):181-3.
7. Bartlett DW, Evans DF, Anggiansah A, Smith BG. A study of the
association between gastro-oesophageal reflux and palatal dental
erosion. Br Dent J 1996 Aug 24;181(4):125-31.
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34
4
Diseases of Bone
Manifested in Jaw
Introduction
Second Classification
Fibro-osseous Lesions
In it, normal bone is replaced by benign fibrous tissue
showing varying amounts of mineralization. The subject
of benign fibro-osseous enlargement of the jaws has many
facets, the most sinister of which is the possibility that a
healthy good looking person may take on a monstrous
appearance.
Classification
Fibro-osseous Lesions of
Medullary Bone Origin
First Classification
Fibrous Dysplasia
Etiopathogenesis
DevelopmentalJaffe and Lichtenstein considered it as
a developmental anomaly caused by aberrant activity
in the bone forming mesenchymal tissue. Most theories
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Classification
First classification
Monostotic fibrous dysplasiain it, only one bone is
involved.
Polyostotic fibrous dysplasiain it, more than one bone is
involved
Jaffe typefibrous dysplasia involving variable
number of bone, accompanied by pigmented lesions
of the skin or Caf-au-Lait spots.
Albrights syndromea severe form of fibrous
dysplasia involving nearly all the bones in the body,
accompanied by pigmented lesions of the skin plus
endocrine disturbances of various types.
Clinical Features
Monostotic fibrous dysplasia
Age and sexfibrous dysplasia discovered in young
patients, usually in children younger than 10 years
affecting both the sexes equally.
Sitesmonostotic fibrous dysplasia involves only one
bone and presents no extra-skeletal effects, other than
occasional pigmented skin lesions. Most frequent sites
are ribs, femur, maxilla and mandible.
Appearanceswelling is seen on affected site (Fig. 34-1).
McCune-Albrights syndrome
SexAlbrights syndrome is exclusively found in
females.
FeaturesAlbrights syndrome, in addition show,
endocrinal disturbances like precocious puberty, goiter,
hyperthyroidism, hyperparathyroidism, Cushings
syndrome and acromegaly.
Caf au lait spotthese are coffee with milk color spot.
There is irregular flat area of increased skin pigmentation.
Symptomsvaginal bleeding has been noted.
Signssecondary sexual characteristics such as pubic
and axillary hair and development of breasts are evident
by the age of 5 years. It may result in crippling deformities
or fracture
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Oral Manifestations
Monostotic
Sitesmaxilla (Fig. 34-2) is more commonly affected than
mandible, with most changes occurring in the posterior
region. Most common area involved is premolar-molar
area.
Fig. 34-4: Malalignment of teeth seen in upper arch on right side due
to fibrous dysplasia (Courtesy Dr Ashok L).
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Fig. 34-6: Mixed type lesion seen in fibrous dysplasia,
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Diagnosis
Clinical diagnosispainless swelling seen in the
maxillary region with intact mucosa. Caf au lait spots
are seen.
Radiological featuresground glass appearance, granular
appearance is seen.
Laboratory diagnosiswhen the polyostotic lesions are
numerous and active, the serum alkaline phosphatase
levels may be elevated in 50% of the cases. Biopsy shows
bone made up of proliferating fibroblast in a compact
stroma of interlacing collagen fibers. Irregular trabeculae
of bone are scattered throughout the lesion, with no
definite pattern of arrangement. Some of these trabeculae
are C-shaped and described as Chinese character
shaped.
Differential Diagnosis
Lesions are likely to be confused in the osteolytic stage of
fibrous dysplasia
Central giant cell granulomait has got faint wispy
trabeculae coursing through it whereas internal
calcifications may occur in fibrous dysplasia and appear
to be stippled and granular appearance.
Traumatic bone cystthere is no cortical bulging and
displacement of teeth.
Dental cystit has a thin, well defined cortex which is
smooth, while in fibrous dysplasia, cortex tends to be
wider and more granular in appearance.
Aneurysmal bone cystthere is hemorrhagic aspirate.
Chronic osteitisit is always associated with the roots of
pulp less teeth.
Chronic osteomyelitisit manifests itself in older age
group (30-80 years) as compared to fibrous dysplasia
(10-20 years). In addition, patients with osteomyelitis
will give a history of trauma, fracture or any debilitating
systemic disease.
Peripheral and central squamous cell carcinomait also
occurs in older age group and shows a predilection for
mandible. Fibrous dysplasia grows by slow expansion
whereas central and peripheral squamous carcinoma
spreads rapidly.
Metastatic tumorseen in older age groups and shows a
predilection for premolar-molar region of mandible.
Reticular cell sarcoma and Ewings sarcoma are rarely seen
in maxilla.
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Management
Surgicalsurgical removal of the lesion should be carried
out.
Osseous contouringit is necessary for correcting the
deformity for esthetics or pre-esthetic purposes.
Classification
Slootweg and colleagues have separated the lesions into
two distinct groups:
Juvenile ossifying fibroma WHO typeit occurs
predominantly in the maxilla and mandible. Here, the
designation of juvenile ossifying fibroma should be
restricted exclusively to those lesions whose histomorphology is consistent with that described in the 1992
WHO monograph on jaw lesions. This trabecular
variant has strands of immature cellular osteoid within
the lesion and usually occurs in childhood with a slight
maxillary predilection.
Juvenile ossifying fibroma with psammoma like ossiclesit
occurs in the paranasal sinuses and extragnathic bones.
The psammomatoid variant has small spherical ossicles
surrounded by osteoid rims within the lesion. It occurs
over a wider age range than the trabecular variant and
usually affects the orbit or paranasal sinuses.
Radiographic Features
Internal structureit may appear as unilocular or
multilocular lesion.
Appearanceit may be radiolucent or show mixed
appearance containing radiopaque foci (Fig. 34-11).
Marginit has got distinct radiopaque border.
Clinical Features
Ageit is seen under the age of 15 years.
Siteno site predilection and with equal frequency in
both the jaws. Although there is report that this is more
commonly found in maxillary region.
Symptomsthe presenting clinical symptom is of
swelling (Fig. 34-10).
Effect on surrounding structureneoplasm can impinge
on neighboring structure. Due to impingement, patient
may noticed nasal obstruction, exophthalmos and proptosis. In some cases, permanent blindness may occur.
Intracranial extensionin some cases, meningitis may
arise due to intracranial extension.
Diagnosis
Clinical diagnosisit is not possible to make clinical
diagnosis.
Radiological diagnosismixed lesion in young patient
will give clue to the diagnosis.
Laboratory diagnosisbiopsy shows non-encapsulated
lesion. There are also myxomatous foci, nuclear
crowding, and multinucleated osteoclasts.
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Clinical Features
Management
Excisioncomplete local excision of tumor is the
treatment of choice.
Cherubism
It is also known as familial fibrous dysplasia of the jaws,
disseminated juvenile fibrous dysplasia, familial multilocular
cystic disease of the jaws and Hereditary fibrous dysplasia of
the jaws. Above terms of cherubism are related to fibrous
dysplasia but there is no similarity between fibrous
dysplasia and cherubism so, this term should be avoided.
The clinical entity was first described by Jones in 1933
who coined the term Cherubism reflecting the characteristic of chubby facial appearance similar to plump cheeked
little angle (cherubs) seen in Renaissance painting. It is
autosomal dominant inherited fibro-osseous disease that
affects only the jaws causing bony expansion.
Classification
It depends on the severity and location of the lesion and
the extent to which jaws are affected.
Grade Ithe fibro-osseous expansion tends to be bilateral
and symmetrical. It is primarily in the ramus of the
mandible.
Grade IIin more severe cases, the ramus and the body
of the mandible are involved resulting in congenital
absence of the third and occasionally the second
mandibular molar teeth. In this group, the tuberosity
region of the maxillae is also affected.
Grade IIIin these cases, the lesions affect the mandible
and maxilla entirely and may result in considerable
facial deformities.
Etiology
Developmental defectanomalous development of dental
structures with disturbance in the development of bone
forming mesenchyme may lead to this condition.
Hormonalcherubism can be present in latent hyperparathyroidism and hormone dependent benign
neoplasm.
Otherother factors which are responsible for
cherubism are trauma and an aberration in ossification.
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Jawsbilateral enlargement of mandible in this condition produces full, round lower face. Bilateral enlargement of maxilla gradually follows.
Eye raised to heavenpulling or stretching of skin of the
cheek, depresses the lower eyelid, exposing a thin line
of sclera and resulting in the so called eyes raised to
heaven look.
Orbital floortumor encroachment on the orbital floor
often causes partial obliteration of the palatal vault with
resulting V shaped cleft.
Alveolar processthe alveolar process are so wide, as to
occupy almost the whole of the roof of the mouth; the
actual palate being reduced to a narrow fissure between
the two approximating alveolar process.
Lymph nodesthere may be enlargement of submandibular lymph nodes.
Progressthere is rapid increase in size up to 7-8 years
of age, after which the lesions become static or progress
very slowly until puberty. After puberty the maxillary
lesions tend to regress. The mandibular lesions progress
slowly up to the age of 20 years and then regress; the
facial appearance almost returns to normal in the 4th
and 5th decades of life.
Teeththe fibrous replacement of bone displaces the
deciduous dentition. The primary teeth may be irregularly spaced and some may be absent. There is
premature loss of primary teeth. The developing
permanent teeth are affected, giving rise to displaced
unerupted or absent teeth along with malocclusion.
Radiographic Features
Radiodensitycyst like radiolucency of mandible, bilaterally symmetrical which is up to several centimeters
in diameter.
Progressinitiation of bone destruction near the angle of
the mandible with later expansion of lesions posteriorly
into ramus and anteriorly into the mandibular body.
Appearanceit appears as a classic multilocular cavity
due to internal radiopaque septa, which tends to coalesce
as they enlarge. On posteroanterior views, teeth are seen
to be hanging in air.
Marginsthey are well defined, well corticated and
smooth around most of the radiolucency.
Effect on surrounding structurethere is also expansion of
buccal and lingual cortical plates (Fig. 34-14). In mandible,
the inferior alveolar canal may be displaced and the
lesion may occupy alveolar process, the angle and the
ramus. The thin cortex may eventually disappear.
Maxillary lesions enlarge at the expense of maxillary
sinus.
Effect on teethdisplacement of numerous teeth but prior
to enamel calcification. Erupted deciduous teeth in the
Diagnosis
Clinical diagnosistypical cherubic appearance of child
with bilateral swelling in the jaw
Radiological diagnosiscyst like radiolucency present
bilateral in the mandible
Laboratory diagnosisin active cases, serum alkaline
levels may be raised. Biopsy shows large multinucleated
giant cell in a loose delicate fibrillar connective tissue
stroma.
Differential Diagnosis
Fibrous dysplasiacherubism is bilateral.
Giant cell granuloma- it occurs frequently in the anterior
segment of mandible in contrast to cherubic lesions,
which are seen in the posterior part of mandible.
ABCthe lesions of ABC are tender, whereas cherubic
lesions are painless.
Central hemangiomathere is localized gingival bleeding
and pumping tooth syndrome.
Giant cell lesions of hyperthyroidismare not bilateral and
they can be differentiated on abnormal blood chemistry
levels.
Metastatic tumorsit is seen in older age group as compared to cherubism and also there will be signs and symptoms or history of primary tumor elsewhere in the body.
Ameloblastomait is seen unilaterally and frequently in
an older age group than that of cherubism
Odontogenic myxomahistory of missing tooth, as it is of
developmental origin.
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Management
Surgical contouringsurgical procedures should be
delayed, as long as possible, as the cystic lesion defect
usually becomes static and regresses during adulthood.
Occasionally, surgical contouring of the lesions is
necessary to improve esthetics and in case of active
growth.
Homogeneous bone graftsin cases of extensive
involvement, homogeneous bone grafts can be given to
prevent pathological fractures of mandible.
Orthodontic careorthodontic care may be required to
ensure proper alignment of the teeth.
Calcitoninthis therapy is under trial nowadays,
awaiting results of some study.
Radiographic Features
Radiodensitysolitary unilocular (Fig. 34-15) or multilocular radiolucency.
4
Fig. 34-15: Unilocular radiolucency seen in mandibular anterior region.
Types
Non-aggressiveit exhibits slow growing benign
behavior.
Aggressiveit shows typical features of rapidly growing,
destructive lesion.
Clinical Features
Agelesion of adolescent and young adult with 60%
cases in younger than 20 years and 74% cases in younger
than 30 years.
Sitesmandible is twice as frequently involved than
maxilla, with anterior half showing greatest incidence
with fairly high percentage crossing the symphysis. The
commonest site being the anterior and bicuspid region
in mandible and the canine fossa and ethmoid region in
maxilla.
Symptomsthe earliest sign of the lesion may be
expansion of bone with premature loosening and
shedding of deciduous teeth. There is jaw swelling
associated with facial asymmetry. Usually painless, but
local discomfort may be noted.
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Diagnosis
Differential Diagnosis
Ameloblastomait is uncommon in a younger age
range, which is most susceptible to giant cell granuloma.
Seen in posterior mandible in contrast to giant cell
granuloma which occurs anterior to the first molar.
Ameloblastoma demonstrates internal, hard curved
arch like septa whereas giant cell granuloma has
lighter wispy septa. Ameloblastoma is usually multiloculated.
Aneurysmal bone cystit does not occur in anterior
segment of mandible. Aspiration produces blood.
Odontogenic myxomamultiloculated and typical honeycomb appearance. Missing or impacted tooth is usually
a finding.
Giant cell tumorit is described in Table 34.1
Traumatic bone cystno bodily movement of teeth is
present. No expansion of overlying bone cortex.
Fluid filled odontogenic cystinternal septa are not
present. No bony spicules protrude from radiographic
margins. Regular smooth bony expansion of cortical
plates while scalloped, undulating bulging of cortex.
Brown tumors of hyperthyroidismserum calcium levels
are elevated.
Cherubismit is bilateral in the posterior part of
mandible and there is history of familial involvement. It
does not cross the midline.
Metastatic tumorsit is seen in older age groups and
also predominant lesions are multilocular with history
and symptoms of primary tumor in addition to local
lesions.
Central hemangiomait shows localized bleeding around
the necks of teeth and also the pumping tooth syndrome.
Post extraction socket, surgical defect and residual cystit
can mimic unilocular appearance of central giant cell
granuloma. Patients with surgical defect will give a
history of previous surgery and history of extraction in
residual cyst and post extraction socket.
Table 34.1: Difference between giant cell tumor and giant cell granuloma
It is preceded by trauma
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Pagets Disease
It is also called as osteitis deformans. It was discovered in
1877 by Sir James Paget. It fondly refers to as collage of
matrix madness. There is abnormal resorption and
apposition of bone in one or more bones. The disease is
initiated by an intense wave of osteolytic activity with
resorption of normal bone resulting in irregularly shaped
resorption cavity followed by vigorous osteoblastic activity
forming woven bone after variable period.
Etiology
Inflammatoryinitially it is thought to be inflammatory
disease, but later on this cause is ruled out.
Circulatory disturbancethe bone in Pagets disease is
excessively vascular and it has been suggested that
vessels are similar to arteriovenous aneurysms.
Slow virus theoryslow viruses are those viruses which
take a long time for incubation. The possibility of an
infective, viral Etiology for Pagets disease is suggested
by ultra-structural demonstration of intra-nuclear
inclusions in abnormal osteoclast.
Genetic and environmental factorsgenetic and environmental factors appear to be important. It is transmitted
as autosomal dominant trait with genetic heterogeneity.
Connective tissue factorsit may be a disorder of
connective tissue biosynthesis.
Othersvasculitis, trauma, hormonal imbalance,
degenerative neurologic disorders.
Clinical Features
Geographical prevalenceit is seen most frequently in
Britain and less frequently in North America and
Western Europe.
Age and sexpredominantly in patients over 40 years of
age with a slight predilection for men. Male to female
ratio is 2:1.
Oral Manifestations
Sitesmaxilla is involved three times more commonly
than mandible. It is bilaterally symmetrical in the
involved jaw.
Symptomsmovement and migration of affected teeth
occurs. Due to migration patient may noticed malocclusion. In case of edentulous patient as alveolar ridge
becomes enlarged patient complaint of poor fit of denture.
Signsincrease in alveolar width associated with
flattening of palate when maxilla is involved (Fig.
34-18).
Appearanceas the disease progresses, the mouth may
remain open exposing the teeth as the lips are too small
to cover the enlarged jaws.
Extraction sitesextraction sites heal slowly and
incidences of osteomyelitis are higher. Extraction may
be further complicated by excessive bleeding from highly
vascular abnormal bones in the lytic phase of disease.
Complicationsosteogenic sarcoma, osteomyelitis,
pathological fracture and facial paralysis. Sarcoma is
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Radiographic Features
Early radiolucent stage
Appearanceinferior cortex of mandible may appear
osteoporotic and possess a laminated structure.
Trabecular arrangementbone pattern in which trabeculae
though reduced in number, run linearly in the direction
of length of bone and have few intersections between
them. This appearance is most commonly seen posterior
to bicuspid. In the anterior region, the bony trabeculae
are coarse and relatively straighter than normal, but they
intersect producing bone spaces that are larger than
normal. Coarse and sparse trabeculae, sometimes, tend
to converge towards the midline of mandible which is
highly suggestive of Pagets disease. In this stage, inferior
border of the mandible may appear osteoporotic and
have a laminated structure.
Effect on rootroot resorption is common.
Osteoporosis circumscriptain the skull, early lytic lesion
may be seen as discrete radiolucent areas termed as
osteoporosis circumscripta. The margins are somewhat
irregular. There is appearance of denser bone around
the radiolucency.
Lincolns sign or black beardthis sign is present in bone
Scintigraphy. Bone scan may demonstrate marked
uptake throughout the entire mandible. This is called as
Lincolns sign or black beard.
Granular or ground glass appearance
Radiopaque patchesthere are rounded radiopaque
patches of abnormal bone of greater density within the
Diagnosis
Clinical diagnosisin this simian appearance, enlargement of skull, bowing of leg and bone pain may give
clue to the diagnosis.
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Differential Diagnosis
Early stageradiolucent appearance
Giant cell lesions of hyperparathyroidismin Pagets
disease, there is an increase in serum alkaline phosphatase only whereas in Giant cell lesions of hyperparathyroidism there is elevation of serum alkaline
phosphatase as well as serum calcium levels with
decrease in serum phosphate levels. Also in case of
hyperparathyroidism, there is overall radiolucency.
Osteoporosisin early stages, it may be confused with
Pagets disease but if the bony area in question is
pathologically enlarged and if straight linear trabeculae
are seen in the affected bone parallel to the long axis,
osteoporosis is ruled out. Blood chemistry is normal.
Osteomalaciapseudofractures are common in cases of
osteomalacia. Serum calcium and serum phosphorus
levels are decreased in osteomalacia whereas in Pagets
disease, they are normal.
Multiple myelomait causes painful enlargement of
the jaws and shows typical radiolucent punched out
lesions on the skull radiograph. Positive test for Bence
Jones proteins.
Second stagemixed radiolucent radiopaque appearance
Osteogenic sarcomait occurs in a younger age group
(10-40) than that of Pagets disease and it shows a variety
of radiographic appearance i.e. sunburst and Codmans
triangle.
Cementifying and ossifying fibromait is predominately
seen in the younger age group and they show well defined
margins in contrast to that of Pagets disease which is
diffuse.
Fibrous dysplasiaage difference, Pagets disease spreads
more diffusely, seen bilaterally, cotton wool appearance.
Maxillary sinus is reduced in size in the case of fibrous
dysplasia but in the case of Pagets disease, it fails to
reduce the air space.
Osteoblastic metastatic carcinomait will give a history of
parent tumor or show signs and symptoms of primary
tumor.
Ossifying sub-periosteal hematomait can be excluded if
the patient gives a recent history of trauma and in
addition it is seen in patients less than 15 years of age.
Management
Medical
Calcitonina parathyroid hormone antagonist
produced by the thyroid gland, suppresses bone
resorption and also relieves pain and decrease serum
alkaline.
Sodium phosphateit retards bone resorption.
Bisphosphonatesthey have also been used, since they
inhibit bone resorption as well as mineralization.
Bisphosphonates which are used are etidronate,
pamidronate, alendronate, tiludronate or risedronate.
Mithramycinit is considered as a second line agent
due to its toxicity; is cytotoxic to osteoclasts.
Plicamycinit inhibits osteoclastic activity
Surgerysurgical approach for esthetics correction
should be carried out.
Radiationin some cases radiation therapy can be
useful.
Fibro-osseous Lesions of
Periodontal Origin
Periapical Cemental Dysplasia
It is described in Chapter 14: Odontogenic Tumor of Jaw.
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Clinical Features
Radiographic Features
Locationlesions of florid osseous dysplasia present
bilaterally in both the jaws. Lesions occur above the
inferior alveolar nerve canal. It involves all four quadrants.
Radiodensityit varies from an equal mixture of
radiolucent and radiopaque region to almost complete
radiopaque.
Sizeindividual lesions do not exceed 2-3 cm in
diameter. The lesions may extend into the mandibular
ramus or into the maxillary sinus.
Marginsmargins are fairly regular and well defined.
Each lesion is surrounded by a radiolucent capsule and
a cortical rim.
Radiolucent stagein this stage, well defined radiolucent
area are superimposed over the apical area of adjacent
tooth.
Mixed stagein this stage radiolucent cavity, partially
filled with one or more dense radiopaque masses. As
lesions mature, the radiopacities increase. This stage
also shows target appearance with central calcified masses
in the radiolucent lesion.
Radiopaque stagethis shows multiple radiopacity
continuous with the surrounding bone, but they were
separated from adjacent teeth periodontal ligament
space. In this stage cotton wool appearance (lobular or lump
shaped and soft radiopaque characters like that of cotton
wool) is seen.
Active hypercementosishypercementosis of tooth in the
affected area is seen. There is an also wide periodontal
ligament space.
Differential Diagnosis
Pagets diseaseno radiolucent capsule and increased
serum alkaline phosphatase levels. Pagets disease
affects entire mandible while florid osseous dysplasia
occur above the inferior alveolar canal.
Chronic sclerosing osteomyelitissigns of infection is
present in osteomyelitis.
Osteopetrosisprofuse thickening of the skull base or
calvarium and diffuse bony radiopacities. It will cause
enlargement of bone, which is not a feature of florid
osseous dysplasia.
Diagnosis
Clinical diagnosispainless expansion in four quadrant
of jaw will give clue to diagnosis.
Radiological diagnosisradiopaque, mixed lesion in all
four quadrants with active hypercementosis will
diagnose this condition.
Management
Effective oral hygieneif teeth present effective oral
hygiene should be maintained since with this disease,
patients exhibit poor healing and osteomyelitis may
develop after tooth loss.
Recontouringpatients with more severe form of the
disease has superficial lesions which are located near
the crest of alveolar ridge, these may require recontouring
to accommodate the denture or to prevent ulceration.
Cemento-ossifying Fibroma
This is the terminology used for cementifying fibroma and
ossifying fibroma. Cemento-ossifying fibroma is a benign
fibro-osseous neoplasm. The description of the ossifying
fibroma of the jaws was first given by Montgomery in 1927.
It is a benign neoplasm that is osteogenic (non-odontogenic), well defined and rarely encapsulated, consisting of
fibrous tissue with variable amounts of mineralized
material similar to bone and/ or cementum. Chromosomal
abnormalities have been identified in the ossifying fibroma;
however, the molecular mechanisms that causes the
development of this tumor remain unknown.
Nomenclature
The previous nomenclature of ossifying fibroma or
cementifying fibroma was based upon the histopathology
which displayed predominantly bone like or cementum
like tissue, characterized by osteoblasts and cementoblasts
respectively. This terminology was first used by Hamner,
but is of little practical value because of the range of the
behavior of these lesions with identical histopathological
appearance. Furthermore many of them contained both
bone and cementum like elements. Therefore these lesions
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Clinical Features
Age and sex distributionit predominantly occurs in
females in third or fourth decades of life.
Bones affectedit can arise from any part of the facial
skeleton and skull with over 70% of cases arising in the
head and neck region. Cemento-ossifying fibromas
ostensibly do not occur outside the craniofacial complex.
Although it has been principally found in the jaws, it
has also been reported in the orbitofrontal bone,
nasopharynx, paranasal sinuses and skull base. Most
lesions arise in the tooth bearing areas of the mandible
and maxilla (Fig. 34-20). It mostly occurs in molar and
premolar mandibular area above the inferior alveolar
canal. In the maxilla, it occurs most often in the canine
fossa and zygomatic arch area.
Symptomsthere is occasional facial asymmetry is seen
in some of the cases. When in maxilla, symptoms may
include nasal stuffiness and epiphora on the affected side.
Signsthere may be associated exophthalmos, with
visual disturbances, depending on the extent of
compression of its orbital content by the tumor.
Giant ossifying fibromalarge lesions increasing in size
to over 80 mm in their greatest diameter have been termed
giant ossifying fibroma(Fig. 34-21).
Teeththe lesion is slow growing and in some cases,
there is displacement of teeth.
Cortexbony cortex and covering mucosa remain intact.
Radiographic Features
Peripherythe borders of cemento-ossifying fibroma
lesions usually are well defined. A thin radiolucent line,
representing a fibrous capsule, may separate it from
surrounding bone. Sometimes, the bone next to the lesion
develops a sclerotic border.
Internal structureit is a mixed radiolucent/ radiopaque
density with a pattern that depends on the amount and
form of the manufactured calcified material. In the early
stages solitary cyst-like osteolytic lesions without
periosteal reaction are seen. In some instances, the
internal structure may appear almost totally radiolucent
with just a tint of calcified material. In the type that
mainly contains abnormal bone, the pattern may be
similar to that seen in fibrous dysplasia, or a wispy
(similar to stretched tufts of cotton) or flocculent pattern
(similar to large, heavy snowflakes) may be seen (Fig.
34-22). Lesions that produce more cementum like
material may contain solid, amorphous radiopacities
(cementicles) similar to those seen in cemental dysplasia.
Effect on surrounding structurecemento-ossifying
fibroma can be distinguished from the previously
mentioned bone dysplasia by its tumor like behavior.
This is reflected in growth of the lesion, which tends to
be concentric within medullary part of bone with
outward expansion approximately equal in all
directions. These neoplasms have propensity for osseous
cortical expansion and encroachment on contiguous
structures. A significant point is that the outer cortical
plate, although displaced and thinned remains intact.
In the mandible, bowing or erosion of the inferior cortex
is seen. It results in displacement of the inferior alveolar
canal. The cemento-ossifying fibroma lesion can grow
into and occupy the entire maxillary sinus, expanding
its walls outward; however, a bony partition always
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Diagnosis
Clinical diagnosisnot so specific. Facial asymmetry is
seen.
Radiological diagnosismixed radiopaque radiolucent
lesion seen with sclerotic border. Displacement of teeth
can also be seen
Laboratory diagnosislarge number of fibroblasts, with
flat elongated nuclei is present within the network of
interlacing collagen fibers. Chinese letter shaped islands
of bone or calcification is also seen.
Differential Diagnosis
Early radiolucent stage
Post extraction socket and residual cysthistory of
extraction and history of surgery
Primordial cystit is always associated with a missing
permanent tooth which is not a case with cementifying/
ossifying/cemento-ossifying fibroma.
Ameloblastomait occurs in posterior most part of the
mandible and is accompanied by paresthesia of the lip.
It often shows a multilocular appearance.
Periapical cemental dysplasiait occurs at the apices of
vital teeth. However, they affect an older age group than
cementifying/ossifying/cemento-ossifying fibroma and
have a predilection for the lower incisor region whereas
cementifying/ossifying/cemento-ossifying fibroma
often occurs in premolar-molar region.
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Mature stage
Periapical spherical type of hypercementosisit is attached
to a part of root and is separated from the periapical
bone by a radiolucent periodontal ligament space which
surrounds the entire root.
Condensing osteitisit can be ruled out because it occurs
at the periapex of a non-vital tooth. It does not have a
radiolucent rim which is seen in fibro-osseous lesions.
Periapical idiopathic osteosclerosisit occurs in the
periapical region of vital teeth. Cementifying/ossifying/
cemento-ossifying fibroma however is smoothly contoured and almost round and ovoid, whereas periapical
idiopathic osteosclerosis is usually quite irregular in
shape and also there is absence of a radiolucent rim.
Complex odontomadensity is not uniform and also it
seldom occur periapically.
Management
Enucleationsmall, clinical encapsulated lesions are
treated by conservatively enucleation.
Resectionit is recommended if there is involvement of
inferior border, extension into maxillary sinus occurs.
4
Fig. 34-23: Peripheral ossifying fibroma
(Courtesy Dr Soni).
Radiographic Features
In edentulous patients, there may appear to be some
superficial erosion of the underlying bone on radiographs.
Intra-oral films taken with low penetration may show
varying amounts of calcification within the lesion.
Diagnosis
Clinical diagnosisnot so specific.
Radiological diagnosiserosion of underlying bone below
the lesion with calcification will give clue to diagnosis.
Osteoporosis
Clinical Features
Even though cemento-ossifying fibroma is considered
as an intraosseous lesion, affects the gum and soft tissue
have also been described.
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846
Types
Primary (associated with aging).
Secondary (reduction of histologically normal bone that
has been accelerated by abnormal or iatrogenic circumstance such as corticosteroid or heparin therapy or
condition such as malnutrition and scurvy.
Clinical Features
Ageeither present at birth (congenital) or developed in
early life (infantile).
Fracturebones are fragile and susceptible to fracture.
These fractures typically affect the forearm (Colles
fracture), spine (vertebral fracture) and hip (femur
fracture).
Congenita form inherited as an autosomal recessive
disorder is invariably fatal in early life due to massive
hemorrhage, anemia and rampant bone infections
occurring due to progressive loss of bone marrow and
their cellular products.
Percussionpercussion over the affected vertebrae is
painful.
Symptomsosteoporotic patient may notice gradual loss
of height due to shortening of trunk. In advanced cases,
clinical onset is often characterized by attack of severe
pain which is aggravated by movements and occurs after
trauma.
Osteomyelitisit may occur due to relatively avascular
and there may be bone pain.
Oral Manifestations
Osteomyelitismarked predilection for development of
osteomyelitis.
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Radiographic Features
Appearancetypical wedge appearance of affected
vertebrae, on a lateral radiograph.
Internal structurereduction in number of trabeculae is
least evident in the alveolar process. Persistent
trabeculae tend to occur along planes of bone stress.
Trabeculae may be arranged in a radial manner, with
wide spaces in between.
Cortexreduced density and thinning of cortical
boundaries, such as inferior mandibular cortex (Figs
34-24 and 34-25).
Lamina durathe lamina dura surrounding the teeth may
appear thinner than normal
Anatomic shadows such as the nasal fossa and
maxillary sinus are less distinct.
Diagnosis
Clinical diagnosisosteomyelitis of the jaw with fragile
bone and fracture of bone will give clue to the diagnosis.
Radiological diagnosiswedge shaped appearance of the
vertebrae with reduce density of bone in the jaw.
Laboratory diagnosisthere is anemia, hepatomegaly,
decrease RBC count and increase serum phosphatase
levels. Biopsy shows lack of physiologic bone resorption.
Osteoblasts are prominent but osteoclasts are seldom
found. Trabeculae are in disorder arrangement.
Differential Diagnosis
Infantile cortical hyperostosispositive history of highly
specific soft tissue and bony abnormalities are found.
Sites of involvement limited to few bones. New bone is
subperiosteal and continuous to inferior border.
Management
Life style changesgood nutrition and regular exercise
helps to prevent osteoporosis. Person should be asked
to stop smoking and alcohol.
Calcium supplementthey are widely used as an adjunct
to other treatment in the prevention and treatment of
osteoporosis. Recommended dose is 1000 mg/day.
Anabolic steroids such as stanozolol, vitamin D and
vitamin D active metabolites are also used.
Bisphosphonatesnew drug for systemic osteophonates
are under evaluation and this includes bisphosphonates. These are synthetics analogue of pyrophosphate
that absorb on to bone surface and become incorporated
into the bone matrix. When the bone contains bisphosphonates is ingested by resorbing osteoclasts, the drug
released within cell in high concentration and thus
exerts a toxic effect, leading to cell death and inhibits the
bone resorption.
Hormone replacement therapyhormone replacement
therapy with estrogen is the treatment of choice of
prevention of osteoporosis. Progesterone should be
added to estrogen in women with intact uterus, to reduce
the risk of endometrial carcinoma.
Alendronate 110 mg daily with calcium supplement is
also effective. Etidronate 400 mg daily for 2 weeks
followed by 13 weeks calcium supplement is also useful.
Calcitonin injectioninjection of calcitonin to reduce bone
resorption can be given. But it is rarely used due to side
effects as hot flushes and nausea.
Grafting procedures to rebuild the residual ridge and
implants to stabilize dentures are being used in advanced
cases of bone loss.
Prevention of bone lossoral bone loss can be prevented
by plaque control, removal of local etiologic factors and
use of antibiotics in case of early onset periodontitis.
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Etiology
Clinical Features
Age and sexit is equal in males and females, with
average onset at 9 weeks of age, with most of the cases
arising before 6 months.
Sitesbones commonly affected are mandible, clavicle,
scapula, frontal bone and ulna. There is bilateral
involvement in every case. Of all these bone clavicle and
mandible are the most common sites.
Symptomsinfants will develop fever and become hyperirritable.
Signssoft tissue swellings have a sudden onset,
especially in the facial area and early in disease, they
may be warm and tender. Swelling is devoid of clinical
signs of inflammation on the overlying skin. Swelling
disappears slowly, but may suddenly recur at the same
place or new site may be involved.
Others featureother features are pseudo-paralysis,
pleurisy and dysphasia.
Oral Manifestations
Sitesmandible is one of the commonest bones affected
in infantile cortical hyperostosis.
Symptomspatient may have malocclusion and enamel
hypoplasia may be present.
Signsresidual asymmetric deformity of mandible,
usually in the angle and ramus area.
Radiographic Features
Incidenceonly after swelling have subsided and ceased
to be tender, many bone changes occur.
Diagnosis
Clinical diagnosisinfant with fever, soft tissue swelling,
with swelling in the jaw will give clue to the diagnosis.
Radiological diagnosisthickening of cortex with laminated appearance.
Laboratory diagnosisanemia, leukocytosis, elevated
erythrocyte sedimentation rate, monocytosis and
increased serum alkaline phosphatase levels.
Differential Diagnosis
Callus formationunilateral or at least asymmetrical,
when seen bilaterally.
Osteomararely discovered in a younger age.
Cherubismmultilocular expansile radiolucency with
no cortical thickening.
Osteoporosisin infantile cortical hyperostosis,
abnormal bone production is subperiosteal while in
osteoporosis, it is cancellous.
Osteomyelitisosteomyelitis of jaw may be associated
with laying down of much subperiosteal new bone. But
infantile cortical hyperostosis occurs within 6 months
of life, as compared to osteomyelitis which occurs very
unusually below 6 months of life. In osteomyelitis, whole
of the mandible is not involved.
Periostitis of jawit is apparently unilaterally involved
and is localized. It is possible to see underlying cause of
the condition. Laminated structure in periostitis is visible
only at the inferior margins as compared to infantile
cortical hyperostosis which is visible all over the bony
surface of jaw.
Fibrous dysplasiaCaffeys disease represent the changes
added to be the bone, while fibrous dysplasia is an
abnormality within the bone.
Hypovitaminosis Ait produce the condition called as
cortical hyperostosis. But it usually affects metacarpal
bone and occurs over the age of 1 year, while infantile
cortical hyperostosis occurs below 6 months and
mandible is commonly affected.
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Oral Manifestations
Types
Radiographic Features
Osteopetrosis
Clinical Features
Ageit can occur in infant and some cases are
diagnosed later in life.
Skeletal featuresalmost every one has a varying degree
of poor skeletal development, if the disease appears early
in life. Subsequent skeletal deformities occur later due to
bending of the long bones and improper healing after
pathological fractures.
Symptomsas a result of continuous bone deposition
and lack of bone resorption, the foramina of cranial
nerves are constricted, hence there is loss of hearing,
disturbed vision, which diminish progressively.
Facial palsyfacial nerve palsy is also seen.
Signsdue to displacement of hematopoietic bone
marrow, anemia ensues and the hematopoietic function
is assumed by the liver, spleen and the lymph nodes
resulting in hyperplasia of lymphoid tissues and hepatosplenomegaly. There is also frontal bossing, obliteration
of maxillary sinus and possible hydrocephalus and
mental retardation.
Prognosisprognosis of infantile osteopetrosis is very
poor as compared to adults osteopetrosis.
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Diagnosis
Clinical diagnosishearing deformity, fracture of bone
with skeletal deformity will give clue to the clinical
diagnosis.
Radiological diagnosismarble bone appearance is seen
which is typical of this disease.
Laboratory diagnosisred blood cell count below
1,000,000 cells per cu mm. Elevated serum acid
phosphate levels have been reported in patients with
benign dominant osteopetrosis. Biopsy shows prominent
osteoblasts, but osteoclasts are seldom found.
Differential Diagnosis
Polyostotic fibrous dysplasiafibrous dysplasia usually
involves a part of bone, rather than the complete bone.
Hence, involved bone generally exhibits asymmetric
enlargement.
Pagets diseaseit can be differentiated from osteopetrosis
by its classic bones. It most often involves the skull, pelvis,
vertebrae, femur, maxilla and mandible. Also, serum
chemistry measurements show markedly elevated
alkaline phosphate levels.
Sclerotic cemental masseshave a stronger predilection
for black women over 30 years of age. The most common
salient feature of this disease is that only jaws are
affected, radiograph of the jaws reveal radiopaque
masses frequently rimmed by radiolucent borders.
Infantile cortical hyperostosisskeletal changes are
subperiosteal and not endosteal. Mandible is more
commonly involved.
Management
Bone marrow transplantationthis is the treatment of
choice in osteopetrosis patient. But to find matched
donor is a difficult process.
Interferon gamma 1bif interferon gamma 1-b is given in
combination with calcitrol will reduce the bone mass.
Other modalitiescorticosteroid, parathormone, macrophage colony stimulating factor and erythropoietin can
also be given.
Supportive treatmentthis is given to combat infection,
osteomyelitis. Antibiotics which are given in infection
are fluoroquinolones and lincomycin. Hyperbaric
oxygen therapy can also be given.
Precautionavoid major surgery in patients with
osteopetrosis. Performing dental extraction osteopetrosis
patient has a risk of osteomyelitis and jaw fracture.
Osteogenesis Imperfecta
It is also called as brittle bone, Lobstein disease. It is a serious
disease of unknown etiology. It represents a hereditary
autosomal dominant trait.
Pathogenesis
There impairment of collagen maturation. Collagen is main
part of bone, dentin, sclera, ligament and skin. So collagen
impairment will result in change in this structure.
Types
Congenital or Vroliks typeit is present at birth.
Tarda or Lobsteins typeit is recognized later in life. It is
also called as osteopsathyrosis.
Clinical Features
Agemany infants with this disease are stillborn or die
shortly after birth.
Bone deformitypatient is having bone deformity and
hyper extensibility of the joint. There is also bowing of
the bone (Figs 34.27A and B).
Fracture of boneextreme fragility and porosity of bones
with an attendant proneness of fracture. Fracture heals
readily but new bone is of similar imperfection. It is
common for fracture to occur while the infant is walking
or crawling. Hyperplastic callus formation, which may
mimic osteosarcoma, take place.
Blue sclerathere is occurrence of pale blue sclera which
is thin; pigmented choroids show and produce the blue
color (Fig. 34-28).
Signsthere is deafness due to osteosclerosis; laxity of
ligament and peculiar shape of the skull. There is also
abnormal electrical reaction of muscle. Increased
tendency for capillary bleeding.
Oral Manifestations
Dentinogenesis imperfectamost of the times, osteogenesis
imperfecta is associated with dentinogenesis imperfecta.
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Clinical Types
Neonatal lethal typeit is characterized by multiple
fractures in infants and the child seldom survives.
Severe non-lethal typedisease is not evident until late
childhood and patient shows fracture of bone with
minimum trauma. Although the fractured bone heals
up rapidly, considerable skeletal deformity and dwarfed
stature often develop.
Moderate and deforming typeit is associated with
dentinogenesis imperfecta and blue sclera.
Mild and non-deformity typethe patients are clinically
normal, but they have increased tendency for bone
fracture, due to trauma.
Radiological Features
Wormian bonespatient may show wormian bone (bones
in skull sutures) (Fig. 34-29).
B
Figs 34-27A and B: Patient of osteogenesis imperfecta
showing bone deformity (Courtesy Dr Lambade).
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Bird faciesarrested development and ensuing hypoplasia of mandible ultimately produce the characteristic
bird facies (Fig. 34-31). Mandibular hypoplasia yields a
retrognathic appearance.
4
Fig. 34-31: Mandibular retrognathism resulting in characteristic bird
face appearance.
Diagnosis
Clinical diagnosissevere bone deformity with blue sclera
are diagnostic features of osteogenesis imperfecta.
Radiological diagnosismultiple wormian bones with
osteopenia will diagnose this condition.
Laboratory diagnosisbone is composed of immature
spongy bone. Osteoblastic activity retarded and there is
failure of fetal collagen to be transformed into mature
collagen.
Management
Management of fracturemanagement of fracture should
be done in patient.
Management of teethteeth management should be same
as that is carried out in dentinogenesis imperfecta.
Fig. 34-32: Cleft palate formation seen in patient with
Pierre Robin syndrome.
Clinical Features
Triadit is triad of cleft palate, mandibular micrognathia and glossoptosis (causes airway obstruction).
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Diagnosis
Clinical diagnosistriad of cleft palate, micrognathia and
glossoptosis will diagnose this condition.
Management
Breathing supportbreathing support and feeding
assistance are necessary during infancy.
Surgicalsurgical closure and orthodontic treatment are
indicated.
Marfans Syndrome
It is also called as Marfan-Achard syndrome, arachnodactyly.
It is hereditary disease transmitted as autosomal dominant
trait. It is basically a disease of connective tissue related to
defective organization of collagen which is abnormally
soluble.
Clinical Features
Spider fingerexcessive length of the tubular bones
resulting in disproportionately long, thin extremities,
the finger and toes are long, thin and tapering so that
the name spider finger has been applied.
Shapethe shape of face and skull is characteristically
long and narrow.
Jointhyperextensibility of joint with habitual
dislocations, kyphosis or scoliosis and flatfoot.
Bilateral ectopia lentisit is caused by weakening or
rupture of the suspensory ligaments.
Cardiovascular complicationscardiovascular complications like aortic aneurysm and aortic regurgitation,
valvular defects and enlargement of the heart are common.
Downs Syndrome
It is also called as Trisomy 21 syndrome and mongolism.
It is associated with subnormal mentality in which an
extremely wide variety of anomalies and functional
disorders may occur. It results from excessive chromosomal
material involving all or a portion of chromosome 21. It is
cause by advanced maternal age, uterine and placental
abnormalities and chromosomal aberration.
Type
Typical typetrisomy21 with 47 chromosomes (95
percent of cases).
Translocation type46 chromosomes.
Chromosomal mosaicism.
Clinical Features
Skullflat face, large anterior fontanelle, open sutures.
There is also brachycephalic skull shaped with frontal
prominence and occipital flattening (Figs 34-33A
and B).
Palpebral fissuresthey are almond shaped with
superior-lateral or Mongolian obliquity.
Eyessmall slanting eyes with epicanthal folds. Eyes
are widely spaced. There is also ocular hypertelorism.
Nosethere is flattened nasal bridge (Fig. 34-33).
Otherssexual underdevelopment, cardiac abnormalities and hypermobility of the joints.
Oral Manifestations
Palatehigh arched palatal vault is very prevalent.
Maxilla and mandiblebifid uvula, malocclusion and
multiple odontogenic cysts of maxilla and mandible.
Temporomandibular jointthere may be temporomandibular dysarthrosis.
Diagnosis
Clinical diagnosisspider finger, with high arched
palate, hyperextensibility of joints.
Management
B
Figs 34-33A and B: Brachycephalic skull shaped with widely
shaped eyes. Nose has flattened bridge.
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Oral Manifestations
Diagnosis
Management
There is no specific treatment for this syndrome and many
patient died during first year of life.
Achondroplasia
It is also called as chondrodystrophia fetalis. It is a disturbance of endochondral bone formation, which results in a
characteristic form of dwarfism. It is a hereditary condition,
which is transmitted as an autosomal dominant trait.
Clinical Features
Appearancepatient is quite short, usually less than 14
meters in height and thickened muscular extremities,
brachycephalic skull and bowed legs.
Handshands are usually small and fingers are stubby.
Skullthe base of the skull is small and constricted as a
result of retarded growth of the cartilaginous portions.
The calvarium is large and bulges frontally and laterally.
Nosethere is also depression of the bridge of nose.
Lumbar lordosislumbar lordosis with prominent
buttocks and protruding abdomen is often present.
Jointsjoints exhibit limitation of motion.
Othersarms do not hang freely at the sides and the
elbows can not be straightened.
Fig. 34-34: Malocclusion with macroglossia of tongue
(Courtesy Dr Parate).
Radiological Features
Periodontal destructionperiodontal destruction of bone
can be observed on the radiograph (Fig. 34-35).
Oral Manifestations
Proganthismmaxilla is often retruded because of
restriction of growth at the base of skull which may
produce relative mandibular prognathism.
Teethcongenital missing teeth with disturbances in
shape of teeth may also occur.
Radiographic Features
Shorter bone and bone clubbinglong bones are shorter
than normal and there is thickening or mild clubbing at
the ends.
Epiphysisepiphysis may close, either early or late.
Narrow foramen magnumbones at the base of the skull
fuse prematurely, producing shortening as well as a
narrow foramen magnum.
Diagnosis
Fig. 34-35: Periodontal destruction of bone seen in the
OPG (Courtesy Dr Parate).
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Management
There is no specific treatment for this disease.
Clinical Features
Symptomsnausea, vomiting and epigastria distress.
Excess salivation, diarrhea and mucus discharge with
headache and sweating. There is pain in joints of hand,
feet and spine.
Signsbarely detectable pulse, hypotension, cardiac
arrhythmias and disturbance in electrolyte balance.
There is also stiffness of gait, limitation of movement
occurs.
Severe casesin most severe cases, there is almost
crippling of movement and extreme pain because the
spine and joints become rigid and virtually, immobilization of the individual occurs.
Complicationrespiratory and metabolic acidosis and
coma.
Clinical Features
Appearancefacial appearance of this patient may be
swollen, particularly with widening of the angles of
mandible and at the bridge of nose.
Symptomsin some patients, there is loss of visual
activity and loss of facial sensation; some degree of facial
paralysis and deafness occurs and all this is due to
cranial nerve involvement through closure of foramina.
Alveolar processintraorally, there is sometimes
overgrowth of alveolar process.
Radiological Features
Increase densitya skeletal radiograph reveals increased
density of many bones of body.
Skull sclerosisthe skull exhibits diffuse sclerosis which
may be present in the jaws.
Radiographic Features
Diagnosis
Diagnosis
Clinical diagnosisexcess salivation, headache,
sweating and joint pain will give clue to diagnosis.
Radiological diagnosiscalcification and thickening of
bone.
Management
There is no treatment although patient may live his normal
life.
Massive Osteolysis
Management
Elimination of fluoride from bodyall attempts should be
to eliminate the toxic dose of fluoride from the body.
Maintenance of vital signssupport all the vital signs.
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Pathogenesis
In this condition, there is progressive destruction of bone.
The bone is replaced by fibro-vascular tissue. It occurs due
to proliferative vascular and connective tissue response to
unknown mechanism.
Clinical Features
Oral Manifestations
Siteintraorally mandible is more commonly affected
as compared to maxilla.
Symptomsthe patients may present with pain or facial
asymmetry. In some cases there is history of gradual
progressive recession of the lower jaw.
Pathological fracturethere is pathologic fracture of bone
following even minor trauma.
Signsthere may be complete destruction of mandible
(Fig. 34-36). Deviation of mandible can also occur in the
affected side. Ulceration of the lesion is usually absent.
Diagnosis
Clinical diagnosispain, facial asymmetry and
pathological fracture without any apparent cause may
suspect massive osteolysis
Radiological diagnosisit will show complete destruction
of bone in the jaws
Laboratory diagnosisbiopsy shows vascular proliferation with osteoclastic reaction.
Management
Suggested Reading
Radiological Features
Radiodensityit has got osteolytic pattern radiologically.
Appearanceradiolucency is present in the mandible
showing complete destruction. Margins of the lesion are
indistinct (Fig. 34-37).
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65.
66.
67.
68.
69.
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AIDS
35
859
AIDS
Introduction
AIDS is a devastating fatal disease which is in epidemic
form throughout the world. It is an incurable viral STD
(sexually transmitted disease) which is caused by human
immunodeficiency virus (HIV). It stands for: AAcquired, i.e. contagious not inherited.
IImmune, i.e. power to resist disease.
DDeficiency.
SSyndrome, i.e. number of signs and complaints
indicative of a particular disease.
The case of AIDS was detected in June 1981 when five
young homosexual men came with the suffering from rare
lung infection due to microorganism called Pneumocystis
carinii. In India, the first description of AIDS came in
Chennai where six women out of 125 who were screened
were HIV positive in high risk group of prostitutes.
HIV attacks the immune system of the body. Due to that
an individual is not able to protect himself from potentially
harmful organism.
AIDS appears to be endemic in central and equatorial
Africa and it may be old disease of Africa that has gone
unrecognized. HIV infection has also become the primary
emphasis of effort at controlling STDs. Moreover, the
knowledge gain about sexual and other behavior associated
with transmission of HIV, as well as strategies that have
been effective in modifying those behaviors, is transferable
to other sexually transmittable and blood-borne infections.
These above factors have revolutionized standard
approaches to the control of these infections.
Oral and perioral lesions are common in patients with
human immunodeficiency virus, which are often the
presenting feature and may have deterioration of general
health and a poor prognosis.
Definition
WHO has given the following definition of AIDS.
Prevalence
It is more common in African country and Western countries
particularly in the United States. The largest population of
AIDS occurs in homosexuals, intravenous drug users, and
heterosexuals with sexual contact with AIDS patient. It
can also occur in patients who received transfusion of blood
or blood pigments donated by the person with risk factors.
About 92% of victims are males, 6.5% females with 1%
children. It is common in the age group of 25 to 49 years.
Transmission
Sexual transmissionit is in 90% of cases. It depends upon
number of sexual partners, receptive anal intercourse
and presence of other STDs. All these are in high risk
group. Prostitution is a major heterosexual factor
associated with AIDS. Homosexuals have more risk of
transmitting HIV than the heterosexual males.
Use of contaminated blood productsintravenous drug
users, HIV-contaminated blood transfusion, blood
clotting concentrate and organ transplantation.
Perinatal transmissionit occurs in 13% among children
born to HIV seropositive mother.
Other nosocomal routestransmission from patient to
patient due to reuse of contaminated and shared needles.
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Professional hazardsthe risk of transmission from HIVinfected patient to health care workers is more than
health care workers to patient.
Saliva transmissionHIV has been found to be present
in saliva. Saliva reduces the ability of HIV to infect its
target cells. So transmission through saliva is rare
possibility. But, there are some rare example which
documented that HIV is transferred from the saliva of
the patient.
Mechanism of Action
Normal mechanismpathogenic viruses identified by
macrophage it activates T lymphocytes it gets
differentiated into effector cell like T helper cell (T4) and
T suppresser cell (T8 ) T 4 cells secrete various
lymphokines which induce lymphocyte to be
differentiated into plasma cell it secretes specific
antibodies against viral antigen it destroys the virus.
Mechanism in AIDS
Antigenic stimulationwhen the virus enters the blood
stream, it evokes antigenic stimulation which activates
CD4, T helper lymphocytes and macrophages.
Secretion of TNF and interleukin 6lymphocytes and
macrophages then secrete growth factors, tumor
necrosis factor (TNF) and interleukin-6. This results
in increase in CD4 cells thereby increasing number of
cells vulnerable for HIV virus.
Adherence of virus to CD4 cellsHIV virus then
adheres to CD4 surface via interaction between viral
gp120 surface glycoprotein and CD4 cell surface
membrane receptors. This surface interaction occurs
with the help of transmembrane protein (chemokine
receptor-5 or CCR-5).
Replication of HIV virusafter this, HIV virus will
replicate in CD4 cell which also proliferates by
antigenic stimulus.
Incubation periodonce the viral genes are integrated
into cells of own DNA, they can apparently remain
dormant for an indefinite period of time, without
causing any effects. This is called as incubation period
Fate of CD4initially CD4 cells reduce the number of
HIV virus by cellular and humoral attacks. But as
continuous replication of virus occurrs in lymph
nodes, it will destroy the lymph nodes. This will lead
into unchecked replication of virus which will lead
to decrease in CD4 count of the human being. When
the number of CD4 count is severely depleted below
200/mm3, the immune system collapses and variety
of infections occur. At this stage, the patient is said to
have AIDS.
Window periodit is time between entry of virus into the
body and the blood test becoming positive. This period
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AIDS
is about 1 to 3 month and person is infectious during
that period.
Homosexuals or bisexuals71.4%
Intravenous drug users18.4%
Hemophilia
Recipient of multiple blood transfusion
Infant born of parents belonging to first 3 high risk
groups
Heterosexual contacts of high risk group.
Classification
1993 Revised Classification System for
HIV Infection
The Centers for Disease Control and Prevention (CDC) has
revised the classification system for HIV infection to
emphasize the clinical importance of the CD4+, Tlymphocyte count in the categarization of HIV-related
clinical conditions. Consistent with the 1993 revised
classification system, CDC has also expanded the AIDS
surveillance case definition to include all HIV-infected persons
who have less than 200 CD4+, T-lymphocytes/L, or a
CD4+, T-lymphocyte percentage of total lymphocytes of
less than 14. This expansion includes the addition of three
clinical conditions pulmonary tuberculosis, recurrent
pneumonia, and invasive cervical cancer.
Measures of CD4+, T-lymphocytes are used to guide
clinical and therapeutic management of HIV-infected
persons. The revised CDC classification system for HIVinfected adolescents and adults categorizes persons on the
basis of clinical conditions associated with HIV infection
and CD4+, T- lymphocyte counts. The system is based on
three ranges of CD4+, T-lymphocyte counts and three
clinical categories.
CD4 + T cell
categories
A
Asymptomatic,
acute HIV and
PGL
B
Symptomatic,
not A or C
conditions
C
AIDS
indicator
condition
A1
B1
C1
Category 2 : 200 to
499/L (14-28%)
A2
B2
C2
A3
B3
C3
Category A
It consists of one or more of the conditions listed below in
an adolescent or adult (greater than or equal to 13 years)
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Category B
It consists of symptomatic conditions in an HIV-infected
adolescent or adult that are not included among conditions
listed in clinical Category C and that meet at least one of
the following criteria:
The conditions are attributed to HIV infection or are
indicative of a defect in cell-mediated immunity.
The conditions are considered by physicians to have a
clinical course or to require management that is
complicated by HIV infection.
Examples of conditions in clinical category B include,
but are not limited to:
Bacillary angiomatosis
Candidiasis, oropharyngeal (thrush)
Candidiasis, vulvovaginal; persistent, frequent, or poorly
responsive to therapy
Cervical dysplasia (moderate or severe)/cervical carcinoma
in situ
Constitutional symptoms, such as fever (38.5C) or diarrhea
lasting greater than 1 month
Oral hairy leukoplakia
Herpes zoster (shingles), involving at least two distinct
episodes or more than one dermatome
Idiopathic thrombocytopenic purpura
Listeriosis
Pelvic inflammatory disease, particularly if complicated by
tubo-ovarian abscess
Peripheral neuropathy
For classification purposes, Category B conditions take
precedence over those in Category A. For example, someone
previously treated for oral or persistent vaginal candidiasis
(and who has not developed a Category C disease) but
who is now asymptomatic should be classified in clinical
Category B.
Category C
Conditions included in the 1993 AIDS surveillance case
definition
Candidiasis of bronchi, trachea, or lungs
Candidiasis, esophageal
Cervical cancer, invasive *
Coccidioidomycosis, disseminated or extrapulmonary
Cryptococcosis, extrapulmonary
Cryptosporidiosis, chronic intestinal (greater than 1 months
duration)
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Clinical Stage 2
Moderate unexplained weight loss (<10% of presumed
or measured body weight) .
Recurrent respiratory infections (respiratory tract
infections, upper respiratory infections, sinusitis,
tonsillitis, bronchitis, otitis media, pharyngitis).
Herpes zoster .
Minor mucocutaneous manifestations (angular cheilitis,
recurrent oral ulcerations, seborrheic dermatitis, prurigo,
papular pruritic eruptions, fungal fingernail infections).
Clinical Stage 3
Unexplained severe weight loss (>10% of presumed or
measured body weight) .
Unexplained chronic diarrhea for >1 month.
Unexplained persistent fever for >1 month (> 37.6C
intermittent or constant).
Persistent oral candidiasis (thrush).
Oral hairy leukoplakia.
Pulmonary tuberculosis within the last 2 years.
Severe presumed bacterial infections (e.g. pneumonia,
empyema, pyomyositis, bone or joint infection,
meningitis, bacteremia).
Acute necrotizing ulcerative stomatitis, gingivitis or
periodontitis.
Conditions for which confirmatory diagnostic testing is
necessary.
Unexplained anemia (hemoglobin <8 g/dL) .
Neutropenia (neutrophils <500 cells/L) .
Chronic thrombocytopenia (platelets <50,000 cells/L).
Clinical Stage 4
The clinical staging and case definition of HIV for resourceconstrained settings were developed by the WHO in 1990
and revised in 2007. Staging is based on clinical findings
that guide the diagnosis, evaluation, and management of
HIV/AIDS, and does not require a CD4 cell count.
Asymptomatic
Acute retroviral syndrome
Clinical Stage 1
Asymptomatic.
Persistent generalized lymphadenopathy.
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AIDS
Visceral herpes simplex infection, cytomegalovirus
infection (retinitis or organ other than liver, spleen, or
lymph node)
Any disseminated mycosis (e.g. histoplasmosis,
coccidioidomycosis, penicilliosis)
Recurrent nontyphoidal Salmonella bacteremia
Lymphoma (cerebral or B-cell non-Hodgkins)
Invasive cervical carcinoma
Visceral leishmaniasis
USPHSCDC Classification
This classification is given by United State Public Health
Service Center of Disease Control
Group Iacute infection
Group IIasymptomatic infection
Group IIIpersistence generalized lymphadenopathy.
Group IVother disease
Subgroup Aconstitutional diseases
Subgroup Bneurological diseases
Subgroup Csecondary infectious diseases
C1specified secondary infectious diseases listed in
CDC surveillance definition for AIDS.
C2other specified secondary infectious stages:
Subgroup Dsecondary cancer
Subgroup EOther conditions
AIDS-related Complex
In some persons before the development of obvious AIDS,
some clinical and laboratory findings are present. This is
called AIDS-related complex. For clinical and research
studies, persons exhibiting complex clinical problems and
immunological or hematological abnormalities on the
laboratory tests, have been classified as having AIDS-related
complex (ARC). ARC requires any two or more symptoms
and two or more abnormal laboratory findings. It must be
present for at least 3 months.
Clinical findingit includes lymphadenopathy, weight
loss of 15 lbs or 10% of body weight, fever of 38.5oC
which is intermittent or continuous, diarrhea, fatigue,
malaise, night sweats and oral candidiasis.
Laboratory findingthere is decreased number of T helper
cell, decreased ratio of T helper cells to T suppressor
cells. There is also anemia, leucopenia, thrombocytopenia, lymphopenia, increased serum globulin level,
decreased blastogenic response of lymphocytes to
mitogen and increased level of circulating immune
complex.
Cutaneous anergycutaneous anergy to multiple skin
test antigens. Anergy is impaired or inability to react to
skin antigens.
863
Clinical Features
Acute symptomsthey are more or less like infectious
mononucleosis. Patient complaint of sore throat, fever,
headache, myalgia, arthralgia, diarrhea, photophobia,
maculopapular rash and peripheral neuropathy.
Protozoa and helminthes infectionthe most common
opportunistic infection is by Pneumocystis carinii which
causes pneumonia, CNS infection or other disseminated
infections and toxoplasmosis, cryptosporidiosis
(intestinal) causing diarrhea for over one month
Fungal infectionCandida organism may cause esophageal candidiasis, bronchial or pulmonary candidiasis. Cryptococcosis causing CNS infection. Patients
may suffer from disseminated histoplasmosis.
Bacterial infectionsMycobacterium avium intracellulare
causing infection disseminated beyond lung and
lymph node. Mycobacterium tuberculosis causing
tuberculosis.
Viral infectionscytomegalovirus, causing infection in
the internal organs other than liver, spleen and lymph
nodes. Herpes simplex virus, causing chronic
mucocutaneous infection with ulcers persisting more
than one month.
AIDS dementia complexthis is most common
manifestation of AIDS. It is progressive encephalopathy.
Persistent generalized lymphadenopathyin silent phase
patients may have persistent generalized lymphadenopathy. Most frequent sites involved in PGL are cervical,
occipital and axillary lymph nodes.
MalignancyKaposis sarcoma is the most common
vascular malignancy seen in AIDS patient. Kaposis
sarcoma usually occurs in homosexuals. Another
malignancy which may occur is non-Hodgkins
lymphoma which most commonly affects CNS.
Oral Manifestations
Oral manifestations of HIV disease are common and include
oral lesions and novel presentations of previously known
opportunistic diseases. Careful history taking and detailed
examination of the patients oral cavity are important parts
of the physical examination and diagnosis requires
appropriate investigative techniques. Early recognition,
diagnosis and treatment of HIV-associated oral lesions may
reduce morbidity. The presence of these lesions may be an
early diagnostic indicator of immunodeficiency and HIV
infection, may change the classification of the stage of HIV
infection and is a predictor of the progression of HIV
disease. About 95% of AIDS patients have head and neck
lesion and about 55% have important oral manifestation.
They are depicted in Table 35-1.
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Fungal
More common
Candidiasis
Less common
Aspergillosis
Histoplasmosis
Cryptococcus neoformans
Geotrichosis
Bacterial
More common
HIV gingivitis
HIV periodontitis
Necrotizing gingivitis
Less common
Mycobacterium avium intracellulare
Klebsiella pnuemoniae
Enterobacterium cloacae
E. coli
Salmonella enteritidis
Sinusitis
Exacerbation of apical periodontitis
Submandibular cellulitis
Viral
More common
Herpes simplex
Varicella zoster
Epstein-Barr including hairy leukoplakia
Less common
HPV virus
CMV virus
Pox virus
Neoplasm
More common
Kaposis sarcoma
Less common
Non-Hodgkins lymphoma
Squamous cell carcinoma
Lymphadenopathy
Neurologic disorders
Less common
Paresthesia
Facial palsy
Hyperesthesia
Dysphagia
Miscellaneous
Less common
Recurrent aphthous ulceration
Progressive necrotizing ulceration
Toxic epidermolysis
Delayed wound healing
Thrombocytopenia
Xerostomia and sicca type syndrome
HIV embryopathy
Hyperpigmentation
Granuloma annulare
Exfoliative cheilitis
Lichenoid and other drug reaction.
Clinical Features
Sitepatient with HIV usually has lesion of hard palate,
tongue and soft palate.
Clinical patternthere are mainly four clinical pattern of
candidiasis seen in AIDS patient. They are pseudomembranous, hyperplastic, erythematous and angular
cheilitis.
Symptomsthese lesions may be associated with a variety
of symptoms, including a burning mouth, problems in
eating spicy food and changes in taste. All three of these
common forms may appear in one individual.
Pseudomembranous candidiasis (thrush)characteristic
creamy white, removable plaques on the oral mucosa
are caused by overgrowth of fungal hyphae mixed with
desquamated epithelium and inflammatory cells. The
mucosa may appear red when the plaque is removed.
This type of candidiasis may involve any part of the
mouth or pharynx.
Erythematous candidiasisErythematous candidiasis
appears as flat, red patches of varying size. It commonly
occurs on the palate and the dorsal surface of the tongue.
Erythematous candidiasis is frequently subtle in
appearance and clinicians may easily overlook lesions,
which may persist for several weeks if untreated.
Angular cheilitisit appears clinically as redness,
ulceration and fissuring, either unilaterally or bilaterally
at the corners of the mouth. It can appear alone or in
conjunction with another form of candidiasis.
Hyperplasic candidiasisin this, candidal lesion has got
firm appearance. It usually does not scrape on pressure.
(Fig. 35-1).
Management
Topical clotrimazoleit is the treatment of choice. Patient
improves a lot after applying topical clotrimazole
application.
Topical itraconazoleitraconazole in as a oral rinse is also
effective in controlling oral candidiasis in HIV patient.
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AIDS
865
Necrotizing ulcerative periodontitisalso called HIVassociated periodontitis in which rapid loss of periodontal
attachment is seen .
Clinical Features
Types
Linear gingival erythemaalso called HIV-related
gingivitis. There is distinctive linear band of erythema
(Fig. 35-2).
Necrotizing ulcerative gingivitisulceration and necrosis
of interdental papillae occurs.
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4
Fig. 35-4: HIV-associated periodontitis showing extensive loss of
periodontal support.
Management
Debridementremoval of necrotic tissue should be
carried out. After necrotic tissue is removed, irrigation
with povidone-iodine solution is done.
Maintenancepatient should be done periodic scaling
and root planning. Oral hygiene should be maintained
with a chlorhexidine mouth rinse once or twice daily.
Antimicrobial therapyin cases of NUP, metronidazole
(250-mg four times daily), amoxicillin/clavulanate
(Augmentin 250-mg three times daily), or Clindamycin
(300-mg three times daily) should be given.
Herpes Zoster
Occurrenceit occurs more frequently in HIV-infected
patients and carries poor prognosis.
Hairy Leukoplakia
Oral hairy leukoplakia, which presents as a non-movable,
corrugated or hairy white lesion on the lateral margins
of the tongue occurs in all risk groups for HIV infections,
although less commonly in children than in adults. It occurs
in about 20% of persons with asymptomatic HIV infection
and becomes more common as the CD4+ T-cell count falls
below 200/mm3. Hairy leukoplakia is almost always a
manifestation of HIV infection and clinicians should
arrange evaluation of HIV disease.
Etiology
Epstein-Barr virusexact etiology is not known but
Epstein-Barr virus (EBV) has been identified in these
lesions. One hypothesis is that basal epithelial cells of
lateral margin of tongue normally harbors EBV in
majority of adult population, who are EBV seropositive
and carrier of that disease. It is found primarily in
homosexual males. Direct infection of Langerhans cell
due to HIV-induced loss of factor essential for their
integrity and function, permit reactivation of EBL with
frequent epithelial hyperplasia.
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Clinical Features
Kaposis Sarcoma
Pathogenesis
Angiogenesis proteinhigher incidence of Kaposis
sarcoma is in homosexual men with AIDS as compared
to heterosexuals with AIDS. It has been suggested that
there is transmissible agent prevalence in homosexual
population, which stimulates certain factors such as
angiogenesis protein that may be critical in the
pathogenesis of neoplasm. The patient with AIDS often
shows clustered lesion in the oral cavity which suggests
direct inoculation of mucosa with sexually transmitted
agent.
Cytomegalovirus infectionsome theories suggest role
of cytomegalovirus in the pathogenesis of Kaposis
sarcoma, but studies on prevalence of antibodies to
cytomegalovirus in patient with classic and epidemic
Kaposis sarcoma have failed to demonstrate role of
cytomegalovirus.
HHV 8 virusesnowadays, human herpes virus 8
(HHV8) is thought to be in association with Kaposis
sarcoma in AIDS patient.
Types
Management
Antiviral drugshairy leukoplakia usually is asymptomatic and does not require treatment. It disappeared
in patients receiving high-dose acyclovir (2.5 to 3 mg
per day for 2 to 3 weeks). Another antiviral drug which
can be used is descyclovir.
ZidovudineHIV therapy with zidovudine affect
EBV and significant regression of hairy leukoplakia
occurs.
Topical treatmenttopical treatment with retinoid and
podophyllin resins also gives temporary remission of
hairy leukoplakia.
Others drugsother drugs which can use in hairy
leukoplakia are phosphonoformate, topical clotrimazole
(10 mg 5 times a day), nystatin (10000 units/gm 5 times
a day) and ketoconazole (200 mg BD) and azidothymidine.
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Clinical Features
Oral Manifestations
Siteit has tendency to involve the oral cavity, with hard
palate as the most common site. But lesions may occur
on any part of the oral mucosa including the gingiva,
soft palate, buccal mucosa and in the oropharynx. It can
involve either alone or in association with skin and
disseminated lesions.
Appearanceit can appear as a red, blue, or purplish
lesion. It may be flat or raised, solitary or multiple.
Occasionally, yellowish mucosa surrounds the lesion.
The lesions may enlarge, ulcerate and become infected.
Symptomspatient may complain of pain and interference of lesion with eating and speaking
Signslesions are tender and painful on palpation. After
some period, the area may develop in plaque and nodule.
In some cases, necrosis of tissue occurs.
Sizeit may vary in size from few millimeters to a
centimeter or more in diameter.
Teeth mobilityneoplasm can invade the bone causing
mobility of the tooth.
Management
Oral prophylaxisit is important to perform thorough
dental prophylaxis before initiating therapy for lesions
involving the gingiva. Response to therapy is improved
if all local plaque and calculus are removed.
Systemic chemotherapysystemic chemotherapy like
vinblastine, vincristine, etoposide, alpha interferon,
adriamycin, actinomycin D, and doxorubicin should be
given.
