1

DISEASES OF
HARD TISSUES OF
TEETH
Dr. Aparna Aarathi Sreekumar
I MDS
CONTENTS

• Introduction
• Classification of diseases of hard tissues of teeth
• Developmental anomalies
• Environmental alterations
• Microbial diseases

2
CONTENTS

• Tooth wear
• Physical & chemical injuries
• Regressive changes
• Conclusion
• References

3
 INTRODUCTION
• Tooth is composed of four dental tissues
• Three of them—enamel, dentin and cementum—are hard tissues
• Fourth tissue—pulp, or core of the tooth that contains nerves, blood
vessels and connective tissue—is a soft, or non-calcified, tissue
• Enamel – highly mineralised tissue which is totally acellular
• Dentin – avascular, mineralised tissue, containing odontoblastic process as
the cellular component – forms major bulk of the tooth
• Cementum – mineralised tissue covering the root – forms supporting
structure – periodontium

4
INTRODUCTION

• Any defect/ delay in development of any of these structures – negatively

affect the form & function of teeth

• Certain errors in metabolism will also affect development of hard tissues

• Most common disease affecting the hard tissues of teeth – DENTAL CARIES

5
CLASSIFICATION OF DISEASES OF HARD TISSUES OF TEETH

1. Based on location
2. Based on number of teeth involved
3. Based on time of appearance of disease
4. Based on aetiology
5. ICD classification

6
 Based on Location:

Diseases affecting Diseases affecting Diseases affecting

enamel dentin cementum

• Amelogenesis • Dentinogenesis • Concrescence

imperfecta imperfecta • Cemental caries
• Enamel hypoplasia • Dentin dysplasia • Ankylosis
• Turner’s hypoplasia • Dentinal caries • Cemental resorption
• Dental fluorosis • Dentinal resorption • Hypercementosis
• Enamel caries • Dentinal sclerosis • Cementicles
• Cemental tear
• Cementoblastoma

7
Based on Number of Teeth Involved:
Localised defects:
• Single/limited no. of teeth (<4
teeth)
• Eg:- fusion, gemination,
concrescence, dilaceration,
Turner’s hypoplasia, caries, etc.
Generalised defects:
• Symmetrical & multiple teeth
• Eg:- AI, DI, regional
ododntodyspalsia, fluorosis,
rampant caries, etc.
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Based on Time of Appearance of Disease:

Pre-eruptive
• Developmental anomalies,
some environmental
Post-eruptive
alterations, etc. • Most of the environmental
alterations, caries, tooth wear,
etc.

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Based on Aetiology:

DEVELOPMENTAL ENVIRONMENTAL
ANOMALIES
MICROBIAL DISEASE
ALTERATIONS

PHYSICAL & REGRESSIVE

TOOTH WEAR
CHEMICAL INJURIES CHANGES

10
ICD Classification:
521.0 Dental caries 521.1 Excessive attrition
• Infantile Melanodontia • Approximal wear
• Arrested caries • Occlusal wear
• Odontoclasia 521.2 Abrasion
• Cemental caries
• Abrasion of teeth:
• White spot lesions of teeth
• dentifrice
• Dentinal caries:
• ritual
• Acute
• habitual
• Chronic
• traditional
• Enamel caries:
• occupational
• Acute
• Wedge defect
• Chronic
• Incipient
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ICD Classification:
521.3 Erosion 521.6 Ankylosis of teeth
• Erosion of teeth due to:
• medicine 521.7 Posteruptive colour changes
• persistent vomiting
• idiopathic • Staining of teeth [Excludes: deposits on
teeth (523.6)]
• occupational
521.8 Other diseases of hard tissues of
521.4 Pathological resorption
teeth
• Internal • Irradiated enamel
• External • Sensitive dentin
521.5 Hypercementosis
521.9 Unspecified
• Cemental hyperplasia

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 DEVELOPMENTAL ANOMALIES
SHAPE OF THE STRUCTURE OF
TEETH THE TEETH
NUMBER OF SIZE OF THE • Gemination • Amelogenesis
THE TEETH TEETH • Fusion imperfecta
• Hypodontia • Microdontia • Concrescence • Dentinogenesis
• Macrodontia • Dilaceration imperfecta
• Hyperdontia
• Talon Cusp • Dentin Dysplasia
• Dens in dente • Regional
Odontodysplasia
• Dens
evaginatus
• Taurodontism

13
 Some Syndromes Associated with
Hypodontia
In Number of Teeth: Down’s syndrome
HYPODONTIA Crouzon syndrome
Ehlers-Danlos syndrome
• Lack of development of one or
more teeth Hurlers syndrome
Ectodermal dysplasia
• Anodontia: total lack of tooth Turner’s syndrome
development Progeria
• Oligodontia: lack of development Gorlin’s syndrome
of 6 or more teeth Focal dermal hypoplasia
• Most common – permanent Cleft lip & palate
maxillary lateral incisors & 3rd
molars
• Cause: mutation of PAX9 gene
(AD), & MSX1 gene (X-LD)
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HYPERDONTIA
• Development of increased number Some Syndromes Associated with
of teeth Hyperdontia
• Supernumerary teeth – additional Apert’s syndrome
teeth formed Cleido-cranial syndrome
Sturge-Weber syndrome
• Most common - single tooth
Gardner’s syndrome
hyperdontia - maxilla – permanent
Oro-facial digital syndrome
dentition
Ellis-van Creveld syndrome
• Supernumerary:
• Mesiodens – maxillary anterior region
• Distomolar/distodens – accessory 4th
molar
• Paramolar – posterior supernumerary
– lingual/buccal to a molar tooth

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 Supernumerary Teeth:
Suppleme Conical –
ntary small, peg-
(normal shaped Mesiodens
shape &
size)
Supernumerary Tuberculate –
teeth barrel shaped
anterior with
>1 cusp

Rudimenta
ry
(abnormal Molariform –
shape & small
smaller premolar-like/
size) molar-like Distomolar Paramolar
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In Size of Teeth:

MICRODONTIA:
• Smaller than normal
• Types:
• True generalised microdontia – all teeth are smaller than normal –
pituitary dwarfism
• Relative generalised microdontia – normal/ slightly smaller than normal
in larger jaws
• Microdontia involving only a single tooth – mostly maxillary lateral
incisor & third molars
• Peg lateral – maxillary lateral incisor – congenital syphilis

17
MACRODONTIA
• Larger than normal
• Types:
• True generalised macrodontia – all teeth are larger than normal –
pituitary gigantism
• Relative generalised macrodontia – normal/ slightly larger than normal
in smaller jaws
• Macrodontia of single tooth – uncommon
• Often associated with facial hemihypertrophy

