Escolar Documentos
Profissional Documentos
Cultura Documentos
periodontics
Name
1. Everyone feels good when they are addressed by their name. The
purpose of asking the name of the patient is to make him feel
comfortable in order to establish a good rapport.
2. The name is also important for record purposes. It makes it easy
to identify the patient for future correspondence. It is also necessary
to have complete records in case of any medico-legal cases.
Age
1. Certain diseases are seen more commonly in certain
age groups.
Periodontal condition Age Reason
2. Capnocytophaga , Prevotella
intermedia and Prevotella
nigrescens which use hormones
as nutrients.
Acute necrotizing 15 30 years Seen at any age, but most
ulcerative gingivitis commonly between 15-30 years.
Children with Downs syndrome
or from low socioeconomic strata
are predisposed.
Desquamative gingivitis 40-50 years Auto-immune conditions are
common in middle aged women.
An exception is dermatitis
herpetiformis which is seen in
males between 20 to 30 years.
Periodontal Aggressive periodontitis <35 years The rate of bone loss here is 3-4
disease times faster than in chronic
periodontitis; hence, the disease
manifests at a younger age.
Chronic periodontitis >35 years Though the condition may begin
in adolescence, due to the slow
rate of progression it becomes
clinically significant after the age
of 35.
Prognosis of the patient depends upon the age. In two patients
with the same level of disease the older patient has a better
prognosis.
For example: If a 20 year old and a 50 year old patient have
generalized 7mm pockets, the 50 year old patient has taken
much longer to lose the same amount of attachment as to the 20
year old. The 20 year old patient would lose far more attachment
by the time she is 50. Obviously the rate of destruction is more
in the younger patient and the prognosis is obviously worse.
3. Anatomic differences:
The periodontium of children exhibits the following features:
Color of gingiva Less pale than in adults due to thinness of keratinized layer which makes
the underlying vessels more visible
1. Occupational hazards.
Abrasion: Notching on incisal edges maybe seen in carpenters and tailors
who hold bobby pins and needles between their teeth.
Erosion: People who work in factories with acidic environments show
eroded teeth.
2. Stressful jobs.
There is an increase in the hormone cortisol in stressful conditions. Cortisol
suppresses the immune system and therefore, increases the susceptibility
to infections like periodontitis.
Address
The chief complaint of the patient should always be in his/ her own words and
should include the symptoms of the patient in a chronological order.
The history of present illness should be elicited from the patient:
1. A detailed description of the patients chief complaint including when the
symptoms started. In case of pain, nature of the pain as well as aggravating
and relieving factors should be included.
2. Apart from the symptoms mentioned by the patient, the dentist should try to
ascertain whether a periodontal problem exists by asking the patient if he has
loose teeth, bleeding gums, food lodgment, bad breath or pain in his gums.
Pain can be identified as that of pulpal or periodontal origin based on the
following:
Pulpal pain Periodontal pain
Severe, lancinating, poorly localized pain. Dull, gnawing well localized pain or pain deep in
the bone.
Temporomandibular joint:
Lips:
Whether the lips are competent or not should be checked
while the patient is relaxed. If the patient is asked to close his
lips, he might forcefully close it and it becomes difficult to
differentiate between potentially competent and competent
lips.
Incompetent lips are usually associated with mouth
breathing. In these patients gingiva appears erythematous
and shiny especially in the maxillary anterior region. This
change has been attributed to surface dehydration.
Test to check mouth breathing
1. Mirror test
2. Butterfly test
3. Water holding test
Intraoral examination
Soft tissue examinations
Parts of oral mucosa:
Buccal mucosa: Lesions of lichen Planus, leukoplakia, erthyroplakia and oral submucous fibrosis
maybe seen on the buccal mucosa.
Physiological alterations that maybe seen include cheek bite (linea alba buccalis) and ectopic
sebaceous glands (Fordyces granules).
Labial mucosa: Vesicles and ulcers on the labial mucosa may be due to Herpes labialis. The scaling
appointment in these patients should be rescheduled and caution should be used during patient
examination since the condition is contagious. When it spreads to the clinicians finger the lesion is
called herpetic whitlow.
Floor of the mouth: Mucous retention cysts (Ranula) might be present in the floor of the mouth.