Intralesional sclerozing agentsintralesional injection of
sodium tetradecyl sulfate has been effective for oral
lesion.
Intralesional vinblastineit is useful for treating small
lesions, particularly on the palate or gingiva. Several
Cytomegalovirus Infection
Clinical featuresit has got predilection for salivary
glands because many HIV-infected patients have
xerostomia. It is a hypothesis that in such patients
salivary glands, cytomegalovirus infection produces
inflammation causing reduced salivary production.
Managementsystemic ganciclovir or Foscarnet should
be given.
Aphthous Ulcer
Clinical featuresaphthous ulcer are reflection of immune
dysfunction. Report says that pituitary suppresses the
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AIDS
reduced host cortisone production, might account
for this lesion. It is more commonly seen on tongue (Fig.
35-7). Major and herpetiform aphthous ulcer is more
commonly seen as compared to minor ulceration.
Managementintralesional injection of corticosteroid
give successful results. Systemic steroid should be
avoided to prevent further immunosuppression. Topical
corticosteroid can also be given in this patient. In case of
resistance cases of aphthous ulcer, thalidomide should
be given. Thalidomide should be used for short-term as
it may enhance the production of HIV.
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Molluscum Contagiosum
Clinical featuresit is skin disease caused by pox virus.
Lesions are waxy, dome-shaped papule with central
crater. Facial skin also becomes commonly involved.
Managementit is managed by curettage, cryosurgery
and cautery. Recurrence is common. Resolution of lesion
is also seen with anti-retroviral therapy.
Lymphoma
Clinical featuresmost of the lymphoma present are nonHodgkins lymphoma. CNS involvement is seen with
lymphoma. Oral lesion presents as soft tissue enlargement of the palate or gingiva. There is also loss of
periodontal structure resulting in mobility of tooth.
Managementit is managed by chemotherapy and
radiation therapy.
Guidelines to Prevent
Transmission to Dentist
Redesigning of instrumentcall for redesign of
instrument of surgical procedures that carry high risk of
intra-operative injury to clinical staff.
Sterilizationthe understanding that all instruments
used in dental procedures must either be sterilized before
further use or be discarded.
Waste managementelimination and protection from
blood contaminated aerosols. Hazardous clinical waste
should be disposed properly by the waste management.
Management of injuriesprotocol for management of
needle stick and other intra-operative injuries aiming
for defining the risk in given circumstances and
administration of appropriate vaccine or other preventive
measures.
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Prevention
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AIDS
Viral Load Testing
The viral load test measures the amount of HIV virus in the
body. A viral load test should not be taken as a diagnostic
test. Along with the CD4 cell count, the viral load test is
used to give information about the progression of HIV
infection, to predict its future course, and to guide
recommendations for treatment.
Mechanismthere are two types of viral load tests: PCR
(polymerase chain reaction), and bDNA (branched
DNA). The tests use different techniques to measure the
same thing, which is the amount of HIV present in
bloodstream. However, it is very important to use the
same type of viral load test every time and not to switch
between the two, since the values on test reports from
the two different types are not comparable.
Reportsthe test report will show the number of HIV
copies in one milliliter of blood. This indicates the current
level of HIV, and the rate at which it is reproducing. The
higher the count and reproductive rate, the faster the
disease is likely to progress.
High viral loada high viral load can be anywhere
between 5,000 and one million copies or more.
Low viral loada low viral load is usually between 200
and 500 copies. However, a low viral load only indicates
slow progression, not an absence of HIV or cured HIV.
Significance of rate of changethe rate of change in viral
load between successive tests is also important. An
increasing count indicates that a worsening infection,
while a decreasing count indicates suppression of
the HIV infection and improvement of the patients
health.
Errorsthere is a chance of a false positive result,
indicating a falsely high viral load, especially when done
by the very sensitive PCR method. There is also a chance
of a false negative when the result is undetectable; an
undetectable result does not mean the patient is cured of
HIV.
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Management of AIDS
Interferonit has got antiviral, antiproliferative and
immunomodulator activity. The interferon is a
glycoprotein produced by a number of different types of
cells. Type I interferon (alpha and beta) are produced by
leukocytes and fibroblasts. Type II interferon (gamma)
is produced by lymphocytes and monocytes. Low doses
of interferon enhance the antibody formation and
lymphocyte blastogenesis. They also prolong cell cycle
and cause inhibition of intracellular enzyme system
(anti-neoplastic effect). The gamma interferons stimulate
macrophage oxidative metabolism and have
antimicrobial effect.
Thymic replacement therapythymic epithelium plays an
important role in transformation of blood-borne
precursor cell into mature T cells. Thymic hormone or
factor mediates this effect, since the immune system in
AIDS is characterized by numerical and functional
defects of T cell lymphocytes, it will correct the immune
defect. Transplant of fetal thymus of cultural thymic
epithelium and injection of thymic hormone have been
successfully utilized in treatment of AIDS.
Lymphokines and cytokineslymphokines are materials
produced by lymphocyte. Interleukin-I is macrophage
product. In in vitro system, interleukin-I enhances
plague forming cells responses and the generation of
cytotoxic T cell alloantigen. In the presence of
macrophage, interleukin-1 stimulates the production of
interleukin-2, which stimulates and maintains the
growth of T cell activated by antigens. Various studies
have conformed that purified interleukin-2 (which
stimulates and maintains growth of T cell activated by
antigen), preparation in vitro system can normalize
lymphocyte reaction in high percentage of individuals
with unexplained lymphadenopathy and immunologic
abnormalities, but the results are not significant in
patients with AIDS.
Bone marrow transplantationsyngeneic (identical twin)
allogenic bone marrow transplantation has been
successful in reconstituting immune function in the
patients with severe congenital immune defects. If this
could be therapeutic in patient with AIDS that have
appropriate marrow donor.
Monoclonal antibodies therapyIn this, antibodies are
directed against T cell differentiation antigens as a result
of that number of circulating leukemic cells are decreased
in patients with adult T cell active lymphoblastic
leukemia.
Intravenous immunoglobulin therapyit reduces incidence
of bacterial and viral infections. Infusion of hyperimmune gamma globulin enriched for neutralizing
antibodies for LAV/HTLV III could be beneficial for
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872
Suggested Reading
1. Carpenter CCJ, Cooper DA, et al. Antiretroviral therapy in adults:
updated recommendation of the international AIDS society-USA
panel. JAMA 2000;283:381-90.
2. Casariego Z, Kelly GR, et al. Disseminated histoplasmosis with
orofacial involvement in HIV I infected patient with AIDS:
manifestation and treatment. Oral Dis 1997;3:184-7.
3. CDC. Classification system for human T-lymphotropic virus
type III/lymphadenopathy-associated virus infections. MMWR
1986;35:334.
4. CDC. Revision of the CDC surveillance case definition for acquired
immunodeficiency syndrome. MMWR 1987; 36:1-15S.
5. Centres for disease control. 1993 revise Classification system for
HIV infection and expanded surveillance definition for AIDS
among adolescent and adults. MMWR 1992:41:RR:17:1-19.
6. EC Clearinghouse. Classification and diagnostic criteria for oral
lesion in HIV infection. Ec-Clearinghouse on oral problems related
to HIV infection and WHO collaborating center for on oral
manifestation of human deficiency virus. J Oral Pathol Med 1993;
22:289-91.
7. Epstein JB, Silverman S Jr. Head and neck malignancy associated
with HIV infection. Oral Surg, Oral Med, Oral Pathol 1992;73:193200.
8. Epstein JB. Management of Kaposi sarcoma and a proposal for
clinical staging. Oral Dis 1997;3(suppl):S124-S128.
9. Ficarra G, Berson AM, Silverman S Jr, et al. Kaposis sarcoma of
the oral cavity: a study of 134 patients with a review of the
pathogenesis, epidemiology, clinical aspects and treatment. Oral
Surg, Oral Med, Oral Pathol 1988;66(5):543-50.
10. Fowler CD, et al. AIDS presenting as a palatal perforation. Oral
Surg, Oral Med, Oral Path 1989;67:313-8.
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AIDS
33. Scully C, Cawson RA. Medical problems in dentistry (5th edn),
Churchill Livingstone: an imprint of Elsevier, 2005.
34. Scully C, Laskaris G, et al. Oral manifestation of HIV Infection
and their Management: I more common lesion. Oral Surg, Oral
Med, Oral Pathol 1991;71:158-66.
35. Scully C, Laskaris G, et al. Oral manifestation of HIV Infection
and their Management: II more common lesion. Oral Surg, Oral
Med, Oral Pathol 1991;71:167-71.
36. Scully C, Laskaris G, Pindborg J, et al. Oral manifestations of
HIV infection and their Management. I. More common lesions.
Oral Surg, Oral Med, Oral Pathol 1991;71(2):158-66.
37. Syrjanen S, Leimola-Virtanen R, et al. Oral ulcer in AIDS patient
873
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36
4
Endocrine Disorders
Introduction
Hormones vary tremendously in chemical composition and
in biologic activity. Various disorders of components of the
endocrine system have generalized adverse effects on
skeletal system due to altered metabolism.
Pituitary Gland
Locationit lies within the sella tursica at the base of
brain and it is divided into three distinct lobes.
Lobes of pituitary glandthe anterior lobe also called
as adenohypophysis originates from epithelium of
Rathkes pouch, the intermediated lobe from dorsal
portion of Rathkes pouch and posterior lobe or nuerohypophysis develops from base of third ventricles.
Hormone secreted by anterior lobehormone secreted
by anterior lobe are growth hormone (GH), adrenocorticotropic hormone (ACTH), thyroid stimulating
hormone (TSH), follicle stimulating hormone (FSH),
leutinizing hormone (LH) and prolactin.
Hormone secreted by intermediated lobe and posterior
lobehormone secreted by intermediated lobe is
melanocytes stimulating hormone and by posterior
lobe vasopressin and oxytocin.
Complex feedback interactionthe secretory activities of
the pituitary gland are modulated by hypothalamus
through a series of complex feedback interaction.
Thyroid Gland
Locationit is situated in midline of body in the neck, at
the level of cricoid cartilage having two lateral lobes
which are joined by isthmus. Third pyramidal lobe also
extends from the isthmus.
Developmentembryologically the thyroid gland
develops as a downgrowth from the portion of four
pharyngeal pouches.
Functionit regulates the basal metabolic rate, stimulates
somatic and psychic growth and plays an important
role in calcium metabolism.
Secretion from glandfollicular cells lining the follicles
of the gland secrete tri-iodothyronin and tetra-iodothyronin (thyroxin) which stimulates basal metabolic rate
and somatic and psychic growth of the individuals. Para
follicular cells lie in between the follicles and they secrete
thyrocalcitonin which promotes deposition of calcium
salts in skeletal and other tissue and tends to produce
hypocalcemia.
Prohormoneeighty-three percent of T3 is produced by
monodeiodination of T4 in others tissue such as liver,
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Parathyroid Glands
Locationthe four parathyroid glands lie behind the
lobes of the thyroid. They are not regulated by pituitary
gland, but respond directly to changes in serum ionized
calcium concentration.
Parathyroid hormoneparathyroid hormone (PTH) is a
single chain polypeptide of 84-amino acid which are
synthesized by the chief cells and released in response
to a fall in serum ionized calcium concentration.
FunctionPTH directly promotes reabsorption of
calcium from renal tubules and bones. PTH also has
indirect effect, mediated by increasing conversion of
1, 25 hydorxy cholecalciferol, which results in increase
calcium absorption from the food and enhanced
mobilization of calcium from bone. The initial effect of
PTH on bone is to stimulate osteolysis, returning from
bone to extracellular fluid.
Hyperpituitarism
It results from hyperfunction of anterior lobe of pituitary
gland, most significantly with increased production of
growth hormone. The usual cause of this condition is a
benign, functioning tumor of the eosinophilic cells in the
anterior lobe of the pituitary gland. GH acts directly on
some tissue but most of its biological effects are accounted
by stimulation of secretion of insulin like growth factor I
(IGF-I) and its binding proteins from the lower.
Types
Gigantismif the increase in level occurs before the
epiphysis of the long bone are closed.
Acromegalyif the increase occurs later in life after
epiphysis closure.
Adrenal Gland
Clinical Features
Gigantism
Stature of individualgeneralized overgrowth of most
tissue in childhood. Most of the soft tissue and bones
respond to the excess hormone by enlarging. Excessive
generalized skeletal growth can occur. Patient may often
have of height to 7 to 8 feet. Patients achieve monstrous
size because of tumors of the pituitary gland.
Symptomslater in life it may show genital underdevelopment and excessive perspiration and they complained of headache, lassitude, fatigue, muscle and joints
pain and hot flashes.
Skullthere is increase in size of calvarium which may
lead to change in the hat size (Fig. 36-1). Pituitary tumors
may also induce deficiency of other pituitary hormones
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Acromegaly
Age and sexit is more common in males and occurs
most frequently in 3rd decade.
Symptomsthere is temporal headache, photophobia
and reduction in vision.
Facial featuresbone overgrowth and thickening of the
soft tissue cause a characteristic coarse (loose texture)
facial appearance.
Hand and feethand and feet become large, with clubbing
of the toes and fingers due to enlargement of the tufts of
the terminal phalanges. The terminal phalanges of the
hands and feets become large and the ribs also increase
in size.
Radiographic Features
Skull changesenlargement of sella tursica, enlargement
of paranasal sinus (Fig. 36-2) and excessive pneumatization of temporal bone squames and petrous ridge.
Diffuse thickening of outer table of skull. Enlargement
and distortion of the pituitary fossa.
Oral Manifestations
Symptomsin edentulous patients enlargement of the
alveolus may prevent the comfortable fit of complete
dentures.
Teethteeth in gigantism are proportional to the sized
of jaw and the rest of the body and root may be longer
than normal. The teeth become spaced, partly because
of enlargement of the tongue and partly because upper
teeth are situated on the inner aspect of the lower dental
arch, due to disproportionate enlargement of the two
jaws
Jaw bonemandibular condylar growth is very prominent. Overgrowth of mandible leading to prognathism.
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Diagnosis
Clinical diagnosisstature of individual gives clue to the
diagnosis.
Radiological featurescharacteristic radiographic
findings may yield to the diagnosis.
Laboratory diagnosisgrowth hormone concentration
can be measured by radioimmunoassay technique.
Management
Surgerytrans-sphenoidal surgery may result in cure
of GH excess especially in patients with macroadenoma.
Medical therapyoctreotide, a long acting analogue of
somatostatin, lowers GH. It is administered as subcutaneous insulin 2 to 3 times/day. Other somatostatin
analogues like lanreotide, vapreotide can also be given
in this patient. Dopamine antagonists are also used.
Radiotherapyexternal radiotherapy stops tumor
growth and lowers GH levels. GH levels fall slowly and
there is a risk of hypopituitarism.
Etiology
Disease of pituitary glandcongenital or due to destructive
disease of pituitary gland such as infarct occurring before
puberty.
Space occupying lesionspace occupying lesions
involving the sella turcia like craniopharyngioma,
adenomas and sarcoidosis.
Sheehans syndromeSheehans syndrome is a form of
hypopituitarism caused by infarction of the pituitary
associated with postpartum hemorrhage.
Clinical Features
Short stature of individualthe underdevelopment is
symmetrical, individual is very small and in some cases
there may be a disproportional shortening of the long
Oral Manifestations
Jaw bonemarked failure of development of maxilla and
mandible with lack of condylar growth with short ramus
and this can lead to severe malocclusion and crowding
of the teeth.
Teeththe two important hormones are excreted by this
glandthe somatotrophic and the thyrotrophic are
responsible for the normal eruption of teeth and the
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Clinical Features
Ageaffected infants appear normal at birth, but the
typical clinical features become manifested within the
first few years.
Symptomspatient exhibits alopecia, pigmented areas
of the trunk, atrophic skin, prominent veins and loss of
subcutaneous fat. The individual have high pitched
squeaky voice beak like nose and hypoplastic mandible.
Signthe face is pointed, with the nose resembling the
beak of a bird. The head is large, while mandible is small.
Exophthalmos may be present and joint deformities. The
lip is thin. The intelligence of this patient is either normal
or above normal and even at early age patient behave
like old person.
Oral Manifestations
Formation of irregular dentinthere is accelerated
formation of irregular dentin.
Delayed eruptiondelayed eruption of teeth can occur.
Fig. 36-4: Malocclusion and delayed eruption of teeth seen in
dwarfism patient
Radiographic Features
Teethcomplete absence of third molar bud. Roots of
teeth are short and apices are wide open and pulp canal
toward the apex.
Alveolar bonethere is loss of alveolar bone.
Diagnosis
Clinical diagnosisshort stature of individual with
respect to age will easily diagnose this condition.
Eruption of teeth is also delayed.
Radiological diagnosisshort root with wide open apices
are present
Laboratory diagnosisradioimmunoassay will show level
of growth hormone significantly below normal.
Radiographic Features
Long bonethere is presence of osteoporosis of the long
bones.
Skull bonethere is relative overdevelopment of the
frontal and parietal bones, while ossification may be
delayed and deficient.
Jaw bonethe mandible and maxilla are small, but the
mandible shows the greatest amount of underdevelopment so that the chin is underhung.
Diagnosis
Clinical diagnosisalopecia, pigmented area on face, beak
of bird nose, squeaky voice and delayed eruption of teeth
may give clue to diagnosis.
Radiological diagnosisosteoporosis, delayed
ossification, and underhung chin is present.
Management
Management
Removal of causemanagement is usually directed
towards removal of the cause.
Growth hormone replacement therapythis can be
produced by recombinant DNA technology.
Progeria
Hyperthyroidism
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Etiology
Exophthalmic goiterit is characterized by diffuse
hyperplasia of the thyroid and by eye signs.
Toxic adenomain it hyperfunction originates by a
benign tumor of the thyroid gland.
Pituitary diseasea pituitary disease involving anterior
portion of the gland.
Other causesectopic thyroid tissue, Graves disease,
multi-nodular goiter, thyroid adenoma, choriocarcinoma, excess pituitary TSH, autonomous stroma ovarii,
and polyostotic fibrous dysplasia.
Clinical Features
Age and sexit has predilection for females between
20 and 40 years of age.
Thyroid featuresthyroid is diffusely enlarged, smooth,
possible asymmetrical and nodular, a thrill may be
present, may be tender (Fig. 36-5).
Neuromuscularit includes nervousness, fine tremors,
and muscle weakness, mood swings from depression to
extreme euphoria, emotional liability, hyper-reflaxia, ill
sustained clonus, proximal myopathy, bulbar myopathy
and periodic paralysis.
Gastrointestinalweight loss despite normal or increased
appetite, diarrhea, bowel alterations, anorexia, vomiting
and hyperdefecation. Abdomen, liver and spleen may
be enlarged.
Oral Manifestations
Teethadvanced rate of dental development and early
eruption with premature loss of primary teeth.
Alveolar bonegeneralized decrease in bone density or
loss of some areas of edentulous alveolar bone.
Radiographic Features
Generalized osteoporosisin older children and adults
well marked generalized osteoporosis sometimes
appears but it is not reveal in the jaw.
Alveolar resorptionin some cases, there may be alveolar
resorption and in some cases there may be greater density
of the trabeculae.
Diagnosis
Clinical diagnosisenlargement of thyroid gland with
other systemic features may give clue to diagnosis.
Advanced rate of tooth development.
Radiological featuresgeneralized osteoporosis with
alveolar resorption.
Laboratory diagnosisplasma levels of T3 and T4 are
increased; free thyroxin index is raised in this disorder.
Thyroid stimulating hormone (TSH) decreased. Anemia
may be moderate to severe degree and is seen in patient
with prolonged duration of the disease. The anemia is
hypochromic and abnormal forms of RBC may be seen.
Management
Fig. 36-5: Thyroid gland swelling seen in neck area due to tumor.
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Antithyroid drugsit would be appropriated to give antithyroid drugs for 12 to 18 months to those in whom a
single episode was anticipated. Carbimazolefor 0-3
weeks, 40-60 mg daily in divided doses; for 4-8 weeks,
20-40 mg daily in divided doses and for maintenance
phase, 5-20 mg daily.
Subtotal thyoidectomypatients must rendered euthyroid
before operation. The antithyroid drug is stopped
2 weeks before surgery and replaced by potassium iodate
170 mg daily orally.
Radioactive iodine 131I acts either by destroying
functional thyroid cells or by inhibiting their ability to
replicate. Dose -185-370 mBq (5-10 mCi) is given orally.
-adrenoreceptor antagonistselective -adrenoreceptor
antagonist such as propranolol (160 mg daily in divided
doses or nadolol 40-80 mg once daily) will alleviate
but not abolish symptoms of hyperthyroidism within
24-48 hours.
Hypothyroidism
It is caused by insufficient secretion of thyroxin by the
thyroid gland. Failure of thyrotrophic function on the part
of the pituitary gland or an atrophy or destruction of the
thyroid gland leads to an inability of the thyroid to produce
sufficient hormone to meet the requirement of the body.
Hypothyroidism is cause by decreased or deficient
secretion of thyroid hormones caused by thyroiditis,
insufficient thyroid replacement, post-thyroidectomy, postradioactive iodine therapy.
Types
Cretinismif failure of hormone occurs in infancy.
Juvenile myxedemaif it occurs in childhood.
Myxedemaif it is occur after the puberty. In it, there is
subcutaneous deposition of glycosaminoglycan ground
substance producing non-pitting edema.
Primary hypothyroidismthyroid gland is abnormal.
Secondary hypothyroidismin this pituitary gland does
not produce adequate amount of thyroid stimulating
hormone.
Clinical Features
Cretinism and juvenile myxedema
Ageit may be present at birth or become evidence within
the first few months after birth.
Symptomshoarse cry, constipation, feeding problems
in neonates. Retarded mental and physical growth.
Patient also noticed huskiness of voice, constipation and
hypothermia is present. Skin is dry to touch.
Bonesdelayed fusion of all body epiphysis and delayed
ossification of paranasal sinus, partially pneumatization.
Complications
Coronary artery disease, congestive heart failure.
Increased susceptibility to infection, mental disturbances
including depression.
Oral Manifestations
Cretinism and juvenile myxodema
Teethdental development delayed and primary teeth
slow to exfoliate. Enamel hypoplasia can also be seen.
Abnormalities of dentin formation lead to enlarge pulp
chamber.
Jaw bonemaxilla is overdeveloped and mandible is
underdeveloped. Retarded condylar growth leads to
characteristic micrognathia and open bite relationship.
Tonguetongue is enlarged by edema fluid and due to it
tongue may protruded continuously and such protrusion
may lead to malocclusion of teeth.
Skullthe base of skull is shortened leading to a
retraction of the bridge of the nose with flaring.
Faceface is wide and fails to develop in longitudinal
direction.
Lipslips are puffy, thickened and protruding.
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Radiographic Features
Diagnosis
Clinical diagnosissparse hair, delayed development of
teeth, enamel hypoplasia and macroglossia should give
clue to the diagnosis.
Radiological diagnosisthinning of lamina dura,
wormian bone, and external root resorption can give
clue to the diagnosis.
Laboratory diagnosisthyroid stimulating hormone
(TSH) increased and T3 and T4 decreased. In ECG, a
classical sinus bradycardia with low voltage complexes
and ST/T wave abnormalities. There is raised cholesterol
level and triglycerides level and low serum sodium.
Management
Thyroid preparationpatients are managed by thyroid
preparation. Mainly used is levothyroxin, which is
available as 25, 50 and 100 mg tablets. It is customary to
start slowly and a dose of 50 mg/day should be given
for 3 weeks and finally to 150 mg/day. In the elders and
in patient with ischemic heart disease, the initial dose
should be 25 g/day. In children it should start as early
as possible to avoid major developmental and intellectual
abnormalities.
Hyperparathyroidism
It is an endocrine disorder in which there is an excess of
circulating parathyroid hormone. Excess PTH stimulates
osteoclast to mobilize calcium from skeleton leading to
hypercalcemia in addition to PTH increased renal tubular
re-absorption of calcium.
Following is the sequence of event which gives an idea
of the reaction promoted by this hormone.
Target organthe bone and the kidney are the target
organs of parathyroid hormone which mediates the
osteoclast to resorb bone actively.
Elevation of serum calcium levelwhen the bone is
resorbed, calcium is released in the extracellular fluid
and the serum calcium level is elevated.
Action of parathyroid hormonethe parathyroid hormone
acts on the epithelium of kidney tubules causing diuresis
of phosphorus resulting in decrease in serum phosphors
level. At the same time it induces an increase in calcium
re-absorption from glomerular filtrate. Parathyroid
hormone may also increase the absorption of calcium
from the intestine but this is not definitely established.
Hence in a healthy person injection of parathyroid
hormone produces an elevated plasma calcium level, a
decreased plasma phosphorus level and an increased
alkaline phosphatase level.
Types
Primarythere is autonomous secretion of parathyroid
hormone (PTH) by hyperplasia, benign and malignant
tumor of one or more of the four parathyroid glands.
Secondarycompensatory increase in output of PTH in
response to hypocalcemia. The underlying hypocalcemia may result from an inadequate dietary intake or
poor absorption of vitamin D or from deficient
metabolism of vitamin D in the liver or kidney. It effects
to restore serum calcium level at the expense of the lots
of calcium in bone.
Tertiaryoccasionally parathyroid tumor after long
standing secondary hyperparathyroidism develops this
condition known as tertiary hyperparathyroidism. The
increased parathyroid level produces increased bone
resorption and a resultant hypercalcemia.
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Clinical Features
Oral Manifestations
Brown tumorit may develop peripherally or centrally.
This can be presented as swelling which may appear
intraorally or extraorally (Figs 36-6 and 36-7).
Teethgradual loosening, drifting and loss of teeth,
malocclusion.
Radiographic Features
Demineralization of skeletonbone matrix contains less
than normal amounts of calcium producing unusually
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Differential Diagnosis
Diagnosis
Clinical diagnosisbrown tumor, symptoms of renal
calculi, peptic ulcer can diagnose this condition.
Radiological featuresdemineralization of skeleton,
pepper pot skull, brown tumor, and osteitis fibrosa cystic
can give clue to the diagnosis.
Laboratory diagnosisbiopsy shows osteoclastic
resorption of the trabeculae of the spongiosa and along
the blood vessels in the haversian system of the cortex.
Fibrosis especially in the marrow spaces is marked. The
serum calcium level is raised and serum phosphorus
Unilocular
Postextraction socket and surgical defectit will give history
of extraction and surgery respectively.
Primordial bone cyst, traumatic bone cyst and odontogenic
cystthey all occur in a younger age group than in
hyperparathyroidism and have normal serum chemistry
values.
Multilocular
Paget diseasecalcium metabolism is normal and bone
formation usually exceeds the bone resorption resulting
in an elevated blood alkaline phosphatase.
Ameloblastomait usually shows a honeycomb
appearance accompanied with paresthesia and normal
serum chemistry level.
Central giant cell granulomait can only be differentiated
by serum chemistry level.
Cherubismthe lesion is bilateral, seen in children and
also there is usually familial involvement which is not
so in giant cell lesion of hyperparathyroidism.
Aneurysmal bone cyst and central hemangiomait occurs
in a younger age group.
Osteomalaciablood calcium levels are decreased.
Fibrous dysplasiaosseous changes are frequently
localized, loss of lamina dura is less common.
Multiple myelomalesions are punched out, generalized
bone demineralization in hyperparathyroidism helps
in distinguishing.
Management
Surgeryhyperplastic tissue should be removed
surgically.
Vitamin D supplementthe oral administration of
vitamin D in secondary type can prevent skeletal
demineralization in most of the cases.
Parathyroidectomyit is indicated in patient where
patient does not respond to treatment.
Precautionrestriction of dietary phosphate, phosphate
binding agent and aluminum salts should be done.
Hypoparathyroidism
It is an uncommon condition in which there is insufficient
secretion of parathyroid hormone. Parathyroid hormone is
needed for regulation of calcium level in extracellular tissue.
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Etiology
Surgical damagesurgical damage to parathyroid
gland and their vascular supply during thyroid gland
procedure.
Damage from radiotherapyparathyroid damage may
occur from radioactive iodine 131.
Autoimmuneautoimmune destruction of parathyroid
gland may take place.
Otherhypoparathyroidism can also be associated
with DiGeorge syndrome and endocrine-candidiasis
syndrome.
Clinical Features
Hypocalcemiahypocalcemia can occur due to loss of
parathyroid function. It can lead to tetany in the form of
carpopedal spasm of the wrist and ankle joint.
Symptomsthere is stiffness in hands, feet and lips.
There is also paresthesia of hand, feet and around the
mouth. Tingling in the circumoral area, fingers and toes.
Patients may complaint of anxiety, depression, epilepsy
and chorea. Reduction in intellectual capacity due to
calcification within the brain.
Trousseaus signit is elicited by occluding blood flow
to the forearm for 3 minutes with sphygmomanometer
cuff applied to the arm and raising the pressure above
systolic level. This will induce carpopedal spasm.
Oral Manifestations
Teethhypoplasia of enamel (Fig. 36-10), delayed
eruption, external root resorption and root dilacerations.
There is also blunting of molar roots.
Radiographic Features
Calcificationcalcification of basal ganglion which
appears flocculent and paired with the cerebral
hemisphere on PA view.
Dental radiographic findingradiograph of jaw may
reveal enamel hypoplasia, external root resorption,
delayed eruption or root calcification.
Diagnosis
Clinical diagnosisTrousseaus sign, Chvostek sign and
features of tetany may diagnose this condition.
Radiological featurescalcification of basal ganglion with
enamel hypoplasia may give clue to diagnosis.
Laboratory diagnosisthe serum calcium level is
decreased usually below 7 mg/dl. Serum phosphate
level correspondingly elevated. Urinary calcium is low
or absent.
Management
Calcium and vitamin D supplementsupplemental
calcium and vitamin D depending on severity of the
hypocalcemia and the nature of the associated signs
and symptoms.
Intravenous calcium gluconatein severe cases
intravenous administration of calcium gluconate is the
treatment of choice.
Pseudohypoparathyroidism
It is also called as Albright Hereditary osteodystrophy,
acrodysostosis. In this normal parathyroid hormone is
present in the body but biochemical pathway responsible
for activating target cells are defective in function.
Types
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Clinical Features
Staturepatient manifest short stature due to early
closure of certain bony epiphysis.
Shortened fingerhand shows shortening of the
metacarpal bones, so that finger are short.
Osteoma cutissubcutaneous calcification may be
present in some patient
Oral Manifestation
Facial featuresmidfacial hypoplasia, The face is
rounded in appearance.
Teeththere is generalized enamel hypoplasia,
oligodontia, and delayed eruption of teeth present.
Radiological Features
Apices of teeththere is blunting of apices of teeth
Dagger shaped calcificationdagger shaped calcification
seen in pulp of teeth.
Pulp chamberwidened pulp chamber is present.
Diagnosis
Clinical diagnosisshort stature, osteoma cutis oligodontia is present.
Radiological featuresdagger shaped calcification is
typical of this disease.
Laboratory diagnosiselevated serum level of PTH with
hypocalcemia, hyperphosphatemia.
Management
Vitamin D and calciumthis can be given to control
pseudohyperparathyroidism.
Types
Type I or Insulin dependent (IDDM)it occurs due to
deficiency. There is lack of insulin production resulting
in severe hyperglycemia and ketoacidosis.
Pathogenesis
Type I diabetes mellitus
Increase blood glucose levelas there is deficiency of
insulin glucose will remain in blood as absorption of it
is hampered. So blood glucose level is increased.
Glucose as main energy sourceas glucose is main source
of energy in the body and it can not get absorbed patient
feels tried and loosed its weight inspite increased food
intake.
Polyuria and polydipsiadue to hyperglycemia, osmolarity of blood and urine increased which will results in
frequent urination which again lead to increase in water
intake (polydipsia).
Type II diabetes mellitus
Decrease in number of insulin receptorin this condition
there is decrease in number of insulin receptor results in
non absorption of glucose in the body. Thus patient
show insulin resistance.
Etiology
Type I diabetes mellitus
Virusesseveral viruses are been implicated including
infection with mumps Coxsackies B4, retrovirus, rubella
and cytomegalovirus and Epstein-Barr virus. Virus
particle known to cause cytopathic or autoimmune
damage to beta cells have been isolated from the
pancreas.
Dietbovine serum albumin (BSA) a major constituent
of cows milk has been implicated in triggering type I
diabetes. It has been shown that a child who has taken
cows milk early in infancy has been more prone to
develop type I diabetes mellitus as compared to other
who has taken breast milk.
Stressit may precipitate the development of type I diabetes by stimulating the secretion of counter regulatory
hormones and possibly by modulating immune activity.
Immunological factorsthere is evidence that type I
diabetes is a T cell mediated autoimmune disease. There
is also HLA linked genetic predisposition. Monocular
cell infiltration of pancreatic islets restoration in selective
destruction of insulin secreting cells and induction of
remission by immunosuppressive drugs such as
cyclosporine suggest its immunological etiology.
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Clinical Features
Oral Manifestations
Effect on periodontiumit will influence the onset and
course of periodontal disease. Patient with diabetes are
more prone to develop periodontal disease than are those
with normal glucose metabolism. As such diabetes
mellitus does not cause periodontal disease directly but
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Radiographic Features
Loss of lamina dura with blurring of alveolar crestslight
discontinuity or blurring of the cortex of alveolar crest to
wide destruction of lamina dura.
Bone lossthere is also horizontal and vertical bone loss.
Complications
Microangiopathyit results in occlusion of small blood
vessels producing peripheral vascular disease. This
results in decreased tissue perfusion which in turn
results in severe infection like gangrene.
Coronary artery diseasevascular occlusion may affect
the coronary artery resulting in myocardial infraction,
cerebrovascular accident and stroke.
Blindnesswhen retinal vessels are affected blindness
may results.
Other complicationketoacidosis, premature mortality,
and diabetic coma may result.
Diagnosis
Clinical diagnosispolyuria, polydipsia and polyphagia
with periodontal problems may give clue to the diagnosis.
Radiological diagnosisnot specific
Plasma glucose concentrationunequivocal elevation of
plasma glucose concentration greater than 140 mg/dl.
The glucose tolerance testplasma glucose concentration
is 200 mg/dl.
Taste paper stripstrips are available for direct estimation
of blood glucose level.
Bloodrandom glucose elevated, fasting glucose
elevated, 2 hour postprandial glucose elevated.
Management
Diet control
Balance calorie intakethe patient with NIDDM,
particularly those who are obese, dietary control
toward a balanced calorie intake and exercise leading
to weight loss is the sole treatment require.
Calories from carbohydratein diabetic patient, it is
recommended that the percentage of calories derives
Diabetic Insipidus
Causesit occurs due to insufficiency of the posterior
pituitary hormone. Traumatic episodes, such as head
trauma or surgical procedures carried out near the
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Dental Consideration
Emergencyemergency can occur due to diabetese coma
or insulin shock. If tolbutamide, chlorpropamide or small
doses of insulin is taken by the patient there will be less
chances of diabetic coma. However, if the patient takes
large daily dose of insulin there is possibility of diabetic
coma or insulin shock. If the patient complains of being
thirsty, nauseous and shortness of breath and has warm
dry skin, the patient is most likely hyperglycemic and
should be immediately refer to the physician. No
treatment will be required by the dentist.
Dental managementdeliver treatment in such a way so
as to minimize disturbances of metabolic balance.
Appointmentappointment should be of short
duration and in the morning. Encourage to maintain
their standard regimen.
Glucose drinkglucose drink should be available if
patient complains of hypoglycemia.
Local anesthesia without epinephrineuse local
anesthesia without epinephrine in the dental
procedure. There is increased incidence of dry socket
is due to decreased blood supply to mandible is
caused by arteriosclerosis in long standing diabetes.
If you are giving epinephrine, it will further reduce
blood supply which further increases chances of dry
socket.
Suturingfollowing extraction suturing of the socket
should be done to aid homeostasis.
Physician referralphysician advice should be taken
before arranging general anesthesia for dental
treatment.
Antibiotics prophylaxisantibiotic prophylaxis before
dental surgery to prevent subsequent infection.
Avoid complicated oral procedurecomplicated oral
procedure in dental emergencies should be avoided
whenever possible in uncontrolled diabetics until
stabilization of blood glucose level is achieved.
Etiology
Autoimmunesporadic and polyglandular syndrome
may cause destruction of adrenal gland. It may be cause
by bilateral destruction of the suprarenal glands.
Infectiontuberculosis and some deep fungal infection
may cause this disease.
Other causemetastatic carcinoma, intradermal hemorrhage, amyloidosis, hemochromatosis, adrenal
infarction and congenital adrenal hypoplasia may be
the causative factors.
Drugs which can cause Addisons disease are aminoglutethimide, ketoconazole and etomidate.
Clinical Features
Age and sexit is more common in males and, while
found in all age groups, it is most frequently seen in the
3rd and 4th decade.
Symptomsfeeble heart action, general debility,
vomiting, and diarrhea and severe anemia. Patient
complains of postural hypotension. There is also
reduced resistance to infection, trauma, and stress.
Signthe disease is characterized by bronzing of skin,
a pigmentation of the mucous membrane.
Metabolic functiondecrease cortisol level interferes with
the manufacture of carbohydrates from protein, causing
hypoglycemia and diminished glycogen storage in the
liver.
Neuromuscular functionneuromuscular function is
inhibited, producing muscle weakness.
Oral Manifestation
Bronze pigmentationthe pale brown or deep chocolate
pigmentation of the oral mucosa, spreading over the
buccal mucosa form the angle of the mouth and/or
developing on the gingiva, tongue (Fig. 36-12), and lips
may be first evidence of disease.
Diagnosis
Clinical diagnosisbronze skin and bronze pigmentation in oral cavity, decreased metabolic function may
give clue to the diagnosis.
Laboratory diagnosisbiopsy of oral lesion show
acanthosis with silver positive granules in the cells of
the stratum germinativum. Anemia is normocytic and
normochromic associated with reticulocytosis. High
blood levels potassium and low concentration of sodium
and chloride. There is also elevated blood urea nitrogen
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Clinical Features
Management
Glucocorticoids replacementcortisol is the drug of choice.
In patient who are not critically ill hydrocortisone
15 mg on waking and 5 mg at 6 pm in evening.
Supplement Mineralocorticoidsit can also be given.
Adrenogenital Syndrome
It refers to any situation in which there is overproduction
of androgens. It results when hyperplasia or tumors of the
adrenal cortex occur. It may appear at 3 different times of
life, i.e. at birth, in childhood and in adult. Clinical features
vary according to appearance of lesion.
At birthin female child it produces pseudohermaphroditism, while in male child it produces macrogenitosomia praecox.
In childhoodin the females it produces masculinization
and in males it produces sexual precocity.
In adultsin females it produces virilism and in males it
produces feminization.
If the disease begins early premature eruption of the teeth
may occur. This disease managed by administration of
corticosteroid or estrogen.
Cushings Syndrome
Cushings syndrome arises from excess secretion of
glucocorticoids by the adrenal glands. It is described by
Harvey Cushing in 1932.
Etiology
Adrenal tumorCushings syndrome is caused by adrenal
adenoma, adrenal carcinoma, adrenal hyperplasia and
basophilic adenoma of the anterior lobe of pituitary gland.
Oral Manifestations
Dental agein children growth and development
including skeletal and dental age may be retarded.
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Adrenal Insufficiency
It is relatively rare and usually occurs in connection with
an acute septicemia and is called as Waterhouse-Friderichsen
syndrome. This occurs in patient who are on long-term
steroid for the treatment of variety of systemic condition
developed adrenal insufficiency.
Types
Radiographic Features
Osteoporosisgeneralized osteoporosis is present. The
bone likely to involve are the vertebrae and the ribs
although the long bones may be affected.
Demineralizationthere is osseous demineralization
with pathological fractures, often superimposed.
Skullit may show diffuse thinning and have mottled
appearance.
Lamina durajaw may show areas of loss of lamina dura.
Diagnosis
Clinical diagnosismoon facies, buffalo hump, purple
striae on abdomen will easily diagnosed this condition.
Radiological featuresgeneralized osteoporosis with loss
of lamina dura may give clue to diagnosis.
Laboratory diagnosisthis is done by measuring serum
ACTH and cortisol level after administration of
dexamethasone. In normal patient this level will be
decreased but it is unaffected in patient with Cushings
syndrome.
Management
Surgerytumors involving the adrenal cortex are
removed surgically and often require postoperative
administration of corticosteroids to maintain normal
glucocorticosteroids level.
Radiotherapyin case of Cushings syndrome due to
adrenocortical hyperplasia, pituitary irradiation is the
best treatment.
Drugs usedmetyrapone in dose of 2-6 gm per day in
divided doses by mouth. Other drug given is
aminoglutethimide, ketoconazole which act by blocking
steroid synthesis.
Etiopathogenesis
Sudden withdrawal of steroidit usually occur following
sudden withdrawal of steroid hormones in a patient
who has primary adrenal insufficiency. Following
sudden withdrawal in a patient with normal adrenal
cortices but with a temporary insufficiency resulting
from cortical suppression by exogenous corticosteroid
administration
Following stressfollowing stress such as physiologic
or psychological stress.
Bilateral adrenalectomyfollowing bilateral adrenalectomy or removing of a functioning adrenal tumor that
had been suppressing the other adrenal gland.
Destruction of pituitary glandfollowing sudden
destruction of the pituitary gland.
Traumafollowing injury to both adrenal glands by
trauma, hemorrhage, infection, thrombosis or tumor.
Clinical Features
Ageit occur primarily in children but can occur in
adults.
Onsetit is characterized by rapidly fulminating septic
course, a pronounced purpura and death within 48 to
72 hours.
Symptomsin this, patient is not able to tolerate the
stress. There is anxiety, fatigue, hypotension, abdominal
pain, nausea, vomiting, cold clammy skin, lethargy, and
partial or complete loss of consciousness. There is also
mental confusion occur in acute adrenal insufficiency.
Signoral, conjunctival, and vaginal mucosae often
show patches of pigmentation. In some patient,
particularly in the dark-skinned races, patchy area of
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Oral Manifestations
Diseases of Gonads
Hypergonadism
Diagnosis
Clinical diagnosisstress intolerance, mental confusion
and hyperpigmentation of buccal and labial mucosa will
give clue to the diagnosis.
Laboratory diagnosisplasma cortisol levels are low and
fail to raise after administration of ACTH. Plasma ACTH
levels are elevated and serum sodium and chloride and
urinary 17-ketosteroid and 17-hydroxy-corticosteroids
are low.
Hypogonadism
Dental Considerations
Pregnancy
Management
Prevention
Historya careful history should be taken if the patient
has been using steroids on long-term basis.
Additional steroid dosesuch patients should be
administered additional dose of steroids prior to surgery
such that dose is increased to double or triple level 2 to
3 days preceding the surgery. Then it should be gradually
taper to the maintain level. Patient who has been on
steroid therapy but presently is off this therapy for the
last one year without any adverse effects, needs no steroid
supplementation.
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Dental Management
Routine dental procedurescaling and prophylaxis
should be performed as often as is necessary to control
local etiologic factors and reduce gingival inflammation.
Second trimester is the safest period during which to
perform routine dental care. Stressful procedure should
be avoided during pregnancy. In a pregnant woman
stress and strain involved can lead to complication
during the treatment.
Radiographdental radiographs or X-rays are not used
for routine dental care. In emergency situations, X-rays
may be needed to diagnose a problem, however proper
safety measures should be taken. These measures
include the lead apron, reduced radiation and the X-ray
beam position. This again is most important in the first
trimester.
Drugswe must also modify drugs that can be
administered to the pregnant or breastfeeding patient.
Certain anesthetics, pain relievers, antibiotics, and
sedative drugs that may be used are considered unsafe
for the developing fetus and must be avoided. For breastfeeding mothers there is concern over certain drugs that
may be absorbed into the mothers milk. The local
anesthetic that we use is considered safe for emergency
dental care needs.
Syncopeif syncope develops turning the patient on left
side will relieve the pressure and put the patient back to
normal. Supine position can lead pressure on inferior
vena cava by the fetus leading to poor venous return
and lead to hypotension further aggravating the
condition.
First and third trimesterall planned surgical procedures
should be avoided in the 1st and 3rd trimester to avoid
fetal stress and premature labor. This is because of the
vulnerability of the growing fetus in the first 3 months
or trimester and the comfort level of the mother in the
last trimester Third trimester dental care is best postponed
due to the comfort level of the patient and to avoid supine
Menopause
It begins when menstrual function ceases and it usually
occur between the ages 40 to 55. There are numerous
symptoms associated with it and they are caused by
deficiency of estrogen.
Irritability, insomnia, nervousness, osteoporosis,
back and joint pain can also occur in menopause. Patient
may complaint of burning mouth and tongue, taste
abnormalities and dryness of the mucous membrane are
also present. There may be desquamative gingivitis in which
there is atrophy and ulceration of the gingival tissue and
bleeding.
Treatment consists of estrogen replacement therapy
depending on the symptoms.
Suggested Reading
1. Buckerfield JP. Primary Hyperparathyroidism causing bony
swelling in the edentulous jaw. BDJ 1971;131:497.
2. Cianciola LJ, Park BH, et al. Prevalence of periodontal disease in
insulin dependent diabetes mellitus (Juvenile diabetes). JADA
1982;104:653-60.
3. Cohen RB, Wilcox CW. A case of acromegaly identified after
patient complaint of apertognathia. Oral Surg, Oral Med, Oral
Pathol 1993;75:583-6.
4. Falk H, Hugoson A, Thorstensson H. Number of teeth, prevalence
of caries and periapical lesions in insulin-dependent diabetics.
Scand J Dent Res 1989;97:198-206.
5. Greenberg MS, Brightman VJ, et al. Idiopathic hypoparathyroidism, chronic candidiasis and dental hypoplasia. Oral Surg,
Oral Med, Oral Pathol 1969;28:42-53.
6. Kosowicz J, Rzymski K. Abnormalities of tooth development in
pituitary dwarfism. Oral Surg, Oral Med, Oral Pathol 1977;44:
853-63.
7. LaFranchi S. Congenital hypothyroidism: etiologies, Diagnosis
and Management. Thyroid 1999;9:735-40.
8. Murrah VA. Diabetes mellitus and associated oral manifestation:
a review. J Oral Pathol 1985;14:271-81.
9. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology
(2nd edn), Saunders Elsevier, 2004.
http://dentalebooks.com
16. Silverman S Jr, Ware WH, Gillooly C: Dental aspect hyperparathyroidism. Oral Surg, Oral Med, Oral Pathol 1968;26: 184-9.
17. Stephenson E, Haug RH, Murphy TA. Management of the diabetes
oral and maxillofacial surgery patient. J Oral Maxillofac Surg
1995;53:175-82.
18. Walls AWG, Soames IV. Dental manifestation of autoimmune
hypoparathyroidism. Oral Surg, Oral Med, Oral Pathol 1993;75:
452-4.
19. Wals AWG, Soames JV. Dental manifestations of autoimmune
hypoparathyroidism. Oral Surg, Oral Med, Oral Path 1993; 75:
445-52.
20. Wysocki GP, Daley T. Benign migratory glossitis in patient with
juvenile diabetes. Oral Surg, Oral Med, Oral Pathol 1987;63:6870.
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37
4
Blood Disorders
Introduction
The cellular elements of the blood as well as its plasma
proteins play an extraordinary role in many physiologic
mechanisms of the body. The circulating blood has a
profound effect on the maintenance of normal oral mucous
membrane, especially in the mucosa of tongue.
Many important disorders of blood present with
symptoms and signs are seen in the oral cavity. The dentist
is frequently the first medical personnel to encounter such
disorders.
Physiology of Blood
Blood is unique bright red (arterial) to dark red (venous)
colored liquid of variable composition, circulating through
the vessels of body.
It participates in all physiologic and pathologic activities
in all organs and is composed of liquid called as plasma
in which there are suspended erythrocytes, leukocytes and
thrombocytes collectively called as hemocytes.
If blood is allowed to clot, an amber colored liquid
remains after the separation of the clot and is known as
serum. It differs from plasma only by the loss of protein
fibrinogen, which is removed in the coagulation process.
Composition
Blood is a highly complex fluid, which is composed of two
parts liquid plasma (55%) and different types of cells (45%).
Cellsit consists of red blood cells or corpuscles or
erythrocytes, white blood corpuscles or leukocytes and
platelets or thrombocytes
Waterit is about 91 to 92%.
Solidit consists of sodium, potassium, calcium,
magnesium, phosphorus, iron, copper, etc.0.9%.
Plasma Proteins
In normal circumstances, total amount of plasma proteins
varies form 6.5 to 7.5% and an average of 7%.
Composition
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Blood Disorders
Specific gravity of blood1.052 to 1.063 and primarily
depends upon the ratio of plasma to red cells.
Viscosity of bloodthe relative viscosity of water, plasma
and whole blood are roughly 1, 1.8 and 4.7.
pHthe pH of blood varies between 7.36 and 7.45, the
average is about 7.4.
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Functions of RBC
Respiratorythey carry oxygen and carbon dioxide.
Acid base balance they help to maintain the acid base
balance.
Viscositythey maintain the viscosity of blood.
Pigmentvarious pigments are derived from hemoglobin after disintegration of RBCs.
Hemoglobin
It is a red conjugated protein. The hemoglobin molecule is
roughly spherical in shape, consisting of two pairs of
polypeptide chains to which a highly colored heme group,
which is a complex of iron and protoporphyrin, is added.
The protein portion of the molecule is called globin.
Functions of Hemoglobin
Oxygen carriageit is essential for oxygen carriage. It
combines easily with oxygen to form oxyhemoglobin.
Oxyhemoglobin holds oxygen loosely which can be
easily displaced by many other gases like CO, CO2, H2S,
etc. to form a more stable compound.
Carbon dioxide transportit helps in carbon dioxide
transport by directly combining with CO2 to form a
carbamino compound.
Acid base balanceit constitutes one of the important
constituents of blood and helps in maintaining acid base
balance of blood.
Pigmentvarious pigments of bile, stool, urine, etc. are
formed from it.
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Physiologic Variations
Types of WBC
Granular leukocytes or granulocytesit consist of
neutrophils62-70%, eosinophils1-4% and basophils
0-1%.
Agranular leukocytes or agranulocytesit consist of
lymphocytes (25 to 30%)they are of two types, i.e. small
lymphocytes and large lymphocytes and monocytes5
to 10%.
Functions of WBC
Phagocytosisthe neutrophils and the monocytes engulf
and digest foreign bodies and bacteria.
Defensive mechanismsleukocytes play an important role
in the defensive mechanism of the body by manufacturing fraction of serum globulin and formation of
fibroblasts.
Trephonesleukocytes manufacture trephones which
have great influence on nutrition, growth and repair of
tissue.
Heparinsecretion of heparin which prevents
intravascular clotting.
Anti-histaminic functionit defends against allergic
reactions.
Formation of fibroblastslymphocytes may be converted
into fibroblasts in areas of inflammation.
Platelets or Thrombocytes
They are non-nucleated, round or oval bi-convex discs
having an average size of about 2.5 microns and are covered
by a unit membrane. The average number of platelets in a
Functions of Platelet
Hemostasis and blood clottingwhen there is bleeding,
platelets disintegrate and liberate thromboplastin
and 5-hydroxytryptamine. Thromboplastin activates
prothrombin to form thrombin whereas 5-hydroxytryptamine has a vasoconstrictor effect and thus help in
hemostasis.
RepairIn circulation, platelets adhere to the damaged
endothelial lining of the capillaries and thus bring about
speedy repair.
Hasten clot retractionspeed of clot retraction is directly
proportional to the number of platelets present.
Blood Coagulation
When blood is shed, it loses its fluidity in few minutes and
sets into semisolid jelly; this process is called as coagulation
or clotting of blood.
Clotting Factors
Factor I or fibrinogenduring clotting, fibrinogen is
converted to fibrin to form clot.
Factor II or prothrombinduring clotting, prothrombin is
converted to thrombin by thromboplastin.
Factor III or thromboplastinit is essential for conversion
of prothrombin into thrombin.
Factor IV calciumit is essential for the formation of both,
intrinsic and extrinsic thromboplastin and also in the
conversion of prothrombin to thrombin.
Factor V or labile factor or accelerator globulin or
proaccelerinit is necessary for complete conversion of
prothrombin into thrombin by extrinsic or intrinsic
thromboplastin.
Factor VI or accelerinit is hypothetical activation
product of proaccelerin.
Factor VII or stable factorfactor X is converted to activated
factor X by tissue thromboplastin released following
tissue trauma, in the presence of factor VII for extrinsic
pathway.
Factor VIII or anti-hemophilic factor or anti-hemophilic
globulin or platelet cofactorit helps in the formation of
intrinsic thromboplastin and prothrombin conversion.
Factor IX or Christmas factor or plasma thromboplastin
component or platelet cofactor IIit is necessary for
intrinsic thromboplastin formation.
Factor X or Stuart factorit has properties similar to factor
VIII.
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Blood Disorders
897
Fig. 37-1A
Blood Group
Human beings may be put into four group according to the
nature of the agglutinogens possessed by their RBC. These
are called as A, B, AB and O (if no agglutinogen is present).
There are different types of Rh antigens each of which is
called as Rhesus (Rh) factor. These types are designated as
C, D, E. If D antigen is prominent, the person is said to be
Rh positive.
Fig. 37-1B
Fig. 37-1C
Figs 37-1A to C: A diagrammatic representation of mechanism of blood coagulation.
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Anemia can be classified on the basics of etiology and morphology. Some of important anemias are described below.
Iron deficiency
Deficiency of vitamin B 12, folic acid (pernicious anemia and
megaloblastic anemia)
Pyridoxine responsive anemia
Protein deficiency
Ascorbic acid deficiency
Posthemorrhagic Anemia
The anemia caused by blood loss may occur in variety of
conditions causing bleeding.
Types
Acutewhen blood loss occurs in large amounts in a
short period of time, anemia may develop even though
iron stores remain adequate. It is called as acute posthemorrhagic anemia.
Chronicthis develops when there is chronic blood loss
in small amount over prolonged period of time and is
due to depletion of iron in body. Other findings are the
same as that of iron deficiency anemia.
Clinical Features
Factors affecting the clinical featuresthe manifestations
of hemorrhagic anemia depend on the rate and
magnitude of bleeding; the time elapsed since it took
place and the sitewhether it is external or internal.
Blood loss (500 to 1000 ml)when the blood loss is about
500 to 1000 ml, most of the patients do not present any
symptoms, but few may present with weakness and
sweating.
Blood loss (1000 to 1500 ml)with rapid loss of 1000 to
1500 ml, a previously healthy individual may experience
lightheadedness and hypotension.
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Blood Disorders
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Type of anemia
Description
Macrocytic
Normocytic
Simple microcytic
Hypochromic microcytic
Iron deficiency
Diagnosis
Clinical diagnosishistory of blood loss with features of
anemia may diagnose this condition.
Laboratory diagnosisplasma volume and red cell mass
are reduced in proportional amount. Anemia is
Management
Restoration of blood volumeblood transfusion should
be given to restore blood volume.
Other therapyintravenous infusion of saline, dextrin,
albumin or plasma.
Causes
Inadequate intakeinadequate intake of iron in the diet
may lead to deficiency.
Malabsorptionmalabsorption of iron due to
hypochlorhydria and diarrhea may lead to deficiency
state.
Increase requirementincreased requirement of iron in a
growing child and in pregnancy.
Increases lossincreased loss of iron due to injury,
recurrent epistaxis and peptic ulcer. Chronic blood loss
such as menstrual and menopausal bleeding parturition.
Gastrotomysubtotal or complete gastrotomy may cause
iron deficiency anemia.
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Clinical Features
Oral Manifestations
Pallor of mucosain iron deficiency there is pallor of oral
mucosa and gingiva. The normal pink color is lost due
to lack of oxygenated blood in the capillary bed in lamina
propria and is associated with lowered levels of
hemoglobin.
Atrophy of oral mucosathe generalized atrophy of oral
mucosa both in tongue and buccal mucosa occurs.
Tongue changesthere is redness, soreness or burning of
tongue. The filliform papillae over the anterior two thirds
of tongue are the first to undergo atrophy (Fig. 37-3). In
severe cases, fungiform papillae are also affected leaving
the tongue completely smooth and waxy or glistening
in appearance (Fig. 37-4).
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Blood Disorders
Angular cheilitisthere is cracking and fissuring at the
corner of mouth.
Ulcerationthere is softening of epithelium which leads
to linear ulceration of the skin, extending up to and
beyond the mucocutaneous junction. There may be pain
or bleeding from ulcerated tissues. Recurrent aphthous
ulceration and candidal lesions can also occur in iron
deficiency anemia.
Slow healingpatient may show slow healing after oral
surgical procedures.
Gingival enlargementin some cases, there may be
gingival enlargement.
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Diagnosis
Clinical diagnosiskoilonychia, neuropathy, angular
chelitis and depapillation of tongue may yield in
diagnosis.
Laboratory diagnosisthe anemia is microcytic and
hypochromic and the peripheral smear show abnormal
forms of RBCs. There is reduced hemoglobin level, as
low as 4g/100ml. There is normal or slightly reduced
RBC count. MCV, MCH and MCHC are all reduced.
Management
Iron supplementalmost all patients can be treated by oral
supplements of iron by giving ferrous fumerate or ferrous
sulphate. It is given in dose of 300 mg three to four times
a day for a period of 6 months. The parenteral route of
administration is suitable for few patients who are unable
to take iron by mouth or who are unable to or absorb iron
by mouth. The recommended single dose of iron sorbitol
is 1.5 mg of iron per kg of body weight, given daily.
Plummer-Vinson Syndrome
It is also called as Paterson-Brown-Kelly syndrome. It is
characterized by dysphagia, iron deficiency anemia,
dystrophy of nails (koilonychia) (Fig. 37-5) and glossitis.
Clinical Features
Ageit is exclusively found in middle aged women.
Appearancepatient of this syndrome have got
characteristic asthenic appearance.
Dysphagiait occurs due to the formation of webs in
esophagus.
Angular cheilitisvermilion borders of the lip are very
thin and there is often angular cheilosis.
Symptomspatients complaint of spasm in throat or
food sticking in throat. There is also complaining of sore
mouth and inability to retain dentures.
TongueA smooth, red, occasionally enlarged and often
sore tongue with fissuring is occurs.
Diagnosis
Clinical diagnosisdysphagia, glossitis, with features
of iron deficiency anemia will diagnose Plummer-Vinson
syndrome.
Laboratory diagnosissame features as that of iron
deficiency anemia. Biopsy will show atrophic epithelium
and atrophy of lamina propria and muscles.
Management
Correction of anemiamanagement is directed management of iron deficiency anemia
Esophageal dilationesophageal dilation is required to
correct dysphagia.
Erythroblastosis Fetalis
It is type of isoimmune hemolytic anemia. It occurs due to
isoimmune antibodies. It is also called as hereditary disease
of new born (HDN). Congenital hemolytic anemia due to
Rh incompatibility results from destruction of fetal blood
brought about by a reaction between maternal and fetal
blood factors. The Rh factor, named after Rhesus monkey,
was discovered by Landsteiner and Wiener in 1940 as a
factor in human RBC which reacts with rabbit antiserum
produced by administration of red bloods cells from Rhesus
monkey.
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902
Pathogenesis
Diagnosis
Clinical Features
Stillbornsome infants are stillborn.
Symptomschildren having pallor, jaundice,
compensatory erythropoiesis (both medullary and extramedullary) and edema resulting in fetal hydrops.
Kernicterusit may manifest itself by apathy and poor
feeding and later by mental retardation, irritability and
cranial nerve palsies.
Management
Antenatalmaternal sensitization is prevented by the
administration of 300 mg of Rh antiglobulin after
amniocentesis has been done. Management of affected
fetus can be done by intensive plasmapheresis of mother
during pregnancy in order to remove maternal antibodies or by intravenous transfusion of blood into the
fetus to prevent fetal anemia.
Post natalin infants, exhibiting only anemia, fresh
packed RBCs are given to correct anemia.
Splenectomyit results in striking and permanent
improvement, both in anemia and symptoms. After
splenectomy, daily penicillin V 250 mg 12 hourly is given
to avoid infections.
Blood transfusionsevere hemolytic crisis needs blood
transfusion. Folic acid should be given 5 mg orally to
support increased erythropoiesis.
Vaccinationthe patient should be vaccinated against
pneumococci and hemophilus influenzae.
Oral Manifestations
Teethit may manifest in teeth by the deposition of blood
pigment in enamel and dentin of developing teeth giving
them a green, brown or blue hue. It occurs in those portions
of the teeth which are being laid down during the time
when icterus was at its height.
Enamel hypoplasiaenamel hypoplasia is also reported
occurring in some cases of erythroblastosis fetalis. It
usually involves incisal edges of the anterior teeth and
middle portion of the deciduous cuspid and first molar
crown.
Rh humpthere is ring like defect called as Rh hump.
Radiographic Features
Radiodensitythere is presence of transverse lines of
increased and decreased radiolucency, occurring at the
ends of some long bones in some areas.
Cranial vaultthere is also increased thickness of cranial
bone which includes maxilla and mandible. The bones
of vault are thickened as a result of increased thickness
of diploe.
Radiating spiculeradiating spicule may also be present.
Pathogenesis
Substitution of amino acidsubstitution of amino acid
glutamine on position 6 present in the chain of the
hemoglobin-A, by valine.
Formation of hemoglobin Sthis will give rise to an
abnormal hemoglobin, i.e. hemoglobin S.
Formation of tactoidswhen Hbs is deoxygenated, it
forms structures know as tactoids.
Sickle shaped cellstactoids will distort the RBC
membrane and produce characteristic sickle shaped cell
which are destroyed by RE cells.
Thrombosis and infarctionsickle cells increase blood
viscosity and tend to reduce blood flow leading to
thrombosis and tissue infarction.
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Blood Disorders
Hemolysisin addition, these cells are phagocyte in large
number by mononuclear-phagocyte system which
reduce their lifespan and give rise with hemolysis.
Folic acid deficiencypatients may develop severe folic
acid deficiency due to increased erythropoiesis.
Types
Sickle cell diseasein homozygous individuals, whole of
hemoglobin-A is replaced by hemoglobin-S and this is
known as sickle cell disease.
Sickle cell traitheterozygous individuals, only 50% of
HbA is replaced by HbS and this is known as sickle cell
trait.
Clinical Features
Sex and ageit is common in females and mostly the
clinical symptoms become evident before the age of 30
years.
Incubation periodclinical manifestations begin only after
several months as fetal hemoglobin protects against
sickling phenomenon.
Precipitating factorsinclude dehydration, chills and
infection but sometime, the attack occurs spontaneously.
Symptomsthere is fatigue, weakness and shortness of
breath. Patient may complaint of severe abdominal pain,
muscle and joint pain, at high temperature which may
result in circulatory collapse. There is painless
hematuria.
Signpallor on palms (Fig. 37-6), there is enlargement
of heart and murmur is found in most of the patients.
There is increased susceptibility to infection. Most of
persons expire before the age of 40 years. There is also
presence of leg ulcer and gallstones. When associated
with folate deficiency, there may be growth retardation
and also delayed puberty.
903
Oral Manifestations
Oral mucosathe oral mucosa will show pallor and
jaundice.
Teeththere may be delayed eruption and hypoplasia
of the dentition, secondary to their general development.
Osteomyelitispatient is more prone to develop osteomyelitis. This may be due to hypovascularity of the bone
marrow secondary to thrombosis.
Nervespatient may present with paresthesia of mental
nerve which may be secondary to occlusion involving
the nerves and blood supply.
Jaw bonesmongoloid facies with high cheek bones and
bimaxillary proganthism. It is due to marrow hyperplasia
resulting in an increase in hard palate length and palate
alveolar ridge angle.
Radiological Findings
Fig. 37-6: Pallor is seen on hand of patient with sickle cell anemia. To
compare between pallor with normal hand, another hand is kept for the
comparison ( Courtesy Dr Milind Chandurkar).
Osteoporosisbecause of chronic increased erythropoietic activity and marrow hyperplasia, there is loss of
trabeculation of the jaw bone resulting in a mild to severe
generalized osteoporosis and appearance of large
irregular marrow spaces.
Ground glass appearancethe increased radiolucency of
the jaws which is seen to have a ground glass appearance
which is attributed to diminution of fine trabeculae as
there is replacement of marrow by compensatory
hyperplasia.
Inferior border of the mandiblethinning of inferior border
of mandible of alveolar cortex.
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Diagnosis
Clinical diagnosissevere abdominal pain, mongoloid
facies with prominent cheek bone and bimaxillary
prognathism.
Radiological diagnosishair on end appearance, step
ladder effect and osteoporosis of jaw bone will diagnose
sickle cell anemia.
Laboratory diagnosisa smear of peripheral blood usually
shows typical sickle shaped red blood cells and hemoglobin level is decreased. The RBC count may reach level
of 10 lac cells or less per cu mm with Hb levels from 5 to
12 gm/dl. The sickle hemoglobin molecule undergoes
gelation or crystallization, when deoxygenated and
this typically distorts the erythrocyte, producing
the sickle shape. This sickle shaped cells then logjam
and produce stasis within the microvasculature.
Damage to erythrocyte membrane also occurs in sickle
cells and leads to their fragmentation and intravascular
hemolysis.
Management
Preventionprevention of episode by avoiding the
precipitating factors is an important aspect of treatment.
Patients should avoid becoming chilled, dehydrated or
exposed to hypoxia (high altitude).
Folic acidregular folic acid supplement (5 mg/daily)
is given to support the greatly increased erythropoietin.
Antibioticsprophylactic antibiotics are given to prevent
infections. Young patient with hyposplenism should be
given phenoxymethyl penicillin.
Analgesicspain caused by tissue infarction is extremely
severe but analgesics should be avoided or if at all necessary, no addictive analgesics like aspirin, paracetamol
should be given because the episodes are recurrent.
Hydroxyureathis is indicated in adult patients in severe
cases. The drug increases fetal form of hemoglobin which
inhibits the polymerization of hemoglobin S and reduce
Dental Considerations
Shorten time for dental proceduredo not prolong or carry
out extensive dental procedures involving the soft tissues
unless absolutely necessary. Keep the dentition as
healthy as possible because there are always chances
that any infection might precipitate an aplastic crisis.
Anesthesiaavoid using general anesthesia or when
used, it is imperative to avoid episodes of hypoxia
because of the cerebral or myocardial thrombosis which
might result.
Thalassemia
It is also called as Cooleys anemia, Mediterranean anemia
and erythroblastic anemia. As majority of the cases of
thalassemia are seen in the region of Mediterranean Sea,
the name thalassemia is given, thalassa stands for sea. It is
autosomal dominant.
It is an inherited impairment of hemoglobin synthesis
in which there is partial or complete failure to synthesize a
specific type of globin chain. Beta thalassemia is more
commonly occur as compared to alpha thalassemia.
Pathogenesis
Absence of alpha or beta chainshemoglobin molecule
composed of two alpha and two beta chains. Either
alpha or beta globulin genes may be affected.
Reduces hemoglobinif one of chains is not made
adequately, the resultant red blood cells have reduced
hemoglobin. This will result in shortened lifespan of
RBCs.
Alteration in structure of cellsthe excess globin chains
accumulate within the erythrocytes, which results in
alteration in structure of cells.
Hemolysisthese abnormal erythrocytes got destructed
in spleen (hemolysis) and patient suffers from hypochromic and microcytic anemia.
Bone marrow hyperplasiathis occur as rare of hematopoiesis is increased to maintain adequate oxygenation.
Types
Alpha thalassemiathere is reduction or absence of
chain synthesis. Alpha chains of hemoglobin are
required not only for HbA but also for HbF, which is the
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Blood Disorders
Clinical Features
Ageoccurs between the ages of 6 to 24 month and after
the age of 6-8 months.
Symptomsthe patient first presents with pallor of skin,
fever, chills, malaise, generalized weakness, prominent
cheek bone and mild hepatosplenomegaly.
Mongoloid appearancebone marrow hyperplasia in
early life may produce frontal head bossing and there
may be marked overdevelopment of malar bone which
is associated with a short nose having a depressed bridge
giving the appearance of mongoloid.
Organs failuredeposition of iron in various organs (due
to multiple transfusions) leads to signs and symptoms
of organ failure.
Prognosismost patients die in childhood due to anemia
and cardiac failure.
Alpha thalassemiathe clinical findings are severe
alveolar bone loss, pronounced spacing of maxillary
anterior teeth and mongoloid appearance.
Oral Manifestations
Jaw bonethere is excessive overgrowth of maxilla
causing excessive lacrimation and nasal stuffiness.
Oral mucosathe oral mucosa is pale and has a lemon
yellow tint because of chronic jaundice. The color is best
seen at the termination of hard palate and in the floor of
mouth.
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Radiographic Features
Teeththe root of mandibular 1st molar and central
incisors may be spike shaped and short. The lamina
dura is thin and the roots of the teeth may be short.
Circular radiolucency may be seen in the lower anterior
region. There is thinning of the crypt of developing teeth.
Alveolar bonethe alveolar bone shows large bone
marrow spaces, osteoporosis and blurring of trabeculae.
The marrow spaces are large and the trabeculae are large
and course.
Compensatory lamellar striationsome areas may show
prominent trabeculae which have been referred to as
compensatory lamellar striation.
Long bonesin the long bone there is generalized
radiolucency, increased width of shaft, and narrowing
of cortices due to the greater amount of marrow substance.
There is also pathological fracture.
Skullskull is thickened as a result of increased width
of the dipole space between the outer and inner tables of
the vault. This occurs due to proliferation of the hemopoietic tissue. Generalized granular appearance in skull.