18
In Shape of Teeth:
GEMINATION:
• Division of a single tooth germ by an
invagination, resulting in incomplete
formation of 2 teeth
• One tooth with 2 completely /
incompletely separated crowns that
have single root & root canal
• In deciduous & permanent dentition
• TWINNING: production of equivalent
structures by division resulting in 1
normal & 1 supernumerary tooth
FUSION:
• Due to union of 2 normally separated
tooth germs
• Depending upon stage of development
of teeth at the time of union:
complete/incomplete fusion
• Before calcification: 2 teeth completely
unites to form a single tooth
• After calcification: union of roots
• Tooth have separate or fused root
canals
• Common in deciduous & permanent
teeth
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20
 Endodontic Considerations:
• Results in:
• Missed canals
• Enlarged pulp chamber
• Persistent infections

21
CONCRESCENCE
• A form of fusion which occurs after root formation has been completed
• Teeth – united by cementum
• Due to traumatic injury/ crowding of teeth with resorption of interdental
bone so that 2 roots are in contact & become fused by deposition of
cementum between them

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23
DILACERATION
• Sharp bend/curvature of root or crown of a formed tooth
• Due to trauma during the period in which tooth is forming with the result is
that position of calcified portion of tooth is changed & remainder of tooth
is formed at an angle
• Cervical portion/ midway along root/ just at the apex of root – depending
on amount of root formed at the time of injury

24
Endodontic Considerations:

• Identification of direction & extent of dilaceration – from pretreatment

radiograph
• Mesial/ distal – seen in IOPAR
• Apical foramen – darker, with a RL halo around – PDL space: “BULL’S EYE”
• Precurving of instruments
• Flowable GP

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 TALON CUSP
• Anomalous structure resembling eagle’s talon
• Projects lingually from cingulum areas of maxillary / mandibular
permanent incisor
• There can be occlusal interference, sometimes exposure of pulp horn
• Prevalent in persons with Rubinstein-Taybi Syndrome
• R/f: cusp is seen overlying central portion of crown & includes enamel &
dentin

Hattab et al’s classification

Sharma G & Nagpal A. Talon cusp: A prevalence study of its types in permanent dentition & report of a rare case of its association
26
with fusion in mandibular incisor. J. Oral Dis., 2014; 26-32
DENS IN DENTE
• Dens invaginatus/ dilated composite odontoma
• Deep surface invagination of crown or root that is lined by enamel
• Due to invagination in surface of tooth crown before calcification has
occurred because of:
• Increased localised external pressure
• Focal growth retardation & stimulation in some areas of tooth bud
• Appears as an accentuation of lingual pit
• Commonly seen in permanent maxillary lateral incisors

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Classification:
• CORONAL - 3 types –
TYPE 1: Confined to the crown
TYPE 2: Extends below CEJ
Ends in a blind sac
May or may not communicate with adjacent dental pulp
TYPE 3 : Extends through root
Perforates in apical or lateral radicular area without any immediate communication
with pulp
• RADICULAR VARIETY (Bhatt & Dholakia)
• Radicular invagination usually results from an infolding of HERS & takes its origin
within root after development is completed
Treatment :
• Prophylactical restoration of teeth with open apices
• Apexification with Ca(OH)2

28
Endodontic Considerations:

• No pulpal pathosis & communication – minor restoration/RCT (DeSmit &

Demaut, 1982)
• Invagination has separate apical/lateral foramen – RCT of invagination
(Grossman, 1974; Wells & Meyer,1993)

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DENS EVAGINATUS
• Occlusal tuberculated premolar/ Leong’s premolar/ Evaginated odontoma/
Occlusal enamel pearl
• An accessory cusp/ a globule of enamel on occlusal surface between buccal
& lingual cusps of premolars
• Due to proliferation & evagination of an area of inner enamel epithelium &
subjacent odontogenic mesenchyme into dental organ during early tooth
development
• Cusp-like structure – wear – expose pulp

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TAURODONTISM
• Enlargement of body & pulp chamber of a
multirooted tooth, with apical displacement of
pulpal floor & bifurcation
• Based on degree of apical displacement of pulpal
floor:
Mild – hypotaurodontism
Moderate – mesotaurodontism
Severe – hypertaurodontism
• Due to failure of HERS to invaginate at proper
horizontal level (Hammer et al)
• Associated with AI, Klinefelter’s syndrome

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Endodontic Considerations:

• Pretreatment radiograph – knowledge of RC system (Yeh & Hsu, 1999)

• Pulp testing – size of pulp chamber – sensitivity (Durr et al, 1980)
• Difficulty in identifying canals & instrumentation
• May have extraordinary root canals ( shape & number)
• Usage of magnification (Yeh & Hsu, 1999)

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AMELOGENESIS IMPERFECTA
• Hereditary enamel dysplasia
• A complicated group of conditions that demonstrate developmental
alterations in structure of enamel in the absence of a systemic disorder

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• Due to mutation of AMELX(amelogenin), ENAM(enamelin), MMP-
20(enamelysin), AMBN(ameloblastin) genes
• R/F: shape- normal, depending upon amount of enamel prism and
amount of occlusal and incisal wear
• Enamel – totally absent / as a very thin layer over cusp tip and
proximal surfaces
• H/F:
• Disturbances in the differentiation or viability of ameloblasts-
hypoplastic type
• Defects in matrix formation/ total absence of matrix-
hypomaturation type
• Defects of matrix structure and mineral deposition- hypocalcified
type

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Hypoplastic AI

• Inadequate deposition of enamel matrix

• Generalised pattern: pinpoint-to-pinhead sized pits – scattered/in rows or
columns across the surface of teeth
• Commonly affected: buccal surface
• Localised pattern: horizontal rows of pits, a linear depression, or a large
area of hypoplastic enamel surrounded by a zone of hypocalcification
• Commonly affected: middle third of buccal surface
• AD Smooth pattern: enamel of all teeth exhibits a smooth surface & is
thin, hard & glossy
• Appear like crown preparations
• Colour: opaque white – translucent brown
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• X-linked Smooth pattern: diffuse, thin, smooth & shiny enamel
• Have shape of tooth preparation
• Colour: brown to yellow-brown

• Rough pattern: enamel is thin, hard & rough-surfaced

• Teeth taper towards incisal-occlusal surface
• Colour: white to yellow-white

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Hypomaturation AI
• Defect in maturation of enamel’s crystal structure
• Affected teeth: normal shape, exhibit mottled, opaque white-brown-
yellow discolouration
• Enamel - softer than normal & tends to chip from underlying dentin
• Pigmented pattern: surface enamel – mottled & agar-brown
• Fractures from underlying dentin, even by dental explorer
• X-linked pattern: deciduous teeth – opaque white with translucent
mottling, permanent teeth – opaque yellow-white, darken with age
• Degree of enamel loss – very rapid