Tongue: The tongue has quite an irregular surface which offers ideal niches for sheltering bacteria and
retaining desquamated cells and food remnants.
Tongue coating is particularly seen in case of hairy tongue (lingua villosa) or fissurated tongue (lingua
plicata). This tongue coating is responsible for oral malodor. Tongue cleaning should be advocated in all
patients to avoid halitosis.
examination
Periodontal indices
Oral hygiene index
Plaque index: Silness and Loe, Quigley Hein
Gingival index: Loe and Silness
Periodontal Index: Russells index, Ramfjords index, CPITN
index
ORAL HYGIENE INDEX SIMPLIFIED
( John C. Greene & Jack R. Vermillion, 1964 )
SCORE CRITERIA SCORE CRITERIA
0 No calculus present
0 No debris or stain present
1 Supragingival calculus covering not more
Soft debris covering not more than one- than third of the exposed tooth surface.
1 third of tooth surface, or presence of Supragingival calculus covering more than
extrinsic stains without other debris one third but not more than two thirds of
regardless of surface area covered 2 the exposed tooth surface or the presence
2 Soft debris covering more than one- of individual flecks of subgingival calculus
third, but not more than two thirds, of around the cervical portion of the tooth or
the exposed tooth surface. both
Supragingival calculus covering more than
3 Soft debris covering more than two 3 two thirds of the exposed tooth surface or a
thirds of the tooth surface. continous heavy band of subgingival
calculus around the cervical portion of the
tooth or both.
INTERPRETATION OF SCORES
Interpretation
SCORE CRITERIA
EXCELLENT 0
0 No plaque present
GOOD 0.1 0.9
A film of plaque adhering to the free gingival
margin and adjacent area of the tooth. The
1 plaque may be seen in situ only after
application of disclosing solution or by using
FAIR 1.0 1.9
the probe on the tooth surface.
Moderate accumulation of soft deposits within
2 the gingival pocket, or the tooth and gingival
margin which can be seen with the naked eye.
POOR 2.0 3.0
3 Abundance of soft matter within the gingival pocket
and/or on the tooth and gingival margin
GINGIVAL INDEX
( Loe H. & Silness J , 1963
SCORE CRITERIA
0 Absence of inflammation/normal gingiva INTERPRETATION OF SCORES
MILD GINGIVITIS 0.1 1.0
1 Mild inflammation, slight change in colour,
slight edema; no bleeding on probing.
2 Moderate inflammation; marked glazing, MODERATE GINGIVITIS 1.1 2.0
redness edema and hypertrophy. Bleeding
on probing.
SEVERE GINGIVITIS 2.1 3.0
3 Severe inflammation; marked redness and
hypertrophy ulceration. Tendency to
spontaneous bleeding.
SULCUS BLEEDING INDEX (SBI)
Muhlemann H.R and Son S. in 1971
SCORE CRITERIA
0 Normal-appearing gingiva, no bleeding upon probing.
1. No colour or contour changes, but bleeding on probing.
2. Bleeding on probing, colour change(reddening),no edematous contour changes.
3. Bleeding on probing, colour change, mild inflammatory edema.
4. Bleeding on probing, colour change, severe inflammatory edema.
5. Spontaneous bleeding on probing, colour change, very severe inflammatory edema
with or without ulceration.
Gingival bleeding index (Ainamo and Bay, 1975)
The gingival bleeding index is based on recordings from all four tooth surfaces of all
teeth.
Recorded as
Bleeding present +
Bleeding absent -
USES:
It is useful for experimental studies and in practice on routine basis in individual
patients.
ADVANTAGES:
Simple and easy to use.
LIMITATIONS:
Does not discriminate areas of bleeding as mesial, distal, facial, lingual surfaces .
PERIODONTAL INDEX
(Rusell A.L, 1956)
Endogenous Exogenous
Melanin which is increased in the Metallic pigmentation due to bismuth, arsenic,
following systemic condition: lead and silver:
Addisons disease (adrenal dysfunction) Pigmentation occurs when inflammation leads
to increased vascular permeability and there is
Peutz Jeghers syndrome (intestinal
precipitation of metallic sulfides into the
polyposis)
connective tissue. Therefore, the treatment
Albrights syndrome (fibrous dysplasia) consists of scaling.