Antrumthe antra is reduced in size by the encroachment of the bone formation, which is sometimes sufficient
to cause complete effacement of the air sinuses.
Premaxillapremaxilla is prominent resulting in malocclusion.
Cortical bordersthere is generalized thinning of cortical
borders.
Hair on end appearancethe trabeculae joining the inner
and outer table of the skull are readily arranged calcified
spicules which appear as calcified hair extending
between the inner and outer tables, which is called as
hair on end appearance (Fig. 37-7).
Diagnosis
Clinical diagnosismongoloid appearance, chipmunk
facies, and rodent facies with discoloration of dentin
may give clue to diagnosis of thalassemia.
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906
Clinical Features
Ageit occurs soon after birth.
Symptomsthe urine is burgundy red in color or turns
red on exposure to light.
Signsphotosensitivity of exposed parts of body leads
to formation of blister and scars.
Anemiathere is also hemolytic anemia and
splenomegaly.
Oral Manifestations
Management
Blood transfusionrepeated blood transfusions are
necessary. Repeated blood transfusion will lead to
increased iron load in the tissue of the body. This will
lead to a condition known as hemochromatosis.
Chelating agentiron overload can be reduced by regular
use of chelating agents like desferrioxamine therapy.
Bone marrow transplantationallogenic bone marrow
transplantation can be done. It is indicated in young
individual, little organ damage and HLA matched donor.
Splenectomysplenectomy is indicated when there is an
increase in the severity of anemia.
Folic acidthe patient may need supplementary folic
acid because of increased requirement owing to
increased erythropoiesis.
Surgical correctionit is indicated in patient who
developed an abnormal facial appearance.
Erythropoietic Porphyria
It is a group of inherited or acquired disorders characterized
by excessive production, accumulation and excretion of
Diagnosis
Clinical diagnosisburgundy red color urine which turns
red upon exposure to light with erythrodontia will
diagnose the disease.
Laboratory diagnosisabout 50% normoblasts, reticulocyte and 50% RBCs exhibit intense red fluorescence
under fluorescence microscope.
Management
Splenectomyin severe cases of hemolysis, splenectomy
may be carried out.
Megaloblastic Anemia
Megaloblastic anemia occurs due to deficiency of
vitamin B12 or folate or both, resulting in disordered cell
proliferation leading to megaloblastic anemia. All
megaloblastic anemias have erythroid precursors known
as megaloblasts.
Causes
Folate deficiencythe condition is prevalent in women
during pregnancy and lactation. It may occur due to
low availability of folate in diets, prolonged cooking of
food, malabsorption syndromes such as tropical sprue
and malaria.
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Blood Disorders
Vitamin B12 deficiencyremoval of vitamin B12 from the
gut either by bacterial proliferation or by parasites. It
may occur due to chronic dietary deficiency of the
vitamin.
Clinical Features
Symptomsthere are symptoms of anemia like weakness,
loss of appetite and palpitations. Patient may get periodic
diarrhea.
Skinin severe cases, skin may show faint lemon yellow
tint and spleen may be palpable.
Neuropathymany cases show paresthesia of finger and
toes and dementia may also be seen.
Oral Manifestations
Symptomsburning sensation in tongue, hypersensitivity, paresthesia and later dryness of the mouth.
Hunters glossitisatrophy of filiform and fungiform
papillae leads to completely atrophic smooth fiery red
surface of tongue (Hunters glossitis) (Fig. 37-8).
Angular cheilitisangular cheilitis and dysphagia due
to pharyngitis and esophagitis.
Oral mucosayellowish brown pigmentation of oral
mucosa may occur due to increased circulating bile
pigments.
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Management
Educationgeneral education on cooking practices and
food habits is undertaken in tropical countries to prevent
nutritional anemia.
Blood transfusionwhen hemoglobin level is less than
4 gm/dl blood, transfusion should be given.
Vitamin B12oral administration of vitamin B12 should
be given.
Folic acidfolic acid supplements should also be given.
Pernicious Anemia
It is also called as primary anemia, Addisons anemia or
Biermers anemia. The term pernicious anemia should be
reserved for patients who have B12 deficiency secondary to
intrinsic factor deficiency.
Causes
Atrophy of gastric mucosait occurs due to atrophy of
gastric mucosa resulting in failure to secrete the still
unidentified intrinsic factor.
Autoimmune disordersit is suggested that it is
autoimmune disorder, because autoantibodies to gastric
parietal cells are often found in patients.
Clinical Features
Diagnosis
Clinical diagnosissymptoms of anemia with Hunter
glossitis with dysphagia may give clue to diagnosis.
Laboratory diagnosisthe peripheral smear shows a
macrocytic blood picture with many abnormal forms of
RBCs. There is associated leukopenia and sometimes,
thrombocytopenia. Bone marrow shows presence of
megaloblasts and erythroid hyperplasia. In advanced
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Oral Manifestations
Symptomsglossitis (Fig. 37-9) and patient complains
of painful and burning lingual sensation which may be
so annoying that the dentist is often consulted first.
Sometimes, inflammation and burning involve the entire
oral mucosa. There is disturbance in taste sensation with
intolerance to dentures and occasional dryness of
mouth.
Diagnosis
Clinical diagnosistriad of generalized weakness, sore
and painful tongue and numbness and tingling of
extremities are typical of pernicious anemia. Patient also
suffers from gastrointestinal problems.
Laboratory diagnosishistologically, oral epithelial cells
in pernicious anemia reveal enlarged, hyperchromatic
nuclei with prominent nucleoli and serrated nuclear
membranes. The red blood count is decreased often to 3
Management
Vitamin B12most of the patients should be given
vitamin B12 parenterally but, some of the patients are
treated with massive oral dose of vitamin B12. The
standard dosage is 100 mg IM every 30 days.
Aplastic Anemia
It is a rare disorder characterized by peripheral blood
pancytopenia (anemia, leukopenia and thrombocytopenia)
associated with bone marrow suppression. It occurs due to
failure of hematopoietic precursor cells in bone marrow to
produce adequate number of all types of blood cells. In
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Blood Disorders
most cases, the cause of bone marrow suppression is not
known and hence is known as idiopathic aplastic anemia.
Aplastic anemia can be associated with Fanconi anemia
and dyskeratosis congenita.
Types
Primary or idiopathic aplastic anemiait is the disease of
unknown origin which occurs most frequently in young
adults, develops more rapidly and usually terminates
fatally.
Secondaryit has known etiology occurs at any age and
presents better prognosis.
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Oral Manifestations
Oral mucosathe mucosa shows pallor due to decreased
number of red blood cells.
Symptomsin some cases, spontaneous hemorrhage
from gingiva is present.
Signpetechiae, often are present on the soft palate and
in severe cases, there may be submucosal ecchymosis.
Large ragged ulcers covered by gray or black necrotic
membrane may be present, which are the result of
generalized lack of resistance to infection and trauma.
Gingival hyperplasiain some cases, gingival hyperplasia may occur in aplastic anemia (Fig. 37-11).
Etiology
Drugs and chemicalscommon drugs which can cause
aplastic anemia are benzene derivatives, chloramphenicol, amidopyrine, organic arsenicals, colloidal
silver, bismuth, mercury, sulfonamides, penicillin and
anticancer drugs. The mechanism due to which drug
can cause aplastic anemia is as follows:
Myelosuppressive effectthe first is characterized by
the myelosuppressive effects of cancer chemotherapeutic agents.
Marrow depressionsome drugs can cause marrow
depression.
Hypersensitivity reactionthe third type is called as
idiosyncratic or hypersensitivity induced aplastic
anemia.
Infectionspatient with bacterial disease such as
tuberculosis and viral infections like hepatitis and
infectious mononucleosis can cause aplastic anemia.
Radiationlong term continuous exposure to small
amounts of external radiation may lead to aplastic anemia.
Other causesin some cases, pregnancy and thymoma
can also cause aplastic anemia.
Clinical Features
Ageit can occur at any age, but is common in young
adults.
Symptoms due to erythrocyte deficiencypatient may feel
weakness after slight physical exertion and exhibits
pallor of skin. There is also breathlessness, headache.
Symptoms due to platelet deficiencythere is marked
tendency to bruising and bleeding. Patient may get retinal
and cerebral hemorrhages.
Deficiency of white blood cellsbacterial and fungal
infection are common occurrence due to white blood
cell deficiency.
Others featurepatient may get ankle edema, numbness
and tingling of extremities, anginal pain, and congestive
cardiac failure.
Diagnosis
Clinical diagnosisclinical features suggesting of thrombocytopenia (bleeding), WBC deficiency (infection)
and erythrocyte deficiency (pallor) will give clue to the
diagnosis.
Laboratory diagnosisRBC count is remarkably
diminished, as low as 1 million cells/mm3. WBC count
is as low as 2000/mm3 and platelet count may fall below
20000/mm3. The classical finding is that of pancytopenia along with reduction of absolute reticulocyte
count. Bleeding time is prolonged and clotting time is
normal. Anemia is normocytic with some degree of macrocytosis. Bone marrow is fatty and few developing cells.
Management
Removal of causewithdrawal of the etiological agent.
Supportive therapyit is in the form of antibiotics and
transfusion.
Hemopoiesisstimulation of hemopoiesis by androgenic
steroid.
Bone marrow transplantationit can be useful in some
cases.
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Fanconis Anemia
It is a rare congenital disease characterized by pancytopenia, bone marrow hypoplasia and congenital anomalies.
Clinical Features
Ageit is usually seen in children.
Skinthere is brown pigmentation of skin.
Hypoplasiathere is, also, hypoplasia of kidney and
spleen.
Symptomspatient suffers from microcephaly, hypoplastic thumb, and short stature, polydactyly and squint.
Other featuresthere may be mental and sexual
retardation.
Oral Manifestations
Gingival bleedingthere is gingival bleeding which may
occur spontaneously.
Infectionfrequent infections of oral cavity can occur.
Diagnosis
Clinical diagnosispancytopenia with congenital
anomalies will diagnose this condition.
Laboratory diagnosisit is same as that of aplastic anemia.
Management
Anti-thrombolytic agentsgingival bleeding can be
reduced by anti-thrombolytic agents such as aminocaproic acid and transexemic acid 20 mg/kg QID
24 hrs before procedure and continued for 3 to 4 days.
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Blood Disorders
Paroxysmal nocturnal hemoglobinuriait is a very rare
disease in which the red cells have acquired susceptibility
to antibodies which are normally in the blood. The
patient has severe to moderate anemia and mild jaundice.
The spleen is usually palpable. There is passage of dark
urine usually in morning sample with subsequent
samples of urine being clear. There are findings of
hemolytic anemia in association with reticulocytosis.
There may be leukopenia and thrombocytopenia.
Administration of alkali may control hemolysis but on
cessation of treatment, massive hemolysis may occur
due to accumulation of sensitive cells during the period
of therapy.
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Clinical Features
Age and sexthe disease is more common in males and
usually occurs in middle age or later.
Symptomscommon symptoms are lassitude, loss of
concentration, headache, dizziness and blackout,
slurring of speech, pruritis, mental confusion and
indigestion. Paresthesia is common, usually involving
the cranial nerves.
Signsthe skin appears flushed or diffusely reddened.
Spleen is palpable in most of the patients. Superficial
veins are dark, enlarged and distended. The tip of the
finger usually has a cyanotic appearance.
Appearancethere is marked purplish red discoloration
especially of the head and neck (Fig. 37-12). Feet and
hands, which give the patient an extremely angry
appearance.
Erythromealgiait is peripheral vascular event occur on
hands and feet. There is burning sensation with
erythema and warmth in hand and feet. This may lead
to thrombotic occlusion of vessels supplying digits
which may results in digital gangrene and necrosis.
Complicationsthrombotic complications may occur and
peptic ulcerations are common.
Polycythemia
It is defined as abnormal increase in the number of red
blood cells in the peripheral blood, usually with an increase
in hemoglobin level.
Types
Polycythemia vera
Relative polycythemia.
Secondary polycythemia
Oral Manifestations
Polycythemia Vera
It is also called as polycythemia rubra vera, Oslers disease,
Vaquezs disease and erythremia. There is an uncontrolled
proliferation of the erythroid stem cells leading to excess of
erythroid cell mass in the body (RBCs). There is accompanying increase in the granulocyte and megakaryocytic
elements though to a lesser degree.
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912
Diagnosis
Quantitative disorders
Management
Increase in number
Granulocytosis
Neutrophilia
Basophilic leukocytosis
Eosinophilic leukocytosis
Lymphocytosis
Monocytosis
Relative Polycythemia
It is also known as stress or spurious (false) polycythemia
and is due to reduction in the plasma volume.
It is an apparent increase in the number of circulating
red blood cells that occurs as a result of loss of blood fluid
with hemoconcentration of cells and is seen in cases of
excessive loss of body fluids such as chronic vomiting,
diarrhea or loss of electrolytes with accompanying loss of
water. The red cell mass is normal.
Secondary Polycythemia
This occurs as a result of hypoxia, which stimulates the
production of erythropoietin, e.g. at high altitudes,
pulmonary diseases or congenital heart diseases.
Secondary polycythemia may also occur in some brain
tumors, usually vascular, Cushings syndrome and renal
and lung carcinoma.
Quantitative Disorders
Agranulocytopenia or Neutropenia
It is also called as granulocytopenia, agranulocytic angina.
It is a serious disease characterized by marked leukopenia
Decrease in number
Granulocytopenia/leukopenia/agranulocytopenia
Neutropenia
Cyclic neutropenia
Primary splenic neutropenia
Chronic hypoplastic neutropenia
Chronic granulocytopenia in childhood
Familial neutropenia
Transitory neonatal neutropenia
Qualitative disorders
Types
Primary agranulocytosisin this, etiology is unknown.
Secondary agranulocytosisin it, cause is recognized.
Mild neutropeniawhen 1000/mm 3 to 2000/mm3
neutrophils are present.
Moderate neutropeniawhen 500/mm3 to 1000/mm3
neutrophils are present.
Severe neutropeniawhen fewer than 500/mm 3
neutrophils are present.
Agranulocytosiswhen no neutrophils are seen in
peripheral smear.
Etiology
Idiosyncrasyidiosyncrasy or sensitization to certain
drugs like aminophylline, chlorpromazine and
phenylbutazone, benzene, bismuth, chloramphenicol,
sulfonamides and use of cytotoxic drugs or antimetabolics.
Deficiencydeficiency of vitamin B12 and folic acid.
Infectionscertain infections decrease the number of
neutrophils in circulating blood because of increased
migration of neutrophils into the tissue, destruction of
neutrophils or direct effect of microorganism and its
toxins on the bone marrow. Infection with hepatitis A
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Blood Disorders
and varicella zoster virus infection are commonly
associated with neutropenia. Overwhelming bacterial
infection, particularly septicemia can be accomplished
by neutropenia because cells are used at rapid rate to
overcome infection.
Diseasesdisease causing sequestration of neutrophils
includes systemic lupus erythematosus and Feltys
syndrome. It can be associated with leukemia,
pancytopenia and hypersplenism.
Hemodialysishemodialysis patient experience decrease
in neutrophils owing destruction by complement
activated by the dialysis membrane.
Irradiationexcessive irradiation can cause neutropenia
due to direct toxic effect on division of bone marrow
cells.
Clinical Features
Age and sexit can occur at any age but is somewhat
more common in adults, particularly in woman.
Occupationit is also common in professional and in
hospital as they have easy access of the offending drugs
and often use drug sample injudiciously.
Symptomsthe onset may be sudden or gradual. The
condition begins with sore throat, high fever and often
rigors, which may be followed by prostration.
Skinthe skin appears pale and anemic and in some
cases, jaundiced.
Signsthere is rapidly advancing necrotic ulceration of
throat and mouth with little evidence of pus formation.
In case of Agranulocytopenia patient dies within 3-5
days due to toxemia and septicemia.
Oral Manifestation
Sitesthe most common sites are gingiva (Fig. 37-13),
palate, tonsil and pharynx.
913
Radiological Findings
Destruction of alveolar bonesupporting alveolar bone is
rapidly destroyed, so that teeth are denuded of bone
and are supported only by soft tissues.
Osteomyelitisvery rarely, infection spreads to deep into
the marrow to cause osteomyelitis.
Diagnosis
Clinical diagnosisgingival ulceration, infection and
anemic patient may give clue to the diagnosis
Laboratory diagnosismajority of patients show a
leukocyte count below 2000 cells per cu mm and
granulocyte count below 100 cells per cu mm.
Hemoglobin and platelet counts are normal.
Differential Diagnosis
Leukemiaanemia, purpura and WBC leukocyte above
1000,000/mm3 with prolonged bleeding and clotting
time.
Cyclic neutropeniamarked cyclic appearance every
20 to 25 days.
Wegeners granulomatouskidney and lung involvement.
ANUGnecrosis starts on papilla tips, not necessary
associated with leukopenia.
Necrotizing sialometaplasialarge ulcerations with
induration on hard and soft palate, flat border and
painless. General condition is not affected.
Erythema multiformetarget lesions and no specific blood
picture.
Management
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914
Cyclic Neutropenia
It is also called as periodic neutropenia or cyclic
hematopoiesis. It is a rare disorder characterized by periodic
or cyclic diminution in circulating neutrophils due to
failure of stem cells of bone marrow. It is also called as
periodic neutropenia. One-third cases are inherited as
autosomal dominant trait and 2/3rd appear spontaneously
during the first few year of life. The patient is healthy
between neutropenic periods; but at regular intervals, the
absolute neutrophils count falls below 500/mm3. In some
patients, it comes to zero.
Clinical Features
Age and sexthe disease is frequently present during
infancy and childhood and both sexes appear to be
equally affected.
Occurrencethe frequency of neutropenic episodes vary
from once in 2 to 4 weeks which last for 3 to 5 days with
21 days gap being the commonest.
Symptomsthe patients manifest fever, sore throat,
stomatitis and regional lymphadenopathy as well as
headache, arthritis, cutaneous infection and
conjunctivitis. Less frequently patient experience lung,
urinary tract infection as well as rectal and vaginal ulcer.
Amyloidosisin some patients, amyloidosis can occur
due to repeated, increased antigenic stimulation during
neutropenic episodes.
Oral Manifestations
Sitelesions are found on the lip, tongue, palate, gums
and buccal mucosa.
Radiological Features
Bone lossit exhibits mild or severe loss of superficial
alveolar bone advancing to periodontitis.
Prepubertal periodontitisin children this loss of bone
around multiple teeth sometimes called as prepubertal
periodontitis.
Diagnosis
Clinical diagnosisrecurrent gingival ulceration,
recurrent infection with prepubertal periodontitis may
yield in diagnosis.
Laboratory diagnosisneutrophils count should be less
than 500/mm3 during each of three successive cycles.
There is increased in monocytes and lymphocytes count.
At the peak of the disease, the neutrophils may
completely disappear for one or two days.
Management
Antibiotic therapythis can be given to control the
infection in the patient.
Corticosteroid therapy and hormonal therapyin some
cases, use of corticosteroids, adrenocorticotropin (ACTH)
or testosterone modulates sharp reduction in marrow
function.
Oral hygiene maintenanceoral hygiene should be
maintained and patient should be recalled for oral
hygiene every 2-3 months.
Cytokine granulocyte colony-stimulating factor (GCSF)this
can be given several times weekly to correct lack of
production of neutrophils. This will decrease time of
neutropenia from 5 days to 1 day thereby decreasing
clinical course of disease.
Other therapyother therapy like splenectomy and
nutritional supplement can be carried out.
Variant of Neutropenia
Chronic idiopathic neutropeniait is an uncommon
disease in which there is decreased production of
neutrophils. The bone marrow shows a number of
immature cells but there is a decrease in number of
mature neutrophils. Most of the patients are asymptomatic because of compensatory monocytosis. In the
oral cavity recurrent ulcerations of the gingival, lips,
buccal mucosa and recurrent dental abscess have been
reported.
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Blood Disorders
Primary splenic neutropeniait is characterized by
neutropenia of a mild degree, splenomegaly and myeloid
hyperplasia of the bone marrow. The common clinical
features are polyarthritis, recurrent oral ulceration,
weight loss and fatigue.
Chronic granulocytopenia in childrenit is a benign
disorder characterized by repeated pyogenic infection.
It is due to increased destruction of neutrophils. Complete
recovery takes place eventually.
Familial neutropeniait is a rare benign disorder
transmitted as a non-sex linked dominant trait. Most of
the patients are asymptomatic but a few may show
periodontal disease and a tendency to develop frequent
furuncles. The total leukocyte count is normal but there
is associated neutropenia.
Transitory neonatal neutropeniait is a disorder caused
by fetal-maternal incompatibility involving only the
neutrophils. Skin infection is the most common clinical
finding. The blood picture shows normal leukocyte
count, severe neutropenia, monocytosis and mild
eosinophilia. The duration of neutropenia varies from 2
to 17 days.
915
Clinical Features
Ageit becomes apparent at the age of 1-2 years when
complication occurs due to infections.
Symptomsthe most common clinical manifestations are
stomatitis, otitis media and bronchitis.
Recurrent infectionchances of recurrent infection in the
patients are high.
Oral Manifestations
Stomatitisit is common oral finding of this disorder.
Periodontitisin some cases, periodontal disease may
be present.
Diagnosis
Clinical diagnosisrecurrent infection, periodontitis and
stomatitis may give clue to diagnosis.
Laboratory diagnosisthe total leukocyte count is slightly
low but the absolute neutrophil count is as low as 100 to
200 cells/mm 3. The bone marrow contains normal
number of mature neutrophils.
Management
Antibioticsantibiotics are given to control the infection.
Chdiak-Higashi Syndrome
It is a congenital autosomal recessive defect of granulocytes
and melanocytes. Abnormal granules are seen in all blood
granulocytes resulting in decreased chemotactic and
bactericidal activity.
Clinical Features
Albinismthe characteristic clinical feature of this
disease consists of oculocutaneous albinism.
Recurrent infectionpatient with Chediak Higashi
syndrome will have recurrent infections of the respiratory
tract and sinuses.
Gastrointestinal disturbancepatient is having hepatosplenomegaly.
Lymph node enlargementthere is cervical lymph node
enlargement present in this patient.
Malignant lymphomathe disease may be associated
with malignant lymphoma.
Other diseasesthere is photophobia, nystagmus,
thrombocytopenia, and neurological problems.
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916
Oral Manifestations
Oral Manifestations
Diagnosis
Management
AntibioticsImmediate and proper treatment with
antibiotics of the infection as soon as they occur is most
important.
Other drugsvincristine, prednisolone and ascorbic acid
have been tried as the treatment of this disorder.
Diagnosis
Clinical diagnosisit is not so specific.
Laboratory diagnosisthe bone marrow of patients
shows a normal number of immature cells but decrease
in number of mature neutrophils. This is called as
maturation arrest. Absolute neutrophils count may be
below 500/mm3.
Management
Corticosteroidsit is not required if the patient is
asymptomatic. Patient who develops severe recurrent
infections may benefit from alternate day corticosteroids
therapy.
Multiple Myeloma
It is described in Chapter 16: Malignant Tumor of Jaw.
Platelet Disorders
Lymphoma
Classification
Purpura
Idiopathic thrombocytopenic purpura
Secondary thrombocytopenic purpura
Congenital purpura
Thrombotic thrombocytopenic purpura
Thrombocytopathic purpura
von-Willebrands disease
Bernard-Soulier syndrome
Aldrich syndrome
Thrombocytosis
Leukemia
It is described in Chapter 16: Malignant Tumor of Jaw.
Clinical Features
Age and sex distributionit is seen in young adults and
seen in predominantly in females.
Symptomsit is usually asymptomatic and free of
infection which is due to compensatory monocytosis,
which accounts of normal number of phagocytes at the
site of tissue injury. In some cases recurring upper
respiratory tract infections, otitis media, bronchitis and
furunculosis can also occur.
Thrombocytopenic Purpura
Purpura is defined as a purplish discoloration of the skin
and mucous membrane due to subcutaneous and
submucus extravasation of blood. Purpura may be due to
deficient or defective platelets or due to an unexplained
increase in capillary fragility.
It is also called as Werlhofs disease, purpura hemorrhagic
and primary thrombocytopenic purpura. It is a disease in
which there is an abnormal reduction in the number of
circulating blood platelets with normal or raised number
of megakaryocytes in the bone marrow. It is thought to be
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Blood Disorders
917
Etiology
Idiopathicin some cases etiology is unknown causing
the decrease in platelet production.
Reduced productionit occurs due to infiltration of bone
marrow by malignant cells. It can occur due cancer
chemotherapeutic drugs.
Platelet destructionthere may be increased in platelet
destruction due to immunological causes. This can be
caused by many drugs like heparin.
Increase consumptionincrease in consumption of
platelet may occur in abnormal blood clot formation.
This is seen in thrombotic thrombocytopenic purpura.
Spleen sequestrationcondition in which splenomegaly
is present, large number of platelet are taken out for
circulation.
Systemic diseasesome systemic disease like lupus
erythematous and HIV infection may cause purpura.
Other diseases like leukemia, sarcoma, lymphoma,
Hodgkins disease myelofibrosis can also cause purpura.
Drugsbarbiturates, analgesics (phenylbutazone and
salicylates), antihistamine (diphenhydramine hydrochloride), myelosuppressive agents used in neoplastic
disease.
Metabolic diseaseuremia, megaloblastic anemia can also
cause purpura.
Othersbone marrow replacement, radiation therapy
can also cause purpura.
Clinical Features
Petechiaethrombocytopenic purpura is characterized
by spontaneous appearance of purpuric hemorrhagic
lesions of skin. The reason for this capillary is not able
to seal off with thrombi. The patient also exhibits a
bruising tendency.
Ecchymosisif large quantity of blood is extravasated
Ecchymosis may result (Fig. 37-14).
Hematomathis can occur in rare case. It also occurs
due to large amount of blood extravasated, which vary
in size from tiny red pinpoint petechiae to large purplish
ecchymosis and sometimes, even massive hematoma.
Other featuresepistaxis, hematuria and melena are
common findings.
Intracranial hemorrhageintracranial hemorrhage is rare,
but can be seen in children and the symptoms are
headache, dizziness and confusion.
Oral Manifestations
Sitesubmucus petechiae and ecchymosis commonly
occur especially at the junction of the hard and soft palate
(Fig. 37-15). In some cases, it can be seen on tongue.
Bleeding after tooth extractionthe first manifestation of
the disease can be seen in oral cavity in the form of
excessive bleeding after tooth extraction.
Petechiaeit appears as numerous tiny, grouped clusters
of reddish spots, only a millimeter or less in diameter.
Petechiae do not blanch on pressure which is the distinguishing feature between purpura and telangiectasia.
Gingival bleedingin severe cases, extensive spontaneous gingival bleeding may be seen and this may
form foci of secondary infection.
Tonguein some cases, petechiae and ecchymosis can
be seen on the tongue (Figs 37-16A and B).
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918
Management
Young childrenin young children, treatment is seldom
necessary unless there is intracranial evidence of
bleeding.
Corticosteroidsin adults, prednisone 60 mg/dl should
be given until the platelet count rises to normal level
when, the dose should be cautiously tapered until the
drug is withdrawn.
Splenectomyif there is no response to prednisolone in
3 to 4 days, splenectomy is indicated.
Transfusionplatelet transfusion can be given.
Removal of causein case of secondary thrombocytopenia
purpura, this will reduce the symptoms and sign of
lesion.
Local hemostasisthe spontaneous gingival hemorrhage
can often be controlled by the local use of hemostatic of
the non-causing type, such as fibrin foam, Gelfoam or
absorbable cellulose with thrombin. Sometimes, 1.5%
hydrogen peroxide mouth wash will stop gingival
bleeding.
Diagnosis
Clinical diagnosispetechiae at the junction of hard and
soft palate is clue to the diagnosis (Fig. 37-17).
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Blood Disorders
quantitative and qualitative deficiency in larger molecule
portion of factor VIII molecule. Von Willebrands factor
activity is responsible for platelet adhesion to subendothelium, regulation of the plasma level of factor VIII
coagulant activity and thereby normal hemostasis.
Clinical Features
Age and sex distributionit is seen in childhood and
adults and females are affected more commonly than
males.
Bleeding tendenciesexcessive bleeding either spontaneously or following even minor trauma is the chief
feature of the disease. Bleeding into the gastrointestinal
tract, epistaxis and severe menorrhagia are also
common. The most common sites of bleeding are nose,
skin and gingiva. Bleeding tendencies usually appear
early in childhood and decrease in middle and old age.
Oral Manifestations
Gingival bleeding and post-extraction bleedinggingival
bleeding and post-extraction bleeding are the most
common oral manifestations. The disease may be
discovered after dental extraction.
Diagnosis
Clinical diagnosisbleeding tendencies either spontaneous or after slight trauma may give clue to the
diagnosis.
Laboratory diagnosisthere is prolonged bleeding time,
normal platelet count, failure of aggregation of platelets
impaired adherence of platelets and depressed levels of
factor VIII are suggestive of this disorder. There is low
Anti-hemophilic globulin (AHG) levels and abnormal
platelet retention to glass beads. The platelet count and
prothrombin consumption are normal. The clotting time
usually is normal but capillary fragility is increased.
Management
TransfusionBleeding episode is best controlled by
transfusion of plasma and or cryoprecipitate and by local
control of homeostasis.
Avoid giving aspirinpatients with von Willebrands
disease should not be given aspirin because of prolongation of the bleeding time that may occur.
Desmopressinit is given as nasal spray to control nasal
bleeding.
919
Clinical Features
Symptomspatients commonly manifest boils, otitis
media, bloody diarrhea and respiratory infection.
Increased susceptibility to infectionthere is eczema and
increased susceptibility to infection.
Malignant lymphomathere is common occurrence of
malignant lymphoma, which is an important feature of
this disease.
Bleedingbleeding occurs from nose, skin and
gastrointestinal tract.
Oral Manifestations
Palatal petechiaepalatal petechiae are frequently present.
Spontaneous bleedingthere is spontaneous bleeding
from the gingiva.
Diagnosis
Clinical diagnosisincrease susceptibility to infection,
spontaneous bleeding, and malignant lymphoma may
give clue to diagnosis.
Laboratory diagnosisprolonged bleeding time, anisocytosis, alteration in the size and shape of platelets with
most platelets smaller than normal. There is decreased
production and defective maturation of platelets since
normal megakaryocytes may be seen in the marrow.
Management
Antibioticspatients are given antibiotics to control the
infection.
Hemostasislocal hemostasis to control gingival
bleeding should be done.
Familial Thrombasthenia
It is also called as Glanzmanns disease. It is hereditary,
chronic hemorrhagic disease transmitted as an autosomal
recessive trait. There is defective platelet aggregation due
to defective membrane protein.
Clinical Features
Sex distributionboth sexes may be affected and onset of
menarche may be a critical event.
Severe bleedingthere is excessive bleeding, either
spontaneous or following minor trauma.
Sign and symptomspurpuric hemorrhages of skin are
common, as are epistaxis and gastrointestinal bleeding.
Hemarthrosis is also noted in some cases.
Aldrich Syndrome
It is also called as Wiskott-Aldrich syndrome. It is X-linked
recessive condition. It is characterized by thrombocytopenia.
Oral Manifestations
Spontaneous gingival bleedingspontaneous bleeding
from the oral cavity particularly gingival bleeding.
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920
Diagnosis
Clinical Features
Management
Oral Manifestations
Onyalai
Diagnosis
Clinical Features
Age and sex distributionindividuals in the second
decade of life seen most commonly affected although,
the disease can develop any time after the first 6 months
of life. There is female predilection.
Onsetthe sudden appearance of hemorrhagic bullae
on the skin and oral mucosa followed by epistaxis or
frank bleeding from mouth.
Signs and symptomsthere is also subconjunctival
hemorrhages, hematemesis, melena, hematuria, vaginal
bleeding and CNS hemorrhage. Hemorrhagic episodes
may be multiple and recurrent attacks result in
anemia.
Diagnosis
Clinical diagnosissudden hemorrhagic bulla appearance will give clue to diagnosis.
Management
Drug managementcorticosteroid therapy, blood
transfusion and platelet transfusion
Thrombocytosis or Thrombocythemia
It is characterized by an increase in the number of platelets
in the blood in excess of 1000 106 /dl. It is of two types, i.e.
primary and secondary.
It is caused by polycythemia and myeloid leukemia,
anemia, tuberculosis, sarcoidosis, hyperadrenalism,
rheumatoid arthritis, and bronchial carcinoma.
Management
Drug managementcertain cytotoxic drugs, heparin,
corticosteroid and aspirin in small dose may help to
counter act the thrombactive tendency.
Radioactive phosphorusit responds to radioactive
phosphorus.
Hemorrhagic Disorders
Hemophilia
Hemophilia stands for hemo (blood), philia (loving). It is a
hereditary disorder of blood coagulation characterized by
excessive hemorrhage due to a prolonged coagulation time.
Deficiency of factor VIII or anti-hemophilic factor is the
cause of hemophilia. It is transmitted as X-linked recessive
character carried on X-chromosome. The males are clinically
affected and the females are carriers of the trait. Hemophilia
A occurs 10 times more commonly than hemophilia B.
Traumatic injury of the oral cavity may lead to the diagnosis
of hemophilia.
Hemophilia B is also called as Christmas disease. It occurs
due to hereditary deficiency of factor IX or functionally
defective factor IX. It is transmitted as X-linked recessive
character through chromosome. It is very rare, compared to
hemophilia A.
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Blood Disorders
921
Moderate1% to 3% of AHG
Moderate to severe0.0% to 0.9% of AHG
Severe0% of AHG
Clinical Features
Age and sex distributionthese manifestations usually
begin after 6 months of age, when the child begins to
move about and tends to fall and sustain injuries, i.e.
when spontaneous hemorrhage is noted by the parents.
Joint hemorrhage or hemarthrosisthe most common
manifestation is hemorrhage into joints which is
spontaneous and associated with warmth and muscle
spasm. Repeated episodes cause damage to the joint with
wasting of the related muscle, leading to deformity and
crippling.
Subcutaneous hemorrhagehemorrhage into subcutaneous tissues, internal organs and musculature also are
frequent and potentially disabling complications.
Superficial trauma gives rise to uncontrolled bleeding.
Intracranial bleedingintracranial bleeding is relatively
rare unless associated with trauma.
Pseudotumor of hemophiliain some cases tissue
hemorrhage can lead to formation of tumor-like mass.
Oral Manifestations
Sitethe anatomic sites involved in persistent oral
bleeding are the frenum of lip and the tongue.
Symptomsthere is prolonged bleeding after tooth
extraction.
Hematoma of floor of mouthhematoma of the floor of
mouth may occur and blood may spread via the fascial
spaces and produce a hematoma of the larynx, with
consequent respiratory embarrassment.
Tooth eruptionphysiological processes of tooth
eruption and exfoliation may be associated with severe
and prolonged hemorrhage.
Gingival hemorrhagegingival hemorrhage may as a
result of gingival injury (Fig. 37-18).
Diagnosis
Clinical diagnosisextensive bleeding after extraction of
tooth and routine periodontal procedure should suspect
hemophilia.
Laboratory diagnosisclotting time is prolonged, but
however the bleeding time, platelet count and
prothrombin time are all normal. The prothrombin
consumption time and the partial thromboplastin time
may be prolonged in severe cases.
Difference between hemophilia A and hemophilia Bin the
laboratory, hemophilia A may be differentiated from
hemophilia B by modification of the prothrombin
consumption time or the partial thromboplastin time.
Management
Fresh frozen plasmareplacement therapy of fresh frozen
plasma should be given. Hypovolemia, allergic reaction,
transfusion hepatitis, hemolytic anemia and
development of factor VIII antibodies are complications
with fresh frozen plasma.
Factor VIII concentratesthe dose and duration of
administration of factor VIII concentrates are planned,
taking into consideration of the site and the type of
bleeding.
Prevention of complicationto reduce complications
caused by cryoprecipitate or plasma various drugs are
used instead of factor VIII products, before dental
extraction, e.g. a synthetic analogue of anti-diuretic
1-deamino-8-d-arginine vasopressin (DDAVP) in
combination with tranexamic acid and Epsilon aminocaproic acid (EACA) can be given.
Genetic counselingit should be provided to patient to
know importance of inheritance.
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922
Diagnosis
Clinical diagnosisspontaneous epistaxis, intraocular
hemorrhage with gingival bleeding.
Laboratory diagnosisboth clotting and prothrombin time
are prolonged but, bleeding time is normal. The basic
defect is reduction in plasma proaccelerin.
Management
Transfusiontransfusion and freshly frozen plasma are
given when there is excessive hemorrhage.
Hypofibrinogenemia
It is uncommon disease in which patient has little or no
fibrinogen present, in either his plasma or tissue.
Types
Congenitalit is rare and autosomal recessive trait.
Acquireit occurs secondary to increase in fibrinogen
consumption during intravascular clotting, defective
fibrinogen formation and destruction or digestion of
fibrinogen by fibrinolytic or proteolytic enzymes
circulating in the bloodstream.
Clinical Features
Sexit occurs in both sexes with slight predilection for
males.
Symptomspatients exhibit severe bleeding episodes
throughout their lives and the disease is clinically indistinguishable from hemophilia. There is also epistaxis,
bleeding into gastrointestinal tract and central nervous
system has been also reported.
Cutaneous lesioncutaneous ecchymosis and hamartomas are frequently seen, although petechiae are rare.
Oral Manifestations
Clinical Features
Age and sex distributionit is inherited as an autosomal
dominant trait affecting both sexes.
Symptomsspontaneous epistaxis, bleeding into the
gastrointestinal tract and menorrhagia are common.
Cutaneous lesioncutaneous ecchymosis and hamartomas are frequently seen, although petechiae are rare.
Othersintraocular hemorrhage and hemorrhage into
the central nervous system have been also reported.
Diagnosis
Clinical diagnosisit is not possible to differentiate it
from hemophilia clinically.
Laboratory diagnosisbleeding time may be normal or
slightly prolonged but prothrombin time and clotting
time are infinite.
Oral Manifestations
Management
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Blood Disorders
Macroglobulinemia
It is also called as macroglobulinemia of Waldenstrom. It is a
plasma cell dyscrasia showing hemorrhagic tendency
similar to other hemorrhagic diseases. The formation of
complex between the abnormal immunoglobulin M,
macroglobulin and clotting factors, thereby inactivating
the clotting factors is responsible for hemorrhage.
Etiology
Multiple myelomait is a variant of multiple myeloma.
Bing-Neel syndromeBing-Neel syndrome (hyperglobulinemia with central nervous system involvement on toxiinfectious basis).
Plasmacytomait is also a variant of plasmacytoma.
Immunologicalit is an altered immunologic basis.
Clinical Features
Age and sex distributionit is most common in persons
over age of 50 years, seldom under 40 years and males
and female affected equally.
Signs and symptomsthe chief clinical signs are
weakness, weight loss, pallor, lymphadenopathy,
hepatomegaly, epistaxis, subarachnoid, and ocular
hemorrhage.
Oral Manifestations
Spontaneous gingival hemorrhageit consists of
spontaneous gingival hemorrhage, often with continued
oozing of blood.
Oral ulcerbleeding oral ulcers on tongue, palate, buccal
mucosa or gingiva and focal areas of hyperemia which
appear edematous are painful.
923
Clinical Features
Agethe lesion may be present in childhood but more
often appear in puberty and become progressively worse
with increasing age.
Sitethey are found most commonly on the skin of the
face, finger, toes, and on the oral mucous membrane.
Appearancethe disease is characterized by multiple
localized angiomatas or telangiectases on the skin.
Signsthe lesion bleeds easily, even after slightest
trauma. Bleeding is not caused by clotting factor
deficiency but as a result of rupture of the weak
capillaries. The lesion blanches on pressure and regains
its color when the pressure removed. As the affected
individual grows, the bleeding episode tends to increase
in frequency and intensity.
Crushed spider appearancethe typical lesion is cherryred to purplish macule or small papule (Fig. 37-19) that
resembles a crushed spider.
Epistaxisthey often give rise to profuse hemorrhage,
such as episodes of epistaxis. Severe bleeding may also
occur from the gastrointestinal tract.
Diagnosis
Clinical diagnosisoral ulcer, gingival bleeding,
lymphadenopathy, weakness, and hepatomegaly will
give clue to diagnosis.
Laboratory diagnosisit generally manifests severe
anemia with hemoglobin level near 4 to 6 gm/dl. An
extremely elevated sedimentation rate with demonstrable euglobulins and frequent gelling of the serum
upon cooling to room temperature or lower are cooling.
The viscosity of blood serum is high. The WBC count,
clotting time, bleeding time and prothrombin time are
normal but lymphocytosis, neutropenia and thrombocytopenia are occasionally seen.
Fig. 37-19: Cherry red lesion seen on lower chin area in hereditary
hemorrhagic telangiectasia.
Management
Oral Manifestations
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924
Diagnosis
Management
Septal dermoplastyit is done in patient who has got
repeated attacks of epistaxis. In this involve mucosa is
removed and replaced by skin graft.
Pressure packspontaneous hemorrhages may be
controlled by pressure packs, particularly nasal bleeding.
Sclerosing agentssclerosing agent such as sodium
morrhuate or sodium tetradecyl sulfate injected into the
lesion is useful.
Electrocauteryelectrocautery is also useful, prophylactically in a lesion that is likely to cause bleeding.
LASER ablationit is also useful in some cases.
Other therapyother therapy like progesterone, estrogen,
iron replacement therapy and occasionally blood
transfusion is also indicated in severe patient.
Suggested Reading
1. Ah-Pin PJ. The use of intraligamental injections in hemophiliacs.
British Dental Journal 1987;162:151.
2. Albert TP. FACA in hemophiliacs undergoing dental extraction.
Oral Surgery 198;51:115.
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Blood Disorders
3. Alexander WN. Alpha Thalassemia, minor Trait accompanied
by clinical oral signs Oral Surg 1977;43:892.
4. Awbrey JJ. Congenital Agranulocytosis. Oral Surgery 1975;35:526.
5. Bachner RL. Oral Manifestation of Acute leukemia. JADA 1977;
95:1148.
6. Cannell H. The development and facial signs of beta thalassemia
major. Br Dent J 1988;164:50-1.
7. Cawson RA. Denture Sore Mouth and Angular Cheilitis. British
Dental Journal 1963;11:446.
8. Chatterjee CC. Human Physiology (9th edn), Volume 1. Medical
Allied Agency, 1982.
9. Cohen MA. Hodgkins disease of the jaws. Oral Surgery 1984;
57:413.
10. Courant P. Oral Manifestation of infectious mononucleosis:
Journal of Periodontology 1969;40:279.
11. Davey KW. Agranulocytosis. Oral Surgery 1969;28:166.
12. Drew SJ, Sachs SA. Management of the thalassemia induced
skeletal facial deformity. J Oral Maxillofac Surg 1997;55:1331-9.
13. Evian CI. Complications of severe bleeding in a patient with
undiagnosed factor 9 deficiency. Oral Surgery 1981;52:12.
14. Guyton AC. Textbook of Medical Physiology (7th edn), WB
Saunders Company, Philadelphia, 1986.
15. Halstead CL. Oral Manifestations of Hemoglobinopathy. Oral
Surgery 1970;30:620.
16. Hansen EH. Oral Aspects of Pernicious Anaemia. British Dental
Journal 1968;125:266.
17. Hattler AB. Hereditary Haemorrhagic Telangiectases. JADA
1981; 103:421.
18. Hoggarth K. Macrocytic anemias: Practitioner. 1993;237:338-41.
19. Izumi Y, Taniguchi T, et al. Effective periodontal treatment in a
patient with type IIA Von Willebrands disease: report of case. J
Periodontal 1999;70:548-53.
20. Jones JH. Oral Manifestations of Systemic Diseases, W B Saunders
Company Ltd London, 1980.
21. Keleher M, Bishop K, Briggs P. Oral complications associated
with sickle cell anemia: A review and case report. Oral Surg, Oral
Med, Oral Pathol, Oral Radiol Endod 1996;82:225-8.
22. Kirson LH. Mental Nerve Paraesthesia Secondary to Sickle Cell
Anaemia. Oral Surgery 1979;48:509.
23. Koppang HS. Oral Manifestations of Porphyria. Oral Surgery
1970;33:926.
24. Kuipers EJ, Vellenga E et al: sulfasalazine induced agranulocytosis
treated with granulocyte macrophage colony stimulating factor.
J Rheumatol 1992;19:621-2.
25. Luker J, Scully C, Oakhill A. Gingival swelling as a manifestation
of aplastic anemia. Oral Surg, Oral Med, Oral Pathol 1991;71:556.
925
26. McCarthy PL. In Lea and Febiger: Diseases of the Oral Mucosa
(2nd edn), Philadelphia 1980.
27. Musselman RJ. Oral Bleeding in classic Hemophilia. Oral Surgery
1982;53:363.
28. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology
(2nd edn), Saunders Elsevier, 2004.
29. Patit JS. Periodontolal Manifestations of acute autoimmune
thrombocytopenic purpura. Journal of Periodontology 1986; 57:
429.
30. Pernu HE, Pajari UH, Lanning M. The importance of regular
dental treatment in patient with cyclic neutropenia: follow up 2
cases: J Periodontol: 1996:67:454-459
31. Poyton HS. Thalassemia: Changes seen in radiographs used in
dentistry. Oral Surgery 1968;25:264.
32. Prince. A alternate to blood product for dental extractions in
mild to moderate hemophilia patient. British Dental Journal
1987;162:256.
33. Provan D, Weatherall D. Red cells II: acquire anemia and
polycythemia. Lancet 2000;355:1260:8.
34. Provan D. Mechanism and Management of iron deficiency anemia.
Br J Hematol 1999;105 (suppl 1):19-26.
35. Robbins SL. Pathologic basis of Disease (2nd edn). WB Saunders
Company, Philadelphia,1982.
36. Schardt-Sacco D. Update on coagulopathieis. Oral Surg, Oral
Med, Oral Pathol, Oral Radiol Endod 2000;90:559-63.
37. Scully C, Cawson RA. Medical problems in dentistry: (5th edn),
Churchill Livingstone: an imprint of Elsevier, 2005.
38. Shah SJ. ARI Textbook of Medicine (4th edn). Association of
Physicians of India, Bombay, 1988.
39. Sinrod. Leukemia as a dental problem. JADA 1957;55:809.
40. Stubbs M, Lloyd JA. Protocol for dental Management of von
Willebrands disease, hemophilia A and hemophilia B. Aust Dent
J 2001;46:37-40.
41. Thompson CC, Tacke RB, et al. Purpuric oral and cutaneous
lesion in a case drug induced thrombocytopenia. JADA 1982;
105:465-7.
42. Tomich CE. Nuclear characteristics of buccal mucosal cell in
sickle cell anaemia. Oral Surgery 1977;43:554.
43. Walker R. Oral Manifestations of hematological disorders. British
Dental Journal. 1965;118:286.
44. Wilde J, Cook RJ. von Willebrands disease and its Management
in oral and maxillofacial surgery. Br J Oral Maxillofac Surg 1998;
36:112-8.
45. Wintrobe MM. In Lea and Febriger; Clinical Hematology (8th
edn), Philadelphia, 1981.
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4
Vitamins
Water soluble
Vitamin B complex
Vitamin B1 (thiamine)
Vitamin B2 (riboflavin)
Vitamin B3 (niacin)
Vitamin B5 (pantothenic acid)
Vitamin B6 (pyridoxine)
Vitamin B8 (biotin)
Vitamin B9 (folic acid)
Vitamin B12 (cyanocobalamin)
Vitamin C (ascorbic acid)
Choline
Inositol
Fat-soluble
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Introduction
B-complex Vitamins
Most of B-complex occurs in nature in the bound form within
the cells of vegetables or animal tissues. The digestion for
the liberation of vitamins and its absorption is a result of
breakdown of cellular structures in the gut. Vitamin Bcomplex is not stored in appreciable amounts in the body
tissues except vitamin B12. Excretion of vitamins occurs in
the kidney.
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Vitamins 927
The oral signs of deficiency of vitamin-B occur in the oral
tissues like tongue, mucous membrane and gingiva. It may
result in dermatitis, stomatitis and gastritis and blood and
bone marrow disorders. Degenerative changes of brain and
nerves are also a characteristic feature of deficiency since
nerve tissue depends on glucose. In hemopoiesis, vitamin
B12 and folate are essential for maturation of red cell
precursors.
Daily requirements
Men1.3 mg daily
Women1.0 mg daily
Children1.1 mg daily
Pregnancy and lactation2 mg daily
Functions in the body
Growthit promotes growth, protects heart muscle and
stimulates brain action.
Nervous systemit plays an important role in the normal
functioning of the entire nervous system.
Digestionit aids in digestion especially that of
carbohydrates.
Diureticit is a mild diuretic and it increases urine
formation.
GITit improves peristalsis and helps prevent
constipation.
Blood cellsit maintains the normal blood count and
improves circulation.
Othersit also reduces fatigue, increases stamina,
prevent premature aging and senility by increasing
mental alertness and promotes a healthy skin.
Deficiency symptoms
Nervous disorderswhen cells cannot metabolize the
glucose aerobically, it affects the nervous system first
since it depends entirely on glucose for its energy
requirements. There is mental depression, nervous
exhaustion and insomnia.
Digestive symptomsit occurs due to defective
hydrochloric acid production in the stomach. Patient
complains of loss of appetite, poor digestion, chronic
constipation and loss of weight.
Heartthere is accumulation of pyruvic acid and lactic
acid derived from it, which produces vasodilatation and
increases cardiac output. The heart muscle becomes lazy
and fatigued and the auricles or the upper chambers of
the heart lose their strength and it gradually enlarges. It
may lead to a condition known as hypertrophy of the
heart.
Beriberiprolonged gross deficiency can cause beriberi.
There are three types of beriberi Wet beriberi
Dry beriberi
Infantile beriberi
Othersother diseases, which can be associated with it
are
Wernickes encephalopathy
Peripheral neuritis
Korsakoffs psychosis
Beriberi
Fig. 38-1: Sources of vitamin B1.
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Etiology
Dietit is caused due to eating polished rice in which
outer husks is removed which contain thiamine.
Alcoholicsit is commonly seen in chronic alcoholics
due to their poor nutrition in general and also because
alcohol interferes with intestinal absorption of thiamine.
Othersit is often precipitated by infection, pregnancy
and lactation.
Pathogenesis
Deficiency of thiamine incomplete metabolism of
glucose accumulation of pyruvic acid and lactic acid
in tissue and body fluid dilation of peripheral blood
vessels fluid may leak out through capillaries,
producing edema high cardiac output, heart dilation.
Clinical Features
Wet beriberi
Symptomspain in legs after walking due to accumulation of lactic acid.
Cardiac signsthere is tachycardia and increased blood
pressure, cardiomegaly, increased JVP and palpitations.
There is also presence of sinus tachycardia and inverted
T waves.
Skinskin is warm due to vasodilation.
Othersedema may develop rapidly to involve leg, face
and trunk.
Dry beriberi
Peripheral neuropathyperipheral neuropathy is a
common feature of this disease.
Wasting of musclein long standing cases, there is
degeneration and demyelination of both sensory and
motor nerve fibers resulting in severe wasting of muscles.
Oral manifestations
Hypertensive mucosathere is hypersensitivity of oral
mucosa.
Symptomspain in the tongue, teeth, jaws and face.
Management
Complete restpatient should advice the complete rest.
Thiaminethiamine 50 mg IM for 3 days then 10 mg 3
times daily by oral route.
Management of infantile beriberiinfantile beriberi is
treated via mothers milk. The mothers should receive
10,000 mcg twice daily. In addition, infants should be
given thiamine in doses of 10,000 to 20,000 mcg IM once
in a day for 3 days.
Precaution while giving thiamine to patientAs such there
are no toxic effects of thiamine. Any excess is excreted in
the urine and not stored in any degree in the tissues or
organs. Rare symptoms of overdose are tremors, herpes,
edema, nervousness, rapid heartbeats and allergies. In
rare cases, excessive supply of this vitamin may also
adversely affect thyroid and insulin production.
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Vitamins 929
Pulses and legumesSoya beans, red gram, split green
gram and peas.
Vegetableslotus stems, turnip greens, spinach,
cauliflower and brinjals.
Nuts and oilseedsalmonds, walnuts, chilgozas and
mustard seeds,.
Fruitspapayas, raisins, custard apples and jack fruits.
Milk and milk productsskimmed milk powder, cows
milk and whole milk powder.
Animalsliver of sheep, eggs, mutton and prawn.
Daily requirement
For infants60 mcg value per kg of body weight daily.
Men1.5 mg daily
Women1.2 mg daily
Children1.3 mg daily
Pregnancy and lactation2 to 2.3 mg daily
Function in the body
Growthit is essential for growth and general health.
Metabolismit is involved in the metabolism of
carbohydrates, fats and proteins. It is essential for
normal tissue maintenance.
Nervous systemit helps in functioning of the nervous
system.
Digestionit helps in digestion and prevents constipation.
Eyesit alleviates eye strain and it is helpful in
counteracting the tendency toward glaucoma.
Othersit promotes a healthy skin, nails and hair and
strengthens the mucous lining of the mouth, lips and
tongue.
Causes of deficiency
Primary deficiencyit occurs due to inadequate diet and
also inadequacy of other essential nutrients including
vitamins and proteins.
Secondary deficiency
It may occur due to diseases of the intestinal tract.
Prolong use of psychological drug that interfere with
production of flavin monophosphate.
Chronic alcoholism, burns and trauma.
Deficiency symptoms
Seborrheic dermatitisit affects the nasolabial fold and
ala of the nose which exhibits a scaly gray dermatitis
and consists of enlarged follicles around the side of the
nose which is plugged with dry sebaceous material.
Ocular changesit consists of corneal vasodilatation,
photophobia and superficial and interstitial keratitis.
There may be itching and burning of the eyes.
Skin and nailsit may also result in dull or oily hair, an
oily skin, premature wrinkles on the face and arms and
split nails.
Management
Riboflavin 25,000 to 50,000 mcg is given daily in divided
doses.
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Sources
Cerealsrice bran, barley, wheat flour, jowar, wheat germ
and finger mallet.
Pulses and legumespeas, soya beans, red gram and split
kesari.
Vegetablesturnip greens, beet green, carrot leaves and
potatoes.
Nuts and oilseedsgroundnuts, sunflower, almonds and
mustard seeds.
Fruitsapricots, passion fruit, custard apple and bael
fruit.
Animalsliver of sheep, mutton, beef and prawns.
Milk and milk productsskimmed milk powder, cows
milk and whole milk powder.
Tryptophanit can be endogenously prepared from
tryptophan 60 mg of tryptophan gives 1 mg of niacin.
Daily requirements
Infants650 mcg per kg body weight daily.
Men17 mg daily.
Women13 mg daily.
Children15 mg daily.
Pregnancy and lactation12-15 mg daily.
Diarrhea
Dementia
Dermatitisthere is an erythema resembling severe
sunburns appears symmetrically overall parts of the
body exposed to sunlight and especially on the neck.
Affected area is well demarcated from the normal. In
acute cases, skin lesions may produce vesiculation,
cracking, exudation, crusting with ulceration and
secondary infection. In chronic cases, dermatitis occurs
as roughening and thickening of skin with brown
pigmentation (Fig. 38-4).
Alimentary tractanorexia, nausea, dysphagia. Glossitis
precedes the skin lesions. Non infective inflammation
may extend through the gastrointestinal tract. Diarrhea
is caused by atrophy of gastric epithelium followed by
submucosal inflammation which is then followed by
ulceration.
Nervous systemdelirium is the most common mental
disturbance in the acute form and dementia in chronic
cases.
Othersthere is also loss of appetite, irritability and
burning sensation in different areas of the body.
Pellagra
Causes of deficiency
Tryptophan deficiencyif insufficient tryptophan is
available for synthesis of niacin.
Dietdietary deficiency of niacin. High dietary levels of
amino acid lucine antagonise the synthesis of NAD and
NADP.
Miscellaneouschronic alcoholism, diarrhea and
carcinoid syndrome.
Clinical Features
Prodormal symptomsit can be developed in 3 weeks
with prodromal symptoms of loss of appetite, vague
gastrointestinal disturbances and numbness or burning
in various locations.
3 D s of diseaseit is called as disease of 3-D s
Dermatitis
Oral manifestations
Oral mucosaentire oral mucosa becomes fiery red and
painful and salivation is profuse.
Glossitisthe epithelium of the entire tongue is desquamated. The filiform papillae are most sensitive and
disappear first; the fungiform papillae may become
enlarged. The tongue becomes red swollen and beefy and
in animals the deficiency leads to black tongue. In early
stages, only the tip and margins of the tongue are swollen
and red. In advanced cases, the tongue losses all the
papillae and the reddening becomes intense. In this stage,
the tongue becomes so swollen that indentation from the
teeth are found along the borders of the tongue.
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Vitamins 931
Stomatitisthe mouth is sore and shows angular
stomatitis, cheilitis. Tenderness, pain and ulceration
begin at the interdental papillae and spreads rapidly.
Other featuressuperimposed ANUG or Vincents
infection involving the gingiva, tongue and mucosa is
common.
Management
Niacin 10 mg or 10,000 mcg per day and vitamin B
complex should also be given.
Alcohol should be stopped.
Daily requirement
Men10 mg
Women10 mg
Children5.5 mg
Function in the body
Metabolismit is a part of enzyme system which plays a
vital role in the metabolism of carbohydrates, fats and
protein and in the synthesis of amino acids and fatty
acids.
Formation porphyrinsit is also essential for the formation
of porphyrins, the pigment portion of the hemoglobin
molecule.
Stimulation of glandit stimulates the adrenal glands
and increases production of cortisone and other adrenal
hormones.
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Deficiency symptoms
Nervousperipheral neuropathy, mental retardation,
irritability, mental confusion and nervousness.
Bloodanemia, albuminuria and leukopenia.
Skindermatitis and eczema.
Otherskidney stones, inflammation of the colon,
damage to the pancreas, loss of muscular control,
migraine headache and premature senility.
Oral manifestation
Cheilosiscracking at the corner of the lip.
Glossitisinflammation of the tongue.
Othersangular stomatitis, tooth decay and halitosis.
Management
10-50 mg daily in divided doses.
Deficiency symptoms
Skinscaly dermatitis, eczema, seborrhea and prickling
of the skin.
Hairit can cause alopecia and dandruff.
Nervousthere is confusion, mental depression and
drowsiness.
Musclethere is muscular weakness, extreme fatigue
and lassitude.
Othersanemia, lack of appetite, hearing abnormalities
and lung infections.
Oralthe fleshy part of the tongue may waste away.
Management
20 mcg of biotin is taken daily for 10 days IM can heal
skin lesions. Oral biotin to be taken in amount of 400
mcg daily for 8-12 weeks. Shampoo coating 1% biotin
can be useful in controlling excessive hair loss.
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Vitamins 933
Nerveit is necessary for the growth and division of all
body cells, including nerve cells and for manufacturing
a number of nerve transmitters.
Hair and skinit is essential for the health of skin and
hair and helps to prevent premature graying of hair.
Pregnancyit is an important nutrient for the pregnant
women and her developing fetus. Folic acid also
improves lactation.
Othersit helps in building of antibodies which prevent
and heals infection. It also produces nucleic acids, RNA
and DNA.
Deficiency causes
Decreased intakeinadequate diet, impaired absorption,
malabsorption states and intrinsic intestinal diseases.
Increased losshemodialysis.
Increased requirementthe body demands exceed the
intake like in pregnancy, infancy, leukemia, hemolytic
anemia.
Othersimpaired utilization, diseases of the upper small
bowel where folate is mainly absorbed and idiopathic.
Clinical features
Anemiadeficiency of folic acid cause anemia which
often occurs in pregnant women and also children.
Skinloss of hair, grayish brown skin pigmentation can
also occurs.
Reproductive disordersspontaneous abortions,
difficulty during labor and high infant death can also
occur. Loss of libido occurs in males.
Nervousdementia, mental depression and fatigue.
Oral manifestations
Atrophic glossitisfiliform papillae disappear first and
fungiform papillae remain prominent. In severe cases,
fungiform papillae are lost and tongue becomes thick,
smooth and fiery red (Fig. 38-6).
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Management
Oralit is used in a dose ranging from 6 to 150 mcg,
helps in the treatment of lack of concentration, fatigue
depression, insomnia, anorexia, poor memory and loss
of weight.
Parenteral1000 mcg of vitamin given twice weekly in
cases of anemia.
Vitamin C
It is also called as ascorbic acid and antibiotic vitamin. It is
a modified simple sugar. It is the most active reducing agent.
Its highest concentration is in the pituitary, adenoid, eye
and WBCs. Stress and corticotrophin leads to loss of
ascorbic acid from the adrenal cortex. It is a powerful
antioxidant. It is necessary for normal maintenance of
intercellular substances of connective tissue in bone and
other tissue of mesenchymal origin.
Absorption and excretion
Absorption of ascorbic acid into the bloodstream takes place
in the upper part of the small intestine. It is excreted by the
kidney through the urine.
Dietary sources (Fig. 38-8)
Cereals, pulses and legumesred gram, peas, maize and
Bengal gram.
Vegetableparsley, drumstick leaves, turnip greens,
cabbage, bitter gourd, radish leaves, carrot leaves, beet
greens cauliflower, cluster beans, tomatoes, spinach and
ladies finger.
Nutscoconut dry and coconut milk.
FruitsIndian gooseberries, guavas, orange juice, limes,
papayas strawberries, lemons, pineapples, custard
apple, raspberry and mangoes.
Fish and meatIndian shard, Rohu, sheep liver and
tengra fish.
Oral manifestations
Tonguethere is sore painful tongue, glossitis and
glossodynia. Tongue is inflamed and is beefy red in color.
Painful and burning lingual sensation. Small shallow
ulcers resembling aphthous ulcers on the tongue with
atrophy of papillae with a loss of normal muscle tone is
called as hunters glossitis. Fiery red appearance of
tongue due to inflammation and burning sensation.
Denture wearing discomfortdiscomfort in wearing
dentures is due to weakened muscular tone.
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Vitamins 935
Milk and milk productkhoa and skimmed milk power
and wholemilk powder.
Daily requirements
Men and women40 mg.
Infants25 mg.
Children40 mg.
Pregnant and lactating women80 mg.
Functions of vitamin C
Synthesisit is important in the formation of collagen,
chondroitin sulfate and neurotransmitter.
Maintenanceit is useful for maintenance of folate pool
and mobility and phagocytic activity of neutrophils. It
is also necessary for maintenance of bones and proper
functioning of the adrenal and thyroid glands.
Absorptionit enhances, the absorption of iron in the body.
Metabolismtryptophan, nor-epinephrine and tyrosine
metabolism require vitamin C.
Othersit promotes healing and protects against all
forms of stress.
Deficiency symptoms
Mild deficiencyit may appear in the form of lassitude
fatigue, anorexia, muscular pain and greater susceptibility to infection.
Severe or prolonged deficiencya prolonged deficiency
may cause scurvy.
Scurvy
Prolonged deficiency of vitamin C may result in scurvy. It
is characterized by weakened blood vessels particularly
microvessels having least muscular supports. There is also
defective synthesis of osteoid which is derivative of collagen
which results in impaired wound healing.
Pathogenesis
Defective collagen formationthere is defective formation
of collagen in connective tissues because of failure of
hydroxylation of proline to hydroxyproline which is a
characteristic amino acid of collagen.
Increase capillary permeabilitythere is also increase in
permeability of capillary (hemorrhage), anemia due to
erythropoiesis and defective collagen formation.
Clinical features
Infantile scurvylassitude, anorexia, painful limbs and
enlargement of costochondral junction.
Folliculosishair follicle rises above skin and there are
perifollicular hemorrhages i.e. tiny points of bleeding
occurring around the orifice of hair follicles with
heaping of keratin like material.
Hemorrhagehemorrhage may occur in the joint, into
nerve sheath under the nails or conjunctiva. Petechial
hemorrhage occurs in buttocks, abdomen, legs, arms,
Diagnosis
Clinical diagnosisscurvy buds with increased
hemorrhagic tendency may give clue to the diagnosis.
Laboratory diagnosisthe calcified matrix material is not
destroyed so that wide zone of calcified but nonossified
matrix, called the scorbutic lattice develops in the
metaphysis. Anemia in scurvy is mild to moderate but
may be severe.
Management
Vitamin C 250 mg 3 times daily can be given.
Choline
It is a colorless crystalline compound which absorbs water
quickly. It is highly soluble in water and alcohol. It is
member of vitamin B group. It is present in foods as well as
in the body in relatively large amount.
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Sources
Fish and sea foodit is available in liberal quantities in
fish and sea foods.
Functions
Fat transportationit helps in the transportation of
fats in the body and prevents accumulation of fat in the
liver.
Nerve cell formationin combination with fatty acid and
phosphorus, it stimulates the formation of lecithin, an
important constituent of nerve cells in the body.
Memoryit goes directly into the brain cells to produce
a chemical that aids memory.
Vitamin A (Retinol)
Carotene is a yellow pigment found in vegetable foods. It is
converted into vitamin A in the body. Vitamin A or retinol
is found in foods of animal origin, while carotene is
provided by foods of both plant and animal origin. Vitamin
A is stored in liver. As a concentrated solution retinol is
light yellow in color. It solidifies when cooled and has a
mild pleasant odor.
Absorption
Management
Deficiency Symptoms
Inositol
It is a crystalline compound which has sweet taste. It is
highly soluble in water and is not destroyed by heat in
neutral, acid and alkaline media.
Functions in the body
Fat transportationit is essential for transportation of
fat in the body.
Brain cells nourishmentit is important in providing
nourishment to the brain cells.
Maintenance of cholesterol levelit helps to lower
cholesterol levels.
Hair growthit also promotes the growth of healthy
hair and helps to prevent its falling.
Prevention of eczemait helps in preventing eczema.
Sourcesthe most important sources is from liver,
brewers yeast, wheat germ, unrefined molasses, peanuts
and cabbage.
Deficiency symptomsit can cause alopecia or patchy
baldness, gastritis hypertension, fatty infiltration in the
liver, hardening of the liver and eczema.
Dosesit is given in the dose of 2 gm a day for 6-10 weeks.
Plant sources
Cereals and pulsesred gram, soya beans, bajra and
lentil.
Vegetablescarrots, green leafy vegetables and
spinach.
Fruitssweet potatoes, papayas, tomatoes, mangoes,
persimmon and raspberries.
Animal sourcessheep liver, cows milk, kidneys, fish
liver oils.
Fats and edible oilsbutter, hydrogenated oil and ghee.
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Vitamins 937
Skin disordersit may result in pimples, acne, boils and
premature wrinkles.
Requirements
Oral Manifestations
Deficiency Symptoms
Effect on growthfailure of growth in young and
collagenous tissue is affected.
Effect on eyesnight blindness, dry conjunctiva, Bitots
spot, corneal xerosis, corneal ulceration or keratomalacia
can occur. Xerophthalmia due to decrease in lacrimal
secretion.
Keratinizing metaplasiathe epithelial cells fail to
differentiate. This means that the cells in the basal layer
lose their specificity and tend to form a stratified
squamous epithelium with keratin production.
Keratinizing metaplasia of epithelial cells is usually
evident in several organs such as bladder, vagina and
skin and predisposes them to infection. Drying of skin
and atrophy of sebaceous glands.
Effect on reproductive organsdegeneration of germinal
epithelium thus affecting reproduction causes sterility
in males and cornification of vaginal epithelium in
females.
Effects on boneimbalance between osteoblasts (bone
forming cells) and osteoclasts (bone resorbing cells)
causing aberrations in the shape of bone.
Management
Depending upon deficiency symptoms it is given in the
dose of 7500-15,000 mcg per day for one month.
Hypervitaminosis A
Causesif more than 30,000 mcg of vitamin A is taken
daily, it can produce toxic effect in adults if continued
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Carotenemia
There is generalized yellowish skin and mucosa seen in
patient. There is also excessive deposition of carotene which
is result of high intake of foods containing carotene.
Increased yellowishness is also seen in hyperlipidemia,
diabetes, nephritis and hypothyroidism and in condition
in which conversion of carotene to vitamin A is impaired
by inborn metabolic error or hepatic disease.
Requirement
Infants and children0.01 mg.
Men and women0.01 mg.
Pregnancy and lactating women0.01 mg.
Management
Restriction of dietthere should be restriction of diet in
the patients.
Vitamin D
It is also called as sunshine vitamin. Vitamin D (1,25dihydroxycholecalciferol) is one of the compound that are
grouped together as the hydroxylated cholecalciferol. If
vitamin D deficiency occurs in children and infants it is
called as rickets and if it occurs in adults it is called as
osteomalacia. Deficiency of vitamin D tends to cause
hypocalcemia.
Fig. 38-12: Sources of vitamin D.
Forms
D3it is present in fish liver oils and animal fats. It is
called as cholecalciferol.
D2it is obtained artificially by irradiation of ergosterol
and called as ergocalciferol.
Absorption
Bile is essential for the absorption of vitamin D, fat helps in
its absorption too. The vitamin is absorbed from the jejunum
of the small intestine and is transported in the lymph
chylomicrons to the bloodstream. Excretion of vitamin D
Pathogenesis
Overgrowththere is overgrowth of epiphyseal
cartilage due to inadequate provisional calcification and
failure of cartilage cells to form a matrix and
disintegrates.
Formation of irregular massesthere is persistence of
distorted, irregular masses of cartilage many of which
projects into the marrow cavity.
Depositiondeposition of osteoid matrix on inadequately
mineralized cartilaginous remnants.