37
• Snow-capped pattern: a zone of white opaque enamel on incisal/occlusal
¼ - 1/3rd of crown
• AD pattern of inheritance

38
Hypocalcified AI

• Enamel matrix - without significant mineralisation

• Enamel – soft & easily lost
• Shape – normal, colour – yellow-brown or orange
• Anterior open bite

39
Treatment:

1. Selective odontotomy
2. Full veneering – shouldn’t oppose a natural teeth
3. Prevention from caries - fluorides, CPP-ACP paste, diet modifications
4. Restorations, if required – GIC, adhesive resin

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DENTINOGENESIS IMPERFECTA

• Hereditary opalescent dentin

• Hereditary developmental disturbances (AD) of dentin in the absence of
any systemic disorder
• Chr.4 - DSPP

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DI 1/ Teeth are blue grey / amber brown / opalescent
Shields
type II

R/F: bulbous crown, narrow roots, pulp chamber & root canal-
normal or completely obliterated

DI 2/ Presence of multiple pulp exposure, normal nonmineralized pulp

chambers & canals
Shields Amber discolouration , attrition, fractured enamel
type III/
R/F: Appearance of shell teeth
Brandywine
type H/F: dentin- composed of irregular tubules with large uncalcified
matrix
Tubules- larger diameter, numerous, sometimes absent
Pulp chamber- may be obliterated by continued deposition of
42
dentin
Treatment:

cast metal crowns - posterior teeth

jacket crowns - anterior teeth

RCT, if indicated

43
Endodontic Considerations:

• Pulp chamber – small

• Root canal - partially/totally obliterated
• Decreased resistance to instruments
• Increased chance for procedural errors
• Chelating agents – not advised
• Rotary instruments – gentle force

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DENTIN DYSPLASIA
• Rootless teeth
• Rare disturbances of dentin
formation characterised by
normal enamel but atypical
dentin formation with abnormal
pulp morphology
Systemic diseases associated with
dentin dyspalsia:
Calcinosis universalis
Rheumatoid arthritis & vitaminosis D
Sclerotic bone
Tumoral calcinosis
45
 • Periapical lesion
Type I (Radicular Type) - • Premature tooth loss may occur because of short
roots or periapical inflammatory lesions
both dentitions - normal
• R/F: roots are extremely short, pulps almost
colour completely obliterated & periapical radiolucencies
(granulomas, cysts, chronic abscesses)
• Coronal pulps - large (thistle tube appearance) &
Type II (Coronal Type) - filled with globules of abnormal dentin
colour of primary dentition • R/F: Deciduous:- roots - extremely short , pulp
is opalescent, permanent chamber - completely obliterated
dentition is normal • Permanent:- abnormally large pulp chambers in
coronal portion

Treatment: intermediary
basing, RCT – unsuccessful
(Tidwell & Cunningham,
1979)

46
REGIONAL ODONTODYSPLASIA
• Odontogenic Dysplasia/
Odontogenesis Imperfecta/
Ghost Teeth
• Localised, non-hereditary
developmental abnormality of
teeth with extensive adverse
effects on formation of enamel, Pathoses associated with regional
dentin, & pulp odontodysplasia:
• Maxillary teeth > mandibular Ectodermal dysplasia
teeth Epidermal & vascular nevi
• Unknown aetiology Neurofibromatosis
• Delay or total failure in eruption Rh factor incompatibility
Hypophosphatasia
• Shape is altered, irregular in
appearance 47
• R/F: marked reduction in radiodensity
• teeth assume a “ghost” appearance
• both enamel & dentin appear very thin
• pulp chamber is exceedingly large

• Treatment: poor cosmetic appearance of teeth – extraction / restoration

followed by prosthetic rehabilitation

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 ENVIRONMENTAL ALTERATIONS

Environmental Postdevelopmental Environmental Localised

effects on tooth loss of tooth discolouration of disturbances in
structure structure: teeth: eruption:
development: • Attrition • Extrinsic stains • Impaction
• Turner’s hypoplasia • Abrasion • Intrinsic stains • Ankylosis
• Hypoplasia due to • Erosion
antineoplastic • Abfraction
therapy • Resorption
• Syphilitic hypoplasia
• Dental fluorosis

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 ENAMEL HYPOPLASIA
• Incomplete or defective formation of
organic enamel matrix of teeth
• TYPES:
I. Hereditary type-both dentition
II. Type caused by environmental
factors-only single tooth
• CLINICAL FEATURES:
I. Mild cases - few grooves, pits &
fissures
II. Moderate - rows of deep pits
III. Severe forms- considerable
portion of enamel may be absent 50
Hypoplasia due to Nutritional Deficiency &
Exanthematous Fevers:
• Deficiencies of vit. A,C,D
• Rickets – strong association with hypoplasia
• Exanthematous fevers – measles, chicken pox, scarlet fever
• Ameloblasts – most sensitive groups of cells in body in terms of metabolic
function
• Pitting type of hypoplasia
• Within 1st year of birth
• Incisors, canines, 1st molars – frequently affected

51
Syphilitic Hypoplasia

• Due to congenital syphilis

• Not of pitting type
• Maxillary & mandibular anterior teeth – Hutchinson’s teeth – screw-driver
shaped

• 1st molars – mulberry molars/ Moon’s molars/ Fournier’s molars – irregular

& agglomerate mass of globules of enamel on occlusal surface & occlusal
third – with well formed cusps

52
Hypoplasia due to Birth Injuries

• Appear as neonatal line/ring (Schour, 1936)

• In deciduous teeth & 1st permanent molars
• Usually found in preterm children (Graham & Larson)

53
Turner’s Hypoplasia

Due to local infection or trauma

Pathogenesis-
• A. Local infection- if deciduous teeth become carious when crown of
succedaneous permanent tooth is formed, bacterial infection involving periapical
tissues disturb ameloblastic layer of permanent tooth bud, resulting in
hypoplastic crown
• B. Trauma- When deciduous teeth have been driven into alveolus & have
disturbed permanent bud while it is still being formed, resulting injury leads to
yellowish or brownish discoloration of enamel usually on labial surface or as true
hypoplastic pitting effect
Most commonly affected teeth are permanent premolars (due to infection),
maxillary incisors (due to trauma)
Brownish discoloration of enamel , severe pitting & irregularity of crown
Cementum may also be yellowish-brown 54
Management:

• Min. size – selective odontotomy, tooth-coloured restorations without

mechanical preparations
• Defect at occlusal /contacting surface – metallic/cast restorations
• Vital bleaching
• Veneers – direct/indirect

55
DENTAL FLUOROSIS

• Mottled enamel (GV Black & Frederick McKay,1916)