SCORE CRITERIA INTERPRETATION OF SCORES
0 No pigmentation
0 No clinical pigmentation ( pink tissue
)
0.03 1 Mild pigmentation
1 Mild clinical pigmentation ( mild light
brown tissue ) 1.03 2 Moderate pigmentation
2 Moderate clinical pigmentation 2.03 3 Heavy pigmentation
( moderate brown tissue )
3 Heavy clinical pigmentation ( deep
brown to black tissue )
Size
The size of any matter depends on what it is made up of; the size of the gingiva is
determined by the sum total of:
1. Cells
2. Intercellular substance
3. Vascular supply
Increase in the size of the gingiva is called gingival enlargement and is classified based on its
etiology as:
Inflammatory Acute : Abscess
Chronic : Plaque induced gingivitis
Drug induced Antiepileptic agents: Phenytoin
Calcium channel blockers: Nifidipine
Immunosuppressants: Cyclosporine
Associated with systemic conditions Conditions in which the reaction to plaque is
Associated with systemic disease increased leading to gingival enlargement:
Pregnancy, puberty, plasma cell gingivitis,
pyogenic granuloma and scurvy
Enlargement is due to the disease itself
irrespective of the plaque, for example due to
leukemia, Wegeners granulomatosis or
sarcoidosis
Neoplastic Benign: Fibroma, papilloma, giant cell
granuloma
Malignant: Carcinoma, malignant melanoma
False enlargement Due to underlying bone lesion: Tori, Pagets
disease, fibrous dysplasia, cherubism, osteoma,
osteosarcoma
Cue to underlying dental tissue: prominence of
enamel during tooth eruption
Inflammatory gingival enlargement has been graded by
Bokencamp et al in 1994 as:
Grade 0: No sign of enlargement
Grade I: Enlargement of interdental papilla
Grade II: Enlargement of papilla and marginal gingiva
Grade III: Enlargement covering three quarters or more of the
crown
New Clinical Index For Gingival Overgrowth [Eva Ingles
1999]
Grade 0:
No overgrowth; firm adaptation of the attached gingiva to the underlying bone. Slight
granular appearance & a knife edged papilla present toward the occlusal surface with
increase size of gingiva
Grade 1:
Early overgrowth as evidenced by an increase in density of gingiva with marked stippling &
granular appearance.
The tip of the papilla is rounded & probing depth is </= 3mm
Grade 2:
Moderate overgrowth, manifested by an increase in size of papilla & rolled margins.
The contour is still concave or straight with buccolingual dimension of up to 2mm. The
papilla is retractable
Grade 3 :
Marked overgrowth, represented by encroachment of gingiva onto the clinical crown.
The contour is convex with buccolingual dimension of 3mm or more.
The probing depth is > 6mm & the papilla is clearly retractable
Grade 4:
Severe overgrowth, characterized by a profound thickening of gingiva with a large
percentage of the clinical crown covered. The papilla is retractable & the probing depth is >
6 mm & bucco lingual dimension is approximately 3mm
Consistency
Normal consistency of the gingiva is firm and resilient due to:
1. Collagenous nature of the lamina propria; and
2. Contiguity with the mucoperiosteum of the alveolar bone.
It is checked with the help of blunt end of the Instrument.
In gingivitis the consistency maybe soft and edematous due to edema, inflammatory cell infiltration
and degeneration of connective tissue elements.
Since gingivitis is a chronic inflammatory condition the outer wall may show repair in the form of
increased fibrosis and keratinization. In these cases the gingiva appears pale pink and firm in
consistency though the inner lining of the sulcus is still atrophic or ulcerated. Here the presence of
bleeding on probing helps us arrive at the diagnosis of gingivitis irrespective of outer changes in color
or consistency.
Contour
The contour of the gingiva is scalloped with knife edge margins.
Gingival contour depends upon the following factors:
1. Shape of the teeth
2. Alignment of the teeth in the arch
3. Proximal contact
4. Dimension of gingival embrasure
Contour is accentuated in labially placed teeth and the gingiva is thickened in lingually placed teeth. Besides these
physiologic variations in contour, in areas of diastema the interdental papilla is missing and the gingiva is firmly adherent
to the underlying bone.