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Vitamins 939
Disruptiondisruption of the orderly replacement of
cartilage by osteoid matrix with enlargement and lateral
expansion of osteochondral junctions.
Microfracturethere is abnormal growth of capillaries
and fibroblasts in the disorganized zone because of
microfracture and stresses on inadequately mineralized,
weak, poorly formed bone.
Deformitydeforming of skeleton due to loss of
structural rigidity of the developing bone.
Oral manifestations
Teethdevelopmental abnormalities of dentine and
enamel, delayed eruption and malalignment of teeth.
Cariesthere is higher caries index in rickets as
compared to normal.
Enamelthere may be hypoplasia of enamel; enamel
may be mottled, yellow gray in color.
Pulpthere are large pulp chamber, high pulp horns
and delayed closure of root apices.
Malocclusionthe osteoid is so soft that teeth are
displaced leading to malocclusion of the teeth.
Radiographic features
Long bonesthe earliest and prominent manifestation is
widening and fraying of epiphysis of the long bones.
Bowing is a characteristic deformity seen in the weight
bearing areas, fine trabeculae are reduced in number.
Green stick fracturesit will be noted in many cases.
Jaw bonea thinning of jaw cortical structure such as
the inferior mandibular canal, the lamina dura and the
follicular walls of developing teeth has been described
in rickets. The trabeculae become reduced in number. In
severe cases, jaws appear completely radiolucent, so that
teeth appear to be suspended in air.
Teethif the disease occurs before 3 years of age, enamel
hypoplasia is fairly common. The pulp cavities of
deciduous teeth are grossly enlarged. The dentin is
reduced to a thin margin separating the pulp cavity from
enamel and cementum. The density of existing dentin
appears to be normal and margins of pulp cavities are
well and sharply defined. There is narrowing of the
periodontal ligament space.
Diagnosis
Clinical diagnosisrachitic rosary, pigeon breast,
Harrison grove with hypocalcification will diagnosed
rickets.
Radiological featuresgreen stick fracture with
narrowing of periodontal space.
Management
Dietary enrichmentdietary enrichment of vitamin D in
the form of milk.
Calcium gluconateif tetany is present, give calcium
gluconate IV. Daily dose between 1000-2000 IU of
vitamin D combined with 500-1000 mg of calcium.
Curative treatment includes 2000 to 4000 IU of calcium
daily for 6 to 12 weeks followed by a daily maintenance
dose of 2000 to 4000 IU for a prolonged period.
Hormonal therapyhormonal therapy like flucytosine.
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Pathogenesis
Vitamin D promotes the absorption of calcium and
phosphorus from the intestinal tract, therefore diet
deficient in vitamin D produces a negative calcium
balance that in turn leads to under mineralization of the
skeletal system. Thus rickets is caused by a lack of
calcification of cartilage and osteoid tissue.
Causes
Decreased renal tubular reabsorptionthe disease is now
recognized as a specific disorder characterized by
hypophosphatemia associated with decreased renal
tubular reabsorption of inorganic phosphates.
Geneticfamilial occurrence being inherited as X linked
dominant trait.
Diminished calcium and phosphate absorptiondiminished
intestinal calcium and phosphate absorption.
Clinical features
Ageit is first recognized in children when they are
about to walk.
Statureslight decrease in height of the patient and
reduced growth and rickets like bone changes.
Signs and symptomsbowing of legs, enlarged epiphysis,
bone pain, muscle weakness and vertebral fracture. Bony
outgrowth at the site of muscular attachment and around
joints may limit the movement
Oral manifestations
Dentinwidespread formation of globular hypocalcified
dentin with clefts and tubular defects occuring in the
region of pulp horns. Gross reduction in amount and
quantity of dentin which results in abnormally wide
root canal and large pulp chambers with faulty calcification and marked interglobular space in dentin.
Pulppulp horns are elongated and extend high often
reaching the dentoenamel junction.
Periapical infectionbecause of this defect there
commonly is invasion of the pulp by microorganisms
without demonstrable destruction of the tubular matrix.
Thus there is often periapical involvement of a grossly
normal appearing deciduous or permanent tooth
followed by the development of multiple gingival fistulae.
Tract is frequently present in dentinoenamel junction or
even outer enamel surface. This tract remains patent and
may result in early pulpal infection developing in
abscess or carious lesion.
Cementumthere is formation of abnormal cementum.
Radiographic features
Lamina duralamina dura around the teeth is frequently
absent or poorly defined. Osteoporotic bone with
thinned dental crypts.
Jaw bonesin some cases, only a relatively faint outline
of the jaw is seen, with almost complete absence of
Osteomalacia
It is also known as adult rickets and only flat bones and
diaphyses of long bones are affected. It is most commonly
seen in post menopause females with a history of low dietary
calcium intake and little exposure to UV light.
Clinical features
Age and sexit is seen in adults and pelvic deformities
are commonly seen in females.
Boneremodeling of bone occurs in the absence of
adequate calcium resulting in softening and distortion
of the skeleton.
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Vitamins 941
Symptomsthe majority of patients has bone pain and
muscle weakness of varying severity.
Othersthere is increased tendency towards fracture,
peculiar waddling or penguin gait, tetany and green
stick bone fractures.
Oral manifestations
Severe periodontitisthere is incidence of severe
periodontitis in some cases of osteomalacia.
Radiographic features
Pseudofracturea poorly calcified ribbon like zone
extending into bone at approximately right angles to the
periosteal margin. They are partial or complete fracture
without displacement in which callus has been formed
but there is no calcium available to be deposited, thus
healing process is not complete and fracture remains
apparent radiographically. It is also called as Loosers
zone. Osteoid tissue is formed in the defect but there is
no calcium available to be deposited in the osteoid.
Jawspseudofracture of the jaws near the angle has also
been noted.
Boneindividual bony trabeculae may be sparse and
unusually coarse in intraoral periapical radiograph.
Lamina durathe lamina dura may be thin or absent in
long standing and severe cases of osteomalacia.
Diagnosis
Clinical diagnosisbone pain, muscle weakness, fracture
and waddling gait.
Radiological diagnosispseudofracture can be seen
radiologically.
Laboratory diagnosisthere is elevation of serum alkaline
phosphatase to three or more times its normal levels.
Serum phosphorus is low due to increased phosphorus
excretion in response to reduction of serum calcium.
Serum calcium levels are usually on the lower side.
Management
Dosespatients with osteomalacia due to intestinal
malabsorption require a larger dose of vitamin D and
calcium i.e. 40,000 to 1, 00,000 IU of vitamin D and 15 to
20 gm of calcium lactate per day.
Effect of hypervitaminosis Dif patient is given in excess
of vitamin D, patient may suffer from nausea, vomiting,
constipation, drowsiness and sign of renal failure. There
is also metastatic calcification in arteriole and kidneys
and other tissues.
Vitamin E (Tocopherol)
It is also called as anti-aging factor. The word tocopherol
is derived from the word tocos meaning child birth and
pheros meaning to bear. It is yellow, oily liquid freely soluble
in fat solvents. Tocopherol alpha, beta, gamma, lambda
Daily Requirements
Men15 mg.
Women12 mg.
Children8.3 mg
Infants4-5 mg.
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Deficiency Symptoms
Reproductiveabortion of fetus in females and atrophy
of spermatogenic structures in males leading to
permanent sterility.
Musclesit causes degenerative changes in muscles.
There is muscle fiber atrophy which is replaced by
connective tissue.
Heartthere is necrosis and fibrosis of heart muscles.
Blood capillariesdeficiency may lead to degenerative
changes in the blood capillaries which in turn lead to
heart and lung diseases, pulmonary embolism and brain
stroke.
Oral Manifestations
Loss of pigmentation, atrophic degenerative changes in
enamel of vitamin E deficient rates.
Effects of Deficiency
Management
Vitamin E is given in the doses of 100 -400 mg daily.
Vitamin K (Phylloquinone)
It is essential for the production of a type of protein called
Prothrombin and other factors involve in the blood clotting
mechanism. Hence it is known as anti-hemorrhagic vitamin.
It is not easily destroyed by light, heat or exposure to air. It
is destroyed by strong, acids, alkalis and oxidizing agents.
Oral Manifestations
Gingival bleeding can also occur in cases of vitamin K
deficiency.
Management
It is given in dose of 10-20 mg daily.
Forms
K1it is the form which occurs in plants.
K2it is produced by most bacteria present in human
intestine if not supplied in the diet.
Requirements
Men and women70-140 mcg.
Children35-75 mcg.
Suggested Reading
1. Dervis E. Oral implication of osteoporosis. Oral Surg, Oral Med,
Oral Pathol, Oral Radiol Endod.
2. Field EA, Speechley JA, et al. Oral signs and symptoms in patient
with undiagnosed vitamin B12 deficiency. J Oral Pathol Med 1995;
24(10):468-70.
3. Firth N, Marvan E. Oral lesion in scurvy: Aus Dent J 2001;46(4):
298-300.
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Vitamins 943
4. Huber MA, Hall EH. Glossodynia in patient with nutritional
deficiency. Ear Nose Throat 1989;68:771-5.
5. McLaren DS. Vitamin A deficiency disorders. J Indian Med Assoc
1999;97(8):320-3.
6. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology
(2nd edn), Saunders Elsevier, 2004.
7. Prousky JE. Pellagra may be a rare secondary complication of
anorexia nervosa: a systematic review of the literature. Altern
Med Rev 2003;8(2):180-5 (medline).
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39
4
Metabolic Disorders
Introduction
Types
Disturbances in Protein
Metabolism
All living tissues, whether plant or animal contains protein.
Proteins constitute the most important group of foodstuffs.
In addition to contributing to cells and intercellular
materials, proteins and their constituent amino acids are
important in the formation of hormone, enzymes, plasma
proteins, antibodies and numerous other physiologically
active substances. 1 gm of protein is required for each kg of
body weight. It is required in increased quantity in later
half of pregnancy, during lactation and infancy, childhood
and adolescence.
Etiology
Prolonged illnessit occurs due to prolonged febrile
illness, massive burns and large chronic ulcer.
Chronic infectionchronic infections like urinary tract
infection, tuberculosis and parasitic infection.
Endocrine diseasehyperthyroidism and hypermetabolic state which interfere with utilization.
Otherstress, starvation and persistent vomiting and
diarrhea.
Clinical Features
Ageit occurs between the age of 1 and 3 years in
children.
Marasmusthere is emaciation due to weight loss,
wasting of subcutaneous fat and muscles. Marasmus
can also cause infantile gastroenteritis.
Kwashiorkor diseasethere is generalized edema, flaky
paint dermatosis, thinning, and reddening of hair. There
is also enlarged fatty liver. Kwashiorkor is distinguished
from Marasmus by the presence of edema and the
relatively less severe degree of body wasting.
Striped flag appearancealternating episodes of under
nutrition and adequate nutrition may cause hair to have
dramatic striped flag appearance. This is seen in
kwashiorkor disease.
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Metabolic Disorders
Oral Manifestations
Tonguebright reddening of tongue with loss of papillae.
In kwashiorkor patient may have edema of tongue and
may develop scalloping around the lateral margins due
to indentation of the teeth. Papillary atrophy may be
present and dorsum of the tongue assumes an
erythematous and smooth appearance.
Perioral findingthere is bilateral angular cheilosis,
fissuring of lip. Loss of circumoral pigmentation.
Xerostomiamouth becomes dry. However, there is
reduced caries activity due to lack of substrate
carbohydrate.
Epitheliumepithelium easily becomes detached from
underlying tissue, leaving raw bleeding surface.
Jawsdecreased overall growth of jaws, delayed
eruption, retarded growth of incisors and molars.
Periodontal membraneThe gingiva and periodontal
ligament membrane exhibit varying degrees of
degeneration.
Teethdeciduous teeth of children exhibits linear
hypoplasia of the teeth.
Maxillofacial gangreneis severe infection that spread
in mouth from necrotizing gingivitis.
Diagnosis
Clinical diagnosisstriped flag appearance, weight loss,
wasting of muscle, and flaky paint will give clue to
diagnosis.
Laboratory diagnosisit may cause mild anemia which
is normocytic and normochromic. The reticulocyte count
is normal and the bone marrow tends to become hypocellular.
Management
Antibioticsinfection should be treated with antibiotics.
Nutritional supplementit is usually supplied with milk
based formulae. Full fat desiccated milk products can be
fortified with corn oil and maltodextrin.
Amyloidosis
It is also called as amyloid disease. It is deposition of amyloid
in the tissue.
Forms of Amyloid
Type A (secondary) amyloid is a fibrillar protein of
unknown origin that is seen in prolonged inflammatory
disease, genetic disease and syndromes such as familial
Mediterranean fever.
Type B (primary) amyloid is thought to be immunologic
in origin because of its sequence homology with the NH2
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Types
Primary amyloidosisthere is no evidence of preceding
or existing disease.
Amyloidosis associated with multiple myelomait usually
affects adult patients.
Secondary amyloidosisassociated with variety of
chronic inflammatory disease.
Localized amyloidosisit is characterized by small
localized deposits of amyloid in the skin, bladder and
respiratory tract.
Familial amyloidosisit is rare condition such as familial
Mediterranean form or familial amyloidosis with
polyneuropathy.
Hormone related amyloidit is associated with tumors of
endocrine cells which secretes peptide hormones.
Etiology
Collagen diseaseslike rheumatoid arthritis.
Chronic infectionchronic infections like tuberculosis,
osteomyelitis, regional enteritis and ulcerative colitis.
Malignant diseasemalignant diseases like multiple
myeloma, Hodgkins lymphoma and renal cell
carcinoma.
Clinical Features
Sitecommonly affected organs are kidneys, heart, G.I.
tract, liver, respiratory tract, skin, eyes, adrenals, nerves
and spleen. There may be primary localized collection
of amyloid.
Symptomsthe general symptoms are fatigue, weakness,
ankle edema, dyspnea, paresthesia, orthostatic hypotension and weight loss.
Signspurpuric spots caused by hemorrhage resulting
in formation of amyloid deposits in the blood vessels.
Superficial waxy lesion occurs on the eyelids, nasolabial
folds, neck, axilla or perineum and they may bleed on
pressure.
Myocardiumcongestive cardiac failure is a common
problem due to amyloid deposits in myocardium.
GIT involvementthere is hepatomegaly, malabsorption
or colitis may develop.
Oral Manifestations
Symptomsthere are difficulties in chewing, swallowing
or talking. The speech difficulty is due to paresis of the
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Diagnosis
Clinical diagnosismacroglossia with amyloid deposits
can be seen on the face of patient.
Scintiscanningscintiscanning with 99mTc to localized
soft tissue deposits.
Laboratory diagnosiscongo red is used to diagnose
amyloid which shows birefringence and dichroism.
Management
Alkylating agentsyou can treat amyloidosis by
alkylating agents like melphalan.
Combination therapycombination therapy using
melphalan, prednisone and fluoxymesterone has
reported significant improvement.
Renal transplantationrenal transplantation may be
indicated. It will arrest the progression of bone lesion.
Debulking of lesiondebulking of lesion can be carried
out in case of macroglossia of tongue.
Clinical Features
Sexit is transmitted as non-sex linked recessive
character and both sexes are equally affected.
Urinethe first sign is excretion of red urine containing
uroporphyrin which may be noted at birth or apparent
at first two year after birth.
Photosensitivityexcessive deposition of the excess
porphyrin in the skin lead to photosensitivity. It is absent
in the neonatal period but may become apparent during
first few years after it becomes exposed to sunlight.
Vesiculobullous lesionvesicular and bullous eruption
appears on face, back and hand, i.e. exposed parts.
Vesicle contains a serous fluid which exhibits red
fluorescence. Ruptured vesicle heals slowly and leaves
depressed pigmented scars.
Anemiathere is often coexisting anemia.
Hepatic porphyriain this disease, there is abdominal
crisis and psychological or metal symptoms. There is
demyelination of nerve fibers.
Oral Manifestations
Teeththe porphyrin has an affinity for calcium
phosphate and due to this, deposition of porphyrin occur
in dentin. Deciduous and permanent teeth show red or
brownish discoloration which under ultraviolet light
exhibits red fluorescence due to incorporation of
porphyrins during development.
Oral mucosabullous, erosive lesions of oral mucosa may
be present.
Cheilitis and periodontitisthere is also atrophic cheilitis
and advanced periodontal diseases.
Diagnosis
Porphyria
It is a group of disorders in which there is defect in enzymes
involved in heme mechanism. These will result in
accumulation of porphyrins.
Classification
Management
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Metabolic Disorders
Classification
Simple lipidsthey are esters of fatty acids with various
alcohols, i.e. natural fats and waxes.
Compound lipidsthey are esters of fatty acids containing
groups other than and in addition to an alcohol and
fatty acids.
Derived lipidsthey are derivatives obtained by
hydrolysis of the simple and compound lipids, which
still possess the general characteristics of lipids.
Miscellaneousit includes carotenoids, vitamin E and K.
Function of Lipids
Fuellipids act as fuel in the body.
Insulation of bodythey insulate the body and protect
various internal organs.
Building blocksthey provide building blocks for
different high molecular weight substance.
Essential fatty acidslipids supply the essential fatty
acids which cannot be synthesized in the body and are
essential in the diet for normal health and growth.
Proper functioning of nervous systemthe nervous system
is particularly rich in lipids and is essential for proper
functioning.
Vitamin maintenancesome vitamins like A, D, E and K
are fat soluble, hence lipid is necessary for these vitamins.
Carrierlipoprotein is also carrier of triglycerides and
cholesterol.
Classification of Disorders
Non-lipid reticuloendotheliosisit is also called as
histiocytosis X, idiopathic histiocytosis and Langerhans
cell disease. It is inflammatory reticuloendothelioma
condition with evidence suggesting that it may be reaction
to some type of infection. There is pathological
accumulation of histiocytes and eosinophilic leukocytes.
It is of 3 types. Nowadays, all these three diseases is called
as Langerhans cell histiocytosis (LCH):
Hand-Schller-Christian disease.
Eosinophilic granuloma of bone (chronic localized
Histiocytosis X)
Letterer Siwe disease (acute disseminated histiocytosis X).
Lipid reticuloendotheliosisit is disturbance in sphingomyelin and glucosyl ceramide metabolism.
Gauchers disease
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Niemann-Pick disease
Tay-Sachs disease.
Variant
Hand-Schller-Christian diseaseit is also called as
multifocal eosinophilic granuloma, chronic disseminated
histiocytosis X or xanthomatosis. It is characterized by
widespread skeletal and extraskeletal lesions and
chronic clinical course. It is result of error in the
metabolism of cholesterol and its esters.
Letterer Siwe diseaseIt is an acute fulminating disease,
which invariably occurs in infants usually before the
age of 3 years.
Eosinophilic granulomait is also called as unifocal
eosinophilic granuloma. It is the lesion of bone which is
primarily histiocytes proliferation with an abundance
of eosinophilic leukocytes by no intra- or extracellular
lipid accumulation.
Clinical Features
Hand-Schller-Christian disease
Age and sexit is more common in boys than girls 2:1.
Occur in early life usually before age of five.
Classic triad
Single or multiple areas of punched out bone
destruction in skull.
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Letterer-Siwe disease
Ageit is fulminating condition that most often occurs
in infants younger than 1 year of age.
Onsetinitial manifestation is skin rash involving trunk,
scalp and extremities. Rash may be erythematous,
purpuric and ecchymotic, some time with ulceration.
Symptomspatient may have persistent low grade
spiking fever with malaise and irritability.
Signssplenomegaly, hepatomegaly and lymphadenopathy are common. Nodular and diffuse involvement of
visceral organs particularly in lung and GI tract. Soft
tissue and bony granulomatous reaction, hemorrhage,
anemia, failure to thrive
Teethdiffuse destruction of bone of maxilla and mandible which may result in loosening and premature loss of
teeth.
Eosinophilic granuloma
Siteit may occur in jaws and overlying soft tissues.
Juvenile periodontitisthere is loss of superficial alveolar
bone often mimicking juvenile periodontitis.
Symptomsgingivitis and bleeding gingiva, pain or
ulceration is present.
Signsloosening and sloughing of teeth often occurs
after destruction of alveolar bone. Sockets fail to heal
normally.
Radiological Features
Hand-Schller-Christian disease
Sitebone lesion usually seen in membrane bone but
can occur in long bones and the mandible.
Skull lesionthe skull lesion may be small or large,
single or multiple (Fig. 39-1) and they may occur
anywhere but anterior portion of the vault and the floor
of anterior and middle cranial fossa are commonest site.
Eosinophilic granuloma
Age and sexit occurs primarily in older children and
young adults and proportion of male to female is 2:1.
Siteskull and mandible are common site but femur,
humerus, ribs may be affected.
Symptomsthere may be local pain which may be dull
and steady, swelling and tenderness may also be there.
General malaise and fever may accompany the
eosinophilic granuloma of bone.
Signlesion is destructive and well demarcated, roughly
round or oval in shape. The area destroyed is replaced
by soft tissue. Tissue of early lesion is soft and brown
and since there is no necrosis, it is not friable. Later, it
become fibrous and grayish.
Fig. 39-1: Multiple skull lesions seen in patient with Langerhans
histiocytosis.
Oral Manifestations
Hand-Schller-Christian disease
Symptomssore mouth with or without ulcerative lesion,
halitosis, and unpleasant taste, loose and sore teeth.
There is also history of precocious exfoliation and failure
of healing of tooth socket following extraction.
Periodontal diseaseloss of supporting alveolar bone
mimics advanced periodontal disease.
Gingivitisinflammation of gingiva is also present.
Letterer-Siwe disease
Gingival hyperplasiaenlargement of the gingival tissue
occurs.
Ulcerthere may be presence of ulcer on the oral mucosa.
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Metabolic Disorders
Floating teeth appearancedestruction of periodontal bone
support of one or more teeth especially in the posterior
areas while producing virtually no resorption of tooth
roots. The result is often a distinctive radiographic
appearance of teeth standing in space (floating teeth
appearance), in the region superior to the mandibular
canal.
Pathological fracturein some cases, there may be
complete loss of continuity of the mandible, so that there
is pathologic fracture.
Effect on surrounding structuredisplacement of erupted
teeth and follicle was the most common radiographic
finding. In some cases, root resorption can be seen.
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Diagnosis
Clinical diagnosispunched out destruction of skull,
diabetes insipidus, ulcerative lesion, skin lesion with
exophthalmos will give clue to diagnosis.
Laboratory diagnosisbiopsy shows Langerhans cells
which contain rod shaped cytoplasmic structure known
as Birbeck granules. Plasma cells, lymphocytes, and
multinucleated giant cells are also seen. Patient also
suffers from anemia and less frequently leukopenia and
thrombocytopenia. Serum cholesterol level is normal but
tissue cholesterol level is raised.
Differential Diagnosis
Eosinophilic granuloma
Sitemandible is more commonly affected than maxilla,
posteriorly more common than anteriorly.
Shapeeosinophilic granuloma may be solitary or
multiple and the lesions are circular or elliptical in shape.
Marginit is moderately well defined at its radiographic
periphery.
Punched out appearancethe lesion in the jaw have fairly
discrete borders, which are rarely hyperostotic. Thus
they have punched out appearance.
Floating teeth appearancejaw lesions of eosinophilic
granuloma are usually seen as areas of pure osteolytic
activity in close vicinity to the alveolar processes.
Periosteal new boneperiosteal new bone formation is
observed in some cases.
Bone sclerosissclerosis is a common observation in
inflammatory lesions of the jaws and the fact that it
appears frequently in the alveolar bone lesions by
communication of the lesions with the oral cavity that
results in superimposed infection.
Management
Curettageit is usually treated by curettage or excision
of lesion.
Radiationthe lesions which are inaccessible are treated
by irradiation.
Corticosteroidsintralesional injection of corticosteroids
may be effective in local lesion.
Chemotherapypatients with acute disseminated
disease, may be given drug treatment like prednisolone,
vinblastine, etoposide, and cyclophosphamide.
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Gauchers Disease
Diagnosis
It may be familial and is thought to be due to faulty metabolism of the lipoid, kerasin. Lack of glucocerebrosidase
results in accumulation of glucosylceramide within
lysosomal cells of macrophages and monocytes lineage.
The reticular cells and histiocytes are increased in number
and many of them become infiltrated with kerasin. They
become accumulate in bone marrow of this patient. It is
autosomal recessive.
Types
Clinical Features
Ageit is mostly seen in adults and progress is slow.
Signsthere is enlargement of the lymph nodes, spleen
and to a lesser extent the liver.
Symptomsthere may be bone pain due to changes in
bone marrow. There is often bleeding from the nose or
from the gums. Teeth extraction from the affected area
may result in bleeding complications.
Signsthere is hepatosplenomegaly and CNS involvement. Patient also suffers from anemia and thrombocytopenia.
Pingueculaethe skin is sometimes pigmented and the
conjunctival fibrous tissue may be thickened and of brownish discoloration, a condition known as pingueculae.
Prognosisthe prognosis of malignant infantile form is
very poor; the disease results in death usually within
the first year.
Radiographic Features
Rarefactionbone changes occur due to destructive
infiltration of the cerebrosidic reticulosis of the bone
marrow. As a result of this and proliferation of cells so
called Gaucher cells, the bone undergoes rarefaction.
Porositythere may be generalized porosity of the
mandible and maxilla, with loss of trabecular structure.
Sometimes, there is porosity in the mental region and
thinned out mandibular cortex and areas of osteolysis
present in maxillary premolar area.
Worm eaten appearancepseudocystic radiolucent areas
in the molars and premolars with worm eaten
appearance can be seen.
Management
Glucocerebrosidaseenzyme replacement therapy with
macrophages targeted glucocerebrosidase is used.
Niemann-Pick Disease
It is also called as sphingomyelin lipidosis. It is characterized
by an abnormal storage of phospholipids due to lack of
sphingomyelinase.
Clinical Features
Siteit involves lungs, liver and the nervous system.
Signsthere is hepatosplenomegaly, retarded physical
and mental growth and severe neurological disturbance.
Diagnosis
Clinical diagnosisnot so specific.
Laboratory diagnosisbiopsy shows presence of foam
cells, usually an enlarged reticuloendothelial cell whose
cytoplasm contains numerous droplets-like inclusion
of lipid.
Management
Symptomaticit is only symptomatic to control the
infection. Death usually occurs within 3 years of age.
Othersenzyme replacement therapy and organ
transplantation are also carried out.
Genetic counselingit should be provided for the affected
family.
Tay-Sachs Disease
It is caused by lack of hexosaminidase A, which results in
the accumulation of ganglioside within lysosomes of
neurons. This condition is heterogeneous. There is
progressive neuronal degeneration developing after birth.
Death occurs at 3 to 5 years of age.
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Metabolic Disorders
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Disturbances in Carbohydrate
Metabolism
Classification
Monosaccharidethese are those carbohydrates which
cannot hydrolyze further to yield smaller carbohydrates.
For example: glucose and fructose.
Oligosaccharidesthese are condensation product of two
to three monosaccharides. For example: sucrose, maltose,
lactose and raffinose.
Polysaccharidesthese are high molecular weight
polymers of monosaccharide. For example: cellulose,
starch, glycogen and dextrin.
Function
Energy sourcecarbohydrates are the best source of
energy for human body.
Fuel for fetusglucose is a major fuel of mammalian
tissue and a universal fuel of fetus.
Cell membranecarbohydrates occur in cell membrane.
Fig. 39-3: Hurler syndrome showing large head and
prominent forehead (Courtesy Dr Shetty).
Hurlers Syndrome
It is disturbance of mucopolysaccharide metabolism, which
is characterized by elevated mucopolysaccharide excretion
ratio and an excessive intracellular accumulation of
chondroitin sulphate B and heparin sulphate in those
tissue and organ where they are normally found. It is
inherited as an autosomal recessive trait.
Clinical Features
Ageit usually becomes apparent within first two
years of life, progresses during early childhood and
adolescence and terminates in death before puberty.
Signshead is large, prominent forehead, broad saddle
nose and wide nostrils, hypertelorism and puffy eyelids
with coarse bushy eyebrows, thick lip, large tongue, open
mouth and nasal congestion and noisy breathing (Fig.
39-3).
Abdomenprogressive corneal clouding, hepatosplenomegaly resulting in protuberance of abdomen.
Claw handa short neck and spinal abnormalities are
typical, while flexion contractures result in the claw
hand (Fig. 39-4).
Radiological Features
Bone destructionlocalized areas of bone destruction in
the jaws may be found which appear to represent hyperplastic dental follicles with large pool of metachromate
material probably mucopolysaccharide.
Dentigerous cyst type appearanceradiolucent area
resembles a dentigerous cyst.
Oral Manifestations
Mandibleshortening and broadening of mandible with
prominent gonions and wide intergonial distance.
Teeththere is typical spacing of teeth. Teeth are small
and misshapen.
Gingivathere may be gingival hyperplasia.
Diagnosis
Clinical featuresopen mouth appearance (Fig. 39-5),
claw hand and puffy eyelid will diagnose this condition.
Radiological diagnosisdestructive lesion of bone is seen
radiologically.
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Clinical Features
Symptomssudden onset of hunger, sweating,
shakiness, tremor, anxiety, restlessness, faintness,
weakness, nausea, palpitations. Progression to mental
confusion, bizarre behavior, personality change, reduced
level of consciousness, loss of consciousness, seizures.
Signspulse rapid, blood pressure may be elevated and
moderate hypothermia may be present due to sweating,
hyperventilation and vasodilatation.
Other featuresbizarre or aggressive behavior may be
present, staggering gait, may appear drunk, cold and
clammy skin.
Diagnosis
Fig. 39-5: Open mouth appearance seen in
Hurler syndrome (Courtesy Dr Shetty).
Management
Death usually occurs before the age of ten due to pneumonia
and cardiac failure.
Lipoid Proteinosis
It is described in Chapter 11: Keratotic and Nonkeratotic
Lesions.
Management
Consult physicianconsult physician, ensure that the
airway is patent and protected and that ventilation is
adequate in the patient with a reduced level of consciousness.
Determination of serum glucosedetermine the serum
glucose with glucometer and give the conscious patient
a glass of orange juice or some other form of rapidly
absorbed sugar.
Glucose administrationwhen patient is unable to take
glucose orally, then give: adultGlucagons 1 mg
IM/SC, if no response may repeat in 5-20 minutes,
childGlucagons 0.025 mg/kg IM/SC, if no response
may repeat in 5-20 minutes.
Glucagonglucagon is well absorbed and a response
should be seen within 5 minutes. It is less sclerosing to
veins than Dextrose 50% in water, start an IV with normal
saline to keep vein open.
Hypoglycemia
It is a subnormal blood glucose level. It is caused by delayed
meal, inadequate total caloric intake, unusual physical
Disturbances in Mineral
Metabolism
Acrodermatitis Enteropathica
It is also called as zinc deficiency. Rare disease of infancy
and childhood, transmitted as autosomal recessive
character. Since supplements appear to be curative even
pathogenesis of the characteristic lesions involves a number
of etiologic factors.
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Metabolic Disorders
Clinical Features
Ageit is usually occur in childhood after weaning.
Symptomsthe primary signs of the disorder are skin
lesion, hair loss, nail changes and diarrhea.
Signserythematous, pustular, moist erosions of the
orofacial areas occur as an early manifestation. In fully
developed conditions, the buttocks, elbows, fingers and
toes are affected by vesiculobullous rash similar to that
affecting the orofacial region. Retarded body growth and
mental changes also occur with some frequency.
Oral Manifestations
Sitethe buccal mucosa, palate, gingiva and tonsils.
Candidiasislarge number of children suffer from
candidiasis.
The perioral area usually being affected by weeping
erosions, angular fissuring and spreading dermatitis.
Papillomathere may be numerous small whitish
papillomas on the buccal mucosa and borders of the
tongue.
The oral changes are sometimes described as stomatitis,
glossitis and stomatitis producing thrush like picture.
Signsbuccal mucosa is present with red and white
spots, erosions, ulcers and desquamation.
Tongue lesionlesion on the tongue is sometime
papillated and halitosis is often severe.
Diagnosis
Clinical diagnosisstomatitis, skin lesion, and hair loss
will give clue to the diagnosis.
Laboratory diagnosisserum level of zinc is decreased.
Management
Zinc sulfate220 mg of zinc sulfate tds daily produces
remarkable improvement.
Phosphorus
Phosphates form an intermediate stage in the metabolism
of fats and carbohydrates by their function in phosphorylation. They are used in building the more permanent
organic phosphates including some catalysts essential to
the structure and function of cells. They are utilized in the
formation of phosphoproteins, such as milk casein and in
the formation of the nerve polypeptides. They provide
the energy rich bonds such as adenosine triphosphate,
which is important in muscle contraction and they
form part of such coenzymes as pyridoxal phosphate,
which is necessary in decarboxylation and transmission
of certain amino acids such as tyrosine, tryptophan and
arginate.
953
Hypophosphatasia
It is a hereditary disease transmitted as a recessive
autosomal characteristic. There is deficiency of serum
alkaline phosphate. It resembles rickets. There is low level
of serum alkaline phosphatase activity and elevated urinary
excretion of phosphorylethanolamine which result in
formation of defective bone matrix.
Types
Perinatal typeit is diagnosed at birth and death occurs
within few hours of birth. Death occurs due to respiratory
failure.
Infantile typeit appears at 6 months of age.
Juvenile typethis appears in childhood and has wide
range of clinical expression.
Adult typeit is mild form and appear late in life.
Clinical Features
Symptomsthere is anorexia, irritability, persistent
vomiting and mild pyrexia.
Infantile formsevere hypocalcemia, bone abnormalities
and failure to thrive manifest the infantile form. Most of
the cases are lethal. Deformities of rib may be seen in
these patients.
Juvenile formhypophosphatasia of childhood is
characterized by increased infection, growth retardation
(Fig. 39-6) and rochite-like deformities including deformed extremities, costochondral junction enlargement
(rochite rosary) and pulmonary gastrointestinal and
renal disorders.
Adults formthe adult form includes fracture with a
prior history of rickets and osseous radiolucency. Stress
fracture of metatarsal bones of feet may be presenting
sign of this condition.
Homozygous involvementdisease with homozygous
involvement begins in utero and patient die within 1st
year. Bowed limb bone and marked deficiency of skull
ossification.
Heterozygous involvementin heterozygous, there is milder effect with poor growth and fracture and deformities.
Skullskull suture close early resulting in bulging suture
and gray marking on internal surface of skull which
occur due to increased intracranial pressure. Shape of
skull is brachiocephalic.
Pseudohypophosphatasiadisease resembling classic
hypophosphatasia but with normal serum alkaline
phosphatase level. There is osteopathy of long bones
and skull. There is premature loss of deciduous teeth.
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Radiographic Features
4
Fig. 39-6: Growth of this child is retarded due to hypophosphatasia (Courtesy Dr Manish Thadani).
Oral Manifestations
Premature loss of teeth and root resorptionthere is almost
total lack of cementum and normally attached
periodontal fiber leading to poor support and premature
loss of teeth in deciduous teeth (Fig. 39-7). There is also
delayed eruption of permanent teeth. The roots either
fails to develop fully or undergo early resorption of the
apices.
Hypoplasiateeth may be hypoplastic.
Pulp chamber and root canalthe pulp chamber and root
canal are sometimes larger than normal.
Diagnosis
Clinical diagnosispremature loss of teeth is typical
feature of this disease.
Radiological diagnosisbeaten copper appearance seen
and there is also thinning of lamina dura.
Laboratory diagnosisreduce level of bone, liver and
kidney isozyme of alkaline phosphatase. There is also
increased level of blood and urinary phosphoethanolamine. Biopsy shows abundant poorly mineralized
osteoids.
Management
Symptomatictreatment of hypophosphatasia usually
is symptomatic as infusion of alkaline phosphatase is
not successful.
Prosthetic appliancethese are given to replace missing
tooth.
Genetic counselingthis should be carried out to identify
carriers of defective gene.
Calcium
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Metabolic Disorders
activities. It is one of the important constituent in
coagulation of the blood.
Daily requirementdaily recommended calcium intake
of 360 mg for newborn and infants and 800 mg for
children and adults. Adolescents and pregnant and
lactating women are advised to increase their daily
dietary calcium intake by 50%, i.e. 1200 mg.
Absorption and excretiononly about 1/3rd of daily intake
of calcium is absorbed under normal conditions. High
protein diet has shown to increase calcium absorption.
Calcium is excreted in both faeces and urine.
Deficiencydeficiency may lead to internal hemorrhage
and generalized paralysis can occur. There may be
hyperirritability and tetany with characteristic carpopedal spasm and sometimes laryngospasm and
convulsion. Derangement of blood coagulation and the
integrity of the capillaries.
Magnesium
Actionmagnesium appears to participate practically
in every phosphorylating mechanism. It is also needed
for activity of certain enzymes such as phosphatase and
carboxylase.
Daily requirementthe recommended daily dietary
allowance for magnesium ranges from 50 mg for infants
to 400 mg for teenage males. A daily increase of 150 mg
is suggested during pregnancy and lactation.
Deficiencydeficiency of magnesium occurs due to
gastrointestinal loss of the mineral resulting from
frequent diarrhea and vomiting.
Neuromuscular hyperirritabilitypatients with deficiency exhibit severe neuromuscular hyperirritability
including carpopedal spasm and a positive Chvostek
sign, athetosis movements, marked susceptibility to
auditory, visual and mechanical stimuli, a decreased
serum magnesium level and normal calcium level.
Personality changesthere may be personality
changes, anorexia, nausea and vomiting.
Tetanythe tetany appears when the serum magnesium level is depressed below 1.30 mEq per liter.
Oral manifestationthere may be localized degeneration with enamel hypoplasia of the teeth.
Management of deficiencytreatment is done by
intramuscular injection of magnesium sulfate
followed by a prompt rise in serum magnesium and a
concomitant disappearance of the tetany and the
convulsion.
Excessthe administration of magnesium containing
antacids to patients with renal insufficiency has resulted
in central nervous system depression. There may be
severe voluntary muscle paralysis. High magnesium
intake will produce rickets in growing animals.
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Sodium
Actionsodium plays an important role in the
maintenance of the acid base equilibrium as well as of
osmotic pressure which depends on total base.
Daily requirementthe minimum requirement of salt is
thought to be about 0.5 gm.
Absorption and excretionthe kidney is the principal
organ for excretion of water and salt. When the diet is
low in salts and when there is profuse sweating, there is
no sodium found in the urine. The regulatory mechanism
controlling the reabsorption of sodium by the renal
tubules is controlled by adrenal gland.
Deficiencysodium deficiency occurs in man probably
when diet very low in salt is used for long period of
time. It is associated with gradual weakness, excessive
fatigue, lassitude, apathy, anorexia, a sense of
exhaustion, nausea, muscle cramps and peripheral
vascular collapse.
Potassium
Daily requirementmost of potassium is intracellular and
average requirement of potassium is 2 to 4 gm daily. The
requirement is greatest during periods of rapid growth.
Excretionabout 90% of potassium is excreted in the
urine.
Deficiencydeficiency may occur due to loss of potassium
through diarrhea and vomiting, malnutrition state,
administration of diuretics and ion exchange resins,
excessive dose of cortisone or hydrocortisone and
diabetic acidosis during insulin therapy. The signs of
potassium deficiency are primarily those of muscular
irritability, muscular weakness, reduced or absent reflex,
mental confusion, paralysis, disturbance in conductivity
and contractility of heart muscle and alterations in the
gastrointestinal tract.
Hyperkalemiait may result from extensive tissue
breakdown, adrenal insufficiency, advanced dehydration on administration of excessive amounts of potassium.
Hyperkalemia will produce mental confusion, numbness
and tingling of the extremities, pallor, cold skin, weakness,
disturbances in cardiac rhythm and peripheral collapse.
Miscellaneous Disorders
Malabsorption Syndrome
It is also called as sprue, idiopathic steatorrhea, celiac
disease. It includes conditions causing poor digestion or
absorption to a variable degree of a number of nutrients,
fats, proteins, carbohydrates, vitamins, minerals and water.
The defective absorption may be due to defective digestive
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956
Clinical Features
Oral Manifestations
Glossitisthere may be severe glossitis with atrophy of
filiform papilla, although the fungiform papillae persist
for some time on the atrophic surface.
Symptomspainful burning sensation of the tongue and
oral mucosa are common.
Signsthere are small projections which are pink or red
in color and the erythematous swelling and palatal
lesions appear as multiple aphthous ulcers.
Diagnosis
Clinical diagnosisintestinal disturbances with glossitis,
and erythematous swelling.
Laboratory diagnosisthere is low blood calcium level.
Management
Vitaminadministration of vitamin B12 and folic acid.
Dietdiet must be carefully supervised and supplemented with vitamins and minerals.
Suggested Reading
1. Caldemeyer KS, Parks ET, Mirowski GW. Langerhans cell
histiocytosis. J Am Acad Dermatol 2001;44(3):509-11.
2. Cleveland DB, Goldberg KM, et al. Langerhans cell histiocytosis:
report of three cases with unsual oral soft tissue involvement.
Oral Surg, Oral Med, Oral Pathol, Oral Radiol Endod 1996;82:
541-8.
3. Cleveland DB, Goldberg KM, Greenspan JS, et al. Langerhans cel
histiocytosis: report of three cases with unusual oral soft tisue
involvement. Oral Surg, Ora1 Med, Oral Pathol, Ora1 Radiol
Endod 1996;82:541-8.
4. Dagenais M, Pharaoh MJ, Sikorski PA. The radiographic
characteristic of histocytocytosis X: a study of 29 cases that
involve the jaws. Oral Surg, Oral Med, Oral Pathol 1992;74:
230-6.
5. De Moor S, Van Marck E, Peetermans J, et al. Cacogeusia in
amyloidosis associated with plasma cell dyscrasia. Eur J Cancer
B Oral Oncol 1994;30B(5):362-4.
6. Falk RH, Comenzo RL, Skinner M. The systemic amyloidoses. N
Engl J Med 1997;337(13):898-909.
7. Hartman KH. A review of 114 cases of histiocytosis X. Oral Surg,
Oral Med, Oral Pathol 1980;49:38-54.
8. Johansson I, Ryberg M, et al. Salivary hypofunction in patient
with familial amyloidotic polyneuropathy. Oral Surg, Oral Med,
Oral Pathol 1992;74:742-8.
9. Loh FC, Ravindranathan N, Yeo JF. Amyloidosis with oral
involvement. Case report. Aust Dent J 1990;35(1):14-8.
10. Lustmann J, Ben-Yehuda D, et al. Gaucher disease affecting the
mandible and maxilla: report of case. Int J Oral Maxillofac Surg
1991;20:7-8.
11. Mardinger O, Rotenberg L, et al. Surgical management of
macroglossia due to primary amyloidosis. Int J Oral Maxillofac
Surg 1999;28:129-31.
12. Milian MA, Bagan JV, Jimenez Y, et al. Langerhans cell
histiocytosis restricted to the oral mucosa. Oral Surg, Oral Med,
Oral Pathol, Oral Radiol Endod 2001;91(1):76-9.
13. Neville, Damm, Allen, Bouquot. Oral and maxillofacial pathology
(2nd edn), Saunders Elsevier, 2004.
14. Olsson A, Matsson L, et al. Hypophosphatasia affecting the
permanent dentition. J Oral Pathol Med 1996;25:343-7.
15. Plagmann HH, Kocher T, et al. Periodontal manifestation of
hypophosphatasia. J Clin Periodontal 1994;21:710-6.
16. Salisbury PL 3rd, Jacoway JR. Oral amyloidosis: a late
complication of multiple myeloma. Oral Surg, Oral Med, Oral
Pathol 1983;56(1):48-50.
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Antibiotics 959
40
Antibiotics
Introduction
Antibiotics are chemical substances produced by
microorganisms (fungi, actinomycetes, bacteria) that
suppress the growth of other microorganisms and may
eventually destroy them. Waksman and Woodruff in 1942
formally defined an antibiotic as a chemical substance
produced by microorganisms, which at a high dilution can
inhibit the growth and/or multiplication or kill another
microorganism.
Antimicrobial drugs are the greatest contribution of the
present century to therapeutics. The purpose of antibiotic/
antimicrobial chemotherapy is to aid the host defenses in
controlling and eliminating microbes that temporarily have
overwhelmed the protective host mechanisms. Antimicrobial agents share pharmacokinetic determinants with other
drugs, including ability to pass through membranes
(absorption), diffuse through extracellular fluids (distribution), undergo biotransformation by hepatic enzymes
(metabolism) and be eliminated from the body by renal or
fecal routes (excretion).
In addition, each antimicrobial agent demonstrates
unique pharmacokinetic properties including the acidic
dissociation constant (pKa), lipid solubility, plasma protein
binding, volume of distribution (degree of dispersal of the
drug through the intracellular and extracellular fluids) and
rate and type of hepatic metabolism or renal excretion. The
volume of distribution and hepatic and renal excretion
ratios constitute the major determinants of a drugs halflife (the time required for the peak concentration of a drug
to fall by one half in a given body fluid).
The antimicrobial therapy, which targets a living
organism with a physiology different from that of host, by
the influence of the variables such as microorganism
density, growth phase, ease of development of resistance
and glycocalyx formation capable of interfering with
antibiotic diffusion.
Classification
Antimicrobial drugs can be classified in many ways:
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960
Interference with cell wall synthesisPenicillin, Cephalosporin, Bacitracin, Vancomycin and Cycloserine C
Damage to cytoplasmic membranesPolypeptides:
Polymyxins, Colistin, Bacitracin
Polyene antibiotics: Amphotericin B, Nystatin, Hamycin
Inhibition of protein synthesis and impairment of function of
the ribosomesAminoglycosides, Tetracycline,
Chloramphenicol, Macrolide and lincomycin
Interference with transcription/ translation of genetic
information (misreading of mRNA code)Quinolones,
Metronidazole, Rifampin and Ethambutol
Antimetabolite actionSulfonamides, Sulfones, PAS and
Trimethoprim
Binding to viral enzymes essential for DNA synthesis
(Interfere with DNA function)Vidarabine, Acyclovir
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Antibiotics 961
at least 2 hours after a meal. In addition, interaction with
other orally administered drugs can decrease the external
absorption of some antibiotics. For example, the absorption
of tetracycline is decreased by milk, by antacids containing
divalent and trivalent metallic cations and by medications
containing iron salts.
Conceptual errors about a preordained course of antimicrobial therapy emanate from several faulty assumptions:
Resistant microorganismprolonged antimicrobial
therapy destroys resistant microorganisms. This is a
contradiction in terms, as antimicrobial agents cannot
affect microorganism resistant to them and the prolonged
use of antimicrobial agents only serves to select for these
resistant species.
Rebound infectionprolonged antibiotic therapy is
necessary for rebound infections that recur since the
organisms are suppressed but not eliminated. Acute
orofacial infections do not rebound particularly if the
source of the infection is probably eradicated.
Variability in infectious processantibiotic dosages and
duration of therapy can be extrapolated from one
infection to another. This is not possible to give the
variability in infectious processes.
Remission and relapse of infectionaccording to Norsby
S. R (1991) the ideal duration of antibiotic therapy is the
shortest that will prevent both clinical and microbiological relapse. According to Leitman P. S (1990), the
only practical guide for determining the effectiveness of
antimicrobial treatment and hence the duration of
therapy is clinical improvement of the patient as judged
by remission of the infection. Acute orofacial infections
have a rapid onset and relatively short duration of 2-7
days or less, particularly if the offending cause is treated
or eliminated. If clinical experience and the nature of the
infection dictate that it is anticipated course, if it will be
3 days, then 3 days of antibiotic therapy is enough; if 5
days, then 5 days of therapy, etc. When clinical evidence
indicates that the infection is reasonably certain to
resolve or is resolved, the antibiotic therapy should be
terminated.
Rule of thumbaccording to the rule of thumb, antibiotic
coverage should last for at least 48 hours after complete
remission of clinical symptoms. Treatment of the usual
oral infections of bacterial origin requires an average of
5-7 days of antibiotic therapy.
Effectiveness of Antibiotics
Age, Type and Extent of Infection
The time duration of the presence of an infection plays a
significant role in determining the effectiveness of antibiotic
therapy. Older, well established infections grow slowly and
thus both bactericidal and bateriostatic antibiotics are less
effective than they would be in new infections.
The larger the size or extent of infection, the less effective
the antibiotic therapy will be, because the increased number
of bacteria generally requires a higher concentration of
antibiotic be present at the site of infection.
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962
Resistance
Patient Compliance
This is a very important factor since patients may miss
doses when clinical symptoms begin to subside and a
patient may choose to discontinue therapy as soon as overt
symptoms are absent. Premature termination of drug
therapy will favor selection of microorganisms that are more
resistant to the drug. Particularly with bateriostatic agents,
patient compliance is a requisite for a successful clinical
outcome.
Prophylactic
More than 1/3rd are used for this purpose.
For postoperative wound infection.
In prevention of endocarditis in high risk patients
undergoing any dental procedures that likely to cause
gingival bleeding.
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Antibiotics 963
Macrolide
The Macrolides are a group of antibiotics that have in
common macrocyclic lactone rings linked with aminosugars. Apart from erythromycin, clindamycin, spiramycin,
roxithromycin, clarithromycin and azithromycin are
used clinically. Azithromycin is from a novel class of
antibiotics called azalides which have been derived from
Macrolides.
Erythromycin
It is isolated from streptomyces erythreus in 1952.
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964
Other Macrolides
Azithromycin is active against Gm-ve anaerobes and
provides higher drug concentrations in the tissues than in
blood or serum. It has been found to be highly effective
against all serotypes of Actinobacillus actinomycetemcomitans (Aa) and against Porphyromonas gingivalis.
Effectiveness of erythromycin against viridans streptococci
is poor. Other Macrolides, such as azithromycin and spiramycin have been used in treating dentoalveolar infections.
Aminoglycoside
Spectrumaminoglycosides are compounds that are
composed of at least one sugar attached to one or more
amino groups. Their main antibacterial spectrum is
against Gm-ve bacilli. Some of the aminoglycoside are
active against staphylococci, but most Gm +ve and most
anaerobic bacteria are resistant. All are potentially
ototoxic and may produce deafness due to their effect on
the 8th cranial nerve.
Drug includesthis group includes Streptomycin,
Gentamycin, Tobramycin, Sisomycin, Kanamycin,
Amikacin, Paromomycin, Framycetin and Neomycin.
Mechanism of actionevidence indicates that the
bactericidal effect of these drugs may be due to their
ability to cause detachment of the ribosomal complex
from the mRNA, which would result in the inability of
the cell to produce essential proteins. The aminoglycosides are inactive under anaerobic conditions because
intracellular transport is severely impaired in the
absence of oxygen. Therefore, all anaerobic bacteria are
markedly resistant even though they contain ribosomes
that are sensitive to these antibiotics.
Dosagethe dosage of these antibiotics required for
clinical effectiveness is only slightly below the levels
that elicit toxicity and potential adverse reactions can
be serious and irreversible. Ototoxicity and nephrotoxicity have been frequently associated with use of the
aminoglycoside with an incidence rate of 2-10%.
Therefore, use of an aminoglycoside is somewhat limited.
Due to the synergistic effect with other antibiotics,
aminoglycoside are usually given in lower doses in
combination with other drugs.
GentamycinIM/ slow IV dose (2-5 mg/kg/day in 3
divided doses) (it can produce bactericidal effect)
TobramycinIM/IV 3-5 mg/kg/day in 3-4 equal
doses (bactericidal)
Streptomycin0.5 to 1 gm 12 hourly for 7 days in acute
infection.
UsePenicillin and Gentamycin are commonly used
together for the treatment of bacterial endocarditis. Most
of the aminoglycosides are only available for parenteral
administration; however, some are available as creams
or ointments for topical application.
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Antibiotics 965
a mutant of a related mould, P. chrysogenum, was found to
give the highest yield of penicillin and is now employed
for commercial production of this antibiotic. Penicillins
belong to a group of antibiotics called as beta-lactams. The
other members include cephalosporin, cephamycin,
monobactams and carenems.
Penicillins are a family of antibiotics, with bactericidal
activity against broad spectrum bacteria. The basic
structure of the penicillin consists of thiazolidine ring fused
with a beta lactam ring which is essential for antibacterial
activity. The 2 rings constitute the fundamental nucleus of
all the penicillins, namely 6-amino-penicillanic acid
(6APA). Substitutions and modifications on the acyl side
chain have resulted in a number of semisynthetic penicillins
with enhanced antimicrobial properties such stability to
gastric acids, resistance to hydrolytic enzymes and
increased absorption from the stomach.
The side chain also determines the stability of the
penicillin against degradation by gastric acid and by
enzyme penicillinase (beta lactamase) produced by certain
microorganisms. (The beta lactamase producing organisms
are Staphylococcus aureus, Pseudomonas, Enterobacter, etc).
The first identified penicillin is benzyl peniciilin-G. If
phenoxyacetic acid was added to the culture, phenoxymethyl penicillin (penicillin V) was produced which is
semi-synthetic one.
Classification
Natural penicillinsPenicillin G (Benzyl penicillin),
Procaine penicillin G and Benzathine penicillin.
Semi-synthetic penicillin
Acid resistant penicillinsphenoxymethyl penicillin
(Penicillin V) and Phenoxyethyl penicillin
(Phenethicillin)
Penicillinase-resistant penicillinsAcid labile
(Methicillin, Naficillin, Cloxacillin, Dicloxacillin) and
Acid resistant (Flucloxacillin)
Penicillins effective against Gm +ve and Gm-ve organisms
Ampicillin, Amoxicillin.
Extended spectrum penicillinsCarboxy penicillin
(carbenicillin, Ticarcillin), Ureidopenicillins
Piperacillin, Amidinopenicillin (Mecllinam).
Penicillins with beta lactamase inhibitorsAmoxicillin
Clavulanic acid (Augmentin), TicarcillinClavulanic
acid (Timentin).
Cloxacillin
Activitythis is Penicillinase resistant penicillin. This
drug has weaker antibacterial activity than penicillin
G. So, it is used in conjunction with ampicillin or
amoxicillin to enhance the synergism.
Ampicillin
Actionit is effective against Gm +ve and Gm-ve
organisms. The antibacterial activity of ampicillin is
generally similar to that of Benzyl penicillin, but it is
more effective than benzyl penicillin against a variety of
Gm-ve bacteria. The Gm +ve cocci are less sensitive to
ampicillin than to benzyl penicillin. Ampicillin is
inactivated by penicillinase.
Absorptionit is incompletely absorbed on oral
administration. Food does not interfere with its
absorption. Plasma levels are reached at peak within 2
hours and 1 hour after oral and IM administration
respectively.
Adverse effectampicillin causes skin rash is usually
maculopapular and not urticarial. Diarrhea is common
with oral ampicillin.
Dosagethe ampicillin capsule contains ampicillin
hydrate equivalent to 250 mg of the base. The usual adult
dose of ampicillin is 250 to 500 mg 6 hourly (qid); doses
as large as 1 gm qid may be required for more refractory
Gm-ve infections. High doses for IM/ IV injection are
used in the treatment of meningitis and bacterial
endocarditis.
Amoxicillin
Actionthis is effective against Gm +ve and Gm-ve
organisms. This is a semisynthetic penicillin (amino-phydroxy-benzyl penicillin) with a broad spectrum of
antibacterial activity and having substantial advantages
over ampicillin.
Absorptionamoxicillin is effective on oral administration and the blood levels are twice as high as those
after similar dose of ampicillin. Its absorption is not
affected by food. The incidence of skin rashes and
diarrhea is less than with ampicillin.
Dosage250-500 mg (tid) in adult. It can also be given
IV/ IM.
Adverse reactionpenicillins are among the least toxic of
any antibiotics. Hypersensitivity is by far the most
common adverse reaction noted with any penicillin.
According to Idsoe et al 0.6-10% of patients treated with
penicillin develop some form of allergic reactions such
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966
Newer Penicillins
Azlocillinit is an acyl ampicillin antibiotic with an
extended spectrum of activity and greater in vitro potency
than the carboxy penicillins. Azlocillin is similar to
mezlocillin and piperacillin. It demonstrates antibacterial activity against a broad-spectrum of bacteria,
including Pseudomonas aeruginosa and, in contrast to most
cephalosporin, exhibits activity against enterococci.
Dicloxacillinit is a narrow spectrum beta-lactam
antibiotic of the penicillin class. It is used to treat
infections caused by susceptible Gram-positive bacteria.
Notably, it is active against beta-lactamase-producing
organisms such as Staphylococcus aureus, which would
otherwise be resistant to most penicillins. It is very
similar to flucloxacillin and these two agents are considered interchangeable. Dicloxacillin is commercially
available as the sodium salt dicloxacillin sodium in
capsules (250 or 500 mg) and injections (powder for
reconstitution, 500 and 1000 mg per vial).
Flucloxacillinit is a narrow spectrum beta-lactam
antibiotic of the penicillin class. It is used to treat
infections caused by susceptible Gram-positive bacteria.
Nowadays, it is no longer recommended against betalactamase-producing organisms such as Staphylococcus
aureus, since like in other penicillins, it is not active
against such infections. It is very similar to dicloxacillin
and these two agents are considered interchangeable.
Cephalosporins
In 1945, Prof. G. Brotzu isolated a fungus called as Cephalosporium acremonium. Cephalosporins are extracted from this
fungus. Cephalosporins have 7-amino cephalosporemic
acid nucleus which bears close resemblance to the 6-APA
nucleus of penicillins.
Antibacterial activitycephalosporins possess a wide
range of activity against Gm +ve and Gm-ve bacteria.
Cephalosporins act by inhibiting bacterial cell wall
synthesis and are bactericidal.
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Antibiotics 967
Absorption, fate and excretioncephalosporins are
administered either orally or IV (IM is painful). Cephalosporins are eliminated mainly by renal excretion (As
with penicillins, renal tubular blocking with probenecid
increases the plasma levels significantly).
Adverse reactionit can cause allergy such as skin rashes,
fever, serum sickness, anaphylactic reaction (Rare),
eosinophilia, neutropenia, transient splenomegaly and
increased SGOT levels. Some of the newer cephalosporins cause disulfiram like effect when combined with
alcohol.
First generation cephalosporinsthe first cephalosporin
introduced into medical practice was cephalothin. This
compound is active against both penicillin-sensitive and
resistant staphylococci, pneumococci, streptococci and
the common Gm-ve pathogens, but they are not effective
against anaerobes. Other 1st generation cephalosporins
are cephacetrile and cefazolin. The 1st orally active
cephalosporin for medical use was cephaloglycin.
Cephalexin is more stable and has better oral absorption.
It is often used as follow-up therapy and for the treatment
of minor infections involving Gm+ve organisms.
Cephatrizine has a similar Gm+ve spectrum, but is more
active against Gm-ve organisms.
Second generation cephalosporinsthese offer a wide range
against Gm-ve bacilli. Their main use would appear to
be in the Gm-ve infections, especially those caused by
lactamase producing organisms. But they have less
activity against most pathogens that cause infection of
wounds.
Third generation cephalosporinsthey have poor activity
against the Gm+ve cocci; but are more active against
Gm-ve bacilli than the first and second generation
cephalosporins. This generation includes ceftazidime,
cefsulodin, ceftriaxone (once a day).
Fourth generation cephalosporinsCefepime is more
resistant to some lactamase. It is active against
streptococci, and methicillin-sensitive staphylococci.
Its main use is in serious Gm-ve infections including
infections of the CNS into which has excellent
penetration. Dose: 2 gm IV bid.
Fifth generation cephalosporinsthis is recently discovered
cephalosporin and it is used in severe infection. Example
of this generation cephalosporin is ceftobiprole.
Cefazolinparenteral administration results in higher
blood level that persists longer. It has a half life of
2 hours due to slower tubular secretion. Dose0.25 gm
8 hourly (mild cases), 1 gm 6 hourly (severe cases) IM
and IV.
Cephalexinit is effective against most gram +ve cocci,
bacilli, E. coli and Klebsiella. It is an orally effective first
generation cephalosporin. Dose0.25 to 1 gm 6-8 hourly
and in children 25-100 mg/kg/day.
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968
Nitroimidazoles
Drugs includemembers of the nitroimidazole group of
antibiotics include Metronidazole, Nimorazole,
Tinidazole, Secnidazole and Ornidazole.
Mechanism of actionthe mechanism of action of these
antibiotics is not clear. Since the drugs are only active
against anaerobic organisms, it was first postulated that
the drug interacted with biochemical pathways are
found only in obligate anaerobes. This theory has been
replaced, since current evidence indicates that these
drugs interact with bacterial DNA. Upon entry into an
anaerobic organism, metronidazole is reduced at the
5-nitro position producing a number of short-lived
cytotoxic intermediates which react with DNA, resulting
in cell death. The reductive pathways are characteristic
of sensitive anaerobic bacteria and protozoa but are
not present in aerobic bacteria. The reported carcinogenicity of this drug in rodents may be related to the fact
that mammalian liver microsomes can reduce metronidazole.
Use in dentistryits primary use is in the treatment of
obligate anaerobes associated with the oral cavity,
intestinal and female genital tracts. Metronidazole has
been used successfully in the treatment of periodontitis
which is probably related to its high activity against the
Gm-ve anaerobic bacilli that are often associated with
the disease. The concurrent oral administration of
metronidazole with either amoxicillin or Augmentin has
been used with some success in the treatment of both
juvenile and adult forms of periodontitis and also
effective in the treatment of A. actinomycetemcomitans
associated periodontitis.
Quinolones
Drugs includethe quinolones constitute a group of 1,
8-naphthyridine derivatives. These are synthetically
produced drugs and therefore are not true antibiotics.
Nalidixic acid was introduced into clinical use in 1964
and is the prototype of the quinolones drugs. Ciprofloxacin, a fluorinated quinolones carboxylic derivative
is an example of the newer drug/2nd generation drug.
Others in this group include Norfloxacin, Ofloxacin,
Pefloxacin, Amifloxacin, Lomfloxacin, Levofloxacin, and
Gatifloxacin.
Mechanism of actionNalidixic acid and Ciprofloxacin
are generally considered bactericidal, since they inhibit
the bacterial DNA replication (The bactericidal effect
can only occur in the presence of competent RNA and
protein synthesis. The imbalance of inhibited DNA
replication and continuing protein synthesis results in
inhibition of cell division). The site of inhibition is a
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Antibiotics 969
specific enzyme, DNA gyrase. This enzyme is responsible for the coiling of the long bacterial chromosome so
that it fits into the bacterial cell, but still maintains its
spatial arrangement. Quinolones interfere with this
gyrase so that the spatial arrangement of the DNA is not
possible and therefore it cannot be transcribed.
Ciprofloxacinciprofloxacin is the 1st oral broadspectrum antimicrobial agent with good activity against
Pseudomonas aeruginosa. It has an excellent activity
against a wide range of Gm-ve organisms, including
many that are resistant to 3rd generation cephalosporins,
broad-spectrum penicillins and the newer aminoglycosides. It also has good activity against Gm+ve bacteria
and is thus useful in the management of mixed
infections. However, most anaerobic bacteria are
resistant. The newer quinolones may not be used routinely by dental professionals due to resistance
encountered with the oral flora. Fortunately ciprofloxacin does not cross-react with most antibiotics. Infact,
an additive effect has been reported with some antibiotics
such as the lactams, aminoglycosides, clindamycin
and metronidazole.
Adverse reactionin comparison to other antibiotics, most
quinolones are well tolerated. Nausea, headache,
vomiting, diarrhea, photosensitivity, skin rashes, etc. are
rarely seen. Ciprofloxacin is excreted in breast milk and
may cross the placental barrier. Therefore, it should not
be given to pregnant women or nursing mothers except
in the case of severe infections. The quinolones are not
recommended for pre-pubertal children.
Drug interactionquinolones inhibit the metabolism of
theophylline and caffeine. Toxicity may occur due to
the inhibitory effect of ciprofloxacin on theophylline
if given together. Concurrent administration with
antacids containing magnesium, Al, Ca, Zn containing
multivitamins or iron containing preparations may
substantially interfere with absorption of ciprofloxacin.
Quinolones enhance the effect of warfarin and other oral
anti-coagulants. It must be remembered that organisms
do develop resistance to them and also since it is costly,
their routine use in all infections is to be discouraged.
DosageCiprofloxacin (250/ 500 mg bid orally, 200/
400 mg IV bid over 30-60 minutes), Ofloxacin (200-400
mg OD orally in the morning preferentially, 200-400 mg
IV bid/ OD), Lomefloxacin (400 mg OD orally, 400 mg
IV), Pefloxacin (400 mg bid orally, 400 mg IV bid over 1
hour), Sparfloxacin (200-400 mg OD/ bid orally).
Classification of Local
Antimicrobial Therapy
Systemic antimicrobial agents enter periodontal pockets
following their intestinal absorption and passage
from the bloodstream into oral tissues, GCF and saliva.
Systemic delivery provides a ready exposure of all
periodontal sites to the antimicrobial agent, but it also
posses a risk of adverse reactions to non oral body sites.
Local antimicrobial therapy in periodontitis involves direct
placement of an antimicrobial agent into subgingival sites,
minimizing the impact of the agent on non-oral body sites.
They are applied as a part of home oral hygiene regimens
and professionally applied as part of office based
treatment procedures. Local delivery may be further
classified as providing either non-sustained or sustained
subgingival drug delivery. Sub-gingival irrigation with
antiseptic agents lacking substantively of oral tissues
(Povidone-iodine) are examples of non-sustained drug
delivery. Sustained or controlled drug release can be
provided with sub gingival irrigation of agents
intrinsically substantive for tooth root surfaces (aqueous
tetracycline) or pocket placement of commercial
antimicrobial fibers, gels or films.
Personally applied (Home self-care)Non-sustained
subgingival drug delivery (Home oral irrigation) and
sustained subgingival drug delivery (None developed
to date).
Professionally applied (Dental office)Non-sustained
subgingival drug delivery (Professional pocket
irrigation) and Sustained subgingival drug delivery
(Controlled-release device)
Agents that exert bactericidal effects within 5 minute
time period are preferable for sub-gingival irrigation. Iodine
showed 5 minute bactericidal action against the test
organisms at concentrations therapeutically attainable at
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970
Drug
Trade names
Dosage form
Dose
Indications
Contraindications
Adverse effects
Tetracycline
Achromycin,
Terramycin
Capsule
Injection
Ointment
1-2 gm daily
divided into
4 doses
Juvenile periodontitis,
Chronic periodontal
disease,
Refractory periodontitis,
Desquamative gingivitis
Pregnancy,
children
below 8 years
GI disturbance,
tooth discoloration,
enamel
hypoplasia
Clindamycin
Clincin
Dalcap
Tablet
Capsule
Injection
150-300 mg
6 hourly
Anaerobic streptococci,
Clostridium infections,
Refractory periodontitis
Hypersensitivity,
infancy
Urticaria, diarrhea,
abdominal pain,
jaundice, liver
abnormalities
Erythromycin
Althrocin
Erythrocin
E. mycin
Tablet
250-500 mg
8 hourly
Refractory periodontitis
Hypersensitivity
Mild epigastric
pain, diarrhea,
allergic reaction
Metronidazole
Flagyl
Metroygyl
Aldezole
Tablet
Suspension
injection
200-400 mg
TDS.
200 mg/5 ml
Ulcerative gingivitis,
periodontitis, ANUG
Neurological
disease, blood
dyscrasias,
pregnancy
Anorexia, nausea,
metallic taste,
glossitis
Quinolone
Ciprofloxacin
Ciplox
Cipin
Tablet,
injection
250-500 mg
12 hourly
Osteomyelitis, ANUG,
joint infection, recurrent
periodontitis
Hypersensitivity,
children and
elderly
Diarrhea, vomiting,
abdominal pain,
arthritis,
restlessness
Penicillin
Amoxicillin
Ampicillin
Kaypen
Ampilin
Amox
Mox
Capsule,
Syrup
250 mg-1 gm
TDS
125 mg/ml
Refractory periodontitis
Sensitivity
Pregnancy
Cephalosporin
Cefotaxime
Cefaclor
Cefixime
Alcephin
Biotax,
Capsule
Injection
Syrup
2-6 gm daily in
2-3 divided dose
4 gm initially
followed by
2 gm IV
Inhibits growth of
gramve anaerobes,
Osteomyelitis
Hypersensitivity,
renal failure
GIT upset,
allergic reaction,
increased SGPT,
candidiasis
Chlorhexidine
Hexidine
Rexidin
Suspension
Oral hygiene
bacterial infection
Allergy to
chlorhexidine
Burning sensation,
candidiasis, bad
taste sensation,
staining of teeth
Dose Calculation
Children Dose can be calculated by following formulas
Age Adult Dose
Youngs Formula =
Age + 12
Prophylactic Antibiotics
According to AHA (American Heart Association,
2002)
OrallyAmoxicillin 2 gm one hour before surgery.
Children50 mg/kg body wt. one hour before surgery.
IV or IMAmpicillin 2 gm half an hour before surgery.
Children50 mg/kg body wt. half an hour before surgery.
If allergic to penicillinClindamycin 600 mg, children
50 mg/kg body wt. If Orally one hour before surgery, If
IV or IM half an hour before surgery.
Others
Adult
Children
Clarithromycin
Azithromycin
500 mg
500 mg
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Antibiotics 971
Suggested Reading
1. Barar FSK. Essentials of pharmacotherapeutics (3rd edn), S Chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central publisher, 2005.
3. Craig CR, Stitizel RE. Moderate pharmacology with clinical
application (5th edn), Little Brown and company, 1997.
4. Gomes MW. Synopsis of medical pharmacology (1st edn),
National Series, 2002.
5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001.