• Extremely common disorder, characterized by hypomineralization of tooth
enamel caused by ingestion of excessive fluoride during enamel formation
• Causes:
• Excess fluoridation of drinking water
• Ingestion of fluoride toothpaste
• Overuse of Fluoride tablets
• Consumption of processed food made with fluoridated water
• ↑ in fluoride intake results in an ↑ in degree & extent of porosity of
enamel
56
• Enamel changes due to damage of secretory ameloblasts by fluoride
• Due to fluoride induce change in composition of enamel matrix or be a
result of disturbance of the cellular processes during enamel maturation
• C/F: Chalk like discoloration of teeth with white spot or lines on tooth
enamel
• In more severe cases, affected area have yellow or brown discoloration
• In extreme forms, fluorosis may result in pitted tooth surface
• Corroded appearance

57
Dean’s Index

58
59
Management:

Optimum F- level in water –

0.7-1.2 ppm

Microabrasion – to remove
outer stained enamel

Bleaching

Veneers

60
RESORPTION OF TEETH

• A condition associated with either a physiologic or a pathologic process

resulting in loss of dentin, cementum, bone
– Glossary of Endodontic Terms, AAE, 2006
• Physiologic resorption: in deciduous teeth during eruption of permanent
teeth
• Pathologic resorption: in both deciduous & permanent teeth due to
underlying pathology
• When protected structures are damaged / removed, multinucleated cells
(osteoclasts) colonize root surface & cause resorption

61
Classification
Andreasen’s Inflammatory
classification
Internal
Replacement

Surface
External Inflammatory
Replacement
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Lindskog’s Classification:
Trauma Surface
induced Transient
resorption Pressure
Orthodontic
Replacement
Infection Internal inflammatory
induced
resorption External inflammatory
Communicating
Hyperplastic Internal replacement
invasive Invasive coronal
resorption Invasive cervical
Invasive radicular
63
Australian Dental Journal Endodontic Supplement, 2007
Cohen & Burns’ Classification:

Inflammatory Pressure
• External • Due to
• Apical orthodontic
movement Resorption due
• Lateral DA ankylotic
Idiopathic • Due to to systemic
• Cervical replacement
impacted causes
• Internal
teeth
• Due to
tumours/cysts

64
Tronstad’s Classification:

• Progressive
Inflammatory
• Transient

• Perforating
Internal
• Non-perforating

65
Weine’s Classification:

Internal
• Perforating
• Non-perforating

External
• Mild
• Aggressive

66
Factors Affecting:

1. Physiologic 3. Systemic factors

2. Local factors 1. Hormonal imbalance
1. Periapical inflammation 2. Paget’s disease
2. Trauma 3. Herpes zoster
3. Tumours/cysts
4. Mechanical/occlusal forces
5. Impacted teeth
6. Intracoronal bleaching
7. Periodontal procedures

67
Mechanism:

Injury

Degradation of
inorganic crystals

Degradation of
organic matrix

68
Internal Resorption

• Chronic perforating hyperplasia of pulp/ Pink tooth of Mummery

• An unusual form of tooth resorption that begins centrally within tooth
apparently initiated in most cases by a peculiar inflammation of pulp (Shafer)
• Aetiology:
1. Long-standing chronic inflammation
2. Trauma
3. Iatrogenic
4. Idiopathic

69
Clinical Features:
• Usually asymptomatic, sometimes pain
• Most common – cervical
• Usually single tooth
• Granulation tissue – PINK SPOT

• R/F:
• Uniform, round to oval RL enlargement of pulp space – Ballooning –
inflammatory resorption
• Irregular RO present inside root canal – replacement resorption

• Management: without perforation – Endodontic therapy

• With perforation – nonsurgical – Ca(OH)2 therapy
• Surgical – surgical flaps, root resection, intentional replantation
70
External Resorption

• Initiated in periodontium & affects external or lateral surface of root

• Aetiology:
• Trauma, reimplanted teeth
• Tumours & cysts
• Periapical infection – granuloma
• Excessive mechanical/occlusal forces
• As a part of repair process
• Idiopathic resorption

• C/F: no significant signs

• R/F: small lesion – difficult to find

• Apical area- shortening of roots
71
DISCOLOURATIONS
• Any change in the hue, colour or translucency of a tooth due to any
cause – Ingle

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73
Tetracycline Staining

• Severity depends on stage of tooth development at time of drug administration

• Other factors:
• Placental crossing – deciduous teeth-affected
• Dosage
• Length of time over which administration has occurred

74
 Clinical features:
• Yellowish/ brownish-grey discolouration – pronounced at time of eruption
– gradually becomes more brownish after exposed to light
• Dentin is more stained than enamel

• Tetracycline
Minocycline Yellow
hydrochloride • Oxy-tetracycline

Brownish
• Chlortetracycline
to grey
Oxy-
tetracycline
(Doxycycline)
75
Critical Period for Discolouration: Moffitt et al

• Based on period of mineralisation of 1st mm of dentin nearest DEJ

• 4 mo in utero – 6 mo postpartum – deciduous maxillary & mandibular

incisors
• 5 mo in utero – 9 mo postpartum – deciduous maxillary & mandibular
canines
• 3-5 mo postpartum – 7 yrs – permanent maxillary & mandibular incisors &
canines

Prediction of tetracycline-induced tooth discoloration, Moffitt et al, JADA 88(3): 547-552

76
Extrinsic stain Intrinsic stain

Treatment: scaling & polishing Treatment: non-vital bleaching, veneering,

crowns

77
 MICROBIAL DISEASE - CARIES
• “Dental caries is an irreversible microbial disease of the calcified tissues of the
teeth, characterised by demineralisation of the inorganic portion & destruction of
the organic substance of the tooth, which often leads to cavitation.” – SHAFER

• “Dental caries is an infectious microbiologic disease of the teeth that results in

localised dissolution & destruction of calcified tissues.” – STURDEVANT

• “Dental caries is defined as localised post eruptive pathological process of external

origin involving softening of the hard tooth tissue & proceeding to the formation
of cavity.” - WHO

78
G V Black’s Classification:
Class I
• Occlusal surfaces of posterior teeth Class IV
• Occlusal 2/3rds of buccal & lingual
surfaces of posterior teeth • Proximal surfaces of anterior teeth
• Lingual surfaces of anterior teeth involving incisal angle

Class II Class V
• Proximal & occluso-proximal • Gingival 1/3rd of facial or lingual
surfaces of posterior teeth surfaces except pit & fissures