Normal gingiva follows scalloped outline. Accentuated scalloped outline where recession is present.
In gingivitis the knife edge is lost. The marginal gingiva is rounded and the interdental papilla is blunt.
Other inflammatory changes include:
Stillmans cleft is an apostrophe shaped area of recession or triangular indentation on the gingival margin.
McCalls festoon is a thickened band of gingiva or life preserver shaped enlargement of the gingiva most commonly in the
cuspid region. These lesions were earlier attributed to traumatic occlusion but are now known to be due to inflammation.
Surface texture
Width of attached gingiva=Total width of Gingiva from the margin to the MGJ - Pocket depth
Methods of determination:
Tension test (when stretching of lip or cheek induces movement of the free gingival margin, gingiva is considered
inadequate).
Pushing adjacent mucosa coronally with a dull instrument.
Painting mucosa with Schillers Potassium Iodine solution.
PROCEDURE:
Facial: Retract cheeks and lips laterally away . Watch MGJn. Move the lips up, down and across, creating tension
at MGJn.
Lingual: Hold mouth mirror to tense mucosa of floor of mouth, gently retract side of tongue so MGJn is clearly
visible.
OBSERVATIONS:
Blanching at MGJn
Frenal attachment
Recession
Movement of free gingival margin; AG
Amount of attached gingiva
This is the distance from the projection on the external surface of the bottom of gingival sulcus or pocket to
the mucogingival junction. Keratinized gingiva includes marginal gingiva.
Assessing width of attached gingiva
Determined by subtracting the sulcus pocket depth from the total width of gingival (gingival margin to
mucogingival line)
Tension test
Kopczyk RA (1974); Glickman (1964)
Purpose
To detect adequacy of width of attached gingiva
Locate frenal attachment and their proximity to the free gingiva
To identify promptly the mucogingival junction
Procedure
Facial
Retract cheeks and lips laterally by grasping the lips with thumb and index finger, watch at the
mucogingival junction.
Move the lips and cheeks up and down and across, creating tension at the mucogingival junction
Lingual
Hold the mouth mirror to tense the mucosa of the floor of the mouth, gently retracting the side of
the tongue, so that the mucogingival junction is clearly visible.
Request the patient to move the tongue to left, right, up to touch the palate.
Observation
Blanching at mucogingival junction
Frenal attachments
Areas of apparent recession where there is very little keratinized gingiva and the base of the sulcus or pocket is
near the mucogingival junction
Areas where color, size, loss of slipping, smooth shininess or other characteristic indicates need or careful probing
to determine amount of attached gingiva.
Area where tension pulls the free gingiva from the tooth, indicating no attached gingiva.
Frenal attachment has been described by Placek. M, Skach M, Mrklas L (1974)
Mucosal attachment refers to the attachment of the frenum to the mucogingival junction
Gingival attachment refers to the attachment of the frenum within the attached gingiva
Papillary attachment refers to the attachment of the frenum within the papilla
Papilla penetrating attachment refers to an attachment of the frenum passing through the papilla while inserting
into the attached gingiva (of the palate)
Pull syndrome Placek et al (1974)
Detaching movement of marginal gingiva transferred from the lip by the frenum has been termed pull syndrome.
Bleeding on probing
: Bleeding on probing is an objective sign indicating periodontal disease.
Other signs such as changes in color or consistency are subjective and might be
interpreted differently by different examiners.
The presence of bleeding on probing and exudation indicate that the disease is active.
Absence of bleeding on probing is a good prognostic indicator as it correlates with
periodontal stabiltiy.
Method to check for bleeding on probing: Running the probe. It might take 30 to 60
seconds for the bleeding to become apparent.
Reduced bleeding on probing: Smokers
Local Chronic Chronic gingivitis and
periodontitis
Acute ANUG
Injuries: Mechanical, chemical
and thermal
Systemic Bleeding disorders Hemophilia, Christmas
disease, Thromocytopenia,
Leukemia
Hypoprothrombinemia, Scurvy,
Hormonal changes Pregnancy, puberty, patients
on oral contraceptives,
diabetes mellitus
Medications Salicylates (aspirin) and
anticoagulants (heparin,
warfarin)
Exudation
Certain changes are observed in the sulcular epithelium due to chronic inflammation. Neutrophils enter
the epithelium from the connective tissue and release hydrolytic enzymes which kill bacteria and
degrade the adjacent epithelial cells as well. On applying digital pressure on the lateral aspect of the
gingival margin the pus consisting of dead and live Neutrophils, dead and live bacteria and
desquamated epithelial cells is expressed as an exudate. Therefore, this exudate does not correlate with
the pocket depth but is merely a lateral wall change which indicates that the disease is active.