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972
41
5
Introduction
In dentistry most common complaint of the patient is
pain. So management of pain with the analgesic is primary
importance of dentist. Pain is ill-defined, unpleasant
sensation usually evoked by external or internal noxious
stimulus. Pain receptors are mainly the free nerve ending
widely spread in superficial layer and deep into the body.
Certain pain receptors are present in the body called as
chemoreceptor like bradykinin, prostaglandin (PG),
prostacyclin (PGI2 ), thromboxane (TXA2 ), histamine,
acetylcholine and proteolytic enzymes elicit pain after tissue
injury. A delta fiber transmits fast-acute pain whereas
c-fibers transmit slow-chronic type of pain.
Definition of Analgesic
Analgesics are the drugs that selectively relieve pain by
acting in CNS or on peripheral pain mechanisms, without
significantly altering consciousness. Transmitters involved
in analgesic system are enkephalin and serotonin.
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Nonselective Cyclo-oxygenase
Inhibitors/Nonsteroidal
Anti-inflammatory Drugs
NSAIDs mainly block the PG generation. PG is the
substance which is produced from arachidonic acid by the
enzyme cyclo-oxygenase (COX) which exist in a constitutive (COX-1) found in blood vessels, stomach and kidney;
and an inducible form which is induced at the site of inflammation by cytokines and other inflammatory mediators.
Prostaglandin play a part in the erythema, edema, and fever
associated with inflammation and generate the pain either
by its direct action or by sensitizing the pain receptors or
by release of substance by tissue damage such as bradykinin
and histamine. NSAIDs inhibit the action of cyclooxygenase (COX-1 and COX-2) enzyme. It interfere with
the synthesis of prostaglandin and hence, causes the
blockage of impluse generation mediating pain.
Nabumetone, a new NSAIDs preferentially inhibit
COX-2. Similarly, newer drugs like Nimesulide and
Meloxicam are also reported to have greater affinity for
COX-2 as compared to COX-1.
Action of NSAIDs
Analgesic actionNSAIDs do not affect the tenderness
which is induced by direct application of PG, but it
blocks the pain sensitizing mechanism induced by
bradykinin, tumor necrosis factor Alfa, interleukins and
other algesic factors. It is used in dental caries and
postextraction pain.
Antipyretic actionfever during infection is produced
due to generation of pyrogens which induces the PG
production. Hence, NSAIDs are used to block the action
of pyrogens and help to reduce the body temperature in
fever.
Anti-inflammatoryPG are only one mediator of the
inflammation. NSAIDs is considered to be inhibition of
PG synthesis at the site of injury. Anti-inflammatory
potency of different compounds correspond with their
potency to inhibit COX. However, Nimesulide is a potent
anti-inflammatory but weak COX inhibitors.
DysmenorrheaPG synthesis in endometrium causes
uncoordinated uterine contraction with compressed
blood vessel results in uterine ischemia and pain. NSAID
decrease PG synthesis and relieves the pain approximately 70%. It also relieves additional symptoms like
headache, muscle ache and nausea.
Antiplatelet Function/BleedingPlatelet aggregation is
due to TXA2. NSAIDs inhibit TXA2. NSAIDs acetylates
COX present in platelets when they are in portal
circulation, before it get acetylated in liver.
Salicylates
Aspirin
Aspirin is acetylsalicylic acid. It is rapidly deacetylated in
body by acetylating other macromolecule like COX in
platelet, before platelet get deacetylated in liver as
physiologically happened. Acetylated platelet reduce
tendency to aggregate and induce bleeding tendency due
to aspirin. It is developed by Bayer in 1899. This includes
species of willow. Salicylates derived from salix, a Latin
name willow tree.
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974
Adverse Effects
Peptic ulcerationCOX-1 has physiological role in
gastrointestinal tract like mucus secretion for protection
of gastric mucosa. Aspirin is COX inhibitor, it decreases
mucus secretion from gastric mucosa by inhibiting
cyclooxygenase. Treatment: Misoprostol (PG analog) is
used to heal these ulcers.
Precipitation of asthmaPGD2, TXA2 are bronchoconstrictors while PGE2 and PGI2 are dilators. Aspirin causes
imbalance between these constrictors and dilators
causing precipitation of asthma.
Hemorrhagetreatment is vitamin K supplements.
Salicylismlarge dose (3-5 g/day is anti-inflammatory
dose) results in headache, dizziness, tinnitus, confusion,
vertigo, reversible impairment of hearing and vision,
sweating, palpitation and hyperventilation. These
syndromes are known as salicylism.
Reyes syndromeuse of Aspirin in children below 12
years with influenza or chickenpox cause lifethreatening condition characterized by vomiting,
lethargy, delirium, coma and even death. If a person
survives, it causes irreversible brain damage. Use of
Aspirin in children is prohibited in India.
Acute salicylates poisoning10-30 g is the suicidal dose
of Aspirin in adults. In children, 4 ml is the fetal dose.
Toxicity is seen with serum salicylates level more than
50 mg/dl.
Clinical featurevomiting, dehydration, electrolyte
imbalance, acidotic breathing, abdominal pain,
anorexia. In severe cases, CNS abnormalities and skin
eruption, hyperpyrexia, restlessness, vertigo, tremors,
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Contraindication
Peptic ulcerin peptic ulcers, bleeding tendencies.
Pregnancyin pregnancy, it causes premature closure
of ductus arteriosus, delayed and prolonged labor,
greater postpartum blood loss, low birth weight babies.
Nursing motherit is not used in breastfeeding mothers.
G6PD deficiencyit causes hemolysis.
Before dental extractionit should be stopped 1 week
before dental extraction or any major surgeries.
Chronic liver diseaseit may cause hepatic necrosis.
DiabetesAspirin has hypoglycemic action.
Hepatic damagein hepatic damage, vitamin K deficiency
or hemophilia, hypoprothrombinemia.
Chicken poxin children suffering from chicken pox or
influenzadue to risk of Reyes syndrome in pediatric
patient.
Pharmacokinetics
Aspirin absorbed from stomach and small intestine.
Approximately 80% plasma protein binding capability. Half
life at therapeutic dose is 15-20 mins, at anti-inflammatory
dose is 8-12 hours and during poisoning 30 hours.
Trade Name
T. Aspirin 350 mg, T. Ecosprin 75, 150, 325 mg, T. Disprin
35 mg, T. Loprin 75 mg.
Naproxen
Plasma t12-15 hours
Dose250 mg BID after meal
Trade nameT. Naprosyn 500 mg, T. xenobid 250 mg.
Drug Interaction
Flurbiprofen
Anthranilic Acid
Mephenamic Acid
Actionanalgesic, antipyretic, anti-inflammatory in
action.
Useas an analgesic primarily in muscles, joints and
soft tissue pain. It is quite effective in dysmenorrhea. It
may be useful in rheumatoid arthritis and osteoarthritis.
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976
Oxicam Derivatives
Piroxicam
Actionit reversibly inhibits COX, so it has analgesic,
antipyretic, anti-inflammatory properties.
Plasma half-life2 days
Adverse effectheart burn, nausea, anorexia.
Indicationrheumatoid and osteoarthritis, ankylosing
spondylitis, postextraction pain, pulpitis in dentistry.
Dose20 mg BD for 2 days followed by 20 mg OD.
Trade nameC. Pirox 10, 20 mg, C. Pirox 10, 20 mg.
Tenoxicam: T. Tabitil 20 mg Dose: 20 mg OD. T. Dolonex.
Pyrrolo-pyrrole Derivative
Ketorolac
Actionit also inhibits PG and relieves pain by
peripheral mechanism.
Half-lifet- 5-7 hour.
IndicationPostoperative, dental and acute musculoskeletal pain, pain due to bony metastasis, migraine.
Adverse effectnausea, abdominal pain, ulceration, loose
stools, drowsiness, pain at injection site, dizziness.
DoseDose: 10-20 mg tablets 6 hourly. 15-30 mg IM or
IV every 4-6 hours
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Opioid Analgesics
The dark brown, resinous material obtained from poppy
capsule is called opium. These are plant products
containing pharmacologically active ingredient i.e.
alkaloid. It contains two types of alkaloids, viz. phenanthrene derivatives and benzoisoquinoline derivatives. They
are also called narcotic drugs. The term narcotic is derived
from the Greek word meaning stupor and was used for
agents that produce sleep. The opioids bind to receptors
located in the central nervous system, producing an altered
perception of and response to pain.
Pharmacological Actions
Analgesiathese drugs relieve severe pain like that of
visceral pain and pain of trauma. Mechanisms by which
they act are as follows:
They increase the threshold for painful stimuli. They
act directly on the receptor site in the CNS to inhibit
release of excitatory transmitters from primary
afferents carrying pain impulses and elevate the pain
perception threshold.
They alter emotional reaction to pain. They produce
sleep which also elevates the pain threshold.
CNSthese drugs have a site specific depressant and
stimulant action in the CNS. It produces euphoria in the
presence of pain. However, in absence of pain, it produces dysphoria; and, with an increased dose it produces
sleep.
Respirationrespiratory depression by reducing the
sensitivity of medullary respiratory center neuron to CO2;
rate and tidal volume are both decreased.
Pupilmiosis resulting in pin-point pupils.
CTZnausea and vomiting can occur resulting from
stimulation of the CTZ (chemoreceptor trigger zone)
especially when the stomach is full.
Coughsuppress cough by depressing the cough center.
Neuroendocrinethe sex hormone and corticosteroid
levels are lowered in the short term, but tolerance
develops in the long term. Morphine can release ADH
and reduce urine volume.
GITthese drugs increase tone and segmentation but
decrease peristaltic propulsive movements. This
produces spasm of intestine and sphincters. Secretion
of HCl and intestinal secretions are decreased. These
drugs increase absorption of H2O, so lead to constipation.
Pharmacokinetics
AbsorptionMost opioid analgesics are absorbed well
when taken orally. Absorption occurs from the lungs
and from the nasal and oral mucosa whereas through
GIT is slow and incomplete. A quick effect occurs
following a subcutaneous injection.
Distributionthey are partially bound to plasma proteins.
The opioids can affect fetus in pregnant women.
Metabolismthey are metabolized by conjugation with
glucuronic acid in the liver.
Excretionthey are excreted by glomerular filtration in
the urine within 24 hours.
Adverse Effects
Constipationthe opioids produce constipation by
producing tonic contractions of the gastrointestinal tract.
Respiratory depressionthe opioid analgesic agonists
depress the respiratory center in a dose-related manner.
The depression is related to decrease in sensitivity of the
brainstem to carbon dioxide.
Nausea and vomitingopioids often produce nausea
and vomiting which is due to their direct stimulation of
the chemoreceptor trigger zone (CTZ), located in the
medulla.
Miosisthe opioid analgesics cause miosis, an
important sign (pinpoint pupils) in the diagnosis of an
opioid overdose or an identical in addicts.
Urinary retentionit increases smooth muscle tone in
the urinary tract, thereby causing urinary retention.
CNS effectsit may produce CNS stimulation exhibited
by anxiety, restlessness, or nervousness.
Cardiovascular effectsit may depress vasomotor center
and stimulate the vagus nerve. With high dose, postural
hypotension, bradycardia, and even syncope may result.
Biliary tract constrictionin high doses, the opioids may
constrict the biliary duct, resulting in biliary colic.
Apneait may occur in newborns, when these drugs are
given to mothers during labor pain.
Addictionit is proportional to their analgesic strength.
As the use of opioids in dentistry is usually very less,
this does not produce problems for dentist.
Allergic reactionit includes skin rashes and urticaria.
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978
Drug
Trade name
Dosage form
Dose
Indication
Contra-indication
Side effect
Salicylates
(Aspirin)
Disprin
Anacin
Colsprin
Biospirin
Tablet
Injection
Analgesic /
antipyretic
0.3-0.6 gm TDS
Dental pain
Headache
Fever
Arthritis
Osteoarthritis
Postmyocardial infarction
Hemophilia
Hypersensitivity
Peptic ulcer
Gout
Asthma
Patient on
anticoagulants
Nausea
Vomiting
GI disturbance
Tinnitus
Vertigo
Para-amino
phenol
derivative
(Paracetamol)
Calpol
Crocin
Metacin
Pacimol
Febrinil
Tablet
Injection
Syrup
Drops
0.5-1 gm TDS
infant50 mg
1-3 year
60-80 mg
4-8 year
240320 mg
9-12 year
300-600 mg
Pain
Fever
No absolute
contraindication
Special precaution
in hepatic and
renal failure
Nausea
Rash
Leucopenia
Indole
derivatives
(Indomethacin)
Indocap
Indoflam
Capsule
Tablet
Injection
25-50 mg
2 to 4 times
a day
neonates
0.2 mg/ kg
Dental pain
Rheumatoid arthritis
Osteoarthritis
Ankylosing
spondylitis
Hypersensitivity
Epilepsy
Kidney disease
Pregnancy
Psychiatric cases
Gastric irritation
Nausea
Anorexia
Diarrhea
Asthma
Propionic acid
derivatives
(Ibuprofen
Naproxen
Ketoprofen)
Brufen
Enflam
Febrilix
Combiflam
Duoflam
Nalyxan
(Naproxen)
Ostofen
(Ketoprofen)
Tablet
Capsule
Ibuprofen
200-600 mg TDS
Naproxen
250 mg BD
Ketoprofen
50 mg BD
Postextraction pain
Soft tissue injuries
Rheumatoid arthritis
Musculoskeletal
disorders
Pregnancy
Peptic ulcer
Gastrointestinal
bleeding
Laceration
Gastrointestinal
disorder
Rash
Hypersensitivity
Oxicam
Piroxcam
Pirox
Dolonex
Movon
Capsule
Tablet
Injection
Gel
20-40 mg in
divided or
single doses
Hypersensitivity
Pregnancy
Lactation
Children below
6 years
Bronchial asthma
Heart burn
Nausea
Anorexia
Rashes
Pruritis
Edema
Nimesulide
Nise
Nulide
Emsulide
Nimsaid
Nimulid
Nimol
Tablet
Peptic ulcer
Hypersensitivity
Hepatic impairment
Pregnancy
Epigastric
distress pain
Nausea
Rashes
Edema
Aryl acetic
acid
derivatives
Diclofenac
sodium
Diclofen
Diclomol
Relaxyl
Voveran
Tablet
Gel
100-150 mg
daily in 2-3
divided doses
Dental pain
Arthritis
Gout
Painful post-operative
condition
Peptic ulcer
Hypersensitivity
Pregnancy
Lactation
Asthma
Epigastric pain
Nausea
Rashes
Edema
Itching
Anthranilic acid
Mephenamic
acid
Mefac
Tablet
Meftal forte
Capsule
Spasmodol forte Suspension
250-500 mg TDS
Pain
Arthritis
Osteoarthritis
Dysmenorrhea
As antipyretic
Hypersensitivity
Epilepsy
Epigastric distress
Rashes
Hemolytic anemia
Diarrhea
Ketorolac
Ketorol
Ketanov
Torolac
20 mg initially
followed by
10 mg 4-6 hourly
30-60 mg IM
followed by
10-30 mg 4-6
hourly
Short term
management of
postoperative pain
Hypersensitivity
Syndrome of
nasal polyps
Peptic ulcer
Coagulation
disorders
Angioedema
Gastric ulceration
Bleeding
Pain edema
Headache
Sweating
Tablet
Injection
Musculoskeletal pain
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Drug
Dosage
Adverse effect
Contraindication
Paracetamol +
Ibuprofen
Adult
oral 325-500 mg
Paracetamol
+ 100 mg
Ibuprofen
Children125 mg
Paracetamol
+ 100 mg
Ibuprofen.
TDS
It is a patent
anti-inflammatory
with analgesic and
antipyretic action.
Chronic pain,
inflammatory dental
conditions
Nausea, vomiting
GIT and vision
disturbances, rash
Aceclofenac +
paracetamol
100 mg + 500 mg
Nausea, vomiting,
headache, vertigo,
tinnitus
Hypersensitivity,
pregnancy, peptic ulcer
Therapeutic Uses
Analgesicsthey are indicated in severe pain of any type.
They provide symptomatic relief without affecting the
cause. Opioids are used in traumatic, visceral, ischemic,
postoperative, burn and cancer pain.
Preanesthetic medicationmorphine and pethidine are
commonly used as preanesthetic medication.
Balanced anesthesia and neurolept analgesiamorphine,
pethidine and fentanyl are important components of
these techniques.
Relief of anxiety and apprehensionespecially used in
myocardial infarction and internal bleeding.
Acute left ventricular failuremorphine affords dramatic
relief by reducing preload on the heart due to
Uses in Dentistry
Postoperative painmain use of narcotic analgesics in
dentistry is for severe postoperative pain unresponsive
to the anti-inflammatory analgesics.
Suggested Reading
1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central publisher, 2005.
3. Craig CR, Stitizel RE. Moderate pharmacology with clinical
application (5th edn), Little Brown and Company, 1997.
4. Gomes MW. Synopsis of medical pharmacology (1st edn),
National Series, 2002.
5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001.
6. Mycek MJ, Harvey R, Champe P. Lippincott illustrated review:
pharmacology, (2nd edn), Lippincott Williams and Wilkins
publisher.
7. Salil and Bhattacharya, Sen A, Ray A. Pharmacology (2nd edn),
Elsevier, 2003.
8. Seth. Textbook of Pharmacology (2nd edn), Elsevier, 1999.
9. Sharma HL, Sharma KK, Gupta DK. Textbook of dental
pharmacology (1st edn), Paras Publisher, 2008.
10. Tripathi KD. Essential of Pharmacology for Dentistry (1st edn),
Jaypee Brothers Medical Publishers, 2005.
11. Yagiela, Neidle, Dowd. Pharmacology and thereaputics for
dentistry (1st edn), Mosby Harcourt India, 2001.
http://dentalebooks.com
980
42
5
Antifungal Drugs
Introduction
Fungi are eukaryotes and lack chlorophyll pigment. It
possesses differentiated nuclei surrounded by nuclear
membrane and reproduce either by budding or forming
spores. It has rigid chitinous cell wall. Morphologically it
may be either oval cells or long tubular septate hyphae
showing true lateral branching. Fungi can be mould type,
yeast type, yeast-like fungi (Candida albicans) and dimorphic
fungi (Fig. 42-1).
Antifungal drugs are used in the treatment of superficial
(Affecting oral mucous membrane, skin, nails, etc) and deep
fungal infection (deeper tissues and organs). Fungal
infections are caused by broad spectrum species of yeast
like fungus including Candida albicans, Cryptococcus
neoformans, Histoplasma capsulatum, Blastomyces dermatitidis,
Coccidioides immitis, Aspergillus fumigatus, and many other
pathogenic fungi.
Among these, Candida albicans has become most common
organisms which is isolated from blood culture causes
mainly oral fungal infection called as oral candidiasis or
oral thrush. Oral candidiasis is most common fungal
infection caused in humans and as variety of clinical
Types of Fungi
Fungi are either commensals or pathogenic. Pathogenic
produces mycotoxins and enzymes causing harm.
Pathogenic fungi:
Superficial
Deep
Truly pathogenic.
Classification
First Classification
Antibiotics
Polyenes
Amphotericin B
Nystatin
Hamycin
Natamycin
Heterocyclic benzofuran
Griseofulvin
Anti-metabolites
Flucytosine
Azoles
Imidazole
Topical
Clotrimazole
Econazole
Miconazole
Systemic
Ketoconazole
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Second Classification
According to its mode of action:
Drugs that disrupt the fungal cell membrane Polyenes: Amphotericin B
Azoles: Imidazole, e.g. Ketoconazole trizoles,
Fluconazole
Allylamine: Terbinafine
Drugs that inhibit mitosis: Griseofulvin
Drugs that inhibit DNA synthesis: Flucytosine
Nystatin
It is polyene antibiotic obtained from Streptomyces noursei.
Trade nameMYCOSTATIN
Preparation availableOral5,00,000 unit tablets;
Topical-100,000 unit/gm cream and ointments, 100,000
units vaginal tablets. It is available currently for topical
use in creams, ointment, suppositories, lotion, suspension, vaginal tablets, and oral pastille.
Mechanism of actiondepending upon concentration
used, it can be either fungistatic or fungicidal agent.
Ergosterol is sterol found in cell membrane of fungi. It
binds to the ergosterol and increases the permeability of
cell membrane facilitating pore formation. These
micropore formation allow leakage of intracellular ions
and macromolecule leading to cell death.
Indication
Oral candidiasis (Oral thrush)Nystatin is drug of
choice. it is commonly used as topical agent to
suppress Candida infection. It is not administered
parentally as it is toxic for systemic use.(1) Thrush is
treated by holding 5 ml of nystatin suspension (for
infants- 2 ml) in oral cavity for several minutes 4 times
daily before swallowing. (2) Alternative treatment is
to retain vaginal tablet in the mouth until it dissolves,
at least 4 times a day. (3) Nystatin oral pastille
(200,000 units) dissolved slowly in the mouth 5 times
a daycan be mixed with glycerin.(4) Mycostatin
creams and ointments (1 lack units) may be used in
Amphotericin-B
Amphotericin B is an antifungal antibiotic produced by
Streptomyces nodosus.
Trade nameFungizon, Abelcet, Ambisome, Amhotec.
Preparation availableParenteral: conventional formulation: Fungizone 50 mg power for injection. Lipid
formulation: Abelcet100 mg/20 ml suspension for
injection. Ambisome50 mg powder for inj. Amphotec
50,100 mg powder for inj. Topical: 3% cream, lotion,
ointment.
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Hamycin
It is polyene antibiotics obtained from Streptomyces pimprina.
Trade nameHAMYCIN
Preparation availableTopical -4 lac unit/gm ointment,
5 lac unit vaginal ovules. 2 lac/ml suspension.
Mechanism of actionsame as Nystatin.
Indicationoral thrush (due to Candida albicans)ointment or suspension is applied to the affected area of
oral mucosa with sterile cotton 2-3 times a day for 7-10
days. It can also be given in cutaneous candidiasis,
monolial or Trichomonas vaginitis, histoplasmosis,
pulmonary mycosis and otomycosis caused by
Aspergillus. Dose recommended is 10-20 mg/kg daily.
Adverse effectmild rashes, irritation.
ContraindicationHypersensitivity.
Natamycin
This is a polyene antibiotic topically effective antifungal
agent.
Trade name NATAMYCIN, PIMAFUCIN
Preparation availableTopical- 5% suspension, 2%
cream, 1% ointment and 25 mg vaginal Tabs.
Mechanism of action- same as Nystatin.
Indication
Oral thrush/ Oral candidiasis: Natamycin vaginal
tab or ointment is applied on affected area of oral
mucosa for several minutes 3-4 times daily.
It can be given in vaginal candidiasis (25 mg vaginal
tab is used topically).
Trichomonas vaginatis (used only topically).
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Griseofulvin
It is extracted from penicillium Griseofulvin. Griseofulvin
was the first orally effective antifungal agent. It is effective
against dermatophytes including Epidermophyton,
Trichophyton, microsporum, etc. It is ineffective against
Candida and P. orbiculare.
Trade nameDermofulvin, Grisactin, Grifulvin.
Preparation availableOral microsize: 125, 250 mg
capsules, 250, 500 mg tablets, 125 mg/5 ml suspension.
Oral ultramicrosize: 125, 165, 250, 330 mg tab.
Mechanism of actionGriseofulvin binds to keratin in
new forming skin cells and protects the skin from new
infection. So, its action is to prevent infection of this new
skin structure. It does not kill fungus which are already
present.
Indication
Dermatophytic infectionsGriseofulvin is effective
against all superficial ringworm infection (skin and
hair infection). It must be applied for 2-6 weeks on
affected skin and hair to allow replacement of infected
keratin.
Fungal infection of nails and scalpLong therapy of
griseofulvin may require to allow regrowth of new
protected nails. For adult, 500 mg daily in single or
divided doses with meal; For children, 10 mg/kg of
body wt daily in single or divided dose with meals.
Oral suspension is also available. Fingernails may
respond to 6 month of therapy whereas toe nails may
require 8-18 months.
Fungal infection of tinea of hand, athletes foot, tinea pedis,
tinea manusit may require long therapy 500 mg daily
in single/divided dose with meals for 3-4 weeks.
Adverse effectmild rashes, nausea, vomiting and
headache, gastrointestinal upset, photophobia, peripheral neuritis.
Contraindicationporphyria, liver disease, systemic
lupus erythematosus.
Flucytosin
It is oral antifungal agent effective against systemic infection
due to yeast and fungi. Its spectrum of action is much
narrower than that of Amphotericin B.
Trade nameANCOBON
Preparation availableOral: 250, 500 mg capsule. 100150 mg/kg/day in patient with normal renal function.
Clotrimazole
It is used exclusively as topical agent. It is toxic on parental
administration.
Trade nameMycoban,Lotrimin Mycelex, Surfaz.
Preparation availableTopical: Mycoban Gel 12% (30
gm), Gynostatum vaginal tab, 1% vaginal cream, lotion,
solution. Oral: 100 mg, 200 mg, 500 mg tab.
Mechanism of actionit inhibits the synthesis of ergosterol
by binding to catalytic haem ion of fungal cytochrome
resulting in damage to cell membrane of fungi.
Indication
Candidiasis caused by Candida albicans, oral candidiasis, cutaneous candidiasis.
Treatment of tinea padis (athletes foot), tinea cruris
(jock itch),tinea corporis (ringworm).
Vaginal infection1 vaginal tab 100mg intravaginally at bed time for 7 consecutive days. Then in
alternative days 1 tab (200 mg) intravaginally at
bedtime for 3 consecutive days.
Dermatophytic infections like candidiasis and seborrheic
dermatitisTopical antifungal-corticosteroid fixed
combination has been recently introduced.
Clotrimazole-betamethasone dipropionate cream
(lotrisone) is used once or twice daily, applied to the
affected area results in the clearing of superficial
dermatophytic infection in 2-3 weeks.
Skin infection caused by corynebacteriait is well
tolerated by topical use.
Oropharyngeal candidiasis : it is used in the dose of 10
mg daily (TDS)
Pityriasis versicolor100 to 500 mg/daily is quite
effective.
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Econazole
Miconazole
It is used mostly as topical antifungal agent. It is more toxic
than ketoconazole.
Trade nameMICOGEL, MONISTAT, MICATIN.
Preparation availableTopical: ointment 2%-15 gm, lotion
2%-15 ml, powder 2%-15 gm, cream 2%-15 gm, gel 2%15 gm, vaginal suppositories- 100, 200 mg.
Mechanism of actionsame as Cotrimazole.
Indication
Severe systemic fungal infection in adult, 1200 to 2400
mg/day in divided doses.
Cutaneous candidiasisapplied cream, ointment to
affected area twice daily for 7days.
Systemic mycosisMiconazole is used by intravenous
route (Monistat).
Ocular infectionTopical (1%) for every hours and
subconjunctival injection of 5 mg miconazole (1%)
MICOPTIC OPICOPS once/twice a day.
Otherchronic mucocutaneous candidiasis, fungal
meningitis, fungal urinary tract infection. vulvovaginal candidiasis, Tinea pityriasis versicolor,
otomycosis.
Adverse effectsChills, fever, itching, nausea, rashes,
phlebitis, anemia, irritation to skin.
Ketoconazole
It was first orally effective azole antifungal agent used in
the treatment of systemic fungal infection. It is less toxic
than Amphotericin B.
Trade nameNizoral, Tocon, Fungicide, Funazole.
Preparation availableOral: Tab 200 mg, Topical: 2%
cream, and shampoo.
Mechanism of actionsame as Cotrimazole.
Indication
Mucocutaneous candidiasisTab 200 mg once a day is
very effective.
Paracoccidioides mycosis and Chromoblastomycosisfor
adults, 200-400 mg once daily preferably after food;
for children after 2 years, 3.3 to 6.6 mg/kg once daily.
Histoplasmosisbecause of toxicity of amphotericin
B, ketoconazole is mostly preferred in histoplasmosis.
Leishmaniasisoral ketoconazole 600 mg/day for 28
days is most effective in cutaneous Leishmaniasis.
South America blastomycosis /Almeidas disease
Ketoconazole has been successfully tried in the recent
year.
Dermatophytosis, candidiasis, seborrheic dermatitis
1) Oral dose of 200 mg daily for 2-3 weeks, can be
given. 2) Ketoconazole (Nizoral) available as a cream
for topical treatment. 3) Shampoo 1% is used for
seborrheic dermatitis (Nizoral AD Shampoo).
Ocular infectionketoconazole 200 mg tab containing
ointment are used.
Adverse effectnausea, vomiting, loss of appetite,
giddiness, headache, rashes, photophobia, paresthesia.
It interferes with biosynthesis of adrenal and gonadal
steroid hormone producing gynaecomastia, infertility,
menstrual irregularities and GIT upset.
Fluconazole
It is new antifungal drug which is more water soluble and
has good penetration into cerebrospinal fluid, ocular fluid,
vaginal tissue and saliva. It can be administered
intravenously or orally.
Trade nameSYSCAN, DIFLUCAN.
PreparationOral 50, 100, 150, 200 mg tablets, Topical:
powder for 10, 40 mg/ml suspension. Parenteral-2 mg/
ml in 100 and 200 ml vial.
Mechanism of actionit acts by inhibiting the enzyme
demethylase resulting in the damage to fungus cell
membrane. It has fungistatic action.
Indication
Cryptococcal meningitis -Fluconazole is drug of choice
for treatment and secondary prophylaxis of
cryptococcal meningitis. Drug available in oral/
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Itraconazole
It is newer antifungal drug which is administered orally.
Its efficiency is enhanced in combination with flucytosine.
Trade nameITROLE, CANDITRAL, SPORANOX.
Preparation availableOral: 100 mg, 200 mg Capsule.
Topical: 10 mg/ml solution. Parenteral: 10 mg/ml for IV
infusion.
Mechanism of actionsame as Fluconazole.
Indication
Oropharyngeal candidiasisoral liquids and intravenous preparation are quite effective in the dose of
200 mg capsule/tablets twice daily for at least
6 month, yields good results.
Dermatophytoses treatment
Onchomycosisdose of 200 mg daily taken with the
food to ensure maximum absorption for 3 consecutive
months.
OtherAspergillosis, histoplasmosis, sporotrichosis
and blastomycosis.
Adverse effectperipheral neuropathy, headache,
dizziness, allergic reaction, jaundice, hepatotoxicity.
Terbinafine
it is new systemic antifungal agent. It has higher efficiency
comparable to itraconazole with decreased risk of
hepatotoxicity.
Trade nameLAMISIL.
Preparation availableTopical: 1% cream. Oral: 10 mg
(tab 250 mg/ day orally).
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Summary Chart
Drug
Trade name
Dosage form
Dose
Indication
Contraindication
Adverse effect
Amphotericin B
Fungizone
Tablet
Injection
50-100 mg QID
0.3 mg /kg body
weight 4-8 hourly
as an infusion
Renal impairment,
Epilepsy
Acute reaction,
chills, fever,
nausea, vomiting,
long term
nephrotoxicity
Nystatin
Mycostatin
Tablet
Hypersensitivity
Nausea, diarrhea
and bad taste
Hamycin
Hamycin
Suspension
Oral thrush
Hypersensitivity
Sensitization,
irritation
Griseofulvin
Dermofulvin
Fungal 500
Tablet
500-1000 mg
daily IM
Porphyria,
severe liver
disease, systemic
lupus erythematous
Headache,
irritation
Ketoconazole
Nizral
Tocon
Tablet
200 mg OD/BD
Systemic candidiasis,
Dermatomycosis
Children
below 2 yrs
Hepatitis, rashes,
GIT upset
Terbinafin
Exifine
Sebifin
Tablet
250 mg /day
OD 2-6 weeks
Fungal infections
of skin, nails and
onychomycosis
Hypersensitivity,
Liver dysfunction
GIT symptoms,
skin rashes and
reaction
Fluconazole
F-zole
Fluzone
Capsule
Tablet
Infusion
200 mg on 1st
day followed by
100 mg OD
Hypersensitivity
Nausea,
headache,
skin rashes
and abdominal
pain
Itraconazole
Itrole
Canditral
Capsule
100-200 mg
OD for 6 months
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Nausea,
headache,
skin rashes and
abdominal pain
Suggested Reading
1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central publisher, 2005.
3. Craig CR, Stitizel RE. Moderate pharmacology with clinical
application (5th edn), Little Brown and company, 1997.
4. Gomes MW. Synopsis of medical pharmacology (1st edn),
National Series, 2002.
5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001.
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43
5
Anticancer Drugs
Introduction
Principles of Chemotherapy
Kinetic Classification of
Anticancer Drugs
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Classification
Alkylating Agents
Alkyl SulfonateBusulfan
Nitrogen MustardsMustine HCl, Cyclophosphamide,
Melphalan and Chlorambucil
NitrorsoureasCarmustine (BCNU), Lomustine
(CCNU), Semustine (Methyl-CCNU)
TriazineDacarbazine
EthylenimineThio- TEPA
Anti-Metabolites
Purine antagonist6-Mercaptopurine, 6-Thioguanine
Folate antagonistMethotrexate
Pyrimidine antagonist5-Fluorouracil, Cytarabine
(cytosine arabinoside).
Antibiotics
Actinomycin-D
Mitoxantrone
Bleomycin
Daunorubicin
Doxorubicin
Mithramycin
Mitomycin C
Vinca alkaloids
Vinblastine
Vincristine
Taxanes
Paclitaxel
Docetaxel
Epipodophyllotoxin
Etoposide
Teniposide
Enzymes
L-Asparaginase
Miscellaneous
Hydroxyurea
Procarbazine
Cisplatin
Hexamethylamine
Carboplatin
Alkylating Agents
They produce their effect by linking an alkyl group (R-CH2)
covalently in protein and nucleic acid. Some of them are
described below:
Alkyl Sulfonate
BusulfanIt is highly specific for myeloid elements,
granulocyte precursors being most sensitive, followed
by those of platelets and RBCs.
UseIt is the drug of choice of chronic myeloid leukemia.
Dose2-6 mg/day orally.
Nitrogen Mustards
Mechanismit has two chloroethyl side chains. One of
them forms a cyclical highly reactive ammonium ion
which binds to nucleic acids, i.e. 7-nitrogen group of
guanine. The other chloroethyl sides of nitrogen
mustards can crosslink with DNA strands, either within
a strand or between strands. Although alkylating agents
may bind to variety of cellular components like
cytoplasmic proteins and RNA at therapeutic doses,
impairment of DNA replication is the major mechanism
of cytotoxicity of these drugs. Damage to DNA is more
serious during the S phase of cell cycle probably
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990
Nitrosoureas
Mechanismthey act partly as alkylating agents linking
to an alkyl group or carbonyl group of cell proteins and
form compounds which are unstable in water and
decompose to form alkylating groups, which are able to
damage the cell proteins.
DoseBCNU50-200 mg/m2, CCNU 100-130 mg/m2,
methyl CCNU100-200 mg/m2.
Triazine
Dacarbazineit is different from other alkylating agents
in having primary inhibitory action on RNA and protein
synthesis. It is activated in the liver. It is used in
malignant melanoma. Dose3.5 mg/kg/day IV for 10
days, repeat after 4 weeks.
Ethylenimine
Thio-TEPAit does not require formation of an active
intermediate. It has high toxicity and seldom used today.
Dose0.3-0.4 mg/kg IV at 1-4 weeks intervals.
Anti-metabolites
Purine Antagonist
Mechanism of actionMercaptopurine and thioguanine
are highly effective anti-cancer drugs. It inhibits
conversion of inosine monophosphate to adenine and
guanine nucleotides.
Usethey are useful in childhood acute leukemia and
choriocarcinoma.
Toxic effectmain toxic effects of antipurines are bone
marrow depression which develops slowly.
Dose6-Mercaptopurine (2.5 mg/kg/day) and
6-Thioguanine (2 mg/kg/day).
Pyrimidine Antagonists
Actionmost commonly used are 5-fluorouracil and
cytarabine. It interferes with nucleic acid synthesis by
antagonizing or mimicking pyrimidine metabolites.
Absorptionit may be given orally but its absorption is
unpredictable. So, the IV route is often used because the
plasma clearance is rapid.
Toxicitynausea, vomiting, stomatitis, alopecia and
myelosuppression.
Indicationsit is given in the treatment of breast and GIT
cancer, Hodgkins lymphoma, non-Hodgkins
lymphoma, acute leukemia to induce remission.
Dosefluorouracil1 gm orally on alternate day for
6 days followed by 1 gm weekly or 12 mg/kg/day IV for
4 days. Cytarabine1.5-3 mg/kg IV BD for 5-10 days.
Antibiotics
Practically all of the antibiotics intercalate between DNA
strands and interfere with template function.
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Mitoxantrone
Actionit binds to DNA and is given intravenously and
has a long terminal half life of 36 hours.
Toxicityit may cause myelosuppression, cardiomyopathy and alopecia.
Indicationsacute non-hemolytic leukemia, chronic
myelogenous leukemia, non-Hodgkin lymphoma and
carcinoma of breast.
Dose12 mg/m2 single IV dose repeat at 3 weeks.
Bleomycin
ActionIt consists of a mixture of closely related
glycopeptide antibiotics. It inhibits DNA synthesis and
causes a break in DNA and is active in G2 phase of the
cell cycle.
AbsorptionIt is given by parenteral, subcutaneous or
intramuscular route because it is non-vesicant. It has
initial half life of 30 minutes and elimination from
plasma takes 2-9 hours. It is excreted by kidney and
does not cross the CSF.
Toxicityskin pigmentation, erythema, vesiculation or
fibrosis.
Indicationsit is used in combination with other
chemotherapeutic drugs in testicular carcinoma, head
and neck cancer and Hodgkins lymphoma.
Dose30 mg per injection twice weekly IV.
Mithramycin
Actionits use is restricted to embryonal testicular tumor,
disseminated cancers, especially those with bony
metastasis and hypercalcemia. It reduces serum calcium
levels, probably by direct action on bone inhibiting
calcium release.
Dose25 g/kg by slow IV infusion daily or on alternate
days.
Mitomycin-C
Actionit is derived from streptomyces species and
inhibits DNA synthesis by both cross linking and
alkylating DNA.
Toxicitymyelosuppression, cumulative thrombocytopenia and renal toxicity.
Indicationsused in combination in cancer of breast,
stomach, cervix, pancreas and those of head and neck.
Dose10 mg/m2 IV.
Vinblastine
Absorptionthese drugs are given IV and are vesicants
if extravasated. Plasma clearance occurs in 3 phases
with half life of 4 minutes, 1 hour and 16 hours. Tissue
binding is extensive and prolongs the actions and the
drug binds to platelets, red cells and plasma proteins.
Indicationsit is used in combination for treatment of
testicular tumors and lymphoma.
Toxicityit causes alopecia, neurotoxicity and
myelosuppression.
Dose0.1-0.15 mg/kg IV weekly in 3 doses.
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Vincristine
Useit is a rapidly acting drug, very useful for inducing
remission in childhood acute leukemia.
Toxicityit causes peripheral neuropathy, alopecia.
Indicationsit is medicated in lymphoma (Hodgkins
disease), acute lymphatic leukemia, small cell cancer of
bronchi and breast cancer.
Dose1.5 mg/m2 IV weekly.
Taxanes
Miscellaneous Agents
Paclitaxel
Hydroxyurea
Docetaxel
Procarbazine
Epipodophyllotoxin
Actionthese are phase specific and prevent cells from
entering mitosis from G2 phase.
Absorptionthe drugs are absorbed erratically from the
gut with the plasma availability up to 50%, rapid
clearance from plasma occurs when given intravenously
followed by a slower phase.
Etoposideit is highly protein bound and is excreted in
the urine in 72 hours.
Teniposideit is active as a single agent in small cell
lung cancer.
Toxicitythey cause alopecia, myelosuppression,
mucositis and neuropathy.
Indicationsit is used in treatment of testicular tumors,
leukemia and lymphoma.
Dose100 mg in 5 ml injection or 120 mg/m2 IV infusion
for 30 minutes.
Enzymes
L-Asparaginasethis enzyme is produced by E. coli.
Actionit acts by removing asparagine from the
circulation, thus depressing those tumor cells which are
Cisplatin
Actionthis drug is the only active cytotoxic agent in its
cis form. Chloride ions are lost from the molecule after it
diffuses into the cell and the compound crosslinks mainly
to guanine groups like an alkylating agent. It should be
protected from light and is given intravenously with an
early half life of about 40 minutes with a later slower
phase of clearance i.e. about 60 hours.
Absorptionabout 90% of cisplatin bound to plasma
protein is taken up in the kidney, gut, liver, testis and
ovary, but it does not cross the blood-brain barrier. It is
excreted by the kidney.
Toxicityit is nephrotoxic, ototoxic and may cause
severe nausea and vomiting. Renal damage may be
cumulative. Magnesium wasting may occur as a result
of renal damage. If it is given in large doses it is
associated with peripheral neuropathy, predominately
affecting sensory nerve endings.
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Hexamethylamine
Indicationsit is active against ovarian and cervical
cancer.
Absorptionit is well absorbed from the gut.
Toxicityit causes abdominal cramps, diarrhea and
leucopenia. CNS toxicity includes altered mental state
and convulsions.
Doseit is given orally at a dose of 12 mg/kg/day for 14
days.
Carboplatin
Actionit is a less reactive second generation platinum
compound that is better tolerated.
Toxicitynephrotoxicity, ototoxicity and neurotoxicity
are low. The dose limiting toxicity is thrombocytopenia
and less often neutropenia.
Indicationsit is primarily indicated in ovarian
carcinoma of epithelial origin, squamous cell carcinoma
of head and neck, small lung cancer and seminoma.
Dose400 mg/m2 as an IV infusion over 15-60 minutes
to be repeated only after 4 weeks.
Pharmacology
The susceptibility of a tumor cell to drugs depends on the
sensitivity of the tumor cells to action of the drug, whether
the cell is in cycle or not and whether the drug reaches the
cell at high enough concentration for a sufficient time to
effect cell kill. The concentration of cytotoxic drugs at the
tumor site, duration and integrity of its action are
determined by several factors such as drug absorption,
binding, distribution, metabolism, excretion tumor size and
its vascularity. The higher dose is better in terms of response
and relapse free interval and overall survival.
Principles of Treatment
Routes of Administration
The route of administration of a cytotoxic drug is
determined by the stability, size, molecular charge and
sclerosant characteristics of that drug. The intravenous
route is most commonly used because a known
concentration of the drug is delivered directly to the central
component of the tumor.
Combination Chemotherapy
Three general principles govern the use of combination
chemotherapy. The drugs should be:
Active against the tumor when used alone.
Have different mechanism of action.
Have minimally overlapping toxicities.
By using several drugs which attack the cells in different
ways it is hoped that the development of resistant cells will
be inhibited. If the above three guidelines are used then the
dose chosen for each individual drug will be closed to that
used when the drug is given as a single agent resulting in
a minimum reduction in dosage intensity.
Schedule
The majority of intravenous drugs are given as intravenous
injections or as a short infusion. Longer infusions may be
preferable either to reduce the incidence of toxicity or to
increase the efficiency.
Toxicity
Many cytotoxic drugs are associated with side effects at
commonly used therapeutic doses. Long term side effect of
chemotherapy result in an increased risk of secondary
malignancy and infertility in some cases.
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994
Local Toxicity
Cardiac Toxicity
Gastrointestinal Toxicity
The precise cause of nausea and vomiting which is
commonly seen with cytotoxic drugs is uncertain; but it is
probably due to a combination of stimuli from the
chemoreceptor trigger zone. The timing of onset of vomiting
varies and may occur within 2 hours. Prophylactic antiemetics are used to abolish vomiting and reduce nausea.
Vinca alkaloids may cause constipation and paralytic ileus
which will usually resolve spontaneously.
Alopecia
Generally, the head hair is lost but the whole of the
body hair may be affected. The hair follicles are affected
because of the high rate of cell turnover. Hair loss due to
daunorubicin may be reduced by scalp cooling which by
causing local vasospasm reduces the amount of drug
reaching the follicles.
Pulmonary Toxicity
It is associated with only a few cytotoxic agents such as
bleomycin, busulphan, cyclophosphamide and methotrexate. The pulmonary changes with infiltrate may be
transient or may progress to pulmonary fibrosis.
Neurological Toxicity
The most common toxicity associated with cytotoxic
drugs is peripheral neuropathy as seen with vinca
alkaloids. Loss of tendon reflexes, paresthesia and
numbness in the finger and toes may be noted only and are
an indication to reduce the dosage. Development of
myalgia, neuritic pain and peripheral sensory loss is an
indication to stop the treatment. Drowsiness, confusion
and encephalopathy may be seen with cyclophosphamide,
procarbazine and dacarbazine.
Suggested Reading
1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central publisher, 2005.
3. Craig CR, Stitizel RE. Moderate pharmacology with clinical
application (5th edn), Little Brown and company, 1997.
4. Gomes MW. Synopsis of medical pharmacology (1st edn),
National Series, 2002.
5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001.
6. Mycek MJ, Harvey R, Champe P. Lippincott illustrated review:
pharmacology, (2nd edn), Lippincott Williams and Wilkins
publisher.
7. Salil and Bhattacharya, Sen A, Ray A. Pharmacology (2nd edn),
Elsevier, 2003.
8. Seth. Textbook of Pharmacology (2nd edn), Elsevier, 1999.
9. Sharma HL, Sharma KK, Gupta DK. Textbook of dental
pharmacology (1st edn), Paras Publisher, 2008.
10. Tripathi KD. Essential of Pharmacology for Dentistry (1st edn),
Jaypee Brothers Medical Publishers, 2005.
11. Yagiela, Neidle, Dowd. Pharmacology and thereaputics for
dentistry (1st edn), Mosby Harcourt India, 2001.
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44
Antiviral Drugs
Introduction
Viruses are the ultimate expression of parasitism. They take
nutrition from the host cell and also direct its metabolic
machinery to synthesize new virus particles. It consists of
double stranded or single stranded DNA or RNA enclosed
in protein coat called capsid.
Some viruses contain enzymes that initiate viral
replication in the host cell. The whole infective particle is a
virion. Their replication depends primarily on synthetic
processes of the host cell. They not only take nutrition from
the host cell but also direct its metabolic machinery to
synthesize new viral particles.
Antiviral agents are most active when viruses are
replicating. Viral replication consists of several steps like
Adsorption to and penetration to susceptible host cells.
Uncoating of viral nucleic acid.
Synthesis of early regulatory protein/structural protein.
Synthesis of RNA and DNA.
Assembly/maturation of viral particles.
Drugs can potentially target any these steps, so antiviral
drugs have to be specific for the different viral mechanism.
In many viral infections, replication of virus peaks at or
before the manifestation of clinical symptoms. To be
effective, therefore, therapy has to be started in the
incubation period, i.e. has to be prophylactic.
Classification
According to their therapeutic use
Anti-herpes virus agents
Acyclovir
Idoxuridine
Gancyclovir
Trifluridine
Vidarabine
Pencyclovir
Famcyclovir
Valcyclovir
Foscarnet
Anti-retroviral agents
Reverse transcriptase inhibitors
Zidovudine (AZT)
Didanosine
Zalcitabine
Stavudine
Protease inhibitors
Saquinavir
Indinavir
Nelfinavir
Ritonavir
Amprenavir
Anti-influenza virus agents
Amantadine
Rimantadine
Nonselective antiviral agents
Ribavirin
Lamivudine
Human interferon
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Idoxuridine
It acts as a thymidine analogue. It was the first pyrimidine
antimetabolite to be used as antiviral drug. It is primarily
active against DNA virus.
Mechanism of actionit competes with thymidine, gets
incorporated into the DNA of virus. Therefore, it disrupts
the DNA synthesis and the faulty DNA is formed which
breaks down easily. This DNA directs the synthesis of
wrong viral proteins (faulty transcription occurs).
Clinical utility is limited to herpes simplex keratitis.
Indication
Ocular infectionit is mainly used for ocular
infections.
Herpes simplex keratoconjunctivitisone drop of 0.1%
solution is put hourly during daytime and 2 hourly
during night. 0.5 % eye ointment may be applied
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Gancyclovir
It is about 100 times more active against herpes viruses
including cytomegalovirus. It is more active than acyclovir
intracellular.
Mechanism of actiongancyclovir requires triphosphorylation for activation prior to inhibiting the viral DNA
polymerase. Activated compound competitively inhibit
viral DNA polymerase and causes termination of viral
elongation and inhibit the synthesis of DNA.As the
concentration of active triphosphate is much higher
inside CMV infected cell. Ganciclovir is much active
against CMV, HSV, VZV, and EBV than that of acyclovir.
Indication:
CMV retinitis with AIDS patientIV ganciclovir 5 mg/
kg every 12 hours for 2 weeks during induction and
then 5mg/kg/day for maintenance therapy is useful.
Dual therapy with foscarnet and ganciclovir has
been shown to be more effective than either drug
administered alone. Recently, gancyclovir intraocular
implant which release gancyclovir into the vitreous
cavity of eye is administered at the rate of 1.4 ug/
hour has been proved for treatment of CMV retinitis.
Surgical replacement is required at approximately
5 to 8 months intervals. Implant achieves high and
prolonged intraocular levels of gancyclovir shown to
delay progression of retinitis to a greater degree than
systemic therapy.
CMV colitis and esophagitisintravenous gancyclovir
is used in AIDS patient.
Before any organ transplantationIV administration
reduces the incidence of symptomatic CMV disease if
administered before organ transplantation.
CMV pneumonitisin immunocompromised patient,
it is often beneficial.
Adverse effect:
Systemic toxicity: bone marrow depression.
Rash, fever, vomiting.
CNS disturbance: headache, seizures.
Neutropenia (20-40 % patient).
Famcyclovir
It is an ester prodrug of guanine nucleoside analogue of
pencyclovir. It has good oral bioavailability. It has potency
against herpes simplex virus and varicella-zoster virus. It
is also inhibitory for hepatitis B virus.
Mechanism of actionlike acyclovir, famciclovir needs
viral thymidine kinase for generation of active DNA
polymerase inhibitor to block DNA synthesis. It is also
inhibitory for hepatitis B virus.
Indication:
Alternative to acyclovirit is used as an alternative to
acyclovir for genital herpes and herpes zoster.
Recurrent orolabial HSV infectionit is used in the dose
of 500 mg twice a daily for 7 days.
Shinglesshingles which caused by herpes zoster is
best treated with famcyclovir tablets in the dose of
500 mg every 8 hours for 7 days.
Genital herpes infectionorally drug 125 mg twice daily
for 5 days is required. For recurrent genital herpes in
immunocompetent patient, need 250 mg twice daily
for upto 1 year.
Adverse effect:
Headache, diarrhea, nausea.
Itching, rashes, mental confusion.
Trade nameFAMTREX, FAMVIR.
PreparationOral: 125, 250, 500 mg tablets.
Foscarnet
It is an inorganic pyrophosphate analogue; inhibit herpes
viral DNA polymerase, RNA polymerase and HIV reverse
transcriptase directly without activation of phosphorylation. Foscarnet is active against herpes virus, CMV and
HIV at 3 g concentration.
Mechanism of actiondrug act on the pyrophosphate
binding sites of enzyme polymerase and reversibly
blocks the site in a noncompetitive manner and inhibits
cleavage of pyrophosphate from deoxynucleotide
triphosphate.
Indication
CMV retinitisin CMV retinitis with AIDS patient,
60 mg/kg every 12 hours for induction followed by
90-120 mg/kg/day for maintenance therapy.
Acyclovir resistant mucocutaneous herpes simplex
(type 2)40 mg/kg every 8 hours or 40 mg/kg every
12 hours yields good results.
Varicella-zoster infection in AIDS patientit decreases
HIV viral titer but not used primary for HIV infection.
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Antiretroviral Agents
These are the drugs active against human immunodeficiency virus (HIV) which is a retrovirus. They are mainly
useful in prolonging life and postponing complication of
AIDS or AIDS related complex but not fully cures the
disease.
Protease Inhibitors
As these agent acts at the late stage of HIV replication, they
are effective in both newly and chronically infected cells
and thus, prevent the infection.
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Drugs
Trade name
Dose
Dosage form
Indications
Contraindications
Adverse effects
Idoxuridine
Ridinox
0.5 % ointment
and 0.1% drops
4 hourly for
3 weeks
Ointment
Drops
Keratoconjunctivitis
Ocular irritation ,
edema of lids,
photophobia,
bone marrow
depression
Acyclovir
Zovirax
Cyclovir
Acivir DT
200 mg tablets
for HSV infection
5 times daily
for 7 days for
HZV infection
800 mg 5 times
daily
5% ointmenttopical application
6 times daily
Tablet
Injection i.v.
Cream,
Ointment
Genital herpes,
Mucocutaneous
herpes simplex,
herpes zoster
chickenpox,
ocular keratitis
Hypersensitivity,
glaucoma,
Psychiatric disease
Depression
Topical-stinging
and burning
sensation oral
headache nausea
malaise
Zidovudine
(AZT)
Retonavir
Zidovir
Capsule
Tablet
Syrup
AIDS
Low Hb level
less than 7.5
g/deci liter,
low neutrophil
cell counts
Anemia,
neutropenia,
nausea, vomiting,
abdominal pain,
headache,
insomnia and
myalgia
Retrovir
Ritovir
250,500 mg bd
Capsule
AIDS
Other AIDS
related infection.
Rash, headache,
GIT intolerance,
abnormal
distribution
of body fat.
Amantadine
Amantrel,
Neaman
Adult100 mg bd,
200 mg OD
Child
5 mg/kg/day,
50 mg/5 ml syrup
Capsule
Syrup
Prophylaxis of
influenza. treatment
of influenzal illness,
Parkinsonism
Epilepsy,
CNS disease,
Pregnancy
Insomnia
Dizziness
Nightmares
Lack of mental
concentration and
hallucination
Ribavirin
Ribavin
Virazide
200 mg qid
50 mg/ 5ml syrup
Capsule
Syrup
Influenza measles
Hepatitis virus infection
Anemia
Hemolysis,
GIT symptoms
Interferon
Alferon,
Realfa,
viraferon
A vial (2 ml)
3,5,10 million
IU/day
Chronic hepatitis.
HSV, HZV, CMV,
papilloma viral
infection,
Kaposis sarcoma.
Severe allergies
Headache
Dizziness
Fever
Lethargy
H. Simplex, H. zoster and CMV infectionin immunocompronised patient, it is used in the dose of 3 million
IV/day or 3 times/weeks.
Rhinoviral coldintranasal interferon is prophylactic.
Condyloma acuminate caused by papillomas virusit is
used by topical application on lesion. It can be used
by an intralesional interferon injection in refractory
cases.
Adverse effect
Flu-like symptoms: fatigue, rashes, pain, malaise,
fever, visual disturbance
Neutropenia/ thrombocytopenia
Neurotoxicity: Numbness, neuropathy, tremor,
sleepiness, convulsions.
Thyroid dysfunctions.
Hypotension, alopecia, liver dysfunction.
Trade nameALFERON, REALFA, VIRAFERON.
Preparationparenteral: 3,5,10 million IV vials for
injections
Ribavarin
It is purine nucleoside analogue. It is active against both
RNA, DNA viruses including myxoviruses, paramyxoviruses, adenoviruses, poxviruses.
Mechanism of actionRibavarin acts at multiple sites to
inhibit viral replication. Ribavarin is phosphorylated
intracellularly by enzyme adenosine kinase; generate
its mono and triphosphate derivatives. It inhibits GTP
and viral RNA synthesis.
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Suggested Reading
Therapeutic Regimen
Treatment should be aggressive (HAART) aiming at
suppressing plasma viral load to undetectable levels
(<50 copies of HIV-RNA/ml).
Choice has to be made on the basis of efficacy, durability,
drug interactions, impact on future options and cost.
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5
Corticosteroids
Introduction
Corticosteroids due to their wide spread of action are widely
employed in medical and dental practice. The adrenal gland
consists of outer cortex that secretes steroidal hormones
which have glucocorticoids, mineralocorticoid and weakly
androgenic activities. Glucocorticoids action is mainly for
hepatic glycogen deposition, while mineralocorticoid
action is for sodium, electrolyte-fluid balance.
Classification
Glucocorticoids
Short acting [biological half life less than 12 hours]
Hydrocortisone (cortisol)
Cortisone
Intermediate acting [biological half life in 12-36 hours]
Prednisolone
Methyl prednisolone
Triamcinolone
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Corticosteroids 1003
Long acting [biological half life more than 36 hours]
Paramethasone
Dexamethasone
Betamethasone
Mineralocorticoids
Deoxycorticosterone acetate (DOCA)
Fludrocortisone
Aldosterone
Anti-inflammatory Action
Glucocorticoids
Mechanism of Action
Cellular Action
Activation of receptorcorticosteroids penetrate the cells
and bind to the specific receptor protein leads to
activation of receptor in the cytoplasm of cell called as
Human-Glucocorticoid receptor resulting from structural
changes in the protein.
Specific protein synthesisthis receptor moves to nucleus,
interacts with specific site on chromatin and induces
transcription of specific mRNA results in specific protein
synthesis. This process takes at least 30-60 min. Once
appropriate proteins are synthesized, effect persists for
long time.
Metabolic Action
Carbohydrate and protein metabolismthey prevent
conversion of amino acid into proteins i.e. antianabolic
effect. They promote gluconeogenesis of new glucose
formation in liver. Glucocorticoids stimulate gluconeogenesis and glycogen synthesis in the fastest state.
Glucocorticoids increase the serum glucose level and
thus stimulate the insulin release and inhibit the uptake
of glucose by muscle cells.
Fat metabolismact directly- breakdown of Triglycerides
to Fatty acids (lipolysis), Indirectly-formation and
storage of fats (lipogenesis). It stimulates the hormonesensitive lipase and thus lipolysis. The increased insulin
stimulate lipogenesis and inhibit lipolysis leads to net
increase in fat deposition and also increases release of
fatty acid and glycerol into the circulation. Prolonged
administration of glucocorticoids causes a redistribution
of fat in the body, with loss from extremities and a
deposition in the neck (buffalo hump) and supraclavicular area and face (moon face). Hence, the release
of amino acid from muscle catabolism, supply of glucose
from gluconeogenesis, inhibition of peripheral glucose
uptake, stimulation of lipolysis, all are contribute to
maintain adequate supply to brain and body.
Other Effect
Catabolic actioncorticoids stimulate protein and RNA
synthesis. They have catabolic action on lymphoid,
connective tissue, muscle fats and skin.
Hemopoietic actionglucocorticoids increases the hemoglobin and red cell content of the blood, but decreases
the blood lymphocytes, eosinophils, monocytes, and
basophils due to their redistribution rather than
destruction. It causes an increase in polymorphonuclear
leukocytes and platelet count in the blood.
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Uses
Substitution therapyit is used as substitution therapy
in Addisons disease and hypopituitarism.
Intensive short term therapyit can save life and reduce
morbidity in certain potentially lethal conditions in
which inflammatory or the metabolic response of the
body itself threatens life. For example, allergic emergencies such as anaphylactic shock, status asthamaticus, acute necrotizing vasculitis, etc.
Prolonged high dose suppressive therapyit is indicated
in acute rheumatic fever, ulcerative colitis, subacute
hepatitis, autoimmune hemolytic anemia, pemphigus,
ITP, Hodgkins disease, etc.
Low dose chronic palliative therapyuse of small doses of
glucocorticoids as an adjunct to some other drugs like
salicylates in rheumatic arthritis. Chronic suppression
of pituitary ACTH secretion is indicated in congenital,
virilizing adrenocortical hyperplasia.
Precaution
Historybefore starting the therapy, enquire about
history suggestive of peptic ulceration.
Glucose estimationexamine urine periodically for sugar.
Weight and blood pressure recordkeep record of weight
and blood pressure.
Do not stop abruptlyinstruct the patient not to stop the
therapy abruptly.
Increase doseif the patient develops an acute infection
or has to undergo therapy, increase the dose of steroids.
Restrict useglucocorticoids must not be used in the
presence of infection unless the latter can be
simultaneously treated with antibiotics.
Hydrocortisone (cortisol)
It is naturally occurring steroid. It acts rapidly but has short
duration of action.
Actionanti-allergy, anti-inflammatory.
Therapeutic uses
OSMFhydrocortisone injected intralesionally in the
areas of fibrosis in dose of 25- 50 mg/ ml fortnightly.
Topically, it is applied intraorally on the oral mucosa
can be combined with orabase. Hydrocortisone 25
mg tablets in dose of 100 mg/day can be given
systemically helps in relieving burning sensation.
Hydrocortisone 25 mg tab. Can be combined with
Dexamethasone 90 mg can be given at biweekly
interval. It is mainly attributed to fibrinolytic, antiallergic, anti-inflammatory action by decreasing
fibroblastic production and deposition of collagen.
Aphthous ulcerTopical application of steroid with
Orabase is effective in case of aphthous ulcer. Presence
of saliva may dilute drug and effectiveness. Intralesional injections of hydrocortisone acetate (25 mg/
ml) into the mucosal lesion is given.
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Corticosteroids 1005
Desquamative gingivitistopical hydrocortisone
cream and ointment (0.25- 0.5%) are applied
intraorally to the affected lesion gives better result.
Osteoarthritisintraarticular injections (25 mg/ ml)
are indicated in acute inflammation. Repeated
injections may be associated with painless destruction
of bone joint.
Addison diseasecortisol is administered 20- 30 mg /
day in divided doses usually 20 mg in morning and
10 mg in afternoon as best replacemental therapy.
Congenital adrenal hyperplasiahydrocortisone is
given orally as 0.6 mg/kg dose in 2-4 divided doses.
Lichen planus, pemphigus, and eczematous skin disease
for oral lesions, topical application of creams and
oral suspensions, ointment 1 % applied locally twice
a day. Severe episodes of pemphigus require systemic
steroid administration which may be life saving drug.
Ulcerative colitis, Crohns diseaseadministered orally
as a lower dose on alternate day with hydrocortisone
100 mg gives better results. Care should be taken in
high doses as it may result in intestinal perforation.
Shock, status asthmatics100 mg I.V bolus + 100 mg
infusion in every 8 hrs may be given.
Trade nameCORTEF, EFCORLIN, WYCORT,
ORABASE-HCA.
PreparationOral: 5, 10, 20 mg tablets. Topical: 1% eye
drop-solution, 0.025 nasal drops and 0.25-2.5% skin
creams, ointment.
Hydrocortisone acetateParenteral: 25, 50 mg/ml suspension for soft tissues intralesional/intraarticular
inj.
Hydrocortisone sodium phosphateParenteral: 50 mg/ml
for IV, IM, SC inj.
Hydrocortisone sodium succinateParenteral: 100, 250,
500, 1000 mg/vial for IV, IM injection.
Cortisone
It is next potent drug than hydrocortisone. Nowa days it is
used very occasionally.
Actionanti-allergy, anti- inflammatory.
Therapeutic uses
Oral submucous fibrosiscortisone can be given orally
in dose of 25 mg tablet. Inj.25 mg/ml can be given
intramuscularly, gives better results.
Addison diseaseDaily dose of 25-40 mg is given as a
maintenance dose.
Hodgkin lymphomasystemic use of cortisone in lower
doses can be used. Thrombocytosis /Thrombocytopenia. Drugs can be used systemically.
Trade nameCORLIN, CORTONE
Preparation availableoral: 5, 10, 25 mg tablets.
Parenteral: 22, 25 mg/ml of solution.
Prednisolone
It is four times more potent than hydrocortisone. It is most
selective glucocorticoid.
Actionit is mainly anti-inflammatory but, has little
sodium retentive activity. It also used as an anti-allergic
and immunosuppressive.
Therapeutic uses
Rheumatoid arthritisinitial dose of prednisone 10
mg/day is given in divided doses. Initial dose should
be small and increases gradually until desired degree
of control is achieved.
Collagen diseasecollagen diseases like Polyarteritis
nodosa, Granulomatous polyarteritis. Prednisone 1
mg/kg daily is given. If favorable results are not
achieved, dose is increased in 20 mg daily and then
reduced gradually to 5 mg/ week.
Systemic lupus erythematousprednisone used
intramuscularly and intravenously. For oral use,
topical application of prednisone 2-3 times daily can
be used.
Leukemiamainly in acute lymphoblastic leukemia,
it is used as maintenance dose. It can be used orally
for at least 2-3 years.
Erythema multiformeprednisone gives in dose of 30
mg/day for several days and terminate after
symptoms subsides. It is life-saving drug in severe
form of erythema multiforme.
Pemphigusprednisone is used topically mainly for
oral lesions. Intralesional injections give better results
to subside oral lesions. It is used systemically to bring
the disease under control. After that, the dose is
reduced. Mainly prednisone with immunosuppressive drugs like cyclosporine is effective in
pemphigus.
Bullous pemphigoidsystemic prednisone with
immunosuppressive drugs with dapsone is given in
lower doses for shorter period of time.
Behets syndromesystemic prednisone with
immunosuppressive drugs is used in life threatening
condition. It can be used to reduce ocular, oral, genital
manifestation. Intralesional drugs are administered
in mucocutaneous lesions. Topical application for
oral mucosal lesion which is not controlled by
systemic therapy.
Rheumatic arthritisprednisone dose of 40 mg/day
in divided doses is given.
Bronchial asthmaOral administration of prednisone
is also useful. prednisone of 40-60 mg is useful to
control status asthmaticus and then withdrawn
gradually. Recently, inhaled corticosteroids are found
for the treatment of bronchial asthma.
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Triamcinolone
Dexamethasone
Methyl Prednisolone
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Corticosteroids 1007
Preparation availableoral: 0.25, 0.5, 0.75, 1, 2, 4, 6 mg
tablets. Topical: 0.1% eye drops, ear drops, skin
ointments. Parenteral: 4, 8, 10, 20 mg/ml for IV, IM,
intralesional and intra-articular injections. To give IV,
only 24 mg/ml suspension is used. And for intraarticular
injections, 16 mg/ml suspensions are used.
Betamethasone
Actionthis drug has similar action that of dexamethasone.
Therapeutic usessame as dexamethasone. It is mainly
preferred in cerebral edema and shock.
Trade nameCelestone, Betnovate, Betnesol, Betnelan.
Preparation availableoraloral drops 0.5 mg/ml,
tablets 0.5-1 mg. Topical0.1% eye drops, ointments,
0.05% nasal drops, 0.12% skin creams. Parenteral
4 mg/ml for IM, IV, intralesional and intraarticular.
Contraindication
Cushing syndrome (absolute contraindication)most
patients who are given daily doses of 100 mg of
hydrocortisone of longer than 2 weeks undergo series of
changes termed as cushing syndrome. It is characterized
by fat deposition, rounding appearance of faces (moon
facies), weight gain, muscle wasting, thinning of the skin
with striae and bruising, hyperglycemia, development
of osteoporosis, diabetes and impaired wound healing.
Diabetes mellitussteroid containing fluorine
intensifying diabetes more than other and so it should
be avoided in diabetes.
Hypertensionit increases intracranial hypertension due
to hypokalemia, hypochloremic alkalosis, there is
increased in blood pressure.
Pregnancy and lactationit is best to avoid in 1st trimester
of pregnancy due to risk of cleft palate and intrauterine
growth retardation in the fetus.
Peptic ulcerrisk of bleeding and silent perforation of
ulcers may occur. Dyspeptic symptoms are frequent with
high dose therapy.
Osteoporosisit appears to antagonize the effect of vit.D
on calcium absorption and on hemopoietic system,
increase in the number of platelets and red blood cells.
Caution
Glucocorticoids should be used cautiously in pregnancy, tuberculosis, epilepsy, in debilitating and other
patients.
Newer Drugs
Budesonide (TN: Budecort)preparation available-topical
100,200,400 mcg/puff inhaler. It is used mainly in
chronic bronchial asthma. Used inhalation in the dose
of 200-1600 mcg/day in adults and 200-800 mcg/day
in 2-4 divided doses in children.
Clobetasol (TN Emosone)preparation available-topical
0.05% ointments, lotion, gel. It is used in dermal
infections by topical application on skin 2-4 times a day.
Fluocinolone (TN: Flucort 0.05%)
Fluticasone (Flixotide 25, 50 mcg/puff inhalers)it is new
inhaled steroid with high inflammatory activity and
negligible systemic absorption. It is used as aerosol 2
times a day for prophylaxis of asthma.
Halocinonide (TN: Clobederm-H 0.025 to 0.1%)
Mometasone (TN: ELOCON 0.1%)they are newer drugs
used mainly for dermal infections twice a day on affected
skin.
Mineralocorticoids
Important mineralocorticoids are aldosterone, fludrocortisone, desoxycortisterone.
Mechanism of Action
Mineralocorticoids have main effect on electrolyte (sodium,
potassium) and fluid balance.
They have sodium retaining and potassium depleting
action. Hence, it influences the salt and fluid water
equilibrium in the body. Mineralocorticoids act by binding
to the receptors present in the cytoplasm of principal cells
forming drug-receptor complex which activate the series of
events similar to described for glucocorticoids. It increases
reabsorption of sodium and secretion of potassium by
electrolyte and water metabolism.
Single dose of aldosterone produces sodium retention
and increased urinary loss of potassium. As a result of
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Systemic hypotension
Weight gain.
Contraindication
Fludrocortisone
It is more potent mineralocorticoid having some
glucocorticoids action.
Actionsodium retention action. Anti-inflammatory
action only at high doses.
Therapeutic uses
Addisons disease0.1mg tablets are used as initial
doses; gradually dose is reduced to 0.1 to 0.2 mg daily
as maintenance dose. It is used to replace the
Aldosterone.
Autonomic neuropathyfludrocortisone is drug of
choice for autonomic neuropathy. It is used to achieve
vasoconstrictor tone. It is used in the dose of 0.5 to 1
mg/day.