Class III Class VI

• Proximal surfaces of anterior teeth • Incisal edge of anterior teeth
not involving incisal angle • Occlusal cusp tip of posterior teeth
80
81
 Sturdevant’s Classification:
• Based on location:
• Occlusal – pit & fissure caries Occlusal Smooth Surface
Odontoclasia
• Proximal & cervical – smooth surface caries Caries Caries
• Linear enamel caries / odontoclasia
• Root caries
• Based on extent:
Incipient Chronic
• Reversible – incipient caries Root Caries
Caries Caries
• Irreversible – cavitated caries
• Occult caries
• Based on rate of spread of caries:
• Acute/ rampant caries Occult Rampant Arrested
• Chronic /slow caries Caries Caries Caries
• Arrested caries
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 Other Classifications:
Based on time • Primary caries
of caries • Recurrent / secondary
attack caries

Based on • Forward caries

direction of
caries spread • Backward caries

Based on no. • Simple

of surfaces • Compound
involved • Complex

84
 Aetiology:

• INITIATION – S. mutans
MICRO- • PROGRESSION – Lactobacillus
ORGANISMS • ROOT CARIES - Actinomyces

• Morphology TOOT
Caries TIME
• Fluoride H

FOOD • Sucrose
• Sticky foods
Saliva – Critical pH = 4.5-5.5
85
Management:

Preventive measures:

• Proper brushing & oral hygiene practices

• Fluorides & pit & fissure sealants

Treatment procedures

86
87
 Protocol for Treatment of Root Caries: Billing’s Index:
Grade 1: Incipient; no surface defect; need
remineralisation therapy

Grade 2: Shallow, surface defect<0.5mm;

need recontouring

Grade 3: Cavitation; surface defect>0.5mm;

need restoration

Grade 4: Pulpal; carious pulp exposure;

need RCT + restoration

Billings RJ, Brown LR, Kaster AG. Contemporary treatment strategies for root surface dental
88
caries. Gerodontics. 1985;1(1):20–27
 TOOTH WEAR

Grippo defined four categories of tooth wear:

• Attrition
• Abrasion
• Abfraction
• Erosion

Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and abfraction revisited: a new perspective on
tooth surface lesions. J Am Dent Assoc. 2004;135:1109–18

89
Attrition:
• Physiologic wearing away of a tooth as a result of tooth-to-tooth contact, as
in mastication (Shafer)
• Surface tooth structure loss resulting from direct frictional forces between
contacting teeth (Marzouk)
• Continuous, age-dependent process, which is usually physiologic
• Occlusal / incisal & proximal surfaces
• Deciduous & permanent dentition
• Shortening of arch length – reduction in mesiodistal diameters of teeth
through proximal attrition – Robinson et.al

Robinson HBG, Boling LR, Lischer BE. EV Cowdry: Problems on Ageing (2nd ed). Williams & Wilkins, Baltimore,1941
90
• Males > females
• ↑ attrition – associated with:
• Coarseness of diet
• Tobacco chewing
• Bruxism
• Persons exposed to abrasive dust
• C/F: Enamel may completely
worn away – appear as yellow
Complete loss of cuspal
interdigitation
Hypersensitivity
• H/F: Exposure of dentinal
tubules
Formation of secondary dentin
pulpal to primary dentin
91
2 types:

Attrition

Proximal surface
Occluding surface
attrition/ Proximal
attrition / Occlusal wear
surface faceting

92
Proximal Surface Faceting:

• Results from surface tooth structure loss & flattening/widening of proximal

contacts
• Proximal surface area ↑, cleansability ↓
• Mesio-distal dimensions ↓→ drifting → arch length↓ → altered occlusion
• ↓ embrasure space → alteration of physiology of interdental papilla →
difficult plaque control → periodontitis

93
Occluding Surface Attrition:
• Loss, flattening, faceting, &/or reverse cusping of occluding elements →
loss of vertical dimension of teeth
• If wear is severe, generalised & occurs in a shorter period → loss of
vertical height of face & vertical dimension
• If wear is over a long period of time, alveolar bone can grow occlusally
→ loss of VD is seen, but not imparted to face
• Deficient masticatory capabilities, blunting of cusps → patient applies
more force on teeth
• Cheek biting: can be a sequelae
• Decay at occluding surface → exposed dentin → tooth sensitivity

94
 Attrition
• Management:

Cessation of Diet Management Aesthetic

habits modification of sensitivity corrections

97
1. Extraction/ RCT of pulpally involved
teeth
2. Parafuntional activities, bruxism should
be controlled
3. Myofunctional, TMJ, or any
stomatognathic system disorders should
be diagnosed & resolved
4. Occlusal equilibrium should be
maintained
5. Protect sensitive dentinal areas & actual
caries should be obliterated
6. Restorative modalities should be done

98
Restorations:

Incisal edges – restored to the original vertical

dimension with direct composite resin (Strassler et al)

Adhesive cast metal restorations – to replace missing

tooth structure (Nohl et al)

If occlusion –severely altered – reconstruction with

crowns & bridges (Stewart et al)
99
 Dahl concept:
Inter-occlusal Space – created by placing restorations
intentionally in supra-occlusion – allowing axial tooth
movement, re-establishing complete occlusion
Partial bite raising appliance – used to create
inter-occlusal space in patients with severe
localized attrition
Removable appliance, cast in Co-Cr - palatal
aspects of upper anterior teeth - worn 24 hr/day

After 8 mo, sufficient space - created to restore

upper anterior teeth

Reduced amount of tooth preparation required -

compromised palatal surface

Restored with full ceramic crowns

Poyser NJ, Porter RW, Briggs PF, Chana HS, Kelleher MG. The Dahl Concept: past, present and future.
100
Br Dent J. 2005 Jun 11;198(11):669-76; quiz 720.
Endodontic Considerations:

RCT in incisors with attrition:

• Access opening – incisal aspect
• Pulpal recession – may seen
• Post – additional retention

101
 Abrasion
• Pathological wearing away of tooth substance through some abnormal mechanical
process (Shafer)
• Surface loss of tooth structure resulting from direct friction forces between the teeth &
the external objects (Marzouk)
• On exposed root surfaces, sometimes on incisal or proximal surfaces
• Most common cause – use of an abrasive dentifrice – wear of cementum & dentin if
toothbrush carrying dentifrice is used injudiciously – horizontal direction -Robinson
• C/F: V or wedge-shaped ditch on root side of CEJ with some gingival recession
Lesions – more wide than deep
Angle formed in the depth of lesion & enamel edge – sharp
Exposed dentin – highly polished

Robinson HBG. Abrasion, attrition & erosion of teeth. Health Center J Ohio State Univ, 3: 21,1949
102
• More abrasion on left side – right handed
people
• Premolars & cuspids – commonly affected
• Also found associated with habits:
• Notching of incisal edge of maxillary central
incisor – opening of bobby pins with teeth
• Improper use of dental floss & tooth picks –
proximal abrasion
• H/F: Exposure of dentinal tubules
Formation of secondary dentin