Abcess
An abscess is a localized accumulation of pus. It is different from exudation as it is well contained.
Classifications:
1. Single or multiple. Multiple periodontal abscess is common in diabetics.
2. Occurring in the supporting tissues or occurring in the gingiva
Classification by Meng, 1999
Gingival abscess: In previously healthy sites and caused by impaction of foreign bodies.
Periodontal abscess: In relation to a periodontal pocket, either acute or chronic.
Pericoronal abscess: In relation to an incompletely erupted tooth.
Differences between acute and chronic
abscess are:
Acute Chronic
Appears as an ovoid swelling and Presents a sinus opening
the gingiva is red, edematous,
smooth and shiny
Accompanied by throbbing pain, Usually asymptomatic. There might be
tenderness on palpation, tooth dull, gnawing pain.
mobility, enlarged lymph nodes,
fever and malaise.
Differences between gingival and
periodontal abscess
Gingival Periodontal
Limited to marginal gingiva and Usually involves attached gingiva
interdental papilla
Caused by bacteria being carried deep Caused due to the localization of inflammation
into the tissues when a foreign substance because of one of the underlying resons:
like a toothbrush bristles is forcefully 1. Extension of infection to lateral wall of
embedded in the gingiva pocket
Periodontal Periapical
Periodontal pocket is present Caries is present
Tooth is vital Tooth is non-vital
Pain is usually dull and localized Pain is severe and difficult to localize
(easy to localize due to the (difficult to localize as pulp basically
presence of tactile fibers in the consists of only pain perceiving fibers)
periodontal ligament)
Tender on lateral percussion Tender on vertical percussion
Usually not visible on the Appears as a periapical radiolucency
radiograph
Periodontal examination
Pocket involves only one surface Pocket involves Pocket starts on one surface,
more than one follows a tortuous course to
surface involve another tooth surface
Probing force
0.75N of probing force has been found to be well tolerated and accurate.
Probing forces:
The probe is inserted along the long axis of the tooth into the pocket with gentle (approximately 25 g) force until
resistance is met. 25-g of force is necessary to indent the pad of the thumb about 1-2 mm. In clinical application, what
would be considered gentle insertion force, do not penetrate apical termination of JE. According to some authors,
forces of 0.75 N have been well tolerated & accurate [Van der Velden, 1979]. The tip of the probe has been assumed to
identify the level of the most apical cells of the dentogingival epithelium. This, however, is not the case always (Saglie
et al, 1975; Polson, 1980).
Probe penetration depends on tissue inflammation. In health, probe tip penetrates most coronal intact fibres of
connective tissue attachment (0.3 mm) into JE [Listgarten et al, 1976]. There may be over-estimation (probe may
penetrate beyond apical termination of dentogingival epithelium due to inflammation) or under-estimation (reduction
in inflammation after successful therapy with concomitant deposition of new collagen prevents complete penetration of
probe) of the true pocket.
Probing technique
The probe is inserted parallel to vertical axis of tooth and walked circumferentially around each
surface of each tooth to detect the areas of deepest penetration.
To detect interdental crater the probe should be placed obliquely from facial and lingual surfaces to
explore the deepest point of the pocket located beneath the contact point
Probing technique:
Probe is to be placed parallel to vertical axis of tooth and walked circumferentially around each
surface.
Gutta percha points or calibrated silver points with radiographs can also be used.
In clinical practice, conventional periodontal probes are widely used to obtain two important
measurements: probing depth (PD) and clinical attachment loss (CAL).
PD is defined as the distance from the gingival margin to the base of the probeable crevice.
Probing depth measurements are clinically important since they provide a useful overall assessment of
the depth of periodontal pockets which are the principal habitats of periodontal pathogens.