Hypotensionas the drug has sodium retention
capacity. It is used mainly in hypotension.
Congenital adrenal hypoplasia: Tablets of 0.1 mg/day is
used because in such patients, salt resting is comparatively more.
Trade nameFlorinef
Preparation availableOral: 0.1 mg tablets.
Adverse Effect
Edema
Hypokalemia
Progressive rise in blood pressure
Fluid and electrolyte balance disturbance
Hypertension
Systemic heart diseases
Osteoporosis
Cushing syndrome.
Dental Consideration
Physician consultationit is preferable to consult patient
physician before carrying out any dental treatment in
patient on steroid therapy to determine any alteration
required in the dose before dental treatment.
Osteoporotic changespatient receiving long term steroid
therapy results in adrenal suppression causes
osteoporotic changes in jaw bone and degenerative
changes in periodontium. So; dentist should look for
such symptoms.
Stressful conditionpatient may show hypotension,
vomiting, glucose intolerance, arthralgia in stressful
conditions. In such conditions, majors should be taken
to support blood pressure, fluid volume and to maintain
normal electrolyte balance.
Minimum stress dental treatmentdental treatment should
be carried out with minimum stress. Minor dental
procedure like minor restoration, minor biopsy, denture
orthodontic adjustment, scaling and prophylaxis may
not required any alteration in the dose of corticosteroids.
Doubling the dosefor moderate stressful dental
procedure in suppressed patients, normal dose should
be doubled 8 hours before the procedure like 3rd molar
impaction, vertical extraction, incision and drainage of
dental infection. The dose should be tapered back to
normal during post operative period after the cessation
of pain, fever and other symptoms of stress.
Major dental surgeryfor major dental surgery under
general anesthesia, due to facial trauma, severe oral
infection and Orthognathic surgery, parental administration of corticoids 100 mg cortisol intramuscularly 8
hours before the procedure followed by intravenous
infusion of hydrocortisone ( 300 mg cortisol) during
procedure is given.
Suggested Reading
1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central publisher, 2005.
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Corticosteroids 1009
Summary chart
Drugs
Trade name
Route
Dose
Indications
Contra-indications
Adverse effects
Hydrocortisone
Topical
Topical
Topical
Oral
Inhalation
3-4 times
3-4 times
3-4 times
100 mg
6 hourly
1-2 ml
per day
Lichen planus
Erythema multiforme,
Pemphigus,
recurrent aphthae,
desquamative
gingivitis, oral
submucous fibrosis,
Asthma, Osteoarthritis,
Addisons disease
Viral infection
HSV I and II
Diabetes mellitus.
TB, Osteoporosis,
pregnancy and
not to be given IV/IM
Cutaneous
atrophy.
Susceptibility to
infection, delayed
healing, glaucoma
Prednisolone
Predicort
Prid
Wysolone,Deltacortef, meticorten,
prelone
Oral
5-60 mg/day
in divided
doses
Lichen planus,
Erythema multiforme,
serum sickness,
Pemphigus,
thrombocytopenia,
Behets syndrome,
post herpetic
neuralgia,
malignancies.
Hypersensitivity,
Viral infection,
Diabetes mellitus,
TB, peptic ulcer
Hyperglycemia,
muscular
weakness,
psychosis, HPA
axis suppression
Triamcinolone
Topical
3-4 times
daily
Inhalation
40-100 mg
day
Oral
4-2 mg /day
Intralesional 02-03 ml/day
Intralesional 02-03 ml/day
Lichen planus,
Viral infection,
Erythema multiforme,
TB, not to be
recurrent aphthae,
given IV/IM
desquamative gingivitis,
oral submucous
fibrosis, Asthma,
contact cheilitis,
hemangioma.
Cutaneous
atrophy,
Susceptibility to
infection, delayed
healing,
Muscular
weakness and
psychosis
Lichen planus
Viral infection
Erythema multiforme,
Live viral
recurrent aphthae,
immunization
desquamative gingivitis,
oral submucous
fibrosis, Asthma,
Mucous membrane
pemphigoid
Secondary
infection,
Delayed healing,
Cutaneous
atrophy
Topical
Topical
Topical
Inhalation
3-4
3-4
3-4
3-4
Fluocinolone
Topical
Topical
times
times
times
times
daily
daily
daily
daily
Viral infection
Secondary
infection
Delayed healing,
Cutaneous
atrophy
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46
5
Desensitizing Agents,
Gum Paints and
Mouthwashes
Dentinal Hypersensitivity
Introduction
It is certain that the teeth of man have been hurting for
many thousands of years. Pain has been so closely
associated with dentistry that the word pain and
dentistry have almost become inseparable and one of
the most important objective of dentistry has been the
control and elimination of the pain.
Clinical experience suggests that dentin hypersensitivity
is a relatively common cause of pain associated with the
teeth. Despite this, the condition has been justifiably
described as an enigma being frequently encountered
but ill understood. Even the suitability of the term dentin
hypersensitivity may be questioned. Such symptoms as
sharp, painful, responses of short duration are associated
with many conditions in which dentin is exposed
including the dental caries. Furthermore, there is no
evidence to indicate that hypersensitive dentin differs in
any way from normal dentin (or that specific pulpal changes
occur). The term dentin sensitivity may be more
appropriate. The international association for the study of
pain (IASP) termed hypersensitivity as allodynia which
is pain resulting from a non-noxious stimuli to normal
skin and hence, it can be appropriate to call dentinal
hypersensitivity as allodontia.
Definition
Prevalence of Dentinal Hypersensitivity
Incidencethe prevalence of dentinal hypersensitivity
has been reported over the years in a variety of ways:
Cross Sectional Surveys have shown dentinal
hypersensitivity to be ranging anywhere in between 8%57% of adult dentate population and up to 30% of adults
at some time during their lifetime. It is claimed that 14.3%
of all dental patients have some degree of dentin
hypersensitivity.
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Modulation Theory
On any irritating stimulus to the dentin, the odontoblasts
may become injured and subsequently release a variety of
neurotransmitting agents as well as vasoactive and pain
producing amines and proteins.
These substances may modulate associated nerve fiber
action potentials by increasing neuronal cramp levels
through cell membrane adenylate cyclase receptors.
Hydrodynamic Theory
It is the most widely accepted theory till date. In 1966,
Branstromm provided the scientific explanation for
hydrodynamic theory. Most dentinal stimuli cause pain
by generating action potentials in intradental nerves
through a hydrodynamic mechanism.
Application of any stimuli to dentin increases the rate of
fluid flow in dentinal tubules (Fig. 46-4). The fluid flow in
turn excites nerve terminals at the inner ends of the tubules
or in the outer layer of the pulp. (Exceptions to this are
electric current and intense cold, which can stimulate
pulpal nerves directly).
Treatment of dentin hypersensitivity aims to interrupt
this sequence of event by:
Creation of tubular plugproviding a chemical ion that
can react with and precipitate one of the components of
the protoplasmic fluid and thus create a tubular plug.
Sealing of dentinal tubulessealing or physically
occluding the outer end of dentinal tubules.
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Tactile examination
Air flow from air-water syringe
Percussion
Biting pressure
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Electrical Stimuli
Instrumentit includes electric pulp tester and dental
pulp stethoscope. Pain response can be obtained from
non-sensitive as well as from sensitive teeth.
Mechanismdentinal fluid movement is not necessary
for transmission of electrical stimulus, rather the presence of lower resistance organic material in cementum,
enamel or dentin. Sensitive teeth show lower pain
thresholds than healthy teeth.
Techniqueelectrode or probe should apply the electrical
stimulus to tooth. Power source is required to vary the
electrical stimulus and means of completing the
electrical circuit.
Reference electrodereference electrode, a saliva ejector
connecting the patient to a pulp stimulating instrument
pulp stethoscope.
Current appliedelectrical stimulus consisting of a direct
current pulsed voltage between 0 and 150 or 0 and 300
volts.
Placing of probe tipplace the probe tip on the tooth
surface, depress on/off switch. Rotate the ramp
adjustment dial. Intensity of electrical stimulus rises
from 0 to 25 rms volts and above patient feels the prepain (signals the operator to remove the probe that
activates the recorder).
Evaporative stimuliit includes cold air blast, air thermal
system, air jet stimulator, temtronic device (microprocessor temp. Air delivery system)
Thermal Stimuli
It is electronic threshold measurement device, cold water
testing and heat.
Why cold stimuli is usedbecause patient are generally
more sensitive to cold than to hot stimuli, the use of cold
water (10, 15, 20, 25, 30C) as a simple, quantitative
stimulus is gaining in popularity.
Mechanismthermal stimuli are effective of differences
in thermal conductivity and coefficient of expansion or
contraction of fluids and their container, enamel and
dentin. Thus application of cold causes more rapid
volumetric contraction of dentinal fluid that occurs in
the dentin. This mismatch of volumetric changes
produces negative intrapulpal and intradental pressures
that displace mechanoreceptors and cause pain. Heating
has the opposite effect but the same result, pain
clinically, cold stimuli are more useful than hot stimuli
for testing dentinal sensitivity. Patients tolerate cold
stimuli better than hot stimuli, and there is danger of
causing pulpal damage.
Isolation of toothin using cold water, each tooth is
isolated with a rubber dam and water at a known
temperature.
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Osmotic
It is subjective pain to a sweet stimulus.
Solution usedfresh saturated solution of sucrose;
allowing it to reach room temperature.
Applicationa cotton applicator saturated with the
solution applied to the root surface, allowed to remain
for 10 seconds.
Results
no pain0
and pain 1.
Method
Ask the patient to indicate on the line where the pain is in
relation to the two extremes. Ask the patient to mark on the
line the point that they feel represents their perception of
their current state (Fig. 46-5). The VAS score is determined
by measuring in millimeters from the left hand end of the
line to the point that the patient marks. When the VAS is
properly explained to subjects, they can easily understand
its use and successfully use it to indicate their level of pain
response to hypersensitive stimuli.
Comparison between VAS and VRSthe VAS should be
the more appropriate device than the VRS for measuring
levels of sensitivity, pain during subject assessment and
for measuring tactile and thermal stimuli of hypersensitivity. For those unable to read or to understand
the linear visual analogue scale, picture of faces showing
increasing distress can be used (Fig. 46-5).
Advantage of VASVAS is found to be reproducible
therefore a very high correlation between successive
measurements of pain severity has been noted.
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Desensitizing agents
Trade name of
toothpaste
Mechanism of action
Strontium chloride
Thermoseal
Eanisam
Desent
Senolin
Toss
Potassium nitrate
Senquel
Sensodent K
Formalin
Sensoform
Dentoform
Protein precipitation
Strontium chloride
and formaldehyde
Stolin
Potassium nitrate
5% sodium monofluorophosphates
0.7% available fluoride
Senquel-F
Drug
Trade name
A.M-P.M.
Betadine, alphadine,
povidax, povidone
Dettolin
Kamillosan-N
Listerine
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Chlorhexidine Mouthwash
Chlorhexidine molecule gets adsorbed onto the oral
surfaces and gets released at bactericidal level over
prolonged periods. Due to this process, Chlorhexidine has
antiplaque properties unsurpassed by other agents. The
antibacterial action of Chlorhexidine is due to an increases
in cellular membrane permeability followed by coagulation
of the cytoplasmic macromolecules. It is effective in vitro
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Structure
Chlorhexidine is a chlorophenyl bisguanide that has been
used as an acetate and more commonly as a gluconate salt.
It is N, N-bis (4-chlorophenyl)-3, 12-dimino-2, 4, 11, 13tetra-azotetradecanedimidamide diD-gluconate.
Mechanisms of Action
Absorption onto oral surfacechlorhexidine molecule gets
adsorbed onto the oral surfaces and is released at
bactericidal levels over prolonged periods. Due to this
process, chlorhexidine has antiplaque properties
unsurpassed by other agents.
Antibacterial actionthis action of chlorhexidine is due
to increase in cellular membrane permeability followed
by coagulation of the cytoplasmic macromolecules. It is
effective in vitro against gram +ve and gram ve bacteria
including aerobes and anaerobes and yeast and fungi.
The positively charged chlorhexidine binds to
negatively charged microbial cell surface. It is followed
by disorganization of cytoplasmic membrane. Low
concentration allows cytoplasmic constituent to leak out
and high concentration coagulates them.
Blocking of acidic groupsthese groups on the salivary
glycoprotein reduce the protein absorption to tooth
surfaces.
Cell wall penetrationin high concentration, chlorhexidine penetrates cell wall and causes precipitation
of the cytoplasm.
Indications
Periodontal diseaseit is used in all forms of periodontal
diseases.
Subgingival irrigationit is also used for sub-gingival
irrigation of periodontal pockets.
Aphthous ulcerit also reduces the severity and duration
of aphthous ulceration.
Substitution of mechanical plaque controlwhere
mechanical plaque control is not useful.
Denture stomatitisdenture stomatitis has been treated
by soaking dentures in 0.2% chlorhexidine overnight
for 5 months combined with daily use of amphotericin B
lozenges for 14 days.
Drugs
Trade name
2% zinc sulfate
Gingisol
Sensoform
Gelora
Zytee
Dentogel
Dologel
Stolin
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Suggested Reading
1. Anderson DJ. The sensitivity of human dentin. J Dent Res 37;699.
2. Brannstoon M. The hydrodynamic theory of dentinal pain,
sensation in preparations, caries and the dentinal crack syndrome.
J Endo 1986;12:453-57.
3. Branstorm, Linden and Astrom. The hydrodynamics of dentin
and pulp fluid. Caries Research 1967;1:310.
4. Colour Atlas of Dental MedicineKlaus M. Reteitschak Herbert
F. Wolf.
5. Curro F. Tooth hypersensitivity in spectrum of pain. Dent Clin
Nortn An 1990;34.
6. Dowel P, Addy M. Dentise Hypersensitivity. A review. J Clin
Periodontal 1983;10(4):341-50,351-63.
7. Everett FG, Hall Phatok NM. Treatment of hypersensitive dentin.
J Oral the Pharmacol 1966;2:300.
8. Grossman L. A systematic method for treatment of hypersensitive
dentin. JADA 1935;22:592.
9. http://ergonomicbasics/ss/painscale.htm
10. Manning M.W. New approach to desensitization of cervical dentin.
Dent survey 1961;37:731.
11. Pashley D. Dentist permeability, dentin sensitively and treatment
through tubule declosion. J Endod 1986;12:465-74.
12. Pashley D. Mechanisms of dentin sensitivity. Dent Clin North
Am 1990;34:449-73.
13. Rosenthal M. Historic review of the Management of tooth
hypersensitivity. Dent Clin North An 1990;34:403-27.
14. Yvichi Kinera, Petra WildesInith, 2000 Journal of Clins
Periodontology 27(10):715-721 Role of interhypersensitivity by
lasersa review.
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47
Drugs used in
Pregnancy
Introduction
Administration of drugs to pregnant patient is of significant
concern. Two main concerns must be addressed when
considering whether to give a drug to pregnant women.
The first is that the drug may be teratogenic and the second
is that drug can affect near term fetus.
One must always be aware of the teratogenic, toxic or
otherwise harmful effects of the drug on the developing
fetus. The physiologic changes during pregnancy and the
consequent alteration in the pharmacokinetics lead to
changes in drug absorption, distribution, metabolism and
excretion.
As a general rule, it is best that no drug should be given
during pregnancy, especially during the first trimester as it
is period of organogenesis. Fortunately, most of drugs
commonly used in dentistry are not contraindicated during
pregnancy. Tetracycline and streptomycin are notably
exceptions.
The fetus may metabolize a particular drug via a different
pathway from that of mother or its metabolic product may
bound more avidly in fetal thus leading to accumulation of
drug or its metabolites in fetus. Also since body systems of
fetus are not fully developed, the fetus cannot process
medicine like mothers system so same drug can cause harm
to fetus.
Pregnancy Trimesters
Pregnancy involves three trimesters each 3 months long.
First trimesterin this trimester, different body organs
in the fetus are forming. It is most critical time for
teratogenicity. Dental prophylaxis with detailed
instructions and a visual examination of the oral cavity
without X-rays should be performed if the patient is
pregnant. Elective dental treatment should be avoided
Pharmacokinetics in Pregnancy
Drug absorptionhigh circulating levels of progesterone
slow the gastric emptying as well as gut motility
resulting in slower drug absorption. Parenteral drug
administration is preferred in order to obtain a quick
response. Drug compliance may be poor because of
nausea and fear of adverse effect.
Drug metabolismhepatic drug metabolizing enzymes
are induced during pregnancy probably by high
concentration of circulating progesterone. This can lead
to more rapid metabolic degradation especially of highly
lipid soluble drugs. However, this is of little clinical
consequence.
Drug excretionduring pregnancy the renal plasma flow
increases by 100% and glomerular filtration rate by 70%.
Hence, drugs which depend for their elimination
mainly on kidney are eliminated more rapidly than in
non-pregnant stage, e.g. ampicillin, gentamicin and
cephalosporin.
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Type
Drugs
1st Trimester
Comment
Local anesthetics
Lidocaine
Yes
Yes
Mepivacaine
Yes
Yes
Bupivacaine
No
No
Benzocaine
Yes
Yes
Vasoconstrictors
Epinephrine
Yes
Yes
Analgesics
Paracetamol
Yes
Yes
Codeine
Limited dose
Limited dose
Aspirin
No
No
Ibuprofen
Yes (cautiously) No
Same as aspirin
Penicillin
Yes
Yes
Safe
Erythromycin
Yes
Yes
Antibiotics
Antifungal
Sedative
Tetracycline
No
No
Clindamycin
No
No
Cephalosporin
Yes
Yes
Metronidazole
No
No
Clotrimazole
No
Ketoconazole
No
No
Embryotoxic in rat
Nystatin
Yes
Yes
Safe
Benzodiazepines
No
No
No
Possible with
adequate O2
Types
Drugs
Acceptable
Local anesthetics
Amides
Yes
Vasoconstrictors
Epinephrine
Yes
Hyperactivity or irritability
Analgesics
Aspirin
Yes with caution Avoid feeding for 1 hour after dose, occasional low dose pose no hazard,
chronic high dose may pose problems
NSAID
Yes with caution Use ibuprofen (concentration in milk is low) avoid long acting NSAIDs
Acetaminophen
Yes
Opioids
Yes
Small doses no problems and in larger doses sedation, poor feeding and
constipation
Penicillin
Yes
Erythromycin
Yes
Cephalosporin
Yes
Tetracycline
No
Tooth staining
Clindamycin
Yes/no
Metronidazole
No
Carcinogenic in animal
Nystatin
Yes
Clotrimazole
Yes
Ketoconazole
No
Antiviral
Acyclovir
Yes
Concentrated in milk
Antianxiety
Nitrous oxide
Yes
Benzodiazepines
No
Antibiotics
Antifungal
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Abnormalities
Thalidomide
Phocomelia
Anticancer drug
Tetracycline
Phenytoin
Phenobarbitone
Various malformations
Carbamazepine
CNS defect
Retinoids
Various abnormalities
Alcohol
Consideration in Lactation
Almost all drugs are excreted into the breast milk to some
extent. An infant normally ingests approximately 1% of
the total material dose of a drug. Dental practitioner must
remember that drugs should be selected which have short
half-life, sustained release formulation should be avoided,
drugs should be taken immediately after nursing.
Suggested Reading
1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S Chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central publisher, 2005.
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48
Emergency Drugs
used in Dentistry
Introduction
Though rare, life-threatening medical emergencies can and
do occur in the dental environment whose incidence is
largely unknown. All health care providers, dentists must
be prepared to recognize and properly manage patients of
medical emergencies in the dental office.
In all cases of emergencies, the best and foremost method
of managing medical emergencies is by preventing them
from occurring. With this in mind, it is essential to take a
comprehensive medical history from any patient who is
about to receive dental care.
The following section reviews the more common
emergency drugs that the dental team may have to
administer in general dental practice.
Emergency Management
First and foremost in emergency management is the ability
to effectively provide basic life support, or BLS (includes
cardio-pulmonary resuscitation), when appropriate. It is
recommended that all dental health care professionals
receive regular training in BLS for health care providers,
because these skills are maintained only through repetition.
For certain individuals, like those who practice in the
remote areas where medical services (routine or emergency)
are not readily available, additional training in advanced
cardiac life support, pediatric advanced life support, or
both may be warranted. Didactic and hands-on training in
the prevention, recognition and management of common
emergencies also is recommended. Examples of common
emergencies include seizures, cardiovascular and
respiratory distress, altered consciousness, chest pain and
drug related emergencies.
Advanced cardiac life support training involves the
following:
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Adrenaline
Indicationit is the drug of choice for the management
of the acute allergic reactions especially in the respiratory
and cardiovascular manifestations of allergic reaction.
Anaphylactic shockan allergic (type 1 hypersensitivity) reaction may be precipitated by any material
or drug to which the patient has been sensitized. Lifethreatening events include cardiovascular collapse
(90%), bronchospasm (30%), angioedema (25%), and
pulmonary edema (49%). Severity varies, and onset
of anaphylaxis may be delayed for up to 6 hours or be
biphasic, reoccurring in 5% of patients after clinical
recovery. In addition to adrenaline, high flow oxygen
should be administered to all patients in anaphylactic
shock. Second-line drugs, used to prevent relapse,
are chlorpheniramine and hydrocortisone.
Acute asthmatic attackadrenaline is also used in acute
asthmatic attacks.
Cardiac arrestadrenaline is used highly advanced
cardiac life support protocols.
Mode of Action
Contraction of vascular smooth muscleadrenaline is a
sympathomimetic amine that activates both alpha
and beta adrenoceptors. Contraction of vascular
smooth muscle (alpha-mediated). An increased blood
pressure helps to maintain cerebral and coronary
perfusion.
Increase cardiac outputincreased force and rate of
cardiac contraction (Beta1-mediated). This action
increases cardiac output, which helps to maintain
the blood pressure. However, this may be damaging
as it increases myocardial oxygen requirements and
may precipitate ischemia.
Relaxation of bronchial musclerelaxation of bronchial
smooth muscle (Beta2-mediated). Increasing the
caliber of the airway in acute anaphylaxis helps to
Volume of 1:1000
adrenaline (ml)
Dose (g)
0.2
200
3-4
0.3
300
0.4
400
6-12
0.5
500
Adult
0.5-1.0
500-1000
Chlorpheniramine
Actionit is an antihistaminic drug alternative drug is
diphenhydramine. Antihistamines are useful in the
treatment of the delayed allergic response and in the
definitive management of acute allergic reaction.
Antihistamines act as a competitive antagonist of
histamine. They do not prevent the release of histamine
from the cell in response to injury, drugs, or antigens
but do prevent access of histamine to its receptor site in
the cell and thereby block the response of the effectors
cell to the histamine. They are also the potent local
anesthetics, diphenhydramine and triphelennamine
being particularly potent in this regard. Potential side
effect of most antihistamines is a degree of cortical
depression which causes sedation. Therefore,
Chlorpheniramine is preferred over diphenhydramine
as it is has less sedative effect.
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Oxygen
Indicationsit is the most important drug in the entire
emergency kit. Oxygen is indicated in all medical
emergencies except hyperventilation. Oxygenation
prevents hypoxia that may be damaging to vital organs
such as the brain and heart.
Administrationensuring Airway Patency before oxygen
is delivered, it is essential to ensure that the airway is
patent. Foreign bodies, blood, vomit, and soft tissues
may occlude the air space. The airway may be reestablished by using the head tilt and chin lift or jaw
thrust techniques. Airway adjuncts such as
oropharyngeal (Guedel) airways may be used in the
unconscious patient to hold the tongue in an anterior
position away from the posterior pharyngeal wall. These
airways are contraindicated in conscious or
semiconscious patients where protective reflexes are
active.
Oxygenationif the patient is breathing spontaneously,
a facemask with an attached oxygen supply, running at
a flow rate between 4 and 6 /min, may be used to deliver
oxygen and help prevent hypoxia. Positive pressure
ventilatory support may be provided in respiratory
arrest.
Doseduring cardiorespiratory arrest, the chest
compression to ventilation ratio for adults 15:2 if one
resuscitator is present and 5:1 if two are present.
Nitrous Oxide
Indicationsnitrous oxide may be used for its analgesic
properties in the initial management of myocardial
infarction (MI). The pain experienced during an MI is
often more severe and of longer duration than that in
angina. It may lead to further deterioration of cardiac
function as it increases sympathetic output, which will
elevate the oxygen demands of an already starved
myocardium.
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Methoxamine/Phenylephrine
Actionthis one more vasopressor drug is included in the
emergency drugs kit because of various shortcomings of
adrenaline. Adrenaline is primarily used in the management
of the acute allergic reactions and in cases of clinically mild to
moderate hypotention. In addition to an increase in blood
pressure, adrenaline cause an increase in workload of the
heart through its effect on heart rate and cardiac contraction;
it also increases the irritability of the myocardium by sensitizing
it to dysrhythmias. For this reason, it seems desirable to utilize
a vasopressor that will produce to utilize a vasopressor which
produce a moderate increase in blood pressure without
unduly stimulating the myocardium. Methoxamine and
phenylephrine elevates blood pressure through peripheral
vasoconstriction.
Indicationin management of hypotension, in which the
status of heart is unknown and the intent is to raise the
Glucose/Dextrose 50%
Indicationsglucose may be administered to the
conscious or unconscious hypoglycemic patient.
Administrationglucose may be given orally or intravenously. Intravenous administration is the most rapid
and effective method of elevating plasma glucose levels.
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Hydrocortisone/Dexamethasone
Actionhydrocortisone, an endogenous adrenal
hormone, possesses predominantly glucocorticoids
activity and is essential for human survival.
Administration of steroids for therapeutic purposes has
a negative feedback effect on the hypothalamus and
anterior pituitary gland, which eventually leads to
atrophy of the adrenal cortex and resultant inability to
secrete hydrocortisone in response to stress (acute
adrenal insufficiency). Under these circumstances, a
patient may collapse due to hypoglycemia and
hypotension if a stressful situation, such as dental
treatment, is encountered.
Indicationtherefore, exogenous hydrocortisone should
be administered preoperatively to susceptible patients
to restore the normal physiological response to stress. If
acute adrenal insufficiency does occur, prompt administration of hydrocortisone and immediate hospitalization
is recommended ( Dexamethasone and methylprednisolone are contraindicated in acute adrenal
insufficiency). Corticosteroids will be administered in
the management of an acute allergic reaction, after the
acute phase has been brought under control. The
primary value of the corticosteroid is in the prevention
of recurrent episodes of anaphylaxis.
Administration and dosehydrocortisone may be
administered by the oral, intramuscular or intravenous
routes. The dose varies according to the age and situation
(25 to 200 mg).
Side effect, contraindication, precautionexcept in life
threatening emergencies steroid is contraindicated in
presence of pre-existing infection, peptic ulcer, and
diabetes mellitus.
Atropine
Actionit is a parasympathetic blocking agent, it is
recommended for the management of symptomatic
bradycardia. By enhancing discharge from the sinoatrial
Lidocaine
Indicationlidocaine (xylocaine) is considered the
primary antidysrhythmic drug in ACLS. It is used
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Dopamine/Dobutamine
Morphine Sulphate/Meperidine
Indicationanalgesics are used in emergency situations
in which acute pain or anxiety is present. Pain or anxiety
increases the myocardial workload which increases the
O2 requirement of the myocardium which may worse
the condition. Two such circumstances include acute
myocardial infarction and congestive cardiac failure. It
is use in acute myocardial infarction, congestive cardiac
failure, intense, prolonged pain or anxiety.
Side effectopioid agonists are potent central nervous
and respiratory system depressants. Monitoring of the
vital signs is mandatory whenever these drugs were
used. Use of opioid agonists are contraindicated in
victims of injury and multiple trauma: and should be
used with caution in patients with compromised
respiratory function.
Dosemorphine is available as 8,10, and 15 mg/ml and
meperidine comes in 50 and 100 mg/ml doses.
Verapamil
Actionit is a calcium channel blocker drug. Verapamil
is extremely effective in management of supraventricular
tachycardia. It slows conduction through the atrioventricular node, reducing ventricular response to atrial flutter
and fibrillation.
Indicationin emergency cardiac care verapamil is
primarily used in treatment of paroxysmal supraventricular tachycardia.
Side effect and contraindicationa transient decrease in
arterial pressure may be noted because of peripheral
vasodilatation. Verapamil is not recommended in
ventricular tachycardia; it may induce severe hypotension and predisposed the patient to ventricular
fibrillation. It is available for injection as 2.5 mg/ml in
2 ml and 4 ml ampules.
Antidotal Drugs
In order to manage the emergency situations like overdose
or toxicity reactions caused by various drugs used primarily
for sedation or general anesthesia four categories of
antidotal drugs are used it includes the following;
Opioid antagonists, e.g. Naloxone or nalbuphine.
Benzodiazepine antagonist, eg. Flumazenil.
Antiemergence delirium drug, e.g. Physostigmine,
Vasodilator, e.g. Procaine.
Naloxone/Nalbuphine
Action and indicationthe most significant side effect of
opioid agonist is there ability to produce respiratory
depression by diminishing the responsiveness of the
brains respiratory center to the arterial carbon dioxide.
Naloxone is the only opioid antagonist free of any
agonistic properties. It also reverse the other properties
of the opioid-like analgesia and sedation. Naloxone may
be administered endotracheally in situations where IV
access is not available. Improved respiratory function is
noted within 2 minutes. Nalbuphine, having opioid
agonist-antagonist properties, is used successfully to
reverse respiratory depression induced by opioid
agonists. And because of its own analgesia-inducing
properties it does not entirely remove postsurgical
analgesia or sedation.
Side effect and contraindicationnaloxones effect lasts
only 30 minutes, respiratory depression may recur if
previously given opioid is of long duration. The IM
administration of second dose of the naloxone is
recommended, its onset is slower but for longer duration
than that of IV dose. This minimizes the recurrence of
respiratory depression. Naloxone must be administered
with extreme care to persons with known or suspected
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Flumazenil
Actionbenzodiazepines are supposed to be most safe
drug for anxiety control and sedation. Some side effects
like emergence delirium, excessive duration of sedation,
and possibly significant respiratory depression do occur.
Presence of antagonist for benzodizepines adds safety
to the IV sedation. Flumazenil produce rapid reversal of
sedation and to improve the patients ability to comprehend and obey commands. The duration of antrograde
amnesia associate with midazolam was also reduced
with use of flumazenil. Flumazenil also decrease the
recovery time from midazolam sedation, increase
alertness, and provide decrease amnesic effect in geriatric
patients. Reversal with flumazenil is not effective
following the oral administration of benzodizepines.
Indicationit is used for reversal of clinical action of
parenterally administered benzodiazepines.
Side effectflumazenil may produce rebound anxiety
state in some patients.
Physostigmine
Actionseveral drugs that are primarily used to induce
sedation have the ability to produce emergence delirium
also called as anticholinergic syndrome. In this
phenomenon the patient appears to lose contact with
reality. There may be increase muscular movement, and
patient makes unintelligible sounds. Physostigmine a
reversible cholinesterase with the ability to cross the
blood-brain barrier has become a drug of choice in the
management of emergence delirium.
Indicationfor reversal of emergence delirium.
Side effect, contraindication and precautionside effects
include increase salivation, possible emesis, and
involuntary urination and defecation. If administered
rapidly physostigmine can produce bradycardia and
hypersalivation. Atropine should always available
whenever physostigmine is administered because it is
antidote to physostigmine. Physostigmine should not
be given in patients with asthma, diabetes, cardiovascular disease, or mechanical obstruction of gastrointestinal or genitourinary tract.
Procaine
Actionwhenever there is IM or IV administration of
the drug is present, a local anesthetic with significant
Emergency Equipment
Along with the emergency drugs the emergency equipments
are equally important. Personnel who are expected to use
these equipments must be well trained in its proper use.
IV set/cannula/scalp vein set
Oxygen cylinder
O2 delivery system
AMBU bag
Syringe and needles
Tourniquets
Macgills forceps
Suction and suction tips
Oropharyngeal airways
Endotracheal tubes
Laryngoscope
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Group
Drug
Use
Concentration
Dose
Route
Anti-allergy
Epinephrine
Anaphylaxis
Acute asthma
1:1000
0.3 mg
Subcutaneously
Opioid antagonist
Naloxone
Opioid overdose
0.4 mg/ml
0.4-2 mg
IV or Subcutaneously
Antihistamine
Benadryl
Allergic reaction
10 mg/ml
50 mg
IM, IV
Anticonvulsant
Diazepam
Prolonged seizure
_____
5-10 mg
IM,IV
Oxygen
Oxygen
Respiratory distress
100% inhalation
___
____
Vasodilator
Nitroglycerine
0.4 mg/spray
0.4 mg
Sublingually
Stimulant
Aromatic ammonia
Syncope
Inhalant
0.3 ml
Inhalation
Anti-hypoglycemic agent
Glucose
Hypoglycemia
Few teaspoonfuls
___
Orally
Analgesic
Morphine
Myocardial infract
10 mg/ml
10 mg
Orally
Suggested Reading
1. Barar FSK. Essential of pharmacotherapeutics (3rd edn), S chand
and Company Ltd, 2000.
2. Chaudheri. Quintessence of medical pharmacology (3rd edn),
Central Publisher, 2005.
3. Craig CR, Stitizel RE. Moderate pharmacology with clinical
application (5th edn), Little Brown and company, 1997.
4. Gomes MW. Synopsis of medical pharmacology (1st edn),
National Series, 2002.
5. Hardman, Limbird, Gilman. Goodman and Gillman: the pharmacological basis of therapeutics (10th edn), McGraw Hill, 2001.
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49
Professional Hazards
of Dentistry
Introduction
Medical faculty ensures service to humanity, personal job
satisfaction and fulfilment of professional requirements
but, it also has certain shortcomings and discrepancies.
Dentistry, being an important branch of medical sciences
is no exception to this.
Classification
Professional hazards to dentist from the patients.
Hazards to the dentist from his working conditions,
methodology of practice and materials used.
Hazards to the dentist from law, i.e. consumer protection
act (CPA).
Preventive Approach
General
Proper medical historymedical history should be taken
thoroughly and should be upto date.
Cleaning instrumentclean the instruments before
sterilization, to remove all visible foreign deposits.
Sterilization methodssterilization methods should be
effective against all known pathogens and/or use of
autoclave for various instruments. Working surfaces and
dental units should be cleaned with chemical disinfectants such as 70% isopropyl alcohol, sodium hypochlorite solution and/or glutaraldehyde.
Disposable itemsdisposables items like suction tips,
impression trays, beakers, needles, towels, masks, and
caps should be used.
Aspiration and ventilationuse of high speed aspirators
which exhaust externally and proper ventilation will
definitely reduce the risk of cross-infection from the
aerosols that are formed during certain dental procedures.
Management of sharp itemssharp items like needles,
scalpels and local anesthetic cartridges should be placed
in a soft container. Collection and incineration of surgical
waste should be arranged.
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Musculoskeletal Complaints
Causeswe all are guilty of adopting bizarre positions
while treating our patients and even though such
technique cause minimal patient discomfort, we as
dentist, are in turn rewarded with muscle fatigue, lower
back aches, shoulder problems, etc.
Preventionreduction of physical stress to the body by
adopting a correct posture is important in everyday
practice. Low seated, closely supported dentistry with
Cardiovascular Complaints
Causesit includes varicose veins, high blood pressure
and occurs due to erect posture adopted during long
standing operating procedures.
Preventionproper positioning of doctor should be
maintained.
Radiation Hazards
Causethey are responsible for causing changes in
blood, skin problems, tumor development, shortening
of life span and mutations.
Preventionuse of lead partitions, lead aprons and
cubicalization of patients in protective cabins of lead
glass. Regular check-up of machines for radiation
leakage. Periodic health checks-up of the operator.
Sound Hazards
Causesair driven, high speed handpieces operating
from 3900 to 12,500 Hz and electric engines are main
contributing factors towards sound pollution. Hearing
loss, acoustic stress and impaired power of concentration first affect the individual who are regularly
exposed to frequencies above 3000 Hz.
Preventionpersonal evaluation by routine otologic and
audiometric examination. Noise attenuation by repair
and replacement of defective items, especially high speed
drills. Treatment rooms should be made acoustically
satisfactory. Personal protection by using ear plugs and
muffs which reduce high intensity sounds by 30 to
35 dB.
Light Hazards
Causesdull light or too much bright light can be
hazardous. Ultraviolet radiation used to polymerize
sealant and composite restorations can be hazardous
and may cause skin cancer and chromosomal changes.
Preventionprotective eye glasses for clinician,
auxiliaries and patient with regular ophthalmic
consultation is a must.
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Introduction
In recent period, the CPA has created a great stir amongst
the medical profession on the ground that it would be
extremely damaging to the profession and the public
service. It was brought into existence in 1986 during which
medical service was not included. In April 1995, the
national commission, on appeal from Kerala state
commission decided that medical service should be covered
under CPA.
Consumers section 2(d) of CPA defines consumer is a
person who buys goods for a consideration which has been
Purpose of Act
CPA 1986 is not a substitute for the existing civil remedies.
The redressal machinery set up under the CPA 1986 is an
additional facility as stated under section (3) of the act itself.
This section says that the act shall be in addition and not
in derogation of provision of any other law for the time
being in force.
The CPA was brought into existence for the protection
of interest of the consumer and for the settlement of
consumer disputes with limited time frame and with fewer
expenses. This enables consumer to make a complaint to a
redressal forum in respect of defective service, if the service
has been paid for.
It provides for establishment of consumer councils and
other authorities for the settlement of consumer disputes
and for matter connected therefore.
The district, state and national commission empowered
as quasi-judicial bodies has been established which looks
into complaints of consumers where deficiency of service
have come to the notice. These quasi-judicial bodies observe
the principle of natural justice and are empowered to give
relief of specific nature and award, wherever appropriate,
compensation to consumer.
Advantages
Freeadministration of justice under the CPA is totally
free. Consumer court do not levy court fee in respect of
legal proceedings.
Speedy justiceconsumer courts are expected to deliver
speedy justice.
Own lawyeryou can be your own lawyer before
consumer courts, though appointment of lawyer is not
prohibited. Consumer court does not encourage
appearance of lawyer and extensive long-winded
arguments.
Procedural simplicityprocedural simplicity and
amicable atmosphere prevailing in consumer courts is
more encouraging to an ordinary litigant as compared
to lengthy and procedure oriented civil court proceedings.
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Procedure
Filing of complaintcomplaint is filed by consumer or
any voluntary consumer organization registered under
Society Registration Act, 1860 or under Company Act,
1056.
What complaint meanscomplaint means any allegation
in writing made by complainant in regard to one or more
of the following:
That he has suffered loss or damage as a result of any
unfaired practices adapted by any doctor.
The service mentioned in complaint suffers from
deficiency in any respect.
Timing of complaintas provided under section 24(A) of
CPA the complaint has to be filed within two years from
the date on which cause of action arises. The complaint
has to be filed in any redressal forum subject to its
jurisdiction.
Contain of complainta complaint should contain
Name and description and address of complainant.
Name and description and address of opposite party.
The fact relating to complaint and when, where it
arose.
Document if any in support of allegation containing
the complaint.
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50
Forensic Dentistry
Introduction
Record Management
Contentthe dental record is a legal document of dentist
which contains information about subjective and
objective finding of the patient. It also includes pathological report, radiographs, and clinical photographs of
the patient.
Treatment plantreatment plan which is given to the
patient should be updated in the record. All the letter of
reference, letter of consent, insurance and financial
statement should be store in the record of the patient.
Progress notethe progress note of the patient should
contain information about the restorative and therapeutic procedure which are carried out on to the patient.
Record of telephonic conversationsummaries of the
telephonic conversation with the patient, consultant,
insurance company representative and legal authorities
should be maintained in the record.
Signing of recordrecord should be signed by the
personnel. Any change made in the record should not
erased but a line should be crossed on it, so that it is
readable. This will help to remove any fraud intention
to alter record.
Electronic maintenance of dental recordit is common
nowadays that dental record to be maintained
electronically. Nowadays some software programs are
developed to maintain patient dental information. This
is advantageous as it can be easily networked and
transferred.
Storage of recordrecord should be kept minimum of 7 to
10 years. In the case pediatric patient record should be
maintain until the patient reaches the age to maturity.
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Identification
Forensic odontology is concerned with the identification
of both living and deceased person.
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Problems in Identification
Condition of material recovered
It depends upon the circumstances surrounding the
death and the care exists in its collection and transport.
Incineration produces damage to teeth ranging from mild
scorching of the surface to severe charring of the enamel
and dentine with crumbling of the crown.
Sustained very high temperature will result in
calcinations of the teeth with considerable overall
shrinkage.
Burnt teeth are usually very fragile and suffer separation
of the enamel and often gross disintegration of the
crowns.
In high impact accidents such as aircraft and high speed
road crashes much mechanical damage can occur and
teeth and jaws may fracture and disintegrate.
Failure to recover significant material may result in
failure to identify a body.
Errors in examinationerrors can easily be made in the
examination and recording of the postmortem dental
material.
Inadequate antemortem dataerrors in charting teeth
treated and insufficient descriptive details about the
treatment provided are common. Other difficulty arises
when a dentist has retired and destroyed his records.
X-ray
All bodies which are found under suspicious circumstances and which are rendered unrecognizable due to
prolonged immersion in water, burning by fire and acid or
by any other destructive means such as explosion should
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The CAPMI (computer-assisted postmortem identification) system compares dental record of victims of mass
disaster and enables rapid identification of air crash, flood
and explosion victims. Radiography can provide
information in relation to age, sex, race, and occupation,
diagnosis of certain conditions and identification and cause
of death.
AgeAge can be established by radiography of bones and
teeth (for root calcification). Calcification of costal cartilage
and osteoarthritic changes in large joints and the spine
also help.
Sex and racemay be deduced by radiography in some cases.
Occupationthis can sometimes be deduced from X-ray.
The whole range of pulmonary occupational diseases such
as silicosis, asbestosis may show specific radiographic
findings. The radial artery in laborers using pneumatic
drill may show calcification; coal carriers and professional
wrestlers are liable to calcified lesions of the ligamentum
nuchae. Football players may show calcified hematoma of
the thigh muscle.
Identificationit is possible by comparison of postmortem
and antemortem X-ray (Fig. 50-3).
Cause of deathfracture of bones seen on X-ray may indicate
their antemortem origin and these include depressed
fracture of skull, fracture of hyoid, fracture dislocation of
cervical vertebrae, severe injury to bones by cutting
instrument or fracture of several ribs which are incompatible
with life. Foreign bodies in the upper respiratory tract
provide valuable clue. Evidence of poisoning by heavy
metals and signs of diseases such as malignant growth
may be apparent.
UV Rays
An ultraviolet lamp can be used to locate and define tattoo
marks and scars on burned and decomposed remains, and
to segregate bones in cases of mix-up. When examined by
UV light washed blood stains are readily seen and seminal
stains give a bluish white fluorescence.
Postmortem Serology
A known postmortem grouping of an individual serves to
narrow the range of possible identities. Even in putrefied
bodies, blood group antigen may be detectable for
serological studies. The bone marrow in skeletal remains
may still retain serologically detectable antigens.
DNA Profiling
This is useful if suitable tissue (blood, semen stored in bank)
is available. If such tissue is available a DNA profiling or
autopsy derived tissue should be compared by single probe
analysis with that of parent, children, sibling and if be
necessary other relatives. This is now used worldwide in
aircraft and other major accidents. The techniques which
are used for DNA profiling are Restriction fragment length
polymorphism (RFLP) and polymerase chain reaction
(PCR). RFLP results in splitting source DNA into thousand
of fragment. PCR can do evaluation of denture DNA or
minute quantity of DNA.
Age Assessment
Chronological age assessment may be an important factor
in establishing the identity of the living or deceased person.
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Bite Marks
Definition
A bite mark is a patterned injury produced by teeth on
animate or inanimate objects, is caused by small enamel
defects on the incisal edge of incisor teeth creating individual
characteristics during biting procedures. It can be:
Tooth markmark left by a tooth (human or non-human).
Arch markmark produced by four or five adjacent teeth
in the same arch (Fig. 50-4).
Causes
Child abuseit can be found anywhere on the body,
favorite sites being the arms, hands, shoulders, cheeks,
buttocks and trunk. Most of the time it is inflicted by the
mother.
Sexual assaultsit usually occurs in cases of rape. Most
common site of it is breast and nipples but neck,
shoulders, thighs, abdomen, pubis and even vulva may
be attacked.
It may also be inflicted on police officers when attempting
to arrest resisting offenders.
Sportsbites can occur in sporting events especially
football and some forms of wrestling. In this, it can occur
anywhere but hands, fingers, nose, forearms, ears and
even lips may be target.
Self inflictedfalls onto the face or a fit may cause the
tongue and lips to be badly bitten. Some persons
deliberately bite themselves, sometime to fabricate
injuries for a variety of motives ranging from gain to
psychiatric disorders.
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The doctor should be asked how the bite mark may be best
preserved. When the substance is plastic such as butter,
cheese, lard, or chocolate, it should be stored in a refrigerator
to prevent melting or gradual flowing. It should not be deep
frozen as this may cause brittleness and cracking. Fruits
should be preserved in Campden solution, a metabisulphite
fluid used for fruit bottling. If it is not there then 5% acetic
acid in 40% aqueous formaldehyde solution can be used.
Whatever preservation is recommended, the object
should be adequately photographed with film plane at
right angles to the bite and a scale placed in the focal plane.
Death freezes a bite mark but a subdermal hemorrhage in
living person disappears within 20 minutes hence it is
important to take an immediate photograph of the bite mark.
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Fig. 50-11: Bite mark of suspect is taken.
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Professional Misconducts
Adultery.
Improper conduct or association with patient or member
of patients family.
Conviction by court of law.
Issuing false certificates.
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Suggested Reading
1. Barsley RE. Forensic and Legal Issue in Oral Diagnosis. Dent
Clinic of North Am 1993;37:143-44.
2. Jakush J. Forensic Dentistry. JADA 1989;119:355-68.
3. Standish SM, Stimson PG. Forensic Dentistry Legal Obligation
and methods of identification for the practitioner: Dent Clin of
North Am 1977;21:1-196.
4. Neville, Damm, Allen, Bouquot. Oral and Maxillofacial Pathology
(2nd edn), 2004; Saunders Elsevier.
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51
1051
Controversial Diseases
and Terminologies
Introduction
As there is changing era with more advance diagnostic
technology coming up, nomenclature of some of the diseases
should be revived and changed. In dentistry, there are many
disease names which are nowadays either discarded or
had been given new names. But, as it is being said difficulty
lies not in new ideas but escaping old one, we many times
not accept the newer terms and stick to older ones. This
chapter will give emphasis on some of older terminologies
and why it should not be used.
Some of the diseases in this chapter are described in
detail. The reason for this is that in many parts of the world
these terminologies are still used. But as a practice, we
should start using new terminologies to avoid confusion
in mind of budding dental professionals.
Why Discarded
Bowens disease nowadays synonymous with carcinoma
in situ. Histologically, Bowens disease is characterized by
disorganized growth, presence of large hyperchromatic
nuclei and multinucleated cells which are the same features
that are seen in carcinoma in situ.
Leontiasis Ossea
Bowens Disease
It is localized intraepidermoid carcinoma that may progress
to invasive carcinoma over many years, which is characterized by progressive scaly or crusted plaque-like lesion.
Etiology
Sun exposurethis is thought to be causative factor for
the Bowens disease.
Arsenic ingestionaccidental ingestion of arsenic can
lead to this disease.
Clinical Features
Age and sex distributionit is common in older age group
with more predilections for males.
Locationit occurs on male and female genital mucosa
and in oral mucosa as erythroplakia, leukoplakia or
erythematous lesion.
Etiology
Bone diseasemost cases of leonine face are result of bone
disease from two conditions i.e. fibrous dysplasia and
Pagets disease.
Metaphysial dysplasiabilateral and symmetrical
involvement of the face and jaws may be seen in
some cases of metaphysial dysplasia and in diphysial
dysplasia.
Periostitis of jaw bonesome cases of leonine ossea are
due to periostitis of the jaw bones or it may be due to
osteitis fibrosa.
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Clinical Features
Why Discarded
Nowadays this term is never used as it requires a lot of
imagination to see lion in it.
Primordial Cyst
It is one of the less common types of odontogenic cysts.
Origin
Radiographic Features
Radiodensitythe affected bones vary in size and density.
Appearancethere may be symmetrical thickening and
increased density of the bones without any leonine faces.
Mandibular lesionsthere is tendency of mandible to
present a characteristic appearance. The inferior
margins of the bone, deep to bicuspid and molar region
projects downward, perhaps very markedly, while the
incisor area is either unchanged or only slightly deeper
than normal.
W appearancethe effect of altered configuration of the
mandible is that it represents a rough caricature of the
letter W.
Cumulus cloudthe surface of the bony projection from
the inferior aspect of the mandible may present irregular
appearance resembling the cumulus cloud.
Nosethe nasal bone is often thickened and nasal
septum may or may not be involved.
Frontal bonein some cases there is marked prominence
of frontal bone over the orbits.
Facethere is gross deformity of the face, with large mass
of bone projecting from the mandible on one side and
another, from the opposite paranasal region.
Skullthe base of the skull tends to be either granular in
structure or homogeneous and structureless, but very dense.
Clinical Features
Occurrenceless common and account for only 5% to
6% of cysts of the odontogenic variety.
Age and sexit is found in children and young adult
between 10 and 30 years of age, although it may persist
in older age group and occurs with equal frequency in
both the sexes.
Siteit can arise in any portion of the jaw, but most
often seen in the ascending ramus of the mandible and
in third molar area. It is occasionally associated with an
over-retained erupted deciduous tooth.
Symptomsit has a tendency to painlessly enlarge and
slowly replace large portions of cancellous bone before
expansion of the cortical plate by way of which it reveals
its presence. Pain which is associated with a large cyst
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Radiographic Features
Radiodensitycyst-like radiolucency that is well defined
and have hyperostotic borders.
Internal structureit may be unilocular or have a
scalloped outline that gives it a multilocular appearance
(Fig. 51-1).
Teethit produces deflection of adjacent tooth root, but
seldom cause any root resorption. The involved tooth is
missing because of failure of the tooth to develop.
Those in maxilla are smaller than their mandibular
counterparts.
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Clinical Features
Why Discarded
Nowadays this term is not used and this cyst is thought to
be odontogenic keratocyst.
Radiographic Features
Globulomaxillary Cyst
It is also called intra-alveolar cyst. It occurs in
globulomaxillary area. There is evidence that the cyst
acutely forms in the bone suture between the premaxilla
and maxilla, the incisive suture, so that location may be
different. Due to this Ferenczy has suggested the term
premaxilla-maxillary cyst.
Pathogenesis
Fissural cystit was considered to be an inclusion or
developmental cyst that arises from entrapped nonodontogenic epithelium in globulomaxillary suture
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Origin
Fig. 51-3: Crop OPG showing radiolucency in lateral and canine
region causing the divergence of teeth (Courtesy Dr Ashok L).
Differential Diagnosis
Lateral periodontal cystradiographically, it appears as
a dome-shaped radiolucency more commonly seen in
mandibular lateral incisor and first premolar region
occurring in an older age group.
Lateral dentigerous cystit is commonly associated with
impacted teeth. The radiolucency is associated with the
crown (attached to the neck of the tooth).
Primordial cystit is more common in mandibular
posterior region.
Giant cell granulomait is more common in anterior
region. Usually, it appears as a mandibular multilocular
radiolucency.
Clinical Features
Siteit has got predilection for the inferior part of the
mandible, in the central incisor region.
Symptomsmost are clinically asymptomatic and are
discovered only during routine radiographic examination.
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Radiographic Features
Appearanceit is unilocular, well-circumscribed
radiolucency, although it appears multilocular.
Shapethe image is well defined, round or ovoid
radiolucency that may be regular or irregular in shape.
Lamina durathe lamina dura around the lower incisor
teeth is intact.
Teethas it expands, it diverges the roots of the
mandibular incisors.
Why Discarded
This cyst is discarded as there is no possibility to have epithelial
entrapment during embryonic fusion in mandible.
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Differential Diagnosis
Radicular cystvitality test and periapical radiographs
demonstrate intact lamina dura and normal periodontal
ligament space in median palatine cyst.
Palatal space abscesssoft, fluctuant swelling and yield
pus on aspiration and non-vital teeth found adjacent to
it which give rise to infection.
Incisive canal cystit occurs in canal above palatine
papillae while midpalatine cyst occurs in midline of
palate posterior to palate.
Retention phenomenonseen laterally and not in midline.
Aspiration would not yield amber colored fluid but
viscous clear sticky liquid.
Malignant and benign tumors of salivary glandlaterally
and not in midline.
Why Discarded
This cyst is nowadays thought to be posterior extension of
nasopalatine cyst.
Clinical Features
Siteit is very rare and develops in the midline of the
hard palate posterior to pre-maxilla.
Symptomspatient notices the swelling in the midline
of palate posterior to palatine papilla. It is usually
asymptomatic but some patients may complain of pain.
Signsit is fluctuant and non-tender. Overlying mucosa
is normal. Corticated plate may be perforated as the cyst
grows. Expansion is rare in this cyst.
Teethmaxillary teeth are vital and aspiration produces
amber colored fluid.
If floor of nasal fossa is eroded, cyst may be superiorly
displaced.
Radiographic Features
Siteradiolucent lesion is behind the incisive canal in
premolarmolar area.
Marginswell-defined borders which are hyperostotic.
Appearancenasal septum image crosses the septum and
appears on occlusal radiographs.
Teethin some cases, divergence of teeth may occur.
Origin
Dental epitheliumthe close resemblance of the columnar
cells to ameloblasts and the frequent association of the
tumor with unerupted teeth indicate its origin from
dental epithelium.
Types
Peripheral adenomatoid odontogenic tumor
Central adenomatoid odontogenic tumor
Follicular typeit is associated with embedded tooth
Extrafollicular typeit is not associated with
embedded tooth.
Clinical Features
Incidenceit represents 3% of odontogenic tumors and
is a developmental outgrowth of odontogenic tissue.
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Radiographic Features
Radiodensitywell-demarcated mixed radiolucent or
opaque lesion.
Sitetumor surrounds the entire tooth, most often canine
in the maxilla. Radiolucency usually extends apically
beyond the cementoenamel junction.
Marginit may or may not be well circumscribed.
Borders are sclerotic.
Internal structureunilocular radiolucency but may
contain faint to dense radiopaque foci which may be
seen peripherally as the lesion matures (Fig. 51-5). Dense
cluster of radiopacities appear as small pebbles.
Differential Diagnosis
Dentigerous cystit is seen in 2nd to 4th decade as
compared to adenomatoid odontogenic tumor which is
seen in young age. It is seen in posterior region as
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Cementoma
It is a true neoplasm of functional cementoblasts, which
forms large masses of cementum or cementum-like tissue
on the tooth root.
Clinical Features
Age and sexit occurs most frequently under the age of
25 years and with no significant sex predilection.
Sitemandible is affected three times more frequently
than the maxilla. Mandibular first molar is the most
frequently affected tooth (Fig. 51-7); other involved teeth
are the mandibular second and third molars.
Symptomsassociated tooth is vital unless coincidentally involved. In some cases, pain may be there.
Signlesion is slow growing and may cause expansion
of cortical plates of bone. Periapical cementomas are
multiple.
True Cementoma
Earlier students were told the true cementoma represents
benign proliferation of cementoblasts present in roots of
premolar and molar teeth.
Gigantiform Cementoma
This is rare case of large round radiopaque mass seen in
jaws.
Radiographic Features
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Clinical Features
Pathogenesis
Radiographic Features
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Differential Diagnosis
Ameloblastomait is more common in older age group
and in the mandibular posterior region.
Giant cell granulomamore common in the anterior
region.
Central hemangiomait is more common in the mandible
and it shows profuse hemorrhage if aspirated. Bruit is
heard in such lesion.
Multilocular cystit is more common in the mandibular
posterior region of jaw and also the borders of the lesion
are well defined.
Odontogenic myxomait is more frequently associated
with congenitally missing or unerupted tooth. It shows
a typical honeycomb appearance.
Cherubismit occurs in a younger age group and it is a
bilateral lesion.
Metastatic tumorit occurs in older age group.
Giant cell lesion of hyperparathyroidismmore common
in the older age group. Serum shows high levels of
alkaline phosphatase.
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Hand-Schuller-Christain
Disease, Letterer Siwe Disease,
Eosinophilic Granuloma and
Histiocytosis X
It is an inflammatory reticuloendothelioma condition with
evidence suggesting that it may be reaction to some type of
infection. There is pathological accumulation of histiocytes
and eosinophilic leukocytes.
Eagle Syndrome
In this syndrome there is neck pain associated with
elongated calcified styloid process.
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Suggested Reading
1. Ellis JD, et al. Aneurysmal bone cyst of the maxilla. J Oral Surg
34; 26:1972.
2. Gruskin ES, et al. Aneurysmal bone cysts of the jaws. J Oral Surg
26;523:1968.
3. Oliver LP. Aneurysmal bone cyst-Report of a case. Oral Surg
35;67:1973.