103
Severity depends on:

1. Direction of brushing strokes

2. Size of abrasive
3. Percentage of abrasives in the dentifrice
4. Type of abrasive
5. Diameter of brush bristles
6. Type of bristle
7. Forces used in brushing
8. Type of tooth tissues being abraded

104
 Signs & Symptoms of Toothbrush Abrasion:
1. Linear in outline, following path of
brush bristles
2. Peripheries of lesion - angularly
demarcated from adjacent tooth
surface
3. Surface of lesion - extremely smooth
& polished
4. No plaque accumulation or carious
activity
5. Surrounding walls of abrasive lesion
tend to make a ‘V’- shape, by meeting
at an acute angle axially
6. Probing or stimulating (hot, cold or
sweets) lesion - elicit sensitivity/pain
105
Incisal Abrasion:

Notching of incisal edges – due to

bobby-pin opening

106
• Treatment is indicated when:
1. Caries is present
2. Sensitivity is present
3. Cervical abrasion contributing to periodontal problem
4. Aesthetic consideration

• Management:
1. Flowable resin
2. GIC
3. Microfilled composites

107
• High modulus restorative materials - unable to flex - cervical regions when
tooth structure is deformed under occlusal load &, therefore restorative
materials can’t be displaced from cavity
Heymann HO ,Sturdevant Jr ,Baynes S ,JADA,122(2) 41-57

• An intermediate material with reduced elastic modulus may function as a

stress absorbing layer & improve marginal sealing
Kemp-Scholte CM ,Davidsson,CL complete marginal seal of class V resin composite restorations
affected by increased flexibility .JDR 1990 ;69:1240 -3

108
Endodontic Considerations:

• Sec. dentin deposition

• Maxillary anteriors – lingual wall of pulp chamber
• Molars – on floor of pulp chamber
• Pulp – appear to recede; small pulpal remnants - remain → less calcific tract → pulp
exposure
Berkley D, Berg RG. The age-old patient: challenges in decision making, JADA, 1996; 127-130

109
Abfraction
• Grippo (1991) coined abfraction
• Pathologic loss of both enamel & dentin caused by biomechanical loading forces
(Shafer)
• Forces – static (swallowing & clenching) or cyclic (chewing)
• Abfractive lesions – caused by flexure & ultimate material fatigue of susceptible
teeth – break down of enamel from crown
• With each bite, occlusal forces causes teeth to flex
• Tooth breaks off from gingival third on buccal surface of crown while tooth
brushing
• Premolars – commonly affected, lingual surface of mandibular teeth – rarely
involved
• Found as isolated lesions, with neighbouring teeth uninvolved
110
 Abfraction: “Stress Lesion”
Changes in stress patterns continuously in same area

Underneath the enamel, compressive ↔ tensile

stresses reach to fatigue limit

Rupture of chem. bond between hydroxyapatite

crystals Occlusal interferences,
premature contacts, habits
of bruxism and clenching
may act as stressors
Abfraction
111
• Also known as idiopathic erosion (Lee et al)
• Microfractures can foster loss of tooth structure from tooth brush abrasion
and from acids in the diet or plaque or both
• Abfraction has a possibility of being the initial factor and the dominant
progressive modifying factor in producing cervical lesions

112
Method of Determining the Activity of Abfraction
Lesions: Scratch Test
• No.12 scalpel blade - used to superficially scratch tooth surface
• Visual observation - indication of rate of tooth structure loss
• Loss of scratch definition or loss of the scratch altogether signifies active
tooth structure loss

Kaidonis JA.The tooth wear: View of anthropologists, Clin. Oral Investig., 2008

113
Restorations:

• When dentin hypersensitivity have developed or likely to be developed

• Aesthetics demands are a concern
• RMGIC should be the first preference (Tyas)
Tyas MJ, the class V lesion – aetiology ,restoration, Aust. Dental Journal.1995

• In esthetically demanding cases - RMGIC/GIC liner laminated with resin

composite
• Vandelwalle and Vigil (1997) recommended use of microfilled resin
composite (low modulus of elasticity) - it will flex with tooth without
compromising retention

114
Occlusal Adjustments:

• Occlusal adjustment may involve:

• Altering cuspal inclines
• Reducing heavy contacts
• Removing premature contacts
• Occlusal splints : Aimed at reducing amount of nocturnal bruxism & non
axial tooth loading when constructed properly
Examining the prevalence and characteristics of abfraction-like cervical lesions in a population of U.S.
veterans, Piotrowski et al., JADA, 132(12), 1694 –1701, 2001

Restoration of non-carious cervical lesions Part II. Restorative material selection to minimise fracture, Ichim IP
et al, Dent Mater, 23(12):1562-9, 2007

115
 Erosion
▪ Irreversible loss of dental hard tissue by a chemical process that doesn’t involve
bacteria (Shafer)
▪ Dissolution of mineralized tooth structure occurs upon contact with acids that
are introduced into oral cavity from intrinsic or extrinsic sources (Marzouk)
▪ Causes:
• Acidic beverages, foods, medications
Extrinsic
or environmental acids, iatrogenic
Sources
exposure

Intrinsic • GERD, Chronic excessive vomiting

Sources (Anorexia nervosa/ Bulimia)

Hellstrom I. Oral complications in anorexia nervosa. Scand J Dent Res, 85: 71, 1977.

116
Any food substance with a critical pH value of < 5.5 can become a
corrodent & demineralize the teeth

Corrosive potential of an acidic food depends on its pH value, buffering

capacity of acid, frequency & duration of ingestion

Lussi A. Dental erosion: clinical diagnosis and case history taking. Eur J Oral Sci 1996, 127-31

117
Clinical Features:
• Broad concavities within smooth
surface enamel
• Cupping of occlusal surfaces &
incisal grooving with dentin
exposure
• Increased incisal translucency
• Wear on non-occluding surfaces
• Enamel cuff in gingival crevice
• Hypersensitivity
• Erosion due to excessive
vomiting – palatal surface of
maxillary incisors
• Erosion due to acidic beverages –
labial surface of maxillary incisors
• Increased salivary pH –
xerostomia – results in erosion
118
Perimolysis:

• Decalcification of teeth caused by exposure to gastric acid in patients

with chronic vomiting, as may occur in anorexia or bulimia
• Palatal surfaces of maxillary dentition in which exposed dentin exhibits
a concave surface & a peripheral white line of enamel
• Loss of palatal enamel & dentin due to acid regurgitation aggravated by
circular movements of tongue
• Associated with stress reflux syndrome

119
 Protocol for Prevention of Progression of Erosion:

1. Diminish frequency & severity of acid challenge

2. Enhance defence mechanisms of body
3. Enhance acid resistance, remineralisation & rehardening of tooth surfaces
4. Improve chemical protection
5. Decrease abrasive forces
6. Provide mechanical protection
7. Monitor stability