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Causes and
Classifications
Classifications of Diseases
White Lesions
Variation in structure and appearance of normal mucosa
Leukoedema
Fordyces granules
Linea alba
White lesion with definite precancerous potential
Leukoplakia
Erythroplakia
Tobacco keratosis, actinic keratosis
Lesion associated with electrogalvanism
Carcinoma in situ
Verrucous carcinoma
Lichen planus
Lichenoid reaction
Oral submucus fibrosis
Dyskeratosis congenita
Lupus erythematosus
Acanthosis nigricans
Precancerous lesion
Leukoplakia
Erythroplakia
Palatal lesion associated with reverse smoking
Verrucous hyperplasia
Carcinoma in situ
Precancerous condition
Traumatic keratosis
Focal epithelial hyperplasia
Psoriasis
Geographic tongue
Pachyonychia congenita
White sponge nevus
Hereditary benign epithelial dysplasia
Stomatitis nicotina
Hyperkeratosis palmoplantaris with gingival hyperkeratosis
Darriers disease
Intraoral skin grafts
Pseudoxanthoma elasticum
Hyalinosis cutis et mucosa oris
Oral condyloma acuminatum
Hairy leukoplakia
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Papillary hyperplasia
Granular cell tumor
Discoid lupus erythematosus
Median rhomboid glossitis
Keratoacanthoma
Necrotizing sialometaplasia
Juxtaoral organ of Chievitz
Chronic hyperplastic candidiasis
Verruciform xanthoma
Verruca vulgaris
Condyloma acuminatum
Hemangioma
Sturge-Weber syndrome
Rendu-Osler-Weber disease
Hereditary hemorrhage telangiectasia
Median rhomboidal glossitis
Geographic tongue
Melkersson-Rosenthal syndrome
Crohns disease
Purpura
Polycythemia
Agranulocytosis
Polyarteritis nodosa
Leukemia
Dermatological
Fungal
Atrophic candidiasis
Angular cheilitis
Acute pseudomembranous candidiasis
Sideropenic dysphagia
Lichen planus
Oral submucus fibrosis
Syphilis
Discoid lupus erythematosis
Xeroderma pigmentosum
Epidermolysis bullosa
Infection
Bacterial
Scarlet fever (red fever)
Gonococcal stomatitis
Vincent infection or gingivostomatitis
Acute pharyngitis, tonsillitis
Allergic/Immunological
Pyogenic granuloma
Giant cell epulis
Pregnancy tumor
Traumatic hemangioma
Inflammatory fibrous hyperplasia
Desquamative gingivitis
Precancerous conditions
Viral
MeaslesKopliks spot
Lymphnodular pharyngitis
Herpes simplex infection
Herpes zoster
Herpangina
Chickenpox
Hand-foot-mouth disease
Pemphigus
Erythema multiforme
Stevens Johnson
Lichen planus
Lichenoid reaction
Epidermolysis bullosa
Psoriasis
Lupus erythematous
Uremic stomatitis
Diabetes stomatitis
Scurvy
Pernicious anemia
Ulcerative stomatitis
Atrophic leukoplakia
Erythroplakia
Squamous cell carcinoma
Carcinoma in situ
Kaposis sarcoma
Hemangioendothelioma
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Erythema multiforme
Stevens-Johnson syndrome
Cysts of the Oral Cavity
Odontogenic
Developmental
Primordial cyst
Odontogenic keratocyst
Gingival cyst of infant
Gingival cyst of adult
Lateral periodontal cyst
Dentigerous cyst
Eruption cyst
Calcifying epithelial odontogenic cyst
Inflammatory
Radicular cyst
Periodontal cyst
Inflammatory collateral cyst
Paradental cyst
Non-odontogenic
Nasopalatine cyst
Median palatine cyst
Median alveolar cyst
Median mandibular cyst
Globulomaxillary cyst
Nasolabial cyst
Nasoalveolar cyst
Simple bone cyst
Hemorrhagic bone cyst
Vesicular lesion
Non-febrile lesion
Recurrent herpes labialis
Recurrent herpes stomatitis
Reiters syndrome
Contact stomatitis
Impetigo
Dyskeratosis congenita
Febrile lesion
Herpetic gingivostomatitis
Herpangina
Hand-foot-mouth disease
Chickenpox
Herpes zoster
Smallpox
Bullous lesion
Pemphigus
Familial benign chronic pemphigus
Bullous pemphigoid
Benign mucous membrane pemphigoid
Epidermolysis bullosa
Dermatitis herpetiformis
Dermoid
Epidermoid
Branchial
Thyroglossal
Anterior median lingual cyst
Oral cyst with gastric epithelium
Cystic hygroma
Parasitic cyst, hydatid cyst, cysticercosis cellulosae
Candidiasis
Histoplasmosis
Toxoplasmosis
Cryptococcosis
Geotrichosis
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Mucormycosis
Aspergillosis
Actinomycosis
Odontogenic carcinoma
Malignant ameloblastoma
Primary intraosseous carcinoma
Malignant variant of other odontogenic epithelial tumor
Malignant changes in odontogenic cyst
Bacterial
HIV gingivitis
HIV necrotizing gingivitis
HIV periodontitis
Sinusitis
STD
Odontogenic sarcoma
Ameloblastic fibrosarcoma
Ameloblastic dentinosarcoma
Viral
2nd Classification
Benign
Herpes simplex
Herpes zoster
Hairy leukoplakia
Verruca vulgaris
Condyloma acuminatum
Focal epithelial hyperplasia
Cytomegalovirus infection
Epithelial
With inductive changes in the connective tissue
AOT
Ameloblastic fibroma
Dentinoma
Calcifying odontogenic tumor
Odontoameloblastoma
Odontoma
Without inductive changes in connective tissue
Ameloblastoma
CEOT
Epithelial atypia
Ameloblastic changes in odontogenic cyst
Neoplasm
Kaposis sarcoma
Squamous cell carcinoma
Non-Hodgkins lymphoma
Neurological
Trigeminal neuralgia
Facial palsy
AIDS dementia
Mesenchymal
Odontogenic myxoma
Odontogenic fibroma
Cementoma
Periapical cemental dysplasia
Cementifying fibroma
Benign cementoblastoma
Miscellaneous
Malignant
Odontogenic Tumor
1st Classification
Benign odontogenic tumor
Odontogenic epithelium without odontogenic ectomesenchyme
Ameloblastoma
Squamous odontogenic tumor
Pindborg tumor
Clear cell odontogenic tumor
Odontogenic epithelium with odontogenic ectomesenchyme with or
without dental hard tissue formation
Ameloblastic fibroma
Ameloblastic fibro-odontoma
Ameloblastic fibrodentinoma
Odontoameloblastoma
Adenomatoid odontogenic tumor
Complex and compound odontome
Odontogenic ectomesenchyme with or without included
odontogenic epithelium
Odontogenic fibroma
Odontogenic myxoma
Benign cementoblastoma
Epithelial
With inductive changes in connective tissue
Ameloblastic fibrosarcoma
Ameloblastic odontosarcoma
Without inductive changes in connective tissue
Malignant ameloblastoma
Primary intraosseous carcinoma
Malignant changes in odontogenic cyst
Benign Tumors of the Jaw
Odontogenic tumors
Epithelial
Ameloblastoma
Adenoameloblastoma
Enameloma
Pindborg tumor (CEOT)
Mesenchymal
Dentinoma
Cementoma
Cementoblastoma
Mixed
Ameloblastic fibroma
Ameloblastic fibro-odontoma
Ameloblastic odontoma
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Odontogenic myxoma
Compound composite odontoma
Complex composite odontoma
Odontogenic fibroma
Developmental
Dense invaginatus or dilated odontome
Dense evaginatus
Oncocytoma
Oxyphilic adenoma
Warthins tumor
Pleomorphic adenoma
Classification of Tumor
Epithelial
tumors
Non-odontogenic tumors
Epithelial tissue
Papilloma
Keratoacanthoma
Adenoma
Fibrous connective tissue
Fibroma
Myxoma
Fibrous hyperplasia
Fibrous epulis
Fibrous histiocytoma
Mesenchymal
Cartilage
Chondroma
Chondroblastoma
Chondromyxoid fibroma
Adipose tissue
Lipoma
Bone
Osteoma
Osteoid osteoma
Osteoblastoma
Exostosis and tori- torus palatinus, torus mandibularis
Enostosis
Vascular tissue
Hemangioma
Lymphangioma
Glomus tumor
Hemangiopericytoma
Neural tissue
Neurofibroma
Neurilemmoma
Schwannoma
Ganglioneuroma
Traumatic neuroma
Melanotic neuroectodermal tumor of infancy
Muscle
Leiomyoma
Rhabdomyoma
Myoblastoma
Giant cell tumors
Central and peripheral giant cell tumor
Giant cell granuloma
Giant cell reparative granuloma
Giant cell tumor of hyperthyroidism
Mixed tumors
Tissue of origin
Benign
Malignant
Squamous
epithelium
Transitional
epithelial
Glandular
epithelium
Basal cell layer
Neuroectodermal
Hepatocyte
Squamous cell
papilloma
Transitional cell
papilloma
Adenoma
Squamous cell
carcinoma
Transitional cell
carcinoma
Adenocarcinoma
Adipose tissue
Adult fibrous tissue
Embryonic fibrous
tissue
Cartilage
Bone
Synovium
Skeletal muscle
Smooth muscle
Mesothelium
Blood vessels
Lymph vessels
Glomus cell
Meninges
Hemopoietic cell
Lymphoid tissue
Nerve sheath
Nerve cell
Salivary gland
Liposarcoma
Fibrosarcoma
Myxosarcoma
Chondroma
Osteoma
Benign synovioma
Rhabdomyoma
Leiomyoma
Chondrosarcoma
Osteosarcoma
Synovial sarcoma
Rhabdomyosarcoma
Leiomyosarcoma
Mesothelioma
Angiosarcoma
Lymphangiosarcoma
Hemangioma
Lymphangioma
Glomus tumor
Meningioma
Neurilemmoma
Ganglioneuroma
Invasive meningioma
Leukemia
Malignant lymphoma
Neurogenic sarcoma
Neuroblastoma
Pleomorphic
adenoma
Malignant salivary
gland tumor
Mature teratoma
Immature teratoma
Teratoma
Adipose tissue
Liposarcoma
Cartilage
Chondrosarcoma
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Lipid
Gauchers disease
Niemann-Pick disease
Vascular
Hemangioendothelioma
Malignant
Wegeners granulomatosis
Midline lethal granuloma
Hodgkins disease
Neural tissue
Neurosarcoma
Neurofibrosarcoma
Muscle
Leiomyosarcoma
Rhabdomyosarcoma
Localized
Marginal
Papillary
Discrete
Lymphoid tissue
Hodgkin and non-Hodgkin lymphoma
Lymphosarcoma
Reticular cell sarcoma
Ewing sarcoma
Burkitts lymphoma
Multiple myeloma
Leukemia
Syphilis
Yaws and Bejel
Tuberculosis
Leprosy
Melkersson Rosenthal syndrome
Heerfordts syndrome
Blastomycosis
Coccidioidomycosis
Cryptococcosis
Rhinosporidiosis
Pyostomatitis vegetans
Actinomycosis
Candidiasis
Aspergillosis
Mucormycosis
Lymphogranuloma venereum
Granuloma inguinale
Non-lipid
Eosinophilic granuloma
HandSchllerChristian disease
Letterer-Siwe disease
Chronic
Local irritants
Calculus
Food lodgment area
Occlusal trauma
Mouth breathing
Overhanging restoration
Foreign bodies
Poor oral hygiene
Infection
Bacterial
Viral
Fungal
Fusospirochetal
Parasitic
Saprophytic
Non-specific
Periapical granuloma
Pyogenic granuloma
Peripheral and central giant cell granuloma
Foreign body granuloma
Traumatic granuloma
Crohns disease
Pulsating granuloma
Histiocytosis
Generalized
Diffuse
Marginal
Papillary
Allergy
Non-inflammatory
Familial or hereditary
Developmental
Congenital
Idiopathic
Drug induced
Dilantin sodium
Phenobarbitone
Nifedipine
Cyclosporine
Combined
Conditional
Hormonal (puberty and thyroid dysfunction)
Leukemic enlargementmyelogenous or monocytic
Polycythemia vera
Vitamin C deficiency
Non-specific conditional enlargement
Epulisfibrous
Epulis fissuratum
Eosinophilic granuloma
Plasma cell granuloma
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Crohns disease
Peripheral giant cell granuloma
Wegeners granulomatosis
Cyst
Eruption
Gingival
Neoplastic
Benign
Fibroma
Granular cell myoblastoma
Papilloma
Hemangioma
Peripheral ameloblastoma
Peripheral odontogenic fibroma
Endogenous
Malignant
Squamous cell carcinoma
Fibrosarcoma
Reticular cell sarcoma
Melanoma
Malignant lymphoma
Malignant hemangioendothelioma or hemangioendotheliosarcoma
Metastasis from lung, colon, testis, kidney and cervix
Syndrome associated with gingival hyperplasia
Rutherford
Cannons disease
Cross
Zimmermann-Laband
Cowdens
Papillon Lefevre
Tuberous sclerosis
Sturge-Weber
Melkersson-Rosenthal
Oral Pigmentation
1st Classification
Exogenous
Occupational
Lead industrylead
Match industryphosphorus
Fluorescent lamp industrymercury
Photographysilver
Physiologic
Ethnic, racial variation
Physiologic melanotic macule and papule
Fordyces granules
Postmenopausal changes in sex hormones
Pregnancy
Pathological
Addisons disease
Acromegaly
Peutz-Jeghers syndrome
Lentigo
Nevi (intradermal, compound, junctional, blue)
Neurofibromatosis
Metastatic carcinoma
Malnutrition
Acanthosis nigricans
Cyanosis
Hemolytic anemia
Jaundice
Hemochromatosis
Hemosiderosis
Porphyria
Carotenemia
Hematoma-ecchymoses-varicosities-purpura
Niemann-Pick disease
Diabetic melanosis
Simmonds disease
2nd Classification
Habits
Tobaccoin the form of smoking, chewing and snuff dipping
Pancatechu, pan and pan masala
Foodfood stuff, black berries, blue grapes, coloring agent
of sweets and chocolates
Therapeutic
Drugsanti-malarial drugs and contraceptives
Metallic saltsgold for tuberculosis, bismuth for diarrhea,
silver for nasal drop, mercury for diuretic
Others
Amalgam tattoos
Other self made tattoosgraphite, methylene blue
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Appearance
History
Age
Frequency
Melanoplakia
No symptoms
Birth to 1 year
Common in dark
race
Amalgam tattoo
Macule on gingiva or
edentulous ridge
Common
Recent trauma
bleeding diathesis
Young children
Occasional
Melanotic macule
41-42 years
M/F 1:2.2
Superficial spreading
melanoma
Enlarging macule on
palate or maxillary sinus
Several years
Slowly enlarging
Rare M/F=2:1
Junctional nevus
Mean age 38
Malaise anemia
Working age
Rare
Peutz-Jeghers syndrome
Melanin intestinal
polyposis
Distinct at puberty
Rare
Albright syndrome
Skeletal endocrine
Firm lesions
Amalgam fragment
Macule on gingiva or
edentulous ridge
Common
Late hematoma
Previous trauma
Occasional
Slowly expanding
Occasional
Pigmented lesion
Occasional
Intramucosal nevus
Rare
Compound nevus
Same
Same
Same
Melanoma
Pigmented or amelanotic
nodule polypoid mass on
palate and maxillary gingiva
Rapidly enlarging
Neuroectodermal tumor
Slowly expanding
mass in anterior
maxilla
Birth to 1 year
Rare
Inflammatory
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Intrinsic
Mucus retention cyst (mucocele)
Serous cyst
Pseudo cyst
Extrinsic
Odontogenic
Radicular
Dentigerous
Primordial
Keratocyst
Non-odontogenic
Globulomaxillary
Traumatic
Aneurysmal bone cyst (ABC)
Syphilis
Yaws and Pinta
Gonorrhea
Genital herpes
Genital warts
Nonspecific genital infection
Trichomoniasis
Pediculosis pubis
Scabies
Molluscum contagiosum
Chancroid
Lymphogranuloma venereum
Lymphogranuloma inguinale
Hepatitis B
Cytomegalovirus inclusion body
Infectious mononucleosis
AIDS
Fibrous dysplasia
Leontiasis ossea
Vulvovaginal candidiasis
Trichomoniasis
Vaginitis, cervicitis and cystitis
Bacterial vaginosis
Intestinal protozoa infection
Ectoparasitic skin infection
Toxoplasmosis
Malaria
Babesiosis
Trypanosomiasis
Autoimmune Disorder
Associated with Mucocutaneous Lesion
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Salivary gland
Mikuliczs disease
Sjgrens syndrome
Disorders of platelet
Purpura
Idiopathic thrombocytopenic purpura
Secondary thrombocytopenic purpura
Thrombotic thrombocytopenia
Drug-associated thrombocytopenia
Thrombocytopathia
Glanzmanns thrombasthenia
von Willebrands disease
Bernard-Soulier syndrome
Aldrich syndrome
Blood disorder
Pernicious anemia
Purpura
Collagen disorder
Systemic lupus erythematous
Scleroderma
Rheumatic arthritis
Miscellaneous
Thrombocytosis
Myasthenia gravis
Dermatomyositis
Oral submucus fibrosis
Disorders of coagulation
Blood Disorders
Disorders of RBC
Deficiency
Iron deficiency anemia
Pernicious anemia
Normocytic anemia
Aplastic anemia
Hemolytic anemia
Fibro-osseous Lesions
Lesions arising from periodontal ligament
Extra-corpuscular causes
Infection and toxin
Hypersplenism
Rh factor incompatibility (hemolytic disease of newborn,
erythroblastosis fetalis)
Chronic liver disease
Autoimmune diseases
Transfusion reaction
Intra-corpuscular causes
Hereditary spherocytosis
Sickle cell anemia
Thalassemia
Cooleys anemia
Glucose-6 phosphate dehydrogenase deficiency
Pyruvate kinase deficiency
Folic acid and B12 deficiency
Polycythemia
Relative
Secondary
Vera (malignant)
Disorders of WBC
Qualitative
Lazy leukocyte syndrome
Chdiak-Higashi syndrome
Quantitative
Agranulocytosis
Cyclic neutropenia
Hemophilia A
Hemophilia B
Factor XI deficiency
Factor X deficiency
von Willebrands disease
Fibrous dysplasia
Monostotic
Polyostotic
Familial
Fibro-osseous neoplasm of uncertain origin or debatable origin
Cementoblastoma
Osteoblastoma
Osteoid osteoma
Juvenile ossifying fibroma
Fibro-osteoma or osteofibroma
Cementifying fibroma
Pagets disease
Ossifying fibrous epulis
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Darriers disease
Peutz-Jeghers syndrome
Dyskeratosis congenita
Hereditary benign intraepithelial dyskeratosis
Pachyonychia congenita
Hyalinosis cutis et mucosa oris
Pseudoxanthoma elasticum
Non-infective disease
Vesicular
Erythema multiforme
Pemphigus
Benign mucous membrane pemphigoid
Bullous pemphigoid
Epidermolysis bullosa
Bullous Lichen planus
Non-vesicular disease
Lichen planus
Benign migratory glossitis
Collagen disorder
Lupus erythematous
Scleroderma
Polyarteritis nodosa
Vasculitis
Ischemic lingual necrosis
Wegner granulomatosis
Midline lethal granuloma
Degenerative and relative disorder
Amyloidosis
Oral submucous fibrosis
Senile solar elastosis
Pigmentation
Racial pigmentation
Endocrinopathy
Addison disease
Albert syndrome
Bronze diabetes
Anemia
Oral Hamartomas
Odontogenic
Those involving teeth
Dens invaginatus
Dens evaginatus
Talons cusp
Those not involving teeth
Enameloma
Odontoma
Gigantiform cementoma
Dental lamina cyst of newborn
Non-odontogenic
Epithelial origin
Epstein pearls and Bohns nodule
Inflammatory
Acute and chronic
Staphylococcus
Streptococcus
Actinomycosis
Tuberculosis
Viral infection
Mumps
Cytomegalovirus inclusion disease
Para-influenza
Sarcoidosis
Melkersson-Rosenthal syndrome
Heerfordts syndrome
Allergy
Secondary to sialolithiasis
Post-irradiation to oral tumor
Salivary fistula
Sialolithiasis
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Syndrome
Mucocele
Ranula
Lymphoepithelial cyst
Branchial cyst
Freys syndrome
Developmental
Sialadenosis
Non-inflammatory swelling of salivary gland
Sjgrens syndrome
Necrotizing sialometaplasia
Traumatic
Neoplasms
Benign epithelial
Adenoma
Oncocytoma
Warthins tumor
Pleomorphic adenoma
Malignant epithelial
Adenocarcinoma
Mucoepidermoid carcinoma
Adenocystic carcinoma
Acinic cell carcinoma
Malignant pleomorphic adenoma
Trauma to disc
Trauma to developing condyle or growth center
Trauma to ligament
Subluxation or dislocation or dislocation within displacement
Ankylosis
Foreign body in the joint space
Trauma to muscle
Inflammatory
Infective
Pyogenic infection from staphylococci
Syphilis
Tuberculosis
Actinomycosis
Rheumatic arthritis
Osteomyelitis
Psoriasis
Secondary to hepatitis B infection
Mesenchymal benign
Hemangioma
Lymphangioma
Neurofibroma
Schwannoma
Xanthoma
Lipoma
Non-infective
Stills disease
Systemic lupus erythematosus
Ankylosis spondylitis
Synovitis
Malignant mesenchymal
Rhabdomyosarcoma
Hemangioendothelioma
Others
LymphomaHodgkin and non-Hodgkin
Metastatic
Non-articular arthritis
Myositis
Myositis ossificans
MPDS
Gout
Chondrocalcinosis
Oxalosis
Amyloidosis
Wilsons disease
Gauchers disease
Neoplasms
Neoplastic
BenignWarthins tumor
Malignantlymphoepithelioma (epithelial) and malignant
lymphoma, Burkitts lymphoma, non-Hodgkin lymphoma
and leukemia (connective tissue)
Benign
Osteoma
Chondroma
Osteochondroma
Fibromyxoma
Synovioma
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Neuropathic
Charcoat joint
Ritters sympathetic dystrophy
Enamel Pathology
Internal derangement
Developmental
Disc displacement
Disc fracture
Amelogenesis imperfecta
Dens invaginatus
Enameloma
Environmental pathology
Traumatic
Attrition
Abrasion
Erosion
Enamel caries
Pit and fissure
Smooth surface
Caries at cementoenamel junction
Infection
Pigmentation
Tuberculosis
Syphilis
Leprosy
Blastomycosis
Sarcoidosis
Histoplasmosis
Candidiasis
Aspergillosis
Actinomycosis
Cryptococcosis
Mucormycosis
Rhinosporidiosis
Lymphogranuloma
Endogenous
Exogenous
Enameloma
Dentin Pathology
Developmental
Cystic
Dentinogenesis imperfecta
Dentinal dysplasia
Regional odontodysplasia
Dentin hypocalcification
Dentinal caries
ABC
Traumatic bone cyst
Calcifying epithelial odontogenic cyst (CEOC)
Neoplastic
Dentinoma
Odontoma
Metabolic
Hyperparathyroidism
Pagets disease
Fibrous dysplasia
Cherubism
Histiocytosis
Regressive changes
Secondary dentin
Dentinal sclerosis
Verrucous-papillary Lesion
Neoplasms
Reactive lesion
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Aglossia or hypoglossia
Ankyloglossia
Bifid tongue
Lingual polyp
Macroglossia
Midline fistula
Teratoma
Median rhomboid glossitis
Infectious
Bacterial
Fungal and saprophytic
Parasitic
Viral
Cystic
Epidermoid
Dermoid
Lymphoepithelial
Mucus
Anterior median lingual cyst
Gastric mucosal cyst
Parasitic cyst
Bronchogenic cyst
Neoplastic
Benign
Fibroma
Granular cell myoblastoma
Glomus tumor
Leiomyoma
Rhabdomyoma
Neurofibroma
Keratoacanthoma
Traumatic neuroma
Papilloma
Pyogenic granuloma
Adenoma
Hemangioma
Lymphangioma
Malignant
Squamous cell carcinoma
Adenocarcinoma
Transitional cell carcinoma
Verrucous carcinoma
Mucoepidermoid carcinoma
Reticular cell carcinoma
Lymphosarcoma
Angiosarcoma
Kaposis sarcoma
Melanoma
Rhabdomyosarcoma
Leukoplakia
Erythroplakia
Lichen planus
Oral submucus fibrosis
Candidiasis
Psoriasis
Focal epithelial hyperplasia
White sponge nevus
Pemphigus
Syphilitic mucus patches
Verruca vulgaris
Neurological
Dyskinesiainvoluntary movements
Glossodynia
Trigeminal neuralgia
Glossopharyngeal neuralgia
Polyneuritis
Neurofibromatosis
Tongue thrusting
Dysgeusia
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Miscellaneous
Congenital
Syphilis
Amyloidosis
Melkersson Rosenthal syndrome
Papillon Lefevre syndrome
Traumatic bite
Pulp calcification
Hypervitaminosis
Chronic osteomyelitis
Systemic sclerosis
Dystrophic calcification in areas of tissue necrosis
Arteritis
Polyarteritis nodosa
Midfacial granuloma syndrome
Wegners granulomatosis
Stewart type of midfacial granuloma
Giant cell arteritis
Radiation arteritis
Lymph nodes
Chronic infection (tuberculosis)
Calcification following necrosis
Calcification in metastatic tumor
Vascular hamartomas
Sialoliths
Telangiectasia
In submandibular gland
In minor salivary gland
Antroliths
Hemangioma
Lymphangioma
Eagles syndrome
Osteomas
Osteoma cutis
Osteoma of the tongue
According to duration
In maxillary antrum
Calcified ligament
Ossifying fibroma
Calcifying epithelial odontogenic cyst
Calcifying epithelial odontogenic tumor
Cementifying fibroma
Calcifying fibroma
Hemangioendothelioma
Hemangiopericytoma
Kaposi sarcoma
Angiolymphoid hyperplasia with eosinophils
Kimuras disease
Acute
Acute herpetic stomatitis
Acute aphthous stomatitis
Erythema multiforme
Allergy
ANUG
Herpes zoster
Herpangina
Chronic
Traumatic ulcer
Tuberculosis ulcer
Syphilitic ulcer
Actinomycosis ulcer
Erosive lichen planus
Malignant ulcer
Recurrent
Recurrent aphthous ulcer
Recurrent herpetic stomatitis
Cyclic neutropenia
Allergic reaction
Erosive lichen planus
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Blood disorders
Agranulocytosis
Cyclic neutropenia
Polycythemia
Leukemia
Aplastic anemia
According to Etiology
Local trauma
Trauma due to sharp and malposed teeth
Trauma due to appliance or restoration
Trauma due to epileptic seizure
Trauma during whooping cough
Trauma from injecting needle
Chemical irritant
Local use of chemical agents like phenol, TCA, formocresol,
eugenol, phosphorus
Local use of caustic drugs
Thermal
Hot foods (pizza burn)
Hot instrument
Reverse smoking
Cold ice, CO2 snow or local anesthetic or ether spray
Actinic radiation
Infection
Viral
Herpes simplex
Herpes zoster
Chickenpox
Smallpox
Measles
Rubella
Hand foot and mouth disease
Herpangina
Acute lymphonodular pharyngitis
Infectious mononucleosis
AIDS
Bacterial
Tuberculosis
Syphilis
ANUG
Scarlet fever
Diphtheria
Fungal infection
Candidiasis
Histoplasmosis
Blastomycosis
Mucormycosis
Cryptococcosis
Allergy
Local (stomatitis venenata)
Systemic (stomatitis medicamentosa)
Neoplastic
Squamous cell carcinoma
Mucoepidermoid carcinoma
Basal cell carcinoma
Melanoma
Malignant lymphoma
Nutritional deficiency
Vitamin B complex
Protein deficiency
Diabetes mellitus
Uremia
Metal poisoning
Xerostomia
Gastric hyperacidity or peptic ulcer
Constipation or malabsorption syndrome
Histiocytosis-X
Disease of unknown origin
Aphthous ulcer
Erythema multiforme
Epidermolysis bullosa
Systemic lupus erythematosus
Lichen planus
Pemphigus
BMMP
Acrodermatitis enteropathica
Syndrome
Stevens-Johnson
Behcets
Reiters
Disorders of Teeth (WHO)
Abnormalities of size and form
Concrescence
Fusion
Gemination
Dens evaginatus
Dens in dente
Dens invaginatus
Enamel pearls
Peg shaped
Taurodontism
Tuberculum paramolar
Macrodontia
Microdontia
Mottled teeth
Dental fluorosis
Mottling of enamel
Non-fluoride enamel opacity
Disturbances in tooth formation
Aplasia and hypoplasia of cementum
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Amelogenesis imperfecta
Dentinogenesis imperfecta
Odontogenesis imperfecta
Dentinal dysplasia shell teeth
Microdontia
Supernumerary teeth
Idiopathic
Peg shaped lateral
Cleft lip and palate
Hereditary hypohidrotic ectodermal dysplasia
Radiotherapy during childhood
Hypopituitarism
Malformed crown
Disturbances in tooth eruption
Dentia praecox
Natal teeth
Neonatal teeth
Premature eruption of tooth
Premature shedding of primary tooth
Retained primary teeth
Supernumerary teeth
Distomolar
Fourth molar
Mesiodens
Paramolar
Supplementary teeth
Mesiodens
Enamel hypoplasia
Peg shaped lateral incisor
Turner tooth
Talon cusp
Amelogenesis imperfecta
Dens evaginatus
Dentinogenesis imperfecta
Regional odontodysplasia
Congenital syphilis
Vitamin D resistant rickets
Renal osteodystrophy
Hypoparathyroidism
Epidermolysis bullosa
Radiotherapy during childhood
Anodontia
Enamel loss
Hypodontia
Oligodontia
Embedded teeth
Impacted teeth
Teething syndrome
Color change during tooth formation
Caries
Attrition
Abrasion
Erosion
Amelogenesis imperfecta
Dentinogenesis imperfecta
Extrinsic stain
Causes
Teeth Pathology
Tobacco
Coffee, tea
Cold drink
Chromogenic bacteria
Hyperdontia
Idiopathic
Cleft lip and cleft palate
Gardners syndrome
Cleidocranial dysplasia
Intrinsic discoloration
Hypodontia
Idiopathic
Cleft lip and palate
Hereditary hypohidrotic ectodermal dysplasia
Incontinentia pigmenti
Radiotherapy during childhood
Aging
Death of pulp
Fluorosis
Tetracycline
Internal resorption
Calcific metamorphoses
Dentinogenesis imperfecta
Amelogenesis imperfecta
Congenital erythropoietic porphyria
Erythroblastosis fetalis
Macrodontia
Idiopathic
Fusion
Gemination
Facial hemihyperplasia
Gigantism
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Cryptococcosis
Toxoplasmosis
Taurodontism
Enamel pearl
Benign cementoblastoma
Radiotherapy during childhood
Dentinogenesis imperfecta
Dentin dysplasia type I
Necrosis
Chemicals like phosphorus, arsenic
Osteoradionecrosis
Noma
Internal resorption
Taurodontism
Dentinogenesis imperfecta
Regional odontodysplasia
Vitamin D resistant rickets
Hypophosphatasia
Dentin dysplasia type II
Odontogenic cysts
Radicular
Residual
Dentigerous
Primordial
Lateral periodontal cyst
Gingival
Pulpal calcification
Non-odontogenic cysts
Early exfoliation
Trauma
Aggressive periodontitis
Immunocompromised stages
Diabetes mellitus
Osteomyelitis
Cyclic or chronic neutropenia
Langerhans cell disease
Dentin dysplasia type I
Regional odontodysplasia
Papillion-Lefevre syndrome
Down syndrome
Hypophosphatasia
Scurvy
Neoplasm
Benign
Malignant
Endocrine and metabolic disorders
Fibrous dysplasia
Pagets disease
Hyperthyroidism
Histiocytosis
Caffeys disease
Pregnancy tumor
Leontiasis ossea
Mucocele
Tumor
Necrotizing sialometaplasia
Traumatic
Developmental
Torus palatinus
Hyperplasia of palatal gland
Inflammatory
Periapical, periodontal, gingival abscess of anterior maxillary
teeth
Osteomyelitisacute and chronic
Syphilis
Tuberculosis
Actinomycosis
Quinsy (peritonsillar abscess)
Infected cyst
Mucormycosis
Aspergillosis
Miscellaneous
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Neoplasm
Traumatic
Allergy
Urticaria
Angioneurotic edema
Allergic macrocheilia
Tumors
Metastasis
Inflammatory
Periapical, pericoronal
Osteomyelitis
Periostitis
Cellulitis
Ludwigs angina
Tuberculosis
Actinomycosis
Congenitaldouble lip
Miscellaneous
Amyloidosis
Keratoacanthoma
Papillomatosis
Tuberous sclerosis
Melkersson-Rosenthal syndrome
Papillon Lefevre syndrome
Cheilitis glandularis
Hematoma
Fracture of alveolar process in symphysis region
Denture granuloma
Foreign body granuloma
Epulis on lingual aspect of mandibular anterior teeth
Epulis fissuratum, denture irritation hyperplasia
Inflammatory
Lymphadenitis
Swelling of the Lip
Traumatic
Developmental
Inflammatory
Secondary to dental infection
Carbuncle or abscess from mucus glands or hair follicle or
acne
Infected traumatic lesion
Tuberculosis
Leprosy
Syphilischancre-gumma
Actinomycosis
Molluscum contagiosum
Secondary to irradiation
Condyloma acuminatum
Cyst
Mucus extravasation or mucocele
Lympho-epithelial cyst
Epidermoid cyst
Nasolabial cyst
Cysts
Odontogenic
Radicular
Dentigerous
Gingival
Residual
Keratocyst
Primordial
Non-odontogenic
Traumatic
Ranula
Mucocele
Sublingual dermoid cyst
Lympho-epithelial cyst
Cystic hygroma
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Neoplasms
Salivary fistula
First or second branchial arch sinus or fistula
Congenital lip pit
Developmental
Inflammatory
Periapical, periodontal and dentoalveolar abscess pointing
extraorally
Chronic osteomyelitis
Syphilis
Tuberculosis of jaw bone
Actinomycosis
Osteoradionecrosis
Salivary fistula from suppurative sialadenitis
Infected lymph node
Infected cyst
Infection secondary to trauma, injury
Infection of various facial space
Oronasal fistula
Neoplastic
Intraoral malignancy with secondary growth
Salivary gland malignancy
Perforations of the Palate
Congenital
Cleft palate
Inflammatory
Sialadenitis
Sialolithiasis
Sjgrens syndrome
Mikuliczs disease
Salivary gland tumors
Cysts of salivary gland
Allergy
Angioneurotic edema
Swelling of Neck
Lateral neck swelling
Lymphadenitis
Metastatic carcinoma to lymph nodes
Lymphoma
Parotid lesion
Metabolic diseases
Carotid body tumor
Epidermoid cyst
Cystic hygroma
Osteomyelitis
Syphilitic gumma
Tuberculosis
Infection of traumatic and chronic wound
Mucormycosis
Toxoplasmosis
Blastomycosis
Leprosy
Wegeners granulomatosis
Traumatic
Fracture of maxilla
Use of suction disc for dentures
Pizza burn, thermal burn
Neoplasm
Glossodynia
Local causes
Traumatic injury
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Systemic diseases
Diabetes
Neuralgialingual, glossopharyngeal and facial
Neuritis
Nutritional deficiency
Allergy
Anemia
Sjgrens syndrome
Chronic gastritis
Hypothyroidism
Mercurialism
AIDS
Pharyngitis
Habitssmoking, tobacco and catechu
Systemic conditions
Odor from nasopharynxdue to adenoma, rhinitis, sinusitis,
postnasal drip, tonsillitis, tonsillar abscess, pharyngitis
From lung and bronchibronchitis, lung abscess, pulmonary
tuberculosis, lung malignancy
Diseases of gastrointestinal tracthyperacidity, gastritis, peptic
ulcer, malignancy
Metabolic disordersdiabetes, uremia and liver disease
Blood disordersanemia, agranulocytosis, leukemia,
thrombocytopenia
Salivary gland dysfunctions causing xerostomia
Dehydration statesdiarrhea, vomiting, diabetes insipidus,
Drugisosorbide dinitrate, iodine derivatives, diuretics
phenothiazines, immunosuppressive drugs and dimethyl
sulfoxide
Enlargement of Cervical Lymph Nodes
Inflammation and Infection
Psychological
Bacterial infections
Specific bacterial infection
Syphilis
Tuberculosis
Non-specific
Periodontal disease
Pericoronitis
Periapical infections
Viral infections
Infection caused by herpes simplex
Human immunodeficiency virus
Cat scratch disease
Infectious mononucleosis
Fungal infection
Histoplasmosis
Oral candidiasis
Halitosis
Physiological
During infancysweet odor
During development of dentitionpungent odor
Menstruation
Food habitsalcohol, garlic, lemon, other aromatic beverages
or food substances
Old agedue to metabolic changes in periodontal tissue
Hunger breath
Parasitic infection
Rickettsial infections
Pathological
Lymphoma
Allergic conditions
Serum sickness
Primary neoplasm
Metastasis tumors
Oral squamous cell carcinoma
Metastasis carcinoma from the breast
Miscellaneous conditions
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Neoplastic
Intra-articular
Benign
Osteoma
Chondroma
Osteochondroma
Myxoma
Benign giant cell tumor
Trotters syndrome
Inflammatory
Intra-articular
Pyogenic infection
Rheumatic fever
Rheumatoid arthritis
Gout
Tuberculosis
Syphilis
Actinomycosis
Osteomyelitis
Synovitis
Malignant
Osteosarcoma
Chondrosarcoma
Fibrosarcoma
Metastatic carcinoma
Extra-articular
Pericoronitis
Acute and chronic osteomyelitis
Acute and chronic dentoalveolar abscess
Extra-articular
Benign and malignant tumors of mandible and maxilla mainly
in premolar and molar area
Radiographic appearance
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Tetanus
Tetany
Fibrous dysplasia
Pagets disease
Acromegaly
Miscellaneous
Hemorrhage
Systemic
Scurvy
Diabetes mellitus
Septic embolism in bacterial endocarditis
Meningococcemia
Systemic viral infection
Allergy
Anti-coagulant therapy
Graft versus host reaction
Sturge-Weber syndrome
Angular cheilitis
Infections
Candidiasis
Herpes labialis
Unhygienic appliances
Malabsorption syndrome
Diabetes
Change in vertical dimension
Xerostomia
Nutritional deficiency
Anemia
Vitamin deficiency
Protein deficiency
Plummer-Vinson syndrome
Split papule of syphilis
Allergic reaction to lipstick
Cold sore
Local causes
Thrombocytopenia
Thrombocytosis
Thrombasthenia
Glanzmanns disease
Aldrich syndrome
Sialorrhea
Xerostomia
Hemophilia
Christmas disease
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Developmental
Inflammatory
Tumor of salivary gland
Sialolithiasis
Sjgrens syndrome
Mikuliczs disease
Atrophy of gland
Dehydration
Diarrhea
Vomiting
Diuresis
Diabetes insipidus
Congestive cardiac failure
Ascites
Liver cirrhosis
Drugs
Anticholinergic
Antidepressants
Sympathomimetics
Opium derivatives
Antipsychotic
Antihistamine
Diuretics
Sedatives
Digitalis
Steroids
Chemotherapeutic agents
Miscellaneous
Malnutrition
Nutritional and vitamin deficiency
Radiation
Toxemia
Habits (smoking, betel nut chewing)
Chronic alcoholism
Habitstobacco, catechu
Chromogenic bacteria
Poor oral hygiene
Oral drugs
Iatrogenic
Tattoo made by patient
Chlorhexidine mouthwash
Medicaments like AgNO3, iodine, iron
Intrinsic
Macroglossia
Congenital or developmental
Mongolism
Lingual thyroid or polyp
Inflammatory
Syphilis
Amoebic dysentery
Ludwigs angina
Pneumonia
Typhoid
Tuberculosis
Blastomycosis
Infected wound
Actinomycosis
Neoplasms
Hemangioma (diffuse type)
Neurofibromatosis
Lymphangioma (diffuse type)
Systemic
Pellagra
Downs syndrome
Myxedema
Acromegaly
Amyloidosis
Uremia
Gardners syndrome
Diabetes
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Scurvy
Dyskinesia chorea
Melkersson-Rosenthal syndrome
Sturge-Weber syndrome
Hurlers syndrome
Beckwiths hypoglycemia syndrome
Tuberous sclerosis
Psychogenic pain
Anxiety and depression
Delusional or hallucination pain
Hysterical or hypochondriac pain
Orofacial pain
Extra-cranial causes
Dental and oral
Dentinal hypersensitivity
Pain from disorders of pulp
Hyperemia
Acute pulpits
Chronic pulpits
Pain from disorders of periodontium
Mucogingival pain
Stomatitis
Gingivitis
Glossitis
Glossodynia
Osseous and periosteal pain
Dry socket
Periostitis
Osteomyelitis
From disorders of ear and eye
Enlargement of salivary glands
Classification by Bells
Somatic
Superficialmucogingival
Deep visceralmusculoskeletal
Neurogenic
Neuropathyneuralgia and neuritis
Deafferentation syndrome
Psychogenic
Conversion hysteria
Delusional pain
Sloughing Pseudomembranous Necrotic White Lesion
Myofacial pain
Temporomandibular joint arthropathy
Cervical spine disorders
Trotters syndrome
Eagles syndrome
Osteoporosis
Intra-cranial causes
Vascular pain
Migraine headache
Cluster headache
Tension headache
Temporal headache
Carotodynia
Angina pectoris or myocardial infarction
Plaque
Traumatic ulcer
Diffuse gangrenous stomatitis
Diphtheria
Noma
Candida endocrinopathy syndrome
Chemical burns
ANUG
Candidiasis
Eosinophilic granuloma
Superficial abscess
Syphilitic chancre and mucous patches
Osteogenesis imperfecta
Post-menopausal osteoporosis
Hyperthyroidism
Diabetes
Old age
Gonadal osteoporosis
Idiopathic osteoporosis
Renal acidosis
Oxalosis
Acromegaly
Adaptation syndrome
Hypervitaminosis D
Hypovitaminosis C
Depapillation of Tongue
Neurogenic pain
Congenital cause
Paroxysmal
Trigeminal neuralgia
Glossopharyngeal neuralgia
Geniculate neuralgia
Familial dystonia
Epidermolysis bullosa
Dyskeratosis congenita
Endocrine candidiasis
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Developmental
Geographic tongue
Median rhomboidal glossitis
Central papillary atrophy
Chronic trauma
Nutritional and hematological abnormalities
Pellagra
Riboflavin
Conditional deficiency
Plummer-Vinson syndrome
Medication
Antibiotic
Anticholinergic agent
Cancer chemotherapeutic agent
Systemic causes
Congenital hypopituitarism
Congenital hypothyroidism
Down syndrome
Cleidocranial dysplasia
After radiation
Rickets
Chronic candidiasis
Tumor
Squamous cell carcinoma
Epidermoid carcinoma
Systemic causes
Miscellaneous
Diabetes mellitus
Oral submucous fibrosis
Atrophic Lesion of Oral Mucosa of Tongue
Down syndrome
Diabetes mellitus
Neutropenia
Hypophosphatasia
Papillon lefevre syndrome
Ehlers-Danlos syndrome
AIDS related disorders
Developmental
Others
Acrodynia
Neoplasm
Eosinophilic granuloma
Systemic condition
Endocrinediabetes mellitus
Vitamins like B2, B5, B6, B9 and B12 deficiency
Blood disorderspernicious anemia and iron deficiency
anemia
Infection
Syphilis
Chronic candidiasis
Malformed Teeth
Hairy Tongue
Oral submucus fibrosis
Mucocutaneous
Dehydration
Debilitated patient
Long illness
Painful oral condition restricted tongue movement
Use of local and systemic medication like systemic antibiotic,
topical H2O2 and perborate
Loss of space
Polycythemia
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Leukopenia
Infections
Bacterial
Typhoid
Paratyphoid fever
Brucellosis
Tularemia (early)
Basophilia
Blood disorders
Chronic myelocytic leukemia
Chronic anemia
Hodgkins disease
Splenectomy
Infection
Chronic inflammation of accessory tissue
Smallpox
Chickenpox
Protozoal
Malaria
Relapsing fever
Kala azar
Myxedema
Neutrophilia
Acute infection
Hemopoietic disorders
Gauchers disease
Pernicious anemia
Aplastic anemia
Chronic hypochromic anemia
Aleukemic leukemia
Agranulocytosis
Coccal
Bacilli
Fungi
Spirochetes
Virus
Rheumatic fever
Diphtheria
Smallpox
Inflammatory
Chemical agents
Agents commonly producing leukopenia in all patient if given
in sufficient dose
Mustards (sulfur and nitrogen mustards)
Urethane
Busulfan
Benzene
Antimetabolites
Coronary thrombosis
Gout
Collagen vascular disease
Burns
Hypersensitivity reaction
Intoxication
Uremia
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Miscellaneous
Pulmonary infiltration with eosinophilia
Tropical eosinophilia
Polyarteritis nodosa
Rheumatoid arthritis
Sarcoidosis
Certain poison
Malignant tumor of
Inherited
Gastrointestinal tract
Liver
Bone marrow
Idiopathic
Blood disorders
Acute infection
Infectious mononucleosis
Acute infectious lymphocytosis
Infectious hepatitis
Myelocytic leukemia
Polycythemia
Myelofibrosis
Myeloid metaplasia
Chronic idiopathic neutropenia
Hereditary neutrophilia
Miscellaneous
Lymphocytosis
Chronic infection
Tuberculosis
Secondary and congenital syphilis
Undulant fever
Lymphocytic leukemia
Lymphosarcoma
Heavy chain disease
Hemopoietic disorders
Neutropenia
Exanthema
Eosinophilia
Allergic
Bronchial asthma
Urticaria
Angioneurotic edema
Hay fever
Allergic rhinitis
Drug sensitivity
Skin disease
Pemphigus
Dermatitis herpetiformis
Bullous pemphigoid
Parasitic infection
Trichinosis
Echinococcosis disease
Blood disorders
Chronic myelocytic leukemia
Polycythemia vera
Hodgkins disease
Pernicious anemia
Infection
Scarlet fever
Chorea
Erythema multiforme
Malignant disease of any type
Following irradiation
Monocytosis
Bacterial infection
Tuberculosis
Subacute bacterial endocarditis
Syphilis
Brucellosis
Typhoid
Malaria
Rocky Mountain spotted fever
Typhus
Kala azar
Trypanosomiasis
Oriental sore
Blood disorders
Lymphoma
Leukemia
Hodgkins disease
Multiple myeloma
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Sarcoidosis
Ulcerative colitis
Regional arteritis
Periapical scar
Giant cell granuloma
Benign and malignant tumor including secondary metastatic
deposits
Lymphoreticular tumors of bone
Langerhans cell disease
Periapical cemental dysplasia
Surgical defect
Osteomyelitis
Monolocular lesion
Peripheral Plasmocytosis
Infection
Viral
Rubella
Rubeola
Varicella
Infectious mononucleosis
Bacterial
Streptococcal
Diplococcal
Syphilis
Tuberculosis
Protozoal
Malaria
Trichinosis
Serum Sickness
Drugs
Penicillin
Sulfisoxazole
Antitoxins
Equine tetanus
Equine diphtheria
Neoplasm
Hematological
Plasma cell leukemia
Chronic lymphocytic leukemia
Nonhematological
Breast
Prostate
Miscellaneous
Transfusion
Hyperimmunization
Trauma
Radicular cyst
Residual cyst
Dentigerous cyst
Lateral periodontal cyst
Nasopalatine duct cyst
Simple bone cyst
Calcifying epithelial odontogenic tumor
Adenomatoid odontogenic tumor
Primary bone tumors
Secondary metastasis tumor
Multiple myeloma
Eosinophilic granuloma
Fibro-cemento-osseous lesion
Stafnes bone cavity
Multilocular lesion
Odontogenic keratocyst
Ameloblastoma
Ameloblastic fibroma
Ameloblastic fibro-odontoma
Odontogenic myxoma
Central giant cell granuloma
Brown tumor
Cherubism
Aneurysmal bone cyst
Metastatic tumor of the jaw
CEOT
Fibrous dysplasia
Burkitts lymphoma
Squamous odontogenic tumor
Pericoronal Radiolucency
Dentigerous cyst
Ameloblastoma
Calcifying odontogenic cyst
Adenomatoid odontogenic tumor
Pericoronal space
Unicystic ameloblastoma
Ameloblastic fibroma
Envelopmental primordial cyst
Periapical Radiolucency
Inter-radicular Radiolucency
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Malignancy
Lateral periodontal cyst
Median mandibular cyst
Paradental cyst
Furcation involvement
Lateral radicular cyst
Traumatic bone cyst
Odontogenic tumor
Globulomaxillary tumor
Incisive canal cyst
Histiocytosis-X
Osteoradionecrosis
Odontoma
Osteomyelitis chronic
Pericoronal Mixed Lesion
Primordial cyst
Traumatic cyst
Residual cyst
Odontogenic keratocyst
Aneurysmal bone cyst
Cementoma
Central fibroma
Ameloblastoma
Giant cell granuloma
Midpalatal cyst
Cementifying ossifying fibroma
Benign non-odontogenic tumor
Central squamous cell carcinoma
Myxoma
Odontomaintermediate stage
AOT
Keratinizing and calcifying odontogenic cyst
CEOT
Odontogenic fibroma
Eruption sequestrum
Cystic odontoma
Ameloblastic fibroma
Chronic osteomyelitis
Osteoradionecrosis
Fibrous dysplasia
Pagets diseaseintermediate stage
Central hemangioma
Osteoid osteoma
Cementifying and ossifying fibroma
Osteogenic sarcoma
Chondroma and chondrosarcoma
Ossifying subperiosteal hematoma
Calcifying epithelial odontogenic tumor
Variable Radiopacities
Multiple myeloma
Basal cell nevus syndrome
Multiple cyst or granuloma
Histiocytosis-X
Cherubism
Nodular central masses
Neurofibromatosis
Hurlers and Hunters syndrome
Hyperparathyroidism
Osteoporosis
Osteogenic imperfecta
Hypervitaminosis D
Diabetes
Osteomalacia
Leukemia
Pagets disease
Multiple myeloma
Lymphosarcoma
Fibro-cemento-osseous
Fibrous dysplasia
Periapical cemental dysplasia
Gigantiform cementoma
Benign cementoblastoma
Cemeto-ossifying fibroma
Other
Pagets disease
Osteopetrosis
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Generalized Radiopacities
Salivary calculi
Calcified lymph node
Calcified vessels
Phleboliths
Calcified ACE scars
Foreign bodies
Intrabony
Within the soft tissue
On or overlying the skin
Periapical radiopacities
True
Condensing osteitis
Periapical idiopathic osteosclerosis
Mature periapical cementoma
Foreign bodies
Hypercementosis
Periapical abscess
Current orthodontic therapy
Increase occlusal friction
Systemic sclerosis
Sarcoma infiltration
Carcinoma infiltration
Projected
Gardeners syndrome
Fluorosis
Caffeys disease
Adenomatoid odontogenic tumor
Metastatic carcinoma of prostate
von Buchan disease
Osteopetrosis
Sialoliths
Phleboliths
Arterial calcification
Retained root tips
Exostosis tori and periapical osteoma
Calcified lymph nodes
Periapical infections
Fibrous dysplasia
Pagets disease
Osteoporosis
Normal anatomical variation
Hyperparathyroidism
Leukemia
Cushing syndrome
Hypophosphatasia
Osteomalacia
Multiple myeloma
Projected
Anatomic radiopacities
Foreign bodies
Pathologic soft tissue
Arterial calcification
Rhinoliths and antroliths
Parallel type
Onion peel appearance
Eosinophilic granuloma
Chronic osteomyelitis
Codmans triangle
Osteosarcoma
Radiating type
Sunray appearance
Osteosarcoma
Hair on end appearance
Pagets disease
Central hemangioma
Irregular type
Osteomyelitis
Fracture
Osteogenic malignancy
Subperiosteal bleeding
Leukemia
Histiocytosis
Arthritis
Rheumatism
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Typical feature
Ameloblastoma
Pyogenic granuloma
Hour-glass appearance
Hodgkins disease
Psoriasis
Auspitzs sign
Lichen planus
Wickhams striae
Pemphigus
Nikolskys sign
Scarlet fever
Diphtheria
Diphtheritic membrane
Wegeners granulomatous
Strawberry gingivitis
Tetany
Risus sardonicus
Behcets syndrome
Measles
Kopliks spot
Tapir-lips
Bells palsy
Rickets
Pseudoxanthoma elasticum
Hound dog
Name of disease
Honeycomb pattern
Hemangioma, osteosarcoma
Sunray appearance
Tennis racket
Odontogenic myxoma
Moth eaten
Ground glass
Orange peel
Fibrous dysplasia
Cotton wool
Pagets disease
Downward bowing
Cemento-ossifying fibroma
Mass of coral
Antral halo
Acute sinusitis
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Name of disease
Elys cyst
Osteoarthritis
Hyperparathyroidism
Snowstorm appearance
Sialectasis
Codmans triangle
Osteogenic sarcoma
Follicular cyst
Candlestick appearance
Eggshell appearance
Filling defect
Mottled appearance
Permeated type
Globulomaxillary cyst
Multiple myeloma
Dentigerous cyst, traumatic bone cyst, ABC and giant cell tumor
Spiked root
Beaten silver
Thumb print
Fibrous dysplasia
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Name of disease
Starry sky
Rushton bodies
Dentigerous cyst
Reed-Sternberg cell
Hodgkins disease
Junctional nevus
Lichen planus
Neurilemmoma
Primordial cyst
Liesegang ring
Safetypin appearance
Granuloma inguinale
Lipschutz bodies
Anitschkow cell
Henderson-Paterson inclusion
Molluscum contagiosum
Multiple myeloma
Drug effect
Drugs used
Teeth
Discoloration
Tetracycline
Chlorhexidine
Phenytoin
Cytotoxic
Root anomalies
Gingiva
Swelling
Phenytoin
Cyclosporine
Nifedipine
Salivary gland
Dry mouth
Tricyclic antidepressant
Phenothiazine
Antihypertensive
Lithium
Taste
Disturbed
Metronidazole
Penicillamine
Facial movements
Dyskinesia
Phenothiazines
Metoclopramide
Mucosa
Thrush
Ulcers
Lichenoid lesions
Erythema multiforme
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Angle
Condylar neck
Body
Canine region
Symphysis
Ramus
Coronoid process
Maxillary
Fracture type/site
Dento-alveolar
Le Fort I
Le Fort II
Le Fort III
Zygomatic complex
Nasoethmoidal
Orbit
Various lymph nodes in the head and neck region and their area of drainage
Lymph nodes
Area of drainage
Discharge
Occipital
Posterior scalp
Retromandibular
Superficial parotid
Lateral and frontal scalp, lateral ear, external auditory canal, eyelids
Deep parotid
Buccal
Medial eyelids, skin and mucous membrane of the nose and cheeks
Mandibular nodes
Mandibular
Submandibular nodes
Submental
Submandibular nodes
Submandibular
Superficial cervical
Parotid nodes
Internal jugular
Spinal accessory
Supraclavicular nodes
Supraclavicular
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Fibromatosis
Torus
Irritation fibroma
Peripheral fibroma
Myxoma
Neurofibroma
Lipoma
Granular cell myoblastoma
Sialadenitis
Tumor of salivary gland
Eruption cyst
Mucocele
Mucous cyst
Ranula
Gingival cyst
Nasoalveolar cyst
Epidermoid cyst
Cavernous
Capillary hemangioma
Lymphangioma
Cystic hygroma
Parulis
Eosinohilic granuloma
Epulis fissuratum
Peripheral giant cell granuloma
Pyogenic granuloma
Pregnancy tumor
Squamous cell carcinoma
Lymphomas
Leukemia
AIDS
Sourdigestive dysfunction
FetidANUG
Urinousuremia, kidney dysfunction
Acetonediabetes mellitus
Strenchgangrene, necrotic lesion
Fruityafter use of ether for GA
Mousychronic liver dysfunction
Bloodyinternal hemorrhage
Exophytic lesion
Condition
Appearance
Fluctuance
Emtibility
Usual history
Age
Frequency
Black hairy
tongue
No
No
Older
than 40
Occasionally
Mucocele
Nodular swelling
Yes
No
Variation in size
rupture and draining
<40
Occasional
Ranula
Nodular swelling on
floor of mouth
Yes
No
Slowly enlarging
smaller in early
morning
Common in
female
Cavernous
hemangioma
Nodular swelling
Usually not
Yes
Occasional
Yes
No
Occasional
Superficial
hematoma
Same
Yes
No
Displace teeth
slowly enlarging
Occasional
Lymphangioma
Nodular swelling
pebbly appearance
Usually not
Partially
Rare
No
Slowly expanding
mass
40
Rare
Multiple neurofibromatosis
no
Rare
No
Yes
12
Rare
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Distribution
History
Age
Accompanied condition
Special test
Cyanosis
Increased
severity
in excretion
1 month to
2 years
Malaise dyspnea
Chloasma
gravidarum
Increased
brownish
color of skin
Older than 13
Pregnancy
Addison disease
Skin exposed
Hypoglycemia
weakness
decreased
resistance
to stress
18 and older
Adrenocorticoids
insufficiency
ve ACTH test
Slowly increasing,
increased iron
uptake multiple
blood transfusion
older than 35
Liver disease,
diabetes,
adrenal
insufficiency
Argyria
Chronic selfadminister of
silver containing
18 and over
Equilibrium and
hearing problems
headache
Same
Verrucous leukoplakia
Verruca vulgaris
Condyloma acuminatum
Papilloma
Keratoacanthoma
Inflammatory papillary hyperplasia
Verrucous carcinoma
Fine needle
Punch
Scrape
Trephine
Types of biopsy
Commonly used
Aspiration
Curettage
Excisional
Incisional
Bite
Brush
Cone
Core
Endoscopic
Irrigation
Pressure
Shave
Sponge
Feature
Pemphigus
Bullous pemphigoid
Erythema multiforme
Under 50 years
Over 60 years
Over 40 years
Any
100%
20%
100%
50-60%
70%
3%
85%
45%
90-100%
10-15%
Under 1%
Under 1%
Tzanck test
+ve
ve
ve
ve
Immunofluorescence
Intercellular
Basal membrane
Basal membrane
ve
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Term
Definition
Clinical Appearance
Attrition
Abrasion
Erosion
Abfraction
Predisposing factors
Mechanism
Stage
Appearance
Notes
Stage 1
Radiolucent (fibrous)
Stage 2
Mixed stage
Stage 3
Radiopaque
(calcifying stage)
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Current designation
Former designation
Age of occurrence
Lesion distribution
Clinical course
Acute disseminated
histiocytosis
Letterer-Siwe disease
Chronic
disseminated
idiopathic
histiocytosis
Hand-Schuler-Christian Children
disease
Gradual progression,
lesion usually controlled
by surgical removal and/
or low dose radiotherapy
Chronic localized
idiopathic
histiocytosis
Eosinophilic
granuloma
Isolate or multiple
lesion limited to bone
Manifestation considered as
either idiopathic inflammatory
or benign neoplastic
disease; usually controlled
by surgical removal,
although progression into the
chronic disseminated form
can occur
Older children,
adolescents and
young adults
Reaction
Drugs responsible
Xerostomia
Swelling
Nonspecific ulceration
Lichen planus-like
Erythema multiforme-like
Pemphigoid-like
Pemphigus-like
Lupus-like
Nonspecific
vesiculoulcerative
mucositis
Nonsteroidal anti-inflammatory drugs (NSAIDs) (i.e. indomethacin, gold salts, naproxen), meprobamate, methyldopa,
penicillamine, phenylbutazone, propranolol, spironolactone, thiazides, and tolbutamide
Pigmentation
Gingival enlargement
Calcium channel blockers (amlodipine, bepridil, diltiazem, felodipine, isradipine, nicardipine, nifedipine, nimodipine,
nisoldipine, nitrendipine, oxidipine, verapamil), other dihydropyridines (bleomycin), cyclosporine, phenytoin, and
sodium valproate
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1102
Reaction
Drugs
Swelling
ACE inhibitors, penicillin and penicillin derivatives, cephalosporins, barbiturates, and aspirin and
other NSAIDs
Gingival enlargement
Pigmentation
Lupus-like reactions
Pemphigus-like reactions
Pemphigoid-like reactions
Thiol-containing drugs and sulfonamide derivatives are among the most commonly involved
medications, as are the therapeutic classes of Nsaids, cardiovascular agents, antimicrobials,
and antirheumatics
Nonspecific ulceration
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Syndromes of
Oral Cavity
Adaptation Syndrome
It is disease of hormone which respond to stimulation.
Patient may suffer from hypertension, periarteritis nodosa
and other hormone related disorders.
Adrenogenital Syndrome
It occurs due to hyperplasia or tumors of renal cortex.
Pseudohermaphroditism, sexual precocity and virilism in
women or feminization in men.
Oral featurespremature eruption of teeth if the disease begins
in early life.
Aglossia-Adactylia Syndrome
Complete absence of tongue.
Focal enlargement of salivary gland usually in hard palate
area.
Albrights Syndrome
It is also called as McCune-Albright syndrome.
Severe fibrous dysplasia involving nearly all bones of the
skeleton.
Pigmented lesions of the skin (cafe au lait spots).
Endocrine disturbanceshyper-function of one or more
endocrine glands.
Aldrichs Syndrome
It is also called as Wiskott-Aldrich syndrome.
It is characterized by thrombocytopenic purpura, eczema,
and increased susceptibility to infection.
Oral featuresspontaneous bleeding from gingiva and palatal
petechiae can be seen.
Amelo-onycho-hypohidrotic Syndrome
Defective nails and hypofunction of the sweat glands. There
is also seborrheic dermatitis.
Oral featuressevere hypoplastic hypocalcified enamel.
Anderson Syndrome
It is also called as familial osteodysplasia.
Craniofacial and skeletal anomalies.
Angio-osteo-hypertrophy Syndrome
Port-wine stain on the face, varices.
Hypertrophy of bone including jaw bone.
Oral featuresfacial asymmetry, malocclusion and altered
eruption pattern of teeth.
Aperts Syndrome
It is also called as acrocephalosyndactyly.
Skeletal deformitiesthere is syndactyly (fusion of finger) of
second, third and fourth digit of hand and acrobrachycephaly
(tower skull). In some cases kleeblattschadel deformity
(cloverleaf skull). The skull is ovoid, brachycephalic and often
presents a horizontal supraorbital groove.
Facial deformitiesthe middle-third of face is undeveloped.
Oral features
High palatal vault and V-shaped maxillary alveolar ridge.
Trapezoid shaped appearance of lip when lip are relaxed.
There is posterior palatal cleft and bifid uvula.
Retarded eruption and dental malocclusion.
Class II malocclusion.
Aschers Syndrome
Patient is having a double lip.
Blepharochalasis, i.e. drooping of the tissue between the
eyebrow and the edge of upper eyelid.
Non-toxic thyroid enlargement.
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Blepharonasofacial Syndrome
It is characterized by mental retardation, joint disorders and
craniofacial anomalies.
Facial featuresaffected individuals show microcephaly, an
anti-mongoloid slant of palpebral fissures.
Oral featuresthere is also hypoplastic maxilla, protruding
lip and malocclusion resulting form midface hypoplasia.
Books Syndrome
Behets Syndrome
Recurrent oral ulcerationit has similar appearance as
aphthous ulcer.
Recurring genital ulcerationulcer of scrotum and penis in
males and ulcers of labia in females.
Skin lesionsthey are manifested as large pustular lesions.
Ocular lesionsit consist of uveitis, retinal vasculitis, optic
atrophy, recurrent conjunctivitis and keratitis.
Bernard-Soulier Syndrome
It is transmitted as autosomal dominant trait with variable
penetration.
The membrane receptors on platelets are absent and it
accounts for bleeding problems.
The bleeding time is prolonged.
Blepharocheilodontic Syndrome
It is transmitted as autosomal dominant inheritance.
Eye anomaliesit includes lagophthalmus, ectropion of lower
eyelid.
Lipthere is bilateral cleft lip and palate.
Teetholigodontia, microdontia including tiny molars.
Bloch-Sulzberger Syndrome
Erythematous and vesiculobullous lesions on the trunk and
extremities.
These are replaced by white keratotic, lichenoid, papillary or
verrucous lesions.
Brownish gray macules in a streaked, patchy distribution
over the trunk and extremities.
Bowen Syndrome
It is also called as cerebrohepatorenal syndrome.
Craniofacial anomalies, hypotonia, hepatomegaly and renal
cortical cysts.
Oral featuresit includes micrognathia, protruding tongue
and high arched palate.
There is increase serum iron level and decrease in serum
immunoglobulin levels.
Caffey-Silverman Syndrome
It is also called as infantile cortical hyperostosis.
Development of tender deeply placed soft tissue swellings
and cortical thickening or hyperostosis involving various
bones of the skeleton.
There is also pain, fever and irritability in infants.
Increased serum levels of alkaline phosphatase and increased
ESR.
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Cerebrocostomandibular Syndrome
Thoracic deformity with barking cough and mental
retardation.
Oral featuresit includes mandibular micrognathism, palatal
defect and absence of uvula or even soft palate.
Carcinoid Syndrome
Intermittent attack of flushing of skin of face.
Watery diarrhea, abdominal pain, attacks of dyspnea.
Right side heart failure due to involvement of tricuspid and
pulmonary valve and endocardium.
Chediak-Higashi Syndrome
It is transmitted as autosomal dominant trait.
Generalit includes oculocutaneous albinism, photophobia,
nystagmus and recurrent infection of respiratory tract and
skin.
Oralulceration of the oral mucosa, severe gingivitis and
glossitis.
Costens Syndrome
There is impairment of hearing, either continuously or
intermittent.
A stuffy sensation in the ears especially at mealtime.
Tinnitus, otalgia, dizziness and headache about the vertex,
occiput and behind the ears.
Burning sensations in the throat, tongue and side of nose.
Cowdens Syndrome
It is autosomal dominant disease characterized by
facial trichilemmomas associated with gastrointestinal tract,
central nervous system, thyroid and musculoskeletal
abnormalities.
Papillomatous lesion as well as pebbly lesions of lip, gingivae,
palate and pharynx occurs.
Fibromas at various sites in the oral cavity.
Lichenoid and papillomatous lesions of perioral, perinasal
and periorbital areas of ear and neck.
Hematoma of skin, gastrointestinal tract, breast and
thyroid.
Cross Syndrome
Oral featuresit include gingival enlargement.
Other featuresit includes hypopigmentation, oligophrenia,
microphthalmos and athetosis.
CREST Syndrome
Associated with scleroderma
CCalcinosis cutis
RRaynauds phenomenon
EEsophageal dysfunction
SSclerodactyly
TTelangiectasia
Crouzon Syndrome
It is also called as craniofacial dysostosis.
Cranial deformitiesprotuberant frontal region with an
anteroposterior ridge overhanging the frontal eminence and
often passing to the roof of nose (triangular frontal defect).
The cranium is brachycephalic.
Facial malformationsthere is hypoplasia of maxilla with
mandibular proganthism.
Parrot beakthe upper lip is short and nose resembles Parrots
beak.
Oral feature includes high arched palate, V-shaped dental
arch, peg shaped teeth and partial anodontia.
Eye changeshypertelorism, exophthalmos with divergent
strabismus, optic neuritis and choked disc resulting frequently
in blindness.
Othersspina bifida occulta.
Cushings Syndrome
It is characterized by adiposity about the upper portion of
the body, mooning of the face and tendency to become round
shouldered.
Buffalo humpit is seen at the base of the neck.
There is dusky plethoric appearance with formation of purple
striae.
There is also muscular weakness, vascular hypertension,
glycosuria and albuminuria.
Childrenthere may be osteoporosis and premature cessation
of epiphyseal growth.
Curry-Hall Syndrome
Short limbs, polydactyly and nail dysplasia.
Oral featuresdeciduous teeth are small and conical. Incisors
are retained as permanent successors may be congenitally
missing.
Dejerine-Roussy Syndrome
Tumors of the pons or occlusion of the posterior cerebral
artery with sensory or motor abnormality on the
contralateral side.
Oral featuresorofacial pain and dysgeusia are also present.
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Downs Syndrome
Systemic
Cardiovascularthere is ventricular septal defect, ALV
communication, patent ductus arteriosus and mitral valve
prolapse.
Hematological featuresit includes impaired immunodeficiency, short lived neutrophils, risk of lymphopenia,
eosinophilia, increased risk of leukemia and increased risk of
hepatitis carrier state.
Musculoskeletalit includes atlantoaxial instability; midface is
underdeveloped with relative prognathism, narrow and
partially obstructed nasal passage and open mouth with
tongue thrusting habit.
Nervousmotor function is delayed, dementia analogues and
phonation distorted.
Behaviorgentleness, anxiety and stubbornness.
Oral
PalateV-shaped high vault and soft palate insufficiency.
Oral openingangle of mouth is pulled down due to hypotonic
musculature, lower lip is everted, mouth breathing with
drooling of saliva, chapped lower lip and angular cheilitis.
Tonguescalloped or fissured tongue, protrusion with
tongue thrusting, macroglossia and desiccated tongue.
Teethmicrodontia, hypodontia, partial anodontia, supernumerary teeth, spacing, taurodontism, crown variation,
agenesis, hypoplasia and hypocalcification and delayed
eruption of teeth.
Occlusionmalalignment, frequent malocclusion, frequent
TMJ dysfunction and bruxism.
Fanconis Syndrome
Congenital or familial aplastic anemia.
Bone abnormalities, microcephaly and generalized olivebrown pigmentation of the skin.
Eagles Syndrome
Favre-Racouchot Syndrome
Edwards Syndrome
It is also called as trisomy 18 syndrome.
The affected individuals are mentally retard and show
hypertonicity.
Facial featuresthere are small eyes and prominent occiput.
The index finger overlaps the 3rd finger and 5th finger
overlaps the 4th finger.
Oral featuresit includes micrognathia, high arched palate,
cleft palate and bifid uvula.
Ehlers-Danlos Syndrome
It is also called as rubber man and is autosomal dominant.
Generalthere is hyperelasticity of skin, hyperextensibility
of joint and fragility of skin and blood vessels.
Oral featuresit includes enamel hypoplasia and periodontal
destruction is severe. There is also hypermobility of TMJ
resulting in repeated dislocation.
Fragile X Syndrome
X-linked mental retardation, macro-orchidism and large ears.
Long narrow face and cleft palate.
Mitral valve prolapsed.
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Goldenhars Syndrome
Franceschettis Syndrome
Antimongoloid palpebral fissure with colobomas of the outer
portion of the lower eyelids and deficiency of eyelashes.
Hypoplasia of facial bone especially malar bone mandible.
Malformation of external ear and middle ear.
High palate and malocclusion is also present.
Blind fistulae between angle of the ears and angle of mouth.
Typical hair growth in form of tongue shape extending
towards the cheek.
Bird like or fish like appearance.
Gardners Syndrome
Systemic featuresmultiple polyposis of large intestine and
polyp of colon and rectum.
Tumorsosteomas of bone including long bones, skull and
jaws. There may be occasional occurrence of desmoid tumors.
Other tumors which can occur are lipoma, leiomyoma and
adenocarcinoma of colon.
Cystsmultiple epidermoid or sebaceous cyst of skin
particularly of scalp and back.
Oral featureshypercementosis, multiple unerupted
supernumerary teeth and compound odontoma.
Goltz-Gorlin Syndrome
It is also called as focal dermal hypoplasia syndrome. It is
transmitted as an autosomal dominant trait.
General features
Focal absence of dermis associated with herniation of
subcutaneous fat into the defects.
There is also skin atrophy, streaky pigmentation and
telangiectasia.
Multiple papillomas of skin or mucosa.
Syndactyly, polydactyly, and adactyly.
Oral featurespapillomas of lip, microdontia, cleft lip and
cleft palate.
Gorlin-Chaudhry-Moss Syndrome
It is characterized by craniofacial dysostosis, patent ductus
arteriosus, hypertrichosis and hypoplasia of labia majora.
Oral feature of this syndrome is hypodontia.
Gorhams Syndrome
It also called as massive osteolysis or Phantom bone.
Osteolysis of single or multiple bones followed by
replacement with fibrous tissue.
Pain in the bone and pathological fractures.
Oral featuresthere may be destruction of mandible or maxilla.
Pain and facial asymmetry can be seen.
Grinspan Syndrome
It is triad of lichen planus, diabetes mellitus and vascular
hypertension.
Gradenigos Syndrome
Suppurative otitis
Trigeminal nerve pain
Abducens nerve palsy
Hanharts Syndrome
Digital deformitiesit includes oligodactyly, syndactyly and
hypoplastic digits.
Oral featuresthere is micrognathia, microglossia and
hypodontia.
Hallermann-Streiff Syndrome
Skeletal and genitalit includes syndactyly and hypogenitalism.
Facial featuresit includes microphthalmia, long thin tapering
nose, strabismus, and double cutaneous chin with central
furrow, hypotrichosis of the scalp and eyebrows and
prominent scalp veins.
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Heerfordts Syndrome
Firm painless, bilateral enlargement of parotid gland.
Inflammation of uveal tract of the eye.
Facial palsy.
Hetch-Beals-Wilson Syndrome
Limited mandibular opening.
Shortened leg, hamstring muscles and club foot.
Hypoglossia-hypodactylia Syndrome
Total or partial absence of the tongue.
Micrognathia, high arched or cleft palate, glossopalatine
ankylosis, defects in the lower lip and hypertrophy of
sublingual glands.
Hypodactylia and hypomelia.
Jaw-Winking Syndrome
It is also called as marcus gun phenomenon.
Rapid elevation of the ptotic eyelid occurring on movement
of the mandible on the contralateral side.
Congenital unilateral ptosis.
Jadassohn-Lewandowsky Syndrome
Horners Syndrome
Miosis or contraction of pupil of the eye due to paresis of
dilators of pupil.
Ptosis or drooping of eyelid due to paresis of smooth muscle
elevators of upper lid.
Anhidrosis and vasodilatation over the face due to
interruption of sudomotor and vasomotor control.
Hortons Syndrome
It is also called as sphenopalatine neuralgia.
Unilateral paroxysms of intense pain in the eye, maxilla, ear,
mastoid region, base of nose and beneath the zygoma.
Absence of trigger zones and occurrence of pain everyday
exactly at the same time- for this reasons it is called as alarm
clock headache.
Hurlers Syndrome
It is disturbance in mucopolysaccharide metabolism.
Facial featuresprominent forehead, broad saddle nose, wide
nostrils, hypertelorism and puffy eye lids. There is also corneal
clouding present.
There is also nasal congestion with noisy breathing.
Claw hand resulting from flexion contractures.
Hepatosplenomegaly results in protuberant abdomen.
Death usually occurs before the age of 10 years.
Oral featuresthick lips, large tongue, open mouth.
Kartageners Syndrome
Hunters Syndrome
Similar feature like Hurlers syndrome but they are mild.
Corneal clouding is absent.
Death usually occurs before the age of 15 years.
Hutchinson-Gilford Syndrome
It is also called as progeria. It is transmitted as autosomal
dominant trait. There is manifestation of old age features,
pro- before, geria- old.
Alopecia, pigmented areas of trunk, atrophic skin, prominent
vein and loss of subcutaneous fat.
The individual has high pitched, squeaky voice and beak-like
nose.
Oral featuresloss of all teeth in very young age, hypoplastic
mandible, and delayed eruption of teeth can also occur.
Bronchiactasis
Situs in versus
Sinusitis
KBG Syndrome
The affected individual show short stature and mental
retardation.
Facial featuresflat bridge of nose, round face, long philtrum
and abnormal auricle, with or without hearing defect.
Oral featuresinclude macrodontia, oligodontia, hypoplasia
of enamel and micrognathia.
Klinefelters Syndrome
It occurs in males whose sex chromosome constitution
includes one or more extra chromosomes.
The patient develops infertility and gynecomastia.
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Klippel-Trenaunay-Weber Syndrome
Larsens Syndrome
It is an autosomal dominant disorder.
There is prominent forehead with frontal bossing, flattened
midface, depressed nasal bridge and hypertelorism.
There is bilateral anterior dislocation of tibia or femur with
displaced patella.
Oral featuresit includes cleft palate and malocclusion.
Laugier-Hunziker Syndrome
Acquired pigmented macules in the lips, oral cavity and
fingers.
Lowes Syndrome
Generalized aminoaciduria, mental retardation, hypotonia,
congenital cataracts.
Abnormal skull shaped.
Maffuccis Syndrome
Multiple chondroma of the jaw bone.
Multiple hemangiomas of skin and oral mucosa. Phleboliths
can also occur.
In oral mucosa, it occurs on the tongue.
Melkersson-Rosenthal Syndrome
It is triad of cheilitis granulomatosa, facial paralysis and scrotal
tongue.
Mieschers Syndrome
It is also called as cheilitis granulomatosa.
Diffuse swelling of lip especially lower lip.
Scarring, fissuring, vesicle or pustule formation on the
vermilion border.
It is associated with Melkersson-Rosenthal syndrome.
Mobius Syndrome
Marfans Syndrome
Skeletalexcessive length of tubular bone resulting in
disproportionate long thin extremities.
Craniofacialskull and face are long and narrow. Ears are
large, eyes appear sunken and frontal bossing is seen.
Ocularocular lens subluxation with a defect in the
suspensory ligament.
Cardiovascularaortic aneurysm and regurgitation.
Oraltemporomandibular joint dysarthrosis, multiple
odontogenic cysts of maxilla and mandible, high arched palate
and bifid uvula.
Magic Syndrome
Mouth and genital ulcers with inflamed cartilage.
Mohrs Syndrome
It is autosomal recessive disorder characterized by several
oral, facial and digital defects. The affected individual is
moderately short.
Digital deformitiesbrachydactyly, syndactyly or polydactyly.
Facial deformitiesmidline cleft lip and bifid tip of nose.
Oral featuresthere is high arched palate, lobate tongue,
hypoplastic body of the mandible and hypodontia.
Morquios Syndrome
Melnick-Needles Syndrome
It is autosomal dominant condition characterized by
generalized bony dysplasia and abnormal facies.
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Neck-tongue Syndrome
MEN 1
Noonans Syndrome
Congenital heart disease, chest deformity and mental
retardation.
Short stature, facial bone anomalies and cryptorchidism.
Gingival fibromatosis.
Multiple hyaline fibromas of head, trunk and extremities.
Suppurative skin lesions and flexion contractures.
Otopalatodigital Syndrome
Nance-Horan Syndrome
Papillion-lefevre Syndrome
Nagers Syndrome
It is also called as acrofacial dysostosis.
Facial featuresthere is hypoplasia of malar bones, antimongoloid obliquity or palpebral fissures. Also absent
eyelashes, deformed ears, defective hearing, syndactyly and
abnormalities of humerus and radius.
Oral featuresorally, there is cleft palate, micrognathism and
malocclusion.
Para-trigeminal Syndrome
Severe headache or pain in the area of trigeminal distribution
with signs of ocular and sympathetic paralysis.
Pataus Syndrome
It is also called as trisomy 13 syndrome.
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Parry-Romberg Syndrome
It is also called as progressive hemifacial atrophy characterized
by unilateral atrophy of face.
There is also atrophy of skin, subcutaneous tissue, muscle
and bone.
Loss of hair and vitiligo can be seen.
Contralateral jacksonian epilepsy and trigeminal neuralgia
also occur.
Oral featuresatrophy of half of the tongue and retarded
dental eruption on the involved side.
Proteus Syndrome
Skull featureshemihypertrophy of the skull, seldom of other
bones of the facial skeleton.
Partial gigantismpartial gigantism especially of hand and/
or feet, asymmetric limb overgrowth and length discrepancy,
Scoliosisscoliosis of the vertebral column,
Other featureshyperostosis, various tumors, lipoma,
lymphangioma, connective-tissue nevi, and vascular
malformations
Teeth featureslate mixed dentition with an unusual
asymmetric dental development and eruption and crowding
with loss of space in teeth.
Raeders Syndrome
It is also called as paratrigeminal syndrome.
Headache or pain in the area of trigeminal distribution.
Ocular sympathetic paralysis.
Peutz-Jeghers Syndrome
It is also called as hereditary intestinal polyposis syndrome.
There is familial generalized intestinal polyposis.
Pigmentation of face, oral cavity and sometimes on hands
and feet.
There may gastric, duodenal and colonic adenocarcinoma.
Pfeiffer Syndrome
Skeletal deformitiesit includes craniosynostosis with turribrachycephaly, broad thumbs and halluces.
Facial deformitiesmidface hypoplasia, shallow orbit,
hypertelorism, proptosis and antimongoloid obliquity.
Oral featuresit includes maxillary underdevelopment
resulting in mandibular proganthism, high arched palate and
bifid uvula.
Ramons Syndrome
Hypertrichosis, epilepsy and mental retardation.
Gingival fibromatosis and cherubism.
Raley-day Syndrome
Congenital absence of tongue papillae.
Vasomotor dysfunction, loss of reflexes and feeding
problems.
Lack of pain and taste sensation.
Plummer-Vinson Syndrome
Reiters Syndrome
Riegers Syndrome
Portsmouth Syndrome
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1112
Rutherfords Syndrome
Congenital enlargement of the gingivae and altered eruption
of teeth.
There is corneal dystrophy, conjunctivitis and mucocutaneous
lesion.
Rubinstein-Taybi Syndrome
It is associated with talons cusp.
Developmental retardation, broad thumb and great toes.
Delayed or incomplete descent of testes in males.
Sanfilippos Syndrome
Severe CNS defect, mild somatic disturbance.
Enamel hypoplasia and excessive dentinogenesis with
obliteration of pulp chambers.