Gandara BK, Truelove EL. J Conte Dent Pract, 1(1), Fall Issue, 1999
120
Restorations:

Metallic restorations - choice of material - more resistant to erosion

Tooth colored materials may also be used with minimal or no tooth

preparation, with the assumption that restoration may require
periodic replacement

121
PHYSICAL & CHEMICAL INJURIES

PHYSICAL INJURIES CHEMICAL INJURIES

• Bruxism • Effect of restorative materials
• Fractures
• Ankylosis

122
Bruxism
• Night-grinding/bruxomania
• Habitual grinding/ clenching of the teeth, either during sleep or as an
unconscious habit during waking hours
• One of the most common sleep disorders
• Aetiology:
1. Local factors – occlusal disturbances, transition of dentition from primary
to permanent
2. Systemic factors – GI disturbances, nutritional deficiencies, allergy,
endocrine disturbances
3. Psychologic factors – most common cause – stress, emotional tension,
anxiety
4. Occupations – athletes, watchmakers
123
 Clinical features (Glaros & Rao):

• Effects on dentition – attrition, abfraction

• Effects on periodontium – mobility & loosening of teeth, gingival recession,
alveolar bone loss
• Effect on masticatory muscles – hypertrophy (masseter), trismus
• Effect on TMJ – dislocations, MFPDS
• Headache & facial pain
• Psychologic & behavioural effects

124
Treatment & Prognosis:

• Removal of underlying cause

• Removable occlusal splints worn at night – to immobilise jaw / guide the
movement to minimise periodontal damage
• Inj. Botox IM (masseter) – weakening of muscle – to stop clenching &
grinding

125
Fractures

• Causes:
1. Physical trauma
2. Occlusal prematurities
3. Repetitive heavy and stressful
chewing
4. Resorption - weakened teeth
5. Iatrogenic dental treatment

126
127
Cracked Teeth
• As a result of parafunctional habits / from weakened tooth structure
• Symptoms that develop subsequent to these cracks ― cracked tooth syndrome
• Acute pain during the mastication of small hard food substances & exacerbates
with cold
• Signs & symptoms of a cracked tooth - consistent with an irreversible pulpitis or
necrosis
• 2 groups of cracked teeth : A) TOOTH INFARCTIONS(incomplete tooth fractures
extending partially through a tooth ) that includes:
• Craze lines
• Cuspal fractures
• Cracked teeth
B) VERTICAL ROOT FRACTURES : that occur in endodontically treated teeth

Cameron CE,JADA,1964 : American Association of Endodontists,2008

131
132
Management:
Ellis Class 1
• Smoothing of edges & peripheries
• Esthetic reshaping
• If relatively large surface areas involved:
• In anterior teeth - GIC restoration
• In posterior teeth – metallic restoration
Ellis Class 2
• In anterior teeth -provisional restoration - Class IV
• In posterior - amalgam restoration
Ellis Class 3
• In anterior - provisional restoration can be Class IV
• In posterior - amalgam restoration 133
Management:
Ellis Class 4
• If tooth crown is intact - Endodontic therapy
• If tooth crown is fractured – pulpectomy/root canal therapy
• If tooth crown is discolored – non vital bleaching/laminated veneering
• If tooth is discolored beyond any bleaching - veneered with cast alloy based/cast
ceramic restoration
Ellis Class 5
• Accidental tooth loss / fracture beyond any restorative capability - replaced with a
prosthesis like:
• Provisional fixed bridge
• Pontic
• Electrochemically etched - non noble alloy based bridge
134
Management:

Ellis Class 6
• Cervically horizontal : endodontic therapy
• Midradicularally horizontal : endodontic treatment &/or splinting
• Apically horizontal:
• Vital tooth – should be left without interference
• Non-vital tooth - endodontic therapy & splint, when surgery is not feasible
• Vertical root fracture - unfavourable prognosis
• Single rooted teeth - extraction
• Multirooted teeth - hemisectioning
Ellis Class 7
• After proper reduction of tooth &/or replacing in its socket; splinted
135
Management:

Ellis Class 8
• Endodontic treatment
• Pulp chamber should be filled with resin & 2 pieces should be brought
together & kept under pressure until primer & composite resin sets

Ellis Class 9
• Relieve tooth from eccentric occlusal contacts
• Orthodontic band
• Any sign of pulpitis – endodontic therapy
136
Ankylosis

• Fusion between tooth & bone

• Cause: when partial root resorption is followed by repair with cementum /
bone
• C/f: dull, muffled sound on percussion
• Usually asymptomatic
• R/f: loss of PDL space with mild sclerosis of bone
• H/f: area of root resorption with repair by calcified material
• Treatment: no treatment

137
Effect of Restorative Materials:
• Amalgam: dark coloured metallic components of silver alloy turn dentin
dark grey & tooth appears discoloured – Amalgam blues

138
Effect of Metals:

LEAD: Deposited in deciduous MERCURY/ ACRODYNIA:

teeth in lead poisoning – index Bruxism, premature shedding of
of body burden of Pb (Altshuller) teeth

139
REGRESSIVE CHANGES AFFECTING TEETH

DENTINAL SCLEROSIS

HYPERCEMENTOSIS

CEMENTICLES

PULP CALCIFICATION

140
DENTINAL SCLEROSIS
• Transparent dentin
• Calcification of dentinal tubules & a thicker layer of peritubular dentin
• Secondary to caries or normal ageing process – deposition inside periphery of
tubules
• Tubules – smaller in diameter – less permeable – lesser transmission of stimuli

141
 HYPERCEMENTOSIS
• Cementum hyperplasia
• Non-neoplastic condition in which excessive cementum is deposited in continuation with
normal radicular cementum
• Aetiology:
• Tooth repair
• Inflammation
• Paget’s disease
• Mechanical stimulation
• Functionless & unerupted teeth
• Idiopathic
• May associated with ankylosis
• R/F: sharpened appearance of root
• Endodontic consideration: CDJ farther
from apex – penetration into cemental canal- difficult 142
CEMENTICLES
• Small foci of calcified tissue, not necessarily true cementum, which lie free
in PDL of lateral & apical root areas
• Aetiology: unknown; represents areas of dystrophic calcification - of nests
of epithelial rests in PDL as a result of degenerative change
• Enlarge by further deposition of Ca salts in adjacent surrounding
connective tissue – ‘circular lamellated structure’
• 2 types – free & attached

143
Cemental Tears:

• Small spicules of cementum torn from root surface

• Usually follows a trauma

• 2 types: complete & partial

• Detached cementum - reunited to root surface / may be completely resorbed /
may undergo partial resorption followed by addition of new layers
144
Cemental tear: To know what we have neglected in dental practice. Jeng P et al., Journal of the Formosan
145
Medical Association,2018, 117(4), 261-267
 PULP CALCIFICATIONS