Saethre-Chotzen Syndrome
It is an autosomal dominant trait characterized by short
stature and mild mental retardation.
Facial deformitiesit includes ocular hypertelorism, ptosis of
eyelids, deviated nasal septum and mild conductive deafness.
Other deformitiesfinger exhibits cutaneous syndactyly and
occasional renal abnormalities can be seen.
Oral featuresit includes prognathism, high arched palate
and resultant malocclusion.
Scheies Syndrome
Stiff joints, corneal clouding, aortic regurgitation and normal
intelligence.
Sturge-Weber Syndrome
Angiomatosis of face (nevus flammeus) and leptomeningeal
angiomas.
There is also intracranial calcifications and contralateral
hemiplegia.
Massive growth of gingiva and asymmetrical jaw growth
and tooth eruption sequence.
Sweet Syndrome
Fever.
Relative increase of neutrophils in the peripheral blood.
Skin lesion such as tender erythematous plaque, nodules,
vesicle and pustules on the face and extremities.
Dense dermal infiltrate with mature neutrophils.
Intraoral ulceration is also seen.
SUNCT Syndrome
Sshort acting
Uunilateral
Nneuralgiform headache
Cconjunctival infection
Ttearing
Scheuthauer-Marie-Sainton Syndrome
It is also called as cleidocranial dysplasia.
Open fontanelle of skull and partial or complete absence of
clavicles.
Underdeveloped maxilla, multiple impacted or unerupted,
permanent or supernumerary teeth.
Senear-Usher Syndrome
Bulla and vesicle on skin and oral mucosa.
Nikolskys sign is positive.
This lesion is terminated in pemphigus vulgaris or foliaceous.
Sjgrens Syndrome
Trotters Syndrome
Stevens-Johnson Syndrome
Trichodental Syndrome
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Trichodentoosseous Syndrome
It is transmitted as an autosomal dominant trait.
Hair and nail deformitiesit includes kinky hair and nails show
white band and are brittle.
Oral featuresit includes hypomaturation type of
amelogenesis imperfecta, enamel hypoplasia, unerupted teeth
and taurodontism. The mandibular angle is obtuse and the
jaw is square.
Trichonychodental Syndrome
It is autosomal dominant trait.
Fine curly hair and thin dysplastic nails.
Oral featurestaurodontism and developmental defect of
enamel and dentin.
Turners Syndrome
Short stature, cabitus vulgus, webbed neck, renal disorders
and sexual infantilism.
Oral featuresit includes micrognathia, high arched palate
and corners of mouth appear pulled down. There is
premature eruption of teeth.
Velocardiofacial Syndrome
Synonymit is also called as Shprintzen Syndrome,
Craniofacial Syndrome, or Conotruncal Anomaly Face
Syndrome. The name Velocardiofacial Syndrome comes from
the Latin words velum meaning palate, cardia meaning
heart, and facies means facial features.
Cleft palatecleft palate (incomplete closure of the roof of the
mouth).
Heart defectmultiple abnormalities of the heart including
Ventricular septal defect (VSD), pulmonary atresia, tetralogy
of Fallot, truncus arteriosus, interrupted or right-sided aortic
arch and transposition of the great arteries.
XXXXY Syndrome
There is hypoplastic midface, short stature, mental
retardation, speckled eyes and hypertelorism.
Oral featuresit includes taurodontism and bifid uvula.
Zimmerman-Laband Syndrome
Gingival fibromatosis and ear, nose and nail defect.
Hepatosplenomegaly and hyperextensible joint.
Zinssers Syndrome
Oral leukoplakia, dystrophic nails and hyperpigmentation of
skin.
Pancytopenia and aplastic anemia.
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Glossary
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Cell mediated immunityit is the type of immunity in which the predominant role is played by T-lymphocytes.
Centralin oral pathology, it is the lesion occurring within bone.
Centromerethe constricted portion of the chromosome that divides the short arms from the long arms.
Chief complaintit is the patients response to the dentists question.
Cheilitisit is the inflammation of lip.
Chemoprophylaxisit is the use of chemical drugs in the prevention of disease.
Chemotherapyit is the treatment of a disease by chemicals which affect pathogenic organisms without harming the patient or it is
the treatment of malignant neoplasia by chemical means.
Cheesylesions texture is similar to curd of cheese.
Chemotaxistaxis or movement in response to chemical stimulation.
Chromatina general term used to refer to the material (DNA) that forms the chromosomes.
Chronicpersisting over a long time; when applied to a disease, chronic means that there has been little change or extremely slow
progression over a long period.
Chillsit is cold sensation with shivering, often characteristic of onset of fever.
Chloromait is a condition characterized by multiple myeloid tumors of greenish color, affecting particularly the face and skull, and
associated with blood picture of leukemia.
Choriostomait refers to excessive amount of normal tissue that is present in abnormal location.
Chondromalaciait is a condition characterized by abnormal softness of the cartilage.
Ciliatedhaving hair like processes or fringe of hair.
Circulationit is the movement or flow in a circle, retracing its course repeatedly, applied especially to the flow of blood through
the body.
Cleft lipit is a birth defect that results in a unilateral or bilateral opening in the upper lip between the mouth and the nose.
Cleft palatecleft palate is a birth defect characterized by an opening in the roof of the mouth caused by lack of tissue development.
Coagulationwhen blood is shed, it loses its fluidity in few minutes and sets into a semisolid jelly. This is called as coagulation or
clotting.
Cold abscessit is a slow developing tuberculous abscess generally about a bone or joint and with little inflammation.
Collar stud abscessit is a superficial abscess connected by a sinus tract to a larger deep abscess.
Complement systemthis consists of a group of serum proteins which by series of reactions produce and release by products
whose functions are to initiate an inflammatory reaction, to regulate and enhance phagocytic function and attack the bacterial cell
membrane.
Congenitalpresent at or before birth but not necessarily inherited.
Coalesceit is a term used to denote to fusion or union of separated parts.
Consanguinityblood relationship. In genetics, the term is generally used to describe marriages among close relatives.
Corrugatedhaving a surface that appears wrinkled.
Cotton woolconfluent radiopacities.
Coarctationit is narrowing or constriction, applied especially to blood vessels.
Colit is a depression in an interdental papilla between the two peaks, one on each side of the contact area.
Comait is a state of complete unconsciousness from which a patient can not be aroused, even by determined external stimulation.
Commensalit is an organism that lives on or within another organism, to its own advantage and without being detrimental to the
host.
Commissureit is the point of union between similar parts or bodies.
Concretionit refers to any hardened or solidified mass in the tissue.
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Diffuseused in the description of a lesion; when borders of the lesion are not well defined and it is not possible to detect the exact
parameters of the lesion, then this term is used.
Diploidhaving two sets of chromosomes; the normal constitution of somatic cells.
Diagnosisit is the determination of the nature or cause of the disease.
Differential diagnosisthe list of similar clinical picture, according to probable identity of condition at hand, is the differential
diagnosis.
Dimorphic anemiait is a condition in iron deficiency and folic acid deficiency anemia can occur concomitantly.
Diploethe spongy layer of bone position between the inner and outer layers of compact bone.
Diverticulithey are small pouches or out pocket of the ductal system of one of the major salivary glands.
Disinfectionthis is the process by which pathogenic microorganisms are removed from the surface, without removing bacterial
spores.
Dilacerationsit refers to angulations or sharp bends or curves in the root and crown of the teeth.
Diseaseit is the departure from the average anatomical structure or is an abnormal degree of failure of physiological function or
some reduction in psychological efficiency, due to either adversity in the genetic endowment of the individual or misuse of his free
will or to adverse factors in the environment in which he lives or some combination of these factors or it is defined as loss of ease.
Distomolarfound in the molar region frequently located distal to 3rd molar.
Discreteseparate. Composed of separate parts, not joined or blended.
Dislocationit is the displacement of any part from its normal position, especially in the cases of bone and joints.
Direct fractureit refers to the fracture that occurs at the site of blow.
DLE (discoid lupus erythematous)it is a circumscribed slightly elevated white patch that may be surrounded by a red telangiectic
halo.
Doseit is one measured portion of any medicine which is to be taken one at a time.
Dominantin genetics, a trait or characteristic that is manifested when it is carried by only one of a pair of homologous chromosomes.
Dorsaldirected towards or situated on the back surface (opposite of ventral).
Dry abscessit is an abscess that disperses without bursting or coming to a head.
Drainageit is the gradual removal of fluid from a cavity or wound.
Dressingit is a medicament used to promote wound healing or as a covering for a wound, used for protection or to assist healing.
Drugit is any medicinal substance.
Drug addictionit is state of periodic or chronic intoxication produced by the repeated consumption of drug and is harmful to
individual and to society.
Drug habituationit is the condition resulting from repeated consumption of drug, in which there is psychological and emotional
dependency on the drug.
Drug dependencea state psychic and sometimes also physical resulting from the interaction between a living organism and a drug,
characterized by behavioral and other response that always includes a compulsion to the drug on a continues or period basis in order
to experience its psychic effect and sometimes to avoid the discomfort of its absence.
Drug abuse/misuseit is the improper or excessive use of therapeutic drugs even in the absence of addiction.
Dyskinesiait is defined as an impairment of voluntary motions, causing movements that are incomplete or only partial.
Dysesthesiait refers to the impairment of feeling or sensations; a condition in which a normal stimulus produces disagreeable
sensations.
Dyskeratosisthis lesion shows abnormal orientation in development of epithelial cells.
Dysodontiasisit refers to the painful, difficult or delayed eruption of the teeth.
Dysostosisit refers to the congenital defective bone formation.
Dysphagiaan experience of having great difficulty in swallowing.
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Erythroplakiathe term is applied to any area of reddened velvety textured mucosa that can not be identified on the basis of clinical
and histopathological examination as a cause of inflammation or any other disease process.
Erythrodontiathere is deposition of porphyrins in dentin and to a lesser extent in the enamel which imparts red or brown color
to the deciduous and permanent teeth and known as erythrodontia.
Erosionit is a shallow crater in the epithelial surface that appears on clinical examination as a very shallow erythematous area with
only superficial changes or a moist red lesion often caused by rupture in vesicles and bullae as well as trauma.
Erosion (teeth)it is loss of tooth substance due to chemical process that does not involve bacterial activity.
Erythroplasiathese are painless erythematous eruptions, papular or macular in nature, affecting the mucous membrane.
Escharit is a dry slough, the result of burning or due to contact with a corrosive agent.
Etiologythe study or theory of the factors that cause disease and their introduction to the host.
Eversiona turning outward or a state being turned outwards.
Excrescenceit refers to an abnormal growth protruding from body or plant.
Exacerbationit refers to an increase in the severity of a disease or any symptoms.
Examinationit refers to investigations carried out for diagnostic purpose.
Exanthemait is an eruptive fever.
Excoriationit is the superficial loss of surface skin or a graze.
Excursionit refers to any movement of a movable part from a resting position during the performance of some functions.
Exfoliationit is the peeling off in layers or in scales.
Exophthalmosit refers to the abnormal protrusion of the eyeball.
Exophyticit refers to a word relating to something growing outwards, used for tumor projecting above the normal surface
contours or it refers to any pathological growth that project above the normal contours of the oral surface.
Expansilecapable of being extended or expanded.
Expressivityin genetics, the degree of clinical manifestation of a trait or characteristic.
Exostosisit is a bony swelling developing on the bone surface or on a tooth root.
Exotoxinit refers to a toxic secretion of bacterial cells which cause damage in sites distant from the focus of infections or they are
heat labile proteins which are secreted by certain bacteria and diffuse readily into surrounding tissue.
Extravasationit is the escape of fluid from vessels into the surrounding tissue.
Extrinsichaving its origin outside and separated from a body, organ or part.
Exudatethe matter that passes out into adjacent tissues through vessel walls in inflammation.
Faciesthe appearance of the face.
Factitial injuriesthese are accidentally self-induced injuries on the basis of habits with frequent psychological backgrounds.
Favorable fractureif the fracture line runs in such a manner that the associated muscle tends to hold the fragments together, the
fracture is described as favorable.
Facetit is a small abraded area on a bone or on tooth surface.
Familialrelating to a family, or affecting several of its members.
Fasciait is the layer of areolar tissue beneath the skin or the layer of areolar tissue investing the muscles, nerves and other organs.
Fenestrateto pierce with one or more holes, sometimes used on the walls of bony defect in an attempt to stimulate repair.
Fenestrationit refers to a surgical procedure by which one or more holes are pierced in hard tissue.
Feverit refers to an abnormal increase in body temperature.
Final diagnosisit is statement with which precise diagnosis has been made on the basis of all required observation, identification
of definitive symptoms and the pathological report and patient response to therapy.
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Periodontitisit is name given to periodontal disease when the superficial inflammation in the gingival tissue extends into the
underlying alveolar bone and there is loss of attachment.
Periodontal abscessan abscess that forms deep in the gums along the tooth root following advanced periodontal disease.
Periodontosischronic non-inflammatory destruction of periodontal ligament and the associated alveolar bone.
Phoenix abscessit an acute exacerbation of a chronic or suppurative apical periodontitis.
Phlegmonacute inflammation of the subcutaneous connective tissue.
Pit- it is defined as hollow fovea or indent blind tracts lined with epithelium.
Pilationit is a hair like fracture found in cranial bones.
Plasmapheresisit is a method of increasing the number of blood cells in the blood count. From the blood plasma is skimmed out
simply on standing and remaining concentrate is reinfused into the patient.
Plaqueit is a solid raised lesion that is over 1cm in diameter.
Pleomorphicthe word pleomorphic means occurring in several distinct shapes.
Pleurodonthaving teeth attached to the side of a bony socket or to the side of the jaw.
Plexusa plexus of nerves or a network of blood or lymphatic vessels.
Pocketit is an abnormal space developing between the tooth root and the gums.
Poisonany substance that when absorbed into the system of a living body is liable to cause injury and to endanger life.
Poikilodermait refers to a combination of atrophy, telangiectasia and pigmentary changes.
Polylophodontthese are teeth with multi-ridged crowns.
Pre-cancerous lesionmorphologically altered tissue in which cancer is more likely to occur than its normal counterpart.
Pre-cancerous conditionit is a generalized state associated with a significantly increased risk of cancer.
Premedicationthe administration of drugs or sedatives before treatment, to help in patient management especially with nervous
patient.
Prescribeto write instruction for the preparation, composition and administration of a medicine.
Prevalencethe number of cases of a disease at any given time in any given place.
Priestleys massa green or brown stain on the anterior teeth of the young or where reduced enamel epithelium remains over the
enamel.
Procheiliait is the condition in which one lip protrudes forwards of its normal position.
Prognosisit is the prediction of the course, duration, and termination of the disease and the likelihood of its response to therapy.
Prosthesisthe word prosthesis is used for a manufactured appliance used to take the place of a natural part or to correct a
congenital abnormality or it may be defined as an appliance which replaces lost or congenitally missing tissue.
Proteolysisthe process of digestion of proteins and its conversion by enzymes into peptones, proteoses, etc.
Protuberancethe word protuberances refers to a swelling, eminence or knob of the tissue.
Pseudomembraneit refers to a false membrane, a skin like layer formed by fibrinous exudates containing leukocytes and bacteria.
Pseudoepitheliomatous hyperplasiain this conditions the rete pegs extend far downward, usually accompanied by acanthosis.
The cells are normal in size, shape and chromaticity.
Psychosomaticrelating to the mind and the body; particularly relating to the interdependence of mental processes and bodily
function.
Pustuleit refers to a raised lesion containing purulent material.
Purpurait refers to reddish to purple flat lesion caused by blood extravasated from a vessel leaking into subcutaneous tissue.
Pulsationit is the rhythmic throb or beating as that of the heart.
Pulsethe expansion and contraction of an artery due to increased tension of its walls following contraction of the heart and
subsequent relaxation.
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Wandering teethit is movement of unerupted teeth for no apparent reasons (distal drift).
Wandering abscessan abscess that tracks through the tissue and finally comes to a point some distance form the original site.
Wealit is a reddish, raised and circumscribed lesion on the skin, generally caused by a blow or a bite.
Working diagnosisfollowing reappraisal of diagnostic data at hand including those of follow-up examination which may be seen
necessary and which may provide new relevant finding and indicating result from any addition diagnostic procedure.
Woundit is any injury to the tissues or organs cause by cut, stab or tear, usually going deeper than the outer skin or integument.
Wolfs lawthis law states that, the bone structure depends on the strain and stresses to which bone is subjected.
Xerostomiait is a subjective clinical condition of less than normal amount of saliva.
Xenograftit is a type of graft derived from a donor of different species.
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Multiple Choice
Questions
B. Herpes ulcer
D. Allergic ulcer
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92. Cafe au lait spots are seen in all of the following disease
except:
A. Neurofibromatosis
B. Fibrous dysplasia
C. Peutz-Jeghers syndrome
D. Addisons disease
93. All are the forms of lichen planus except:
A. Erosive
B. Atrophic
C. Hypertrophic
D. Verrucous
94. Freys syndrome patient exhibit gustatory sweating and
flushing due to damage to:
A. Chorda tympani nerve
B. Auriculotemporal nerve
C. Facial nerve
D. Facial artery
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114. Cherubism is a:
A. Bilateral lesion
B. Unilateral lesion
C. Shows early eruption of permanent teeth
D. Seen at the age of 20-25 years
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153. Regressive changes that occurs in the teeth that starts from
inner surface to outer of the teeth:
A. Abfraction
B. Attrition
C. Erosion
D. Internal resorption
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219. Ranula is a:
A. Retention cyst
C. Begin tumor
B. Implantation
D. Malignant tumor
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226. Sialoliths are the stones found in salivary duct and duct is
mainly composed of:
A. Hydroxyapatite
B. Potassium chloride
C. Unknown compounds of phosphate
D. Calcium chloride
237. A 20 years female came to the clinic with severe pain and
redness over the dorsum of the foot. Past history of severe
abdominal pain episodes were present. Peripheral smear
showed anemia with presence of poikilocytes your likely
diagnosis is:
A. Hemoglobin C disease
B. Thalassemia
C. Sickle cell anemia
D. G6PD deficiency
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1148
1A
2B
3C
4D
5A
6A
7B
8A
9A
10 D
11 B
12 D
13 B
14 C
15 A
16 D
17 C
18 A
19 C
20 A
21 B
22 D
23 A
24 D
25 B
26 B
27 D
28 D
29 B
30 A
31 B
32 D
33 B
34 B
35 A
36 B
37 B
38 A
39 D
40 A
41 B
42 C
43 D
44 B
45 B
46 A
47 D
48 D
49 C
50 A
51 B
52 B
53 A
54 A
55 B
56 B
57 B
58 B
59 B
60 C
61 A
62 B
63 A
64 B
65 A
66 B
67 C
68 A
69 C
70 C
71 C
72 B
73 A
74 A
75 A
76 C
77 C
78 D
79 B
80 D
81 D
82 D
83 C
84 C
85 A
86 B
87 D
88 B
89 B
90 D
91 A
92 D
93 D
94 B
95 B
96 D
97 C
98 D
99 A
100 A
101 A
102 C
103 D
104 B
105 B
106 C
107 D
108 C
109 A
110 B
111 B
112 B
113 B
114 A
115 B
116 A
117 C
118 B
119 C
120 B
121 D
122 B
123 D
124 D
125 A
126 A
127 D
128 A
129 C
130 B
131 C
132 C
133 D
134 D
135 A
136 D
137 D
138 A
139 B
140 A
141 B
142 E
143 B
144 B
145 A
146 B
147 D
148 C
149 D
150 B
151 B
152 B
153 D
154 B
155 C
156 A
157 C
158 B
159 D
160 D
161 B
162 C
163 B
164 D
165 C
166 A
167 B
168 B
169 D
170 B
171 C
172 C
173 B
174 B
175 A
176 B
177 C
178 B
179 A
180 C
181 D
182 D
183 C
184 B
185 C
186 D
187 B
188 B
189 D
190 B
191 B
192 B
193 B
194 D
195 A
196 C
197 C
198 C
199 D
200 D
201 C
202 B
203 D
204 B
205 A
206 C
207 C
208 D
209 D
210 D
211 D
212 D
213 A
214 C
215 B
216 B
217 B
218 B
219 A
220 C
221 C
222 A
223 D
224 A
225 A
226 A
227 C
228 A
229 B
230 C
231 D
232 B
233 A
234 C
235 A
236 B
237 C
238 D
239 A
240 C
241 A
242 C
243 D
244 C
245 C
246 B
247 A
248 A
249 A
250 C
251 C
252 B
253 B
254 D
255 D
256 C
257 A
258 C
259 B
260 D
261 A
262 D
263 B
264 A
265 B
266 D
267 A
268 A
269 A
270 A
271 B
272 A
273 B
274 C
275 B
276 A
277 B
278 A
279 B
280 D
281 D
282 B
283 C
284 B
285 B
286 B
287 D
288 D
289 D
290 A
291 A
292 B
293 B
294 A
295 C
296 A
297 C
298 A
299 C
300 C
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Index
A
Abdominal
actinomycosis 747
striae 889
Aberrancy 643
Abfraction 145
Ablation 202
Abnormal root 1079
Abrasion 49, 143, 1048
Acanthosis nigricans 816
Accessory
duct 645
ligament 604
Accidental pigmentation 508
Achondroplasia 854
Acidogenic theory 517
Acidophilic adenoma 668
Acinic cell
adenoma 672
tumor 672
Ackermans tumor 349
Acquire immunodeficiency
syndrome 859
Acquired immunity 18, 19
Acquired melanocytic nevus 296
Acquired preneoplastic condition 25
Acquired syphilis 733
Acral lentiginous melanoma 347,
348, 499
Acridine binding method 88
Acrocephalosyndactyly 1103
Acrodermatitis enteropathica 952
Acrodynia 510
Acrodysostosis 884
Acrofacial dysostosis 1110
Acromegaly 875, 876
Actinic
cheilosis 566
cheilitis 566
elastosis 570
keratosis 205
lentigo 818
Lichen planus 212
Actinomycin D 991
Actinomycosis 746
Actinomycotic osteomyelitis 472
Active immunity 19
Acupuncture 635
Acute
Acute
Acute
Acute
Acute
Acute
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Angio-osteo-hypertrophy
syndrome 1103
Angioreticuloendothelioma 493,
867
Angiosarcoma 360
Angular cheilosis 564
Angular cheilitis 182, 564, 864,
907, 1085
Ankyloglossia 66, 540
Ankyloglossum superius syndrome
541
Ankylosed deciduous teeth 46
Ankylosing spondylitis 617
Ankylosis 139, 620
Annular lichen planus 211, 212
Annulus migrans 546
Anodontia 124
Anomalous dysplasia 132
Antemortem record 1041
Anterior
alveolar cyst 255
deep temporal nerve 16
disc displacement with reduction
627
disc displacement without
reduction 627
dislocation 624
ethmoid nerve-15
median lingual cyst 259
superior alveolar nerve-16
Anthranilic acid 975
Anti aging factors 931, 941
Antibiotic vitamin 934
Antibiotics 959
sore mouth 180
Antibody 20
Anticancer drugs 988
Anticonvulsant drugs 1028
Antidotal drugs 1030
Antifungal drugs 980
Antigen 20
antibody reaction 20
Anti-hemorrhagic vitamin 942
Antiherpes virus agents 996
Antihypoglycemic drugs 1028
Anti-influenza virus agents 999
Anti-metabolites 990
Antimicrobial dosing principle 961
Antiretroviral agents 998
Antral halo appearance 683
Antral lavage 684
Antral papillomas 688
Antral polyps 687
Antral pseudocyst 684
Antroliths 695
Aortic arch syndrome 1103
Aperts syndrome 1103
Aphthous fever 771
Aphthous pharyngitis 768
Aphthous stomatitis 395
Aphthous ulcer 868
Aphthous ulcer with Behcets
syndrome 396
Apical periodontal cyst 247
Aplasia of salivary gland 644
Aplastic anemia 908
Apparent macroglossia 539
Applied kinesiology 635
Arachnodactyly 853
ARC 863
therapy 378
Arch mark 1044
Argyll Robertson pupil 735
Argyria 511
Argyrosis 511
Arhinencephaly 164
Aromatic ammonia 1029
Arrested caries 529
Arsenism 512
Arterial Hemangioma 311, 313
Arterial supply of tongue 535
Arteriography 643
Arteriovenous
fistula 317
malformation 317
shunt 317
Arthritis 486
Arthroscopy 606
Articular branches 16
Articular disc 603
Aryl-acetic acid derivative 976
Aschers syndrome 558, 1103
Ascorbic acid 934
Ascorbic acid deficiency gingivitis
578
Ash-leaf spot 817
Aspergilloma 782
Aspergillosis 781
Aspiration 78
Aspirin 973
Ataxia telangiectasia 823
Atheroma 724
Atresia 645
Atrial septal defect 793
Atrophic lesion of tongue 1088
Atrophic lichen planus 212
Atrophica idiopathic mucosae oris
217
Atrophy 490
Atropine 1029
Attached denticle 485
Attrition 49, 141
Atypical
facial pain 428
gingivitis 579
gingivostomatitis 579
periodontal disease 865
trigeminal neuralgia 428
Aura phase 808
Auric stomatitis 512
Auricular branches 17
Auriculotemporal
nerve 16
syndrome 804, 1104
Auscultation 55, 78
Auspitzs sign 186
Autofluorescence spectroscopy 88
Autoimmune
disorders 1071
hemolytic anemia 910
Autoimmunity 517
Automutilation 548
Autosedation 437
Autosomal dominant inheritance
153
Autosomal recessive inheritance
153
Autosomes 153
Avulsion 701
Azidothymidine 998
Azithromycin 964
Azlocillin 966
B
B complex vitamin 926
B lymphocytes 441
Baby bottle syndrome 1104
Bacteremia 483
Bacterial
meningitis 480
origin gingival disease 586
sialadenitis 658, 659
Baelzs disease 563
Bartholins duct 639
Basal cell
adenoma 667
carcinoma 345
epithelioma 345
papilloma 294
Baseloid mixed tumor 672
Basic life support 784
Basophilia 1089
Basophilic leukocytosis 915
Bathing trunk nevus 296
Beaking 612
Beaten copper appearance 954
Beaten silver appearance 161
Beauty vitamin 928
Becker disease 820
Beckers nevus 158
Beckwiths hypoglycemic
syndrome 1104
Bednars ulcer 389
Beefy red tongue 908
Behavior management technique
46
Behcets syndrome 410, 1104
Bejel 737
Bell stage 6
Bells palsy 805
Benign
cementoblastoma 284
juvenile melanoma 296, 297
lymphoepithelial lesion 662
melanocytic nevus 296
migratory glossitis 545
mucosa antral cyst 684
mucosal cyst of maxillary
antrum 684
mucous membrane
pemphigoid 404
osteopetrosis 849
tumor of jaw 1066
tumors of TMJ 630
Benzoic acid 986
Beriberi 927
Bernard-Soulier syndrome 1104
Besnier-Boeck-Schaumann
disease 810
Beta thalassemia 905
Betamethasone 1007
Bidigital palpation 55
Biermers anemia 907
Bifid condyle 609
Bifid tongue 541
Bilateral palpation 55
Bilobed appearance 609
Bimanual palpation 55, 67, 642
Binder syndrome 681
Biofeedback 437, 634
Biologic carcinogenesis-27
Biology of tumor growth-28
Biopsy 88
Biotin 932
Bird face appearance 621
Bismuth line 509
Bismuthism 509
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Index 1151
Bruxism 54, 702
Bruxomania 702
Buba 738
Buccal bifurcation cyst 251
Buccal caries 523
Buccal fat pad 10
Buccal gland 640
Buccal pit 523
Buccal space infection 474
Buccolingual masticatory
syndrome 551
Buclosamide 986
Bud stage 5
Budesonide 1007
Buffalo hump 799, 889, 1105
Buffer capacity test 96
Build 56
Bulbar trigeminal tractotomy 431
Bull neck 455, 750
Bulls eye 399
Bullous Lichen planus 211, 212
Bullous pemphigoid 404
Burkitts lymphoma 367
Burning mouth syndrome 435, 1104
Burns 174
Burrow 490
Burtonian line 510
Butenafine 986
C
Caf au lait spot 321, 505, 829
Craniofacial fibrous dysplasia 830
Caffey Silverman syndrome 848,
1104
Caffeys disease 848
Calcific degeneration 485
Calcification of oral soft tissue 1077
Calcified carotid artery 724
Calcified lymph nodes 722
Calcifying ameloblastoma 268
Calcifying epithelial odontogenic
cyst 245, 268
Calcifying fibrous epulis 280
Calcifying ghost cell odontogenic
cyst 245
Calcinosis cutis 822
Calcinosis universalis 822
Calcium 954
Calculus 68
Caliber persistent artery 570
Canalicular adenoma 667
Cancellous osteoma 305
Cancer vaccine 384
Cancrum oris 73, 748
Candidal balanitis 185
Candidal onychia 185
Candidal paronychia 185
Candidal vulvovaginitis 185
Candidial leukoplakia 181
Candidiasis 177, 586, 864, 886
Candidosis 177
Candidosis endocrinopathy
syndrome 1104
Canine space infection 473
Canities 490
Cannons disease 188
Cap stage 6
Capadeponts teeth 130
Capillary blood specimen 97
Capillary fragility test 101
Capillary hemangioma 311, 312
Capillary lymphangioma 316
CAPMI 1043
Capsular ligament 604
Capsular pain 425
Carabelli cusp 737
Carboplatin 993
Carcinogenesis-25
Carcinoid syndrome 1105
Carcinoma 24
Carcinoma ex odontogenic cyst 290
Carcinoma in situ 205
Carcinoma of
buccal mucosa 340
floor of mouth 339
gingiva 588
labial mucosa 340
lip 568
oropharynx 341
palate 341
penis 50
scrotum 49
Carcinosarcoma 351
Cardiac failure 792
Cardiac rhabdomyoma 817
Cardiac toxicity 994
Cardiac transplantation 793
Cardiovascular complaint 1036
Cardiovascular disease 786
prophylaxis 786
Cardiovascular syphilis 735
Caries activity text 95
Caries detector dye 519
Carotene 936
Carotenemia 506, 938
Carotid artery syndrome 433, 1104
Carotid body tumor 434
Carotidynia 428
Carpenters syndrome 1105
Carpet track extension 225
Cat scratch disease 750
Cat scratch fever 750
Cavernous
hemangioma 311, 312
lymphangioma 316
sinus thrombosis 481
Caviar tongue 492
CDC classification for AIDS 861
Cefaclor 967
Cefadroxil 967
Cefazolin 967
Cefixime 967
Ceftobiprole 967
Cefuroxime 967
Celiac disease 955
Cell kill hypothesis of Skipper 988
Cellular blue nevus 495
Cellular immunity 441
Cellular oncogens 29
Cellulitis 453
Cemental caries 525
Cementifying fibroma 842
Cementoma 1057
Cemento-ossifying fibroma 842
Cementum hyperplasia 123
Central cyanosis 59, 65
Central dislocation 624
Central giant cell granuloma 837
Central giant cell tumor 326
Central gumma 736
Central mandibular carcinoma
289
Central mucoepidermoid
carcinoma 671
Central odontogenic fibroma 281
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1152
D
Dacarbazine 990
Dagger shaped calcification 885
Dane system 68
Danger space 479
Dariers disease 190
Darier-White disease 190
Darlings disease 775
Decubitus ulcer 389
Dedifferentiation 351
Deep lymphangioma 316
Deep pain 423
Degenerative arthritis 610
Dejerine-Roussy syndrome 1105
Delayed eruption 46, 136
Delusional pain 435
Dens evaginatus 119
Dens invaginatus 117
Dense bone island 310
Dense in dente 117
Dental amalgam contact allergy 393
Dental arch irregularities 70
Dental crown fracture 704
Dental floss injury 144
Dental fluorosis 135
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Index 1153
Diagnostic test of cancer detection
86
Diascopy 491
Diazepam 1028
DIC 924
Dichotomy theory 125
Dicloxacillin 966
Didanosine 998
Differential leukocyte count 99
Diffuse
calcification 485
gangrenous stomatitis 412
gingivitis 576
infiltrative lymphocytosis
syndrome 869
lipoma 304
sclerosing osteomyelitis 469
Digastric fossa 15
DiGeorges syndrome 822
Digital palpation 61
Dilacerations 117
Dilantin sodium induced gingival
enlargement -581
Dilated composite odontome 117
Dilling rule 47
DILS 869
Diphtheria 749
Dipped into white paints
appearance 130
Direct immunofluorescence 94
Disappearing bone 855
Disc
dislocation 627
displacement 626
perforation 627, 628
Discal ligament 603
Discoid lupus erythematosus 225
Discoloration of teeth 148, 1086
Discoloring agents 148, 150
Discrete pulp stone 484
DISH syndrome 433
Disinfection 38
Dislocation 624
Disseminated
blastomycosis 776
herpes infection of newborn 758
intravascular coagulation 924
juvenile fibrous dysplasia 835
sclerosis 806
Distal
step 71
metastasis 29
Distomolar 113, 125
Disturbance in
carbohydrate mechanism 951
lipid metabolism 947
mineral metabolism 952
protein mechanism 944
Diurnal bruxism 702
Diverticuli 645
DNA oncogenic virus-27
DNA profiling 1043
DNM 482
Dobutamine 1030
DOCA 1008
Docetaxel 992
Doctors position 63
Donovanosis 753
Dopamine 1030
Doppler ultrasound 536
Double condyle 609
Double fracture line 711
Double lip 558
E
Eagle syndrome 433, 725, 1106,
1059
Early loss of teeth 1088
Early periodontitis 598
Early syphilis 733
Ears 63
Earthy tongue 547
Ebbing tide type of leukoplakia 197
Ebnuration 612
Ecchondroma 302
Ecchymoses 490, 506, 697
Echinococcosis 260
Econazole 984
Ectodermal dysplasia 165
Ectopic
enamel 121
eruption 140
geographic tongue 546
salivary gland 643
salivary neoplasm 65
Eczematous cheilitis 565
Edema 60
Edwards syndrome 1106
Effect of infection on host 442
Effectiveness of antibiotics 961
Egg shell
crackling 230, 275
of bone 277
Ehlers-Danlos syndrome 817,
1106
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1154
Examination of
cranial nerve 81
deep cervical nodes 62
fistula 80
heart 786
maxillary sinus 678
salivary gland 642
sinus 80
swelling 73
tongue 536
ulcer 78
Excisional biopsy 90
Excrescence 206
Exfoliation 1080
Exfoliative cheilitis 567
Exfolitive cytology 91
Exocrine gland 638
Exogenous pigmentation 508
Exophytic lesion 1098
Exostosis 310
of root 123
Expansible
pulsation 74
swelling 77
External
internal resorption 146
jugular vein 63
nasal branches 15, 16
resorption 145, 530
Exteroceptors 417
Extracapsular fracture 617
Extraductal causes 651
Extraoral
discharging sinus 1082
examination 60
Extraosseous ameloblastoma 278
Extraosseous osteosarcoma 358
Extravasation cyst 255
Extrinsic asthma 794
Extrinsic stain 1079
Extrusive luxation of teeth 699, 701
Eye raised to heaven appearance
836
Eye wear 39
Eyes 63
F
Face shield-39
Facial hemiatrophy 156, 549
Facial hemihypertrophy 155
Facial nerve 82
Facies leprosa 743
Factitious cheilitis 567
Factitious injury 588, 698
Factor V deficiency 922
Factor XI deficiency 924
False cyst 684
False gemination 114
False polycythemia 912
Famcyclovir 997
Familial benign chronic pemphigus
406
Familial fibrous dysplasia of jaws
835
Familial hypophosphatemia 939
Familial multilocular cystic disease
of jaw 835
Familial neutropenia 915
Familial osteodysplasia 1103
Familial otodentodysplasia 122
Mulberry molar 123
Familial thrombasthenia 919
Family history 55
Fanconis anemia 910
Fanconis syndrome 1106
Farmers lip 566
Fascial space infection 473
Fasting blood glucose 104
Fat soluble vitamin 936
Fatigue 1036
Favre-Racouchot syndrome 1106
FDI system 68
Feedback deletion 29
Ferguson Smith type
keratoacanthoma 295
Fetal deciduous teeth 127
Fever blister 758
Fiberoptic transilluminator 519
Fibers of gingiva 573
Fibrin stabilizing factor deficiency 924
Fibroadamanblastoma 267
Fibrocementoma 282
Fibrocystic disease 828
Fibroepithelial polyps 299
Fibroma 297
molluscum 320
Fibromatosis gingiva 574
Fibro-osseous lesion 828, 1072
Fibro-osteodystrophy 828
Fibrosarcoma 352
Fibrous
adamantinoma 267
ankylosis 622
dysplasia 828
epulis 299
healing of wound 720
histiocytoma 299
hyperplasia 298
papule 818
Fibroxanthoma 299
Field arrangement in radiotherapy
378
Filliform papillae 534
Final diagnosis 83
Fine needle aspiration cytology 92
First Arch syndrome 1106
Fissured tongue 543
Fistulae of oral cavity 486
Fixed drug reaction 391
Flame shaped pulp canal 131
Flat torus 308
Floating fracture 713
Floating teeth appearance 593,
949
Flocculent appearance 355
Floor of mouth 11, 66
Floppy infant 1106
Florid osseous dysplasia 841
Flow rate studies 643
Flucloxacillin 966
Fluconazole 984
Fluctuation 76
Flucytosin 983
Fludrocortisones 1008
Fluid thrill 76
Flumazenil 1031
Fluocinolone 1007
Fluorescence 519
photography 88
Flurbiprofen 975
Fluride toxicity 855
Flush terminal plane 71
Fluticasone 1007
Fly-catchers tongue 551
Focal acantholytic dyskeratosis 191
G
G1 phase 24
G2 phase 24
Gancyclovir 997
Ganglioneuroma 324
Ganglionic nerve 16
Gangosa 739
Gangrenous stomatitis 748
Gardner syndrome 167, 1107
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Index 1155
Glandular Cheilitis 563
Glandular fever 770
Glandular odontogenic cyst 246
Glanzmanns disease 919
Glassblowers white patch 185
Glenoid fossa 602
Globodontia 122
Globulomaxillary cyst 1053
Glomangioma 318
Glomeruli 803
Glomus tumor 318
Glossalgia 550
Glossitis 929, 930
areata exfoliativa 545
Glossodynia 422, 550, 1082
Glossopalatine gland 640
Glossopharyngeal neuralgia 432
Glossoplegia 551
Glossopyrosis 550
Glosssopharyngeal nerve 82
Gloves 39
Glucagon 1028
Glucocorticoids 1003
Glucose 1028
Glucose 6 phosphatase deficiency
anemia 910
Glyceryl trinitrate 1027
Godtfredsens syndrome 434
Gold poisoning 512
Goldenhar syndrome 1107
Goldie Goldman model 989
Goltz-Gorlin syndrome 1107
Gonococcal arthritis 740
Gonococcal ophthalmia
neonatorum 739
Gonorrhea 739
Gorham syndrome 855, 1107
Gorlin cyst 245
Gorlin Goltz syndrome 1108
Gorlin sign 542, 817
Gorlins and Goltzs syndrome 262
Gorlin-Chaudhry-Moss syndrome
1107
Goundou 739
Gout 629
Graded von Frey hair 82
Gradenigo syndrome 1107
Grading of tumors 31
Graft versus host disease 216
Graham little syndrome 210
Graham-Little syndrome 1107
Gram negative sepsis and shock 483
Grand mal epilepsy 808
Granular appearance 355, 358, 831
Granular cell myoblastoma 325
Granular cell odontogenic
fibroma 282
tumor 282
Granular cell schwannoma 325
Granular cell tumor 325
Granular erythroplakia 203, 204
Granulocytes 896
Granulocytopenia 912
Granulocytosis 915
Granuloma inguinale 753
Granuloma pyogenicum 329
Granuloma venereum 753
Granulomatous Cheilitis 564
Granulomatous diseases 1068
Granulomatous disorders 809
Graze 1048
Green stain 151
Greenstick fracture 618, 718
H
HAART 872, 1001
Habits 54
Hailey-Hailey disease 406
Hair lip 560
Hair on end appearance 904,
905
Hairy leukemia 373
Hairy leukoplakia 866
Hairy tongue 547, 1088
Hajadu Cheney syndrome 1107
Halitosis 1083
Hallermann-Streiff syndrome 1107
Hallopeau type 402
Halo nevus 296, 297
Halocinonide 1007
Haloprogin 986
Hamartomas 1073
Hamycin 982
Hand-foot and mouth disease 769
Hand-Schller-Christian disease
947, 1059
Hanging drop appearance 692
Hanhart syndrome 1107
Hansen disease 741
Hapten 20
Hard fibroma 298
Hard palate 10
Harrison grooves 939
Hatch-Beals-Wilson syndrome 1108
Hazards due to material used 1036
HDN 901
Head 60
Headache 60
Healing cyst 252
Heart sound 786
Heat testing 72
Hebra nose 753
Heck disease 187
Heefordts syndrome 663, 822,
1108
Hemangioma 311, 490
Hemangiomata 924
Hemangiopericytoma 319
Hematocrit 99
Hematological
disorders 587
investigation 97
toxicity 994
Hematoma 490, 507, 697
Hemifacial microstomia 156
Hemifacial spasm 820
Hemihyperpalsia 155
Hemi-maxillofacial dysplasia 157
Hemisepta 599
Hemochromatosis 506
Hemoglobin 895
Hemoglobin Bart disease 905
Hemoglobin H disease 905
Hemoglobin S 902
Hemolytic jaundice 802
Hemophilia 920
Hemophilia C 924
Hemorrhage 1085
Hemorrhage of iatrogenic cause 924
Hemorrhagic bone cyst 255
Hepadna virus 28
Heparin 896
Hepatic porphyria 946
Hepatitis 799
A 799
B 49, 799
C 800
D 800
G 800
Hepatocellular jaundice 802
Herd immunity 18,19
Hereditary benign intraepithelial
dyskeratosis 189
Hereditary brown enamel 128
Hereditary brown opalescent teeth
128
Hereditary disease of newborn 901
Hereditary elliptocytosis 910
Hereditary enamel dysplasia 128
Hereditary fibrous dysplasia of jaw
835
Hereditary fructose intolerance 952
Hereditary gingival fibromatosis 574
Hereditary hemorrhagic
talangiectasia 494, 923
Hereditary hypohidrotic (anhidrotic)
ectodermal dysplasia 165
Hereditary intestinal polyposis
syndrome 504, 1111
Hereditary opalescent dentin 130
Hereditary spherocytosis 910
Hereditary thymic dysplasia 185
Herlitzs disease 406
Herpangina 768
Herpes gladiatorum 758
Herpes labialis 758, 866
Herpes simplex infection 757, 866
Herpes virus 28
Herpes zoster 586, 762, 763, 866
Herpetic conjunctivitis 758
Herpetic eczema 758
Herpetic genitalis 758
Herpetic gingivostomatitis 586
Herpetic meningoencephalitis 758
Herpetic whitlow 758
Herptiform ulcer 396
Heterotopic calcification 721
Heterozygous 153
Hexamethylamine 993
Hibernoma 305
Hidebound disease 813
High condylar fracture 617
High transverse fracture 714
Higoumenakiss sign 737
Hippocrates oath 1048
Histaminic cephalgia 426
Histiocytosis X 947, 1059, 1101
Histiocytosis Y 295
Histoplasmosis 586, 775
History of pain 50
History of present illness 50
History of swelling 52
History of ulcer 52
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1156
Hypervitaminosis A 937
Hypnotherapy 635
Hypodontia 124, 1079
Hypofibrinogenemia 922
Hypoglossal nerve 82
Hypoglossia-hypodactylia
syndrome 1108
Hypoglycemia 952
Hypognathous 153
Hypogonadism 891
Hypomelanosis 490
Hypoparathyroidism 883
Hypophosphatasia 953
Hypopigmentation 513
Hypopituitarism 877
Hypoplasia due to
birth injury 134
exanthematous disease 134
hypocalcaemia 134
nutritional deficiency 134
Hypoplasia of condyle 606
Hypoplasia of enamel 530
Hypoplasia of salivary gland 644
Hypoprothrombinemia 924
Hypotaurodont 120
Hypotherapy 437
Hypothermia 58
Hypothyroidism 880
I
Iatrogenic immunosuppression
associated Kaposis
sarcoma 868
Iatrogenic pigmentation 508
Ibuprofen 975
Iceberg tumor 665
Icterus 59
Id reaction 182
IDDM 885
Identification of victim 1041
Idiopathic bone cavity 255
Idiopathic bone cyst 255
Idiopathic calcification 724
Idiopathic facial pain 428
Idiopathic facial paralysis 805
Idiopathic hypertension 790
Idiopathic leukoplakia 196
Idiopathic steatorrhea 955
Idiopathic thrombocytopenic
purpura 869
Idoxuridine 996
Ig-A 20
Ig-D 20
Ig-E 20
Ig-G 20
Ig-M 20
Ill effect of CPA 1039
Immune surveillance theory 30
Immunity 18
Immunofluorescence 23, 94
Immunoglobulin 441
Immunological disorders 822
Immunotherapy 384
Impacted mandibular third molar 137
Impacted teeth 137
Impetigo 456
Impetigo vulgaris 456
Imprint abrasion 1048
Impulse on coughing 77
IMRT 384
Incipient carcinoma 203
Incipient caries 521, 524
J
Jacksonian epilepsy 808
Jackson-Lawler syndrome 189
Jacods syndrome 433
Jadassohn-Lewandowsky
syndrome 189, 1108
Jadassohn-Tieche nevus 296, 297
Jaffys disease 829
James Ramsay Hunt syndrome
762, 767
Jaundice 802
Jaundice 507
Jaw cyst-basal cell nevus-bifid rib
syndrome 262, 1108
Jaws 60
Jaw-Winking syndrome 1108
Joint mice 612
Jones diagnostic criteria 789
Jugular foramen syndrome 1108
Junctional bullous epidermatosis
406
Junctional epidermolysis bullosa
406,407
Junctional nevus 296
Juvenile aggressive ossifying
fibroma 834
Juvenile myxoedema 880
Juvenile nasopharyngeal
angiofibroma 319
Juvenile onset respiratory
papillomatosis 771
Juvenile ossifying fibroma 834
Juvenile polyarthritis 615
Juvenile rheumatoid arthritis 615
Juvenile type Hypophosphatasia
953
Juxtacortical osteosarcoma 358
K
Kallman syndrome 168
Kaposi vericelliform eruption 758
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L
Labial gland 640
Labial melanotic macule 495
Laceration 1048
Lacrimal nerve-15
Lactation 1023
Lactobacillus count test 95
Laminated appearance 848
Lane tumor 351
Langerhans cell histiocytosis 947
Larsen syndrome 1109
LASER 202
Laser peel 202
L-asparaginase 992
Late syphilis 733
Latent bone cyst 645
Lateral luxation of teeth 701
Lateral nasal branches 16
Lateral periodontal cyst 242
Lateral pharyngeal space infection
478
Lateral pterygoid muscle 61
Lateral pterygoid-12
Laugier-Hunziker syndrome 1109
Lazy leukocyte syndrome 915
Le Fort I fracture 713, 714, 715
Le Fort II fracture 714, 716
Le Fort III fracture 714, 715, 716
Lead line 510
Lead pipe type movement 807
Lead poisoning 509
Leaf like denture fibroma 299
Leg sign 480
Leiomyoma 324
Leiomyosarcoma 362
Leishmaniasis 782
Lemmoma 322
Lentigo 495
Index 1157
Lentigo maligna melanoma 347,
348, 499
Lentigo solaris 818
Leongs premolar 119
Leonine facies 742
Leontiasis ossea 1051
Leproma 742, 743
Lepromatous leprosy 742
Lepromin test 743
Leprosy 741
Leser-Trelat sign 818
Letterer Siwe disease 947, 948,
1059
Leucosis 368
Leukemia 368
associated gingivitis 578
blast 369
Leukemoid reaction 368
Leukocytes 895
Leukoderma 490
Leukoedema 171
Leukokeratosis nicotina glossi 548
Leukopenia 1089
Leukoplakia 194, 552
Leukoplakia erosiva 195, 198
Leukoplakia simplex 195, 198
Leukoplakia verrucosa 195, 199
Leutic glossitis 736
Lichen planus 208
Lichen planus pemphigoides 213
Lichen planus pigmentosus 212
Lichen planus-lupus erythematosus
overlap 213
Lichenoid contact dermatitis 213
Lichenoid dermatitis 217
Lichenoid foreign body gingivitis
217
Lichenoid mucositis 217
Lichenoid reaction 216
Lidocaine 1029
Liesegang ring 270
Light hazards 1036
Lincolns sign 840
Linea Alba 173
Linear enamel caries 530
Linear gingival erythema 586, 865
Linear lichen planus 212
Linear scars 737
Lingua dissecta 543
Lingua nigra 547
Lingua villosa 547
Lingual caries 523
Lingual cortical mandibular defect
645
Lingual cyst 543
Lingual dysesthesia 550
Lingual frenulum 534
Lingual mandibular bone cavity
645
Lingual nerve 17
Lingual paresthesia 550
Lingual thyroid nodule 541
Lingual varices 541
Lip 9, 65
Lip biting 173
Lipid reticuloendotheliosis 947
Lipoblastomatosis 305
Lipoid proteinosis 192
Lipoma 304
Lipomatosis 304
Liposarcoma 354
Lipping 612
Liquefaction necrosis 484
M
Macrochelia 65
Macrodontia 112, 1079
Macroglobulinemia 923
of Waldenstrom 923
Macroglossia 539, 946, 1086
Macrognathia 155
Macrolide 963
Macrophage inhibiting factors 441
Macule 490
Maffucci syndrome 1109
Magic syndrome 1109
Magnesium 955
Magnetic resonance imaging 643
Major aphthae 396
Making treatment plan 83
Malabsorption syndrome 955
Malformed crown 1079
Malformed teeth 1088
Malignant ameloblastoma 288
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1158
Morphea 813
Morpheaform basal cell carcinoma
346
Morphine sulphate 1030
Morquios syndrome 1109
Morsicatio buccarum 173
Morsicatio labiorum 173
Morsicatio linguarum 173
Moth eaten appearance 344,
368, 373, 465, 500, 882
Mother of pearl appearance 171
Motor function lest 82
Motor system disease 806
Mottled enamel 135
Mould therapy 379
Mouse facies 813
Mouth breathing 54
Mouth piece of flute appearance
614
Mouthwashes 1016
antiplaque mouthwash 1018
Mouthwashes containing
bisguanide antiseptic 1018
essential oil 1018
oxygenating agents 1018
sanguinarine 1018
triclosan 1018
Mucobuccal fold 68
Mucocele 652
Mucocutaneous disorders 586,
1072
Mucocutaneous leishmaniasis 782
Mucocutaneous lymph node
syndrome 1110
Mucoepidermoid carcinoma 669,
671
Mucoepidermoid cyst 246
Mucogingival pain 422
Mucormycosis 777
Mucosal lentiginous melanoma
348
Mucositis 681
Mucus duct cyst 654
Mucus escape reaction 652
Mucus extravasation phenomenon
652
Mucus patches 734
Mucus plug 651
Mucus retention cyst 654
Mucus salivary gland 638
Mulberry molar 134
Multibacillary leprosy 742
Multicentric oral carcinoma 352
Multifocal eosinophlic granuloma
947
Multilocular cyst 274
Multilocular radiolucency 1091
Multiple endocrine neoplasia
syndrome 1110
Multiple idiopathic hemorrhagic
sarcoma of Kaposis 493
Multiple mutations 29
Multiple myeloma 373
Multiple radiolucency 1092
Multiple radiopacities 1093
Multiple sclerosis 434, 806, 841
Multistep theory 30
Mumps 656
Mural ameloblastoma 276
Mural growth theory 232
Murray Puretic dresher syndrome
1110
Muscle disorders 819
N
Nafcillin 966
Naftifine 985
Nager syndrome 1110
Nalbuphine 1030
Naloxone 1030
Nance Horan syndrome 1110
Naproxen 975
Nasendoscopy 679
Nasoalveolar cyst 254
Nasociliary nerve-15
Nasoethmoidal injuries 718
Nasolabial cyst 254
Nasolabial sulcus-9
Nasopalatine cyst 253
Nasopalatine duct cyst 253
Nasopharyngeal
angiofibroma 319
carcinoma 351
cyst 260
Natal teeth 127
Natamycin 982
Natural immunity 18
Neck 63
sign 480
Neck tongue syndrome 1110
Necrosis of pulp 484
Necrotizing
fascitis 483
sialometaplasia 674
stomatitis 748
ulcerative gingivitis 583, 865
ulcerative mucositis 748
ulcerative periodontitis 596, 865
Nelfinavir 998
Neonatal chickenpox 763
Neonatal hepatitis 149
Neonatal teeth 127
Neonatal tetanus 753
Nerve sheath myxoma 302
Nerve supply of
gingiva 573
lip 558
TMJ 605
tongue 535
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Nervous spinosum 16
Neumann type 402
Neurilemmoma 322, 1059
Neurinoma 322, 1059
Neuroblastoma 361
Neurofibroma 320
Neurofibromatosis 320, 504
Neurofibrosarcoma 361
Neurogenic sarcoma 361
Neurogenous pain 429
Neuro-lemmoma 1059
Neurological toxicity 994
Neuroma 323
Neuromelanin 489
Neuromuscular disorders 804
Neuropathic pain 420
Neurophysiology of pain 415
Neurosyphilis 735
Neutron beam 376
Neutron therapy 381
Neutron-tropic ulcer 389
Neutropenia 912, 914
Neutrophilia 915, 1089
Nevoid basal cell carcinoma 262,
346
Nevus flammeus 315
Nezelofs syndrome 822
Niacin 929
Niacin deficiency 549
Nickolskys sign 401
Nicotinic acid 929
Niemann-Pick disease 950
Nifedipine induce gingival
enlargement 581
Night grinding 702
Nimesulide 976
Nitrates 1027
Nitrites 1027
Nitrogen mustards 989
Nitroglycerine 1027
Nitroimidazoles 968
Nitrosoureas 990
Nitrous oxide 1027
Nocturnal angina 787
Nocturnal bruxism 702
Nodes of Ranvier 416
Nodular basal cell carcinoma 345
Nodular elastoidosis 570
Nodular fascitis 333
Nodular leukoplakia 194, 198
Nodular melanoma 347, 348, 499
Nodular subepithelial fibrosis 299
Nodular torus 309
Noduloulcerative basal cell
carcinoma 345
Noma 748
Noma neonatorum 748
Non-bullous impetigo 456
Non-critical surface-36
Non-Hodgkins lymphoma 364
Non-homogenous leukoplakia 194
Non-neuropathic pain 420
Non-paroxysmal pain 420
Non-radiation physical
carcinogenesis-27
Non-specific immunity-19
Non-venereal treponematoses 737
Non-lipid reticuloendotheliosis 947
Non-opalescent and opalescent
dentin 132
Nonselective cyclo-oxygenase
inhibitors 972
Index 1159
Nonsteroidal anti-inflammatory
drugs 972
Noonan syndrome 1110
Normal cell cycle-24
Normal periodontium 572
Norton Simon hypothesis 988
Nose 63
NSAID 972
Numb chin syndrome 344
Nursing bottle caries 526, 1104
Nystatin 981
O
Obliteration of pulp chamber 149
Obstructive jaundice 802
Occipital myotomes 533
Occipital neuralgia 432
Occlusal caries 524
Occlusal enamel pearl 119
Ocular disease 486
Oculoglandular syndrome of
parinaud 751
Odontoameloblastoma 286
Odontoblastic transduction theory
1011
Odontogenic dysplasia 132
Odontogenic fibrosarcoma 290
Odontogenic firbomyxoma 279
Odontogenic infection of orbit 481
Odontogenic keratocyst 238
Odontogenic myxoma 279
Odontogenic tumor 1066
Odontoma 270
Olfactory nerve 81
Olfactory neuroblastoma 320
Oligodontia 124
Oligosaccharide 951
Oncocytoma 668
Oncocytosis 668
Oncogens 29
Onion peel appearance 358, 373,
Onion skin appearance 360, 471
Onyalai 920
OPD syndrome 1110
Ophthalmic nerve 15
Opioid analgesics 977
Opisthotonos 752
Opium 977
Optic nerve 81
Oral alimentary tract cyst 259
Oral amyloidosis 374
Oral cavity development 9
Oral cavity proper 9,10
Oral cyst of gastric or intestinal
epithelium 259
Oral diagnosis 3
Oral epithelial nevus 188
Oral florid papillomatosis 194
Oral focal mucinosis 301
Oral foci of infection 485
Oral genodermatoses 188
Oral glucose tolerance test 104
Oral hamartomas 1073
Oral lichen planus 210
Oral lymphoepithelial cyst 259
Oral lymphoid tissue lesion 1074
Oral manifestation of AIDS 864,
1065
Oral melanotic macule 495
Oral microflora 442
Oral myofunctional therapy 635
Oral submucus fibrosis 217
P
P24 antigen capture assay 871
Pachyderma oralis 188
Pachyonychia congenita 189
Paclitaxel 992
Pagets disease 839
Pagets test 76
Pain conduction 417
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1160
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Index 1161
Pseudosarcomatous fascitis 333
Pseudoxanthoma elasticum 192
Psoriasis 186
Psoriatic arthritis 615
Psychogenic intensification pain
434
Psychogenic pain 434
Psychogenic syncope 825
Psychological stress 1036
Psychomotor epilepsy 808
Pterygoid nerve 16
Pterygomandibular space infection
478
Pterygopalatine fossa syndrome
433
Pterygopharyngeal space 478
Ptylism 646
Puberty associated gingivitis 578
Puberty induced gingival
enlargement 583
Pulmonary actinomycosis 747
Pulmonary foreign bodies 796
Pulmonary stenosis 793
Pulmonary toxicity 994
Pulmonary tuberculosis 745
Pulp calcification 484
Pulp nodules 484
Pulp polyp 458
Pulp stone 485
Pulp testing 72
Pulpal calcification 1080
Pulpal infection 484
Pulpal pain 423
Pulpitis aperta 458
Pulsatility 77
Pulsation 74
Pulse 56
Pulsed ultrasound 536
Pulseless disease 1103
Pumping tooth syndrome 312
Punch biopsy 91
Punched out edges 79
Purine antagonist 990
Purpura 490
Purpura hemorrhagic 916
Purpuric macule 697
Purse string appearance 814
Pustular psoriasis 186
Pustule 487
PUVA therapy 214
PVL 199
Pyogenic granuloma 329
Pyostomatitis vegetans 458
Pyramidal fracture 714
Pyridoxine 931
Pyrimidine antagonists 990
Pyruvate kinase deficiency anemia
910
Q
Quantification of nuclear DNA
content 93
Quaternary syphilis 733
Quatrain 58
Quinckes edema 394
Quinolones 968
Quotidian 58
R
Rabbit fever 751
Rabbit syndrome 551
Replication 28
Repolarization 418
Residual cyst 250
Resorption of teeth 145
Respiration 58
Respiratory disorders 794
Respiratory stimulant 1029
Resting state 417
Retarded eruption of teeth 1088
Retention cyst 684
Reticular lichen planus 210
Retinal anlage tumor 324
Retinol 936
Retrodiscal pad pain 425
Retromolar gland 640
Retropharyngeal space 479
Reverse smoker palate 205
Reverse smoking 205
Reverse transcriptase inhibitors 998
Rh hump 902
Rhabdomyoma 325
Rhabdomyosarcoma 362
Rheumatic heart disease 789
Rheumatic heart fever 789
Rheumatoid arthritis 613
Rheumatoid nodule 613
Rheumatoid spondylitis 617
Rhinopharyngitis mutilans 738
Rhinoscleroma 753
Rhinoscopy 679
Rhinosporidiosis 781
Rhizotomy 431
RHL 760
Ribavarin 1000
Riboflavin 928
Rickets 939
Riegers syndrome 1111
Riga fede ulcer 127
Rights of registered dental
practitioner 1049
RIH 760
Risus sardonicus 752, 753
Ritonavir 998
RNA oncogenic virus 27
Robin anomalad 852
Rodent facies 905
Rodent ulcer 345,346
Role of teeth in establishing
identity 1041
Rolled edge 79
Romberg hemifacial atrophy 156
Romberg sign 735
Root caries 525
Root fracture 699
Root in antrum 691
Rootless teeth 132
Rose Bengal staining test 662
Rotation therapy 378
Round cell sarcoma 359
Routes of drug administration
960
Routes of infection transfer 35
Rubber man 817, 1106
Rubella 768
Rubeola 767
Rubinstein Taybi syndrome 115,
1112
Rudimentary supernumerary teeth
125
Rule of thumb 961
Rumple leede test 101
clotting time 102
Rutherford syndrome 1112
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S
S phase 24
Sabre tibia 738
Saddle nose 743
Saddle nose defect 739
Saethre-Chotzen syndrome 1112
Sailors lip 566
Saint Anthonys fire 457
Saints triad 687
Salbutamol 1028
Saliva 640
Salivary duct cyst 654
Salivary gland 11, 66
Salivary gland calculus 649
Salivary gland disorders 1073
Salivary gland fistula 487
Salivary gland scanning 643
Salivary gland sinus 487
Salivary gland stone 649
Salivary gland virus disease 657
Sallicylates 973
Salmons patch 311, 313
Salt and pepper appearance 345
Sandwich technique of
immunofluorenscence 94
Sanfilippo syndrome 1112
SAPHO syndrome 472
Sarcoidosis 810
Sarcoma 24
Satellite cyst 241
Saucer shaped destruction 464
Saucerization 467
Sausage link appearance 660
Scalded mouth syndrome 790
Scalded skin syndrome 1112
Scale 490
Scanning electron microscope 536
Scarlet fever 749
Scheie syndrome 1112
Scheuthauer Marie Sainton
syndrome 1112
Schilling test 102, 908
Schirmer test 662
Schwachman syndrome 915
Schwannoma 322
Scintigraphy 643
Scleroderma 550, 813
Sclerosing basal cell carcinoma 346
Sclerosing cementum 282
Sclerosing hemangioma 299
Sclerosing osteitis 453, 841
Sclerosing sialadenitis 659
Sclerotic cemental masses 841
Scorbutic child 935
Scratch 1048
Screw driver shaped incisor 737
Scrofula 744, 745
Scrotal tongue 543
Scrumpox 758
Scurvy 935
Scurvy bud 935
Sebaceous cyst 77
Sebaceous hyperplasia 818
Seborrheic dermatitis 929
Seborrheic keratosis 818
Seborrhoeic papilloma 294
Second branchial arch sinus 487
Secondary carcinoma 344
Secondary herpetic infection 760
Secondary hypertension 790
Secondary immunodeficiency 823
Secondary polycythemia 912
1162
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Index 1163
Swelling in submandibular region
1081
Swelling of lip 1081
Swelling of palate 1080
Swift disease 510
Swiss type agammaglobulinemia
185
Swoon 825
Symphysis menti 15
Symptomatic neuralgia 432
Syncope 825
Synodontia 113
Synovial chondromatosis 631
Synovial fluid 605
Synovial sarcoma 353
Syphilis 550, 733
Syphilis periostitis 736
Syphilitic hypoplasia 134
Syphilitic rhagades 737
Systemic blastomycosis 776
Systemic candidiasis 184
Systemic lupus erythematosus
225, 226
Systemic sclerosis 813
T
T cell lymphoma 366
T lymphocytes 441
Tabes dorsalis 735
Tabetic crises 735
Tachypnea 58
Tactile stimuli 1013
Telangiectasia 490
Talon cusp 115, 1112
Tapir lip 820
Tardive dyskinesia 551
Target appearance 1056
Target lesion 399
Targeted radiotherapy 384
Taste buds 534
Taste testing 536
Taurodontism 120
Taxanes 992
Tay Sachs disease 950
Technique for identification in
mass disaster 1042
Teeth 10, 68
Teeth clenching 702
Teeth grinding 702
Teletherapy 377
Temperature 58
Temporal arteritis 427
Temporal space infection 477
Temporalis muscle 12
Temporomandibular joint 61
Temporomandibular
joint disorders 1074
joint pain 425
ligament 604
Tennis elbow 49
Tennis racket appearance 280
TENS 438, 635
Tension headache 427
Teratoblastoma 328
Teratoid tumor 328
Teratoma 257, 328
Terbinafine 985
Tertian 58
Tertiary syphilis 733,735
Test cavity 73
Tetanus 752
Tetanus neonatorum 752
Tetracycline 962
Tetracycline hypoplasia 136
Tetracycline staining 149
Thalassemia 904
Thalassemia intermedia 905
Thalassemia major 905
Thalassemia minor 905
Thalassemia trait 905
Thallium stress test 788
Theories of cariogenesis 517
Theories of cyst enlargement 231
Theories of dentinal
hypersensitivity 1011
Theories of pain conduction 418
Therapeutic modalities of pain 436
Thermal burns 174
Thermal stimuli 1013
Thermal testing 72
Thiamine 927
Thick leukoplakia 198
Thickened periodontal ligament
space 1093
Thin leukoplakia 198
Thistle tube appearance 132
Thomsen disease 820
Thrombocytes 896
Thrombocythemia 920
Thrombocytopenic purpura 916
Thrombocytosis 920
Thrombotic thrombocytopenic
purpura 917
Thrombus 492
Thrush 179, 864
Thumb print appearance 831
Thymic cyst 260
Thymic hyperplasia 822
Thymic replacement therapy 871
Thyroglossal duct cyst 259
Thyroid crisis 879
Thyroid function test 105
Thyroid gland 874
Thyroid storm 879
Thyrotoxicosis 878
Tic Douloureux 429
Ticarcillin 966
TMJ dysfunction syndrome 632
TNM staging 33
Tobacco pouch keratosis 207
Tobacco pouch mouth 814
Tocopherol 941
Tolnafate 985
Toluidine blue testing 86
Tombstone appearance 240
Tongue 11, 63
Tongue disorders 1076
Tongue thrusting 54, 65, 542
Tongue tie 540
Tonic phase 808
Tonsil 66
concretions 722
Tonsillar calculi 722
Tonsillolithiasis 722
Tonsilloliths 722
Tooth ankylosis 707
Tooth brush injury 143
Tooth mark 1044
Tooth mobility 69, 596
Tooth pick injury 144
Tooth tissue loss 1100
Topical antibiotics 969
Topical antiseptic 969
Torulosis 778
Torus mandibularis 309
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U
Ulcerated granuloma
eosinophilicum diutinum
548
Ulcerated leukoplakia 194, 198
Ulcerative colitis 801
Ulcerative lichen planus 212
Ultrasonography 643
Uncomplicated crown fracture 699
Uncomplicated ulcer 389
Undecylenic acid 986
Undermined edge 78
Undifferentiated carcinoma 673
Unequal blood pressure 57
Unicameral cyst 255
Unifocal eosinophilic granuloma 947
Universal system 68
Unstable angina 787
Urbach-Wiethe syndrome 192
Uremia 798
Uremic stomatitis 177
Urinary bladder neoplasm 49
Urine glucose estimation 103
USPHS-CDC classification for
AIDS 863
UV rays 1043
Uveoparotid fever 663
V
Vaccination-38
Vaccinia autonoculata 394
Vaginogingival syndrome 209
Vagoglosso-pharyngeal neuralgia
432
Vagus nerve 82
Valley fever 779
Valvular heart disease 486
Van Buchem syndrome 1113
Vander Woudes syndrome 558,
1113
Vanishing bone 855
Vaquezs disease 911
Varicella 762
Varicella zoster infection 762
Varices 492
Varicose aneurysm 318
Varicose veins 49
Variola 773
Varix 492
VAS 1014
Vascular hemophilia 918
1164
W
W appearance 1052
Waddling gait 819, 839
Wakeful bruxism 702
Walter Reed staging system for
AIDS 862
Wandering rash 545
Warthins tumor 667
Warty appearance 331
Warty deskeratoma 191
Water soluble vitamins 926
Waterhouse-Friderichsen
syndrome 890
WBC count 99
Webbed neck 167
Weber Cockayne syndrome 406,
1113
Wegeners granulomatosis 809
Werlhofs disease 916
Wernickes encephalopathy 928
Western Blot method 870
Wet beriberi 928
Whartons duct 67, 639
Wheal 490
Wheel like spoke pattern 285
Whistling face syndrome 1113
White blood corpuscles 895
White folded gingivostomatitis 188
White lesion 1063
White line 173
White sponge nevus 188
WHO classification of
cancer and precancer 1063
teeth disorders 1078
WHO staging of AIDS 862
Whorl 310
Wickhams striae 210
Widow formation 230
Winters line 138
Wiskott-Aldrich syndrome 919, 1103
Witkop-Von Sallmann syndrome 189
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X
Xanthomatosis 947
Xeroderma pigmentosum 819
Xerostomia 647, 1085
X-linked dominant 153
X-linked recessive 153
XO syndrome 167
X-ray 1042
XXXXY syndrome 1113
Y
Yaws 738
Yeaple probe 1013
Young ossifying fibroma 834
Young rule 47
Yttrium 90 380
Z
Zalcitabine 998
Zidovudine 998
Zimmerman-laband syndrome 1113
Zinc deficiency 952
Zinc pigmentation 513
Zinssners syndrome 1113
Zinssner-Engman-Cole syndrome 224
Zona 763
Zoster infection 550
Zoster sine eruptione 764
Zoster sine herpete 764
Zsingmondys method 68
Zygomatic complex fracture 693
Zygomatic nerve-16
Zygomatic process-13
Zygomaticomaxillary complex
fracture 716
Zygomycosis 777