• Physiological manifestation
• May increase in number &/or size due to local or systemic pathology
• Aetiology:
• Pulp degeneration
• Inductive interactions between epithelium & pulp tissue
• Age
• Circulatory disturbances in pulp
• Periodontal diseases & caries
• Dentinogenesis imperfecta
• Restorative procedures & fluoride prophylaxis
• Orthodontic tooth movement
• Genetic predisposition
• Idiopathic factors
• Systemic factors: cardiac disease, renal stones, hypoparathyroidism

146
Pathophysiology:

147
Types of Calcifications:

• Central cavity filled with epithelial remnants &

Denticles surrounded peripherally by odontoblasts

• Compact degenerative masses of calcified

Pulp stones tissues

• Amorphous & unorganised linear strands of calcification

Diffuse in pulp tissue
• Usually following collagen fibre bundles or blood vessels
calcifications • Commonly found in root canals & less often in coronal
areas
148
Types of Denticles: Based on Morphology:

TRUE DENTICLES FALSE DENTICLES

• Localised masses of calcified tissue
that resembles dentin
• Resembles more of secondary
dentin
• Common in pulp chamber
• Size: >1mm
• Don’t exhibit dentinal tubules
• Appear as lamellae deposited
around a central nidus
• Larger than true denticles
• May fill entire pulp chamber

149
Types of Denticles: Based on Location:

EMBEDDED PULP STONES

• Formed in pulp but with ongoing physiological dentin formation, they
become enclosed within canal walls

FREE PULP STONES

• Found within pulp tissue proper
• Most commonly found type on radiograph

150
Endodontic Considerations:
• Reduced pulp chamber volume –
intrapulpal anaesthesia – difficult &
lasts for a max. of 20 min
• Difficult to identify canals
• Long shank burs, guided access – for
access preparation
• Pilot files, explorers(JW-17) – to locate
canals
• Missed canals – champagne bubble test,
bleeding points
• Under magnification

151
152
CEMENTOBLASTOMA
• True cementoma
• Odontogenic neoplasm of cementoblasts
• C/F: common in mandible – molar & premolar region
• Rarely affect deciduous teeth
• Occur before 30 yrs
• Symptoms- pain, swelling
• Signs of local invasion- bony expansion, cortical erosion, displacement of
adjacent teeth, maxillary sinus involvement, infiltration into root canal & pulp
chamber
• R/F: RO mass fused to one or more roots, surrounded by thin RL rim
• Treatment: surgical extraction of tooth together with attached clinical
mass
153
CONCLUSION

• Tooth is prone to various physical & chemical threats

• Even before eruption
• Various environmental & genetic factors cause abnormalities on teeth
• In shape, size, number, structure
• Ranges from very common caries to very rare genetic diseases affecting the
condition of teeth
• Different factors affect variedly to different hard tissues – enamel, dentin &
cementum

154
REFERENCES
• Sturdevant’s Art & Science of Operative Dentistry, 5th ed, Theodore Roberson, Herald
Heymann, Ed Swift, p65-131
• Operative dentistry-modern theory and practice –MA Marzouk
• Grossman’s Endodontic Practices, 12th Ed
• Shafer’s Textbook of Oral Pathology, 6th ed, Shafer, Hine, Levy, p3-62,517-563,569-588
• Orban’s Oral Histology & Embryology – 12th Ed – G.S.Kumar,p10-14,237-239
• Oral & Maxillofacial Pathology- 3rd Ed – Neville, Damm, Allen, Bouquot(9-16,362-
433,741-752)
• Differential Diagnosis of Oral and Maxillofacial Lesions, 5th Ed -Norman K. Wood, Paul W.
Goaz (90-95)
• Problems in Endodontics - Etiology, Diagnosis & Treatment, Michael Hulsman, Edgar
Schafer (485-530)
• Pathology of the Hard Dental Tissues – Albert Schuurs

155
REFERENCES
• Clinical Operative Dentistry – Principles & Practice – Ramya Raghu -2nd Edition
• Hart PS, Hart TC. Disorders of human dentin. Cells Tissues Organs.
2007;186(1):70-7.
• Billings RJ, Brown LR, Kaster AG. Contemporary treatment strategies for root
surface dental caries. Gerodontics. 1985;1(1):20–27
• Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and abfraction
revisited: a new perspective on tooth surface lesions. J Am Dent
Assoc. 2004;135:1109–18
• Robinson HBG, Boling LR, Lischer BE. EV Cowdry: Problems on Ageing (2nd ed).
Williams & Wilkins, Baltimore,1941
• Hanif A, Rashid H, Nasim M. Tooth surface loss revisited:Classification, etiology,
and management. J Res Dent 2015;3:37-43
• Poyser NJ, Porter RW, Briggs PF, Chana HS, Kelleher MG. The Dahl Concept: past,
present and future. Br Dent J. 2005 Jun 11;198(11):669-76; quiz 720.

156
REFERENCES
• Heymann HO ,Sturdevant Jr ,Baynes S ,JADA,122(2) 41-57
• Kemp-Scholte CM ,Davidsson,CL complete marginal seal of class V resin
composite restorations affected by increased flexibility .JDR 1990 ;69:1240 -3
• Berkley D, Berg RG. The age-old patient: challenges in decision making, JADA,
1996; 127-130
• Kaidonis JA.The tooth wear: View of anthropologists, Clin. Oral Investig.,
2008
• Tyas MJ,the class V lesion –aetiology ,restoration, Aust. Dental Journal.1995
• Examining the prevalence and characteristics of abfraction-like cervical
lesions in a population of U.S. veterans, Piotrowski et al., JADA, 132(12),
1694 –1701, 2001
• Restoration of non-carious cervical lesions Part II. Restorative material
selection to minimise fracture, Ichim IP et al, Dent Mater, 23(12):1562-9,
2007
• Hellstrom I. Oral complications in anorexia nervosa. Scand J Dent Res, 85: 71,
1977.
157
REFERENCES
• Lussi A. Dental erosion: clinical diagnosis and case history taking. Eur J Oral Sci
1996, 127-31
• Gandara BK, Truelove EL. J Conte Dent Pract, 1(1), Fall Issue, 1999
• Australian Dental Journal Endodontic Supplement, 2007
• Prediction of tetracycline-induced tooth discoloration, Moffitt et al, JADA 88(3):
547-552
• Cameron CE,JADA,1964 : American Association of Endodontists,2008
• Cemental tear: To know what we have neglected in dental practice. Jeng P et al.,
Journal of the Formosan Medical Association,2018, 117(4), 261-267
• Sharma G & Nagpal A. Talon cusp: A prevalence study of its types in permanent
dentition & report of a rare case of its association with fusion in mandibular
incisor. J. Oral Dis., 2014; 26-32

158
159