In addition, PD measurements can be rapidly recorded and give a good assessment of the distribution of
periodontal problems within a given patient. They are an essential component of a complete periodontal
examination
Positioning of the probe:
Manual probing is subject to measurement error because of variations in the angulation and site of
insertion of the probe and because of the difficulty in obtaining a fixed landmark as a reference point.
The probe should be kept as parallel as possible to the long axis of the root.
The tip should continuously follow the root surface, to prevent penetration of the pocket epithelium and
connective tissue, resulting in underestimation of attachment loss.
Each tooth is examined at 6 locations: MB, B, DB, DL, L, and ML. The probe may be angled approx. 10 in
interproximal areas.
Level of attachment
Clinical attachment level the level of attachment is the distance between the base of the pocket
and the cemento-enamel junction.
Determining the level of attachment
When gingival margin is located on the anatomic crown, the level of attachment is determined by
subtracting from depth of the pocket the distance from gingival margin to the cemento-enamel
junction. If both are same loss of attachment is 0.
When the gingival margin coincides with the cemento-enamel junction, the loss of attachment
equals the pocket depth.
When gingival margin is located apical to the cemento-enamel junction, the loss of attachment
will be greater then pocket depth, therefore the distance from cemento-enamel junction to
gingival margin should be added to the pocket depth.
Vertical probing attachment loss (PAL)/Clinical attachment loss (CAL):
CAL is the distance from the cementoenamel junction to the base of the probeable crevice.
In single-rooted teeth, LOA occurs only vertically. In multirooted teeth, loss of attachment
can also occur horizontally, indicating furcation involvement.
Changes in CAL can be due only to gain or loss of attachment & afford a greater/better
indication of the degree of periodontal destruction. Shallow pockets attached at the apical
third of root are more destructive than deep pockets attached at the middle third of root.
CAL assessments are more difficult to accurately measure, but they give a better overall
estimate of the amount of damage to the periodontium than do PD measurements. In
prospective studies, CAL measurements are the most valid method of assessing treatment
outcomes.
Probing depth as well as loss of attachment (LOA) can be measured by manual probing or
by more sophisticated, automated, computer-linked, pressure-sensitive periodontal
probes.
Alveolar bone loss
The alveolar bone levels are evaluated by clinical and radiographic examination.
Transgingival probing (sounding) helps to provide information of bone architecture. Area is
anaestheitized the probe should be walked along the tooth-tissue interface so that the operator
can feel the bony topography. The probe can also be passed horizontally through tissue to
provide more three dimensional information (thickness, height, shape).
Radiographic evaluation
Access
Bone condition
Tooth condition
Root anatomy
BONE SOUNDING/TRANSGINIVAL PROBING:
In order to arrive at a correct diagnosis with respect to the alveolar bone level, presence of
angular bony defects and interdental osseous craters, etc, sounding may be done.
Procedure:
Local anaesthesia
Tip of probe is inserted into the pocket and forced through supraalveolar connective tissue to
make contact with the bone and the distance from CEJ to bone level is assessed.
Hard Tissue examinations
Universal system: 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
32 3130 29 28 27 26 25 24 23 22 21 20 19 18 17
FDI system: two digit system :
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
Stains and calculus:
Normal proximal contacts do not allow any food impaction in between the teeth.
The interdental papilla fills the space up to tooth contact in normal conditions. However due to
periodontal disease there is loss of interdental soft tissue and bone levels.
Due to this, the position of interdental papilla recedes from its normal position.
Normal: The interdental papilla occupies the entire embrassure space apical to the interdental
contact
point / area.
Class I: The tip of the interdental papilla is located between the interdental contact point and
the level of
the CEJ on the proximal surface of the tooth.
Class II: The tip of the interdental papilla is located at or apical to the level of the CEJ on the
proximal
surface of the tooth but coronal to the level of the CEJ midbuccally.
Classification of interdental embrasures, by Perry and Schmid
(1996)
Type I embrasure: The gingival papilla fills up the embrasure
space completely.
Type II embrasure: The gingival papilla partially fills the
embrasure space due to papillary recession.
Type III embrasure: The embrasure space is not filled. The
gingival papilla has receded extensively or it is completely lost.
Pathologic migration
Definition: Tooth displacement that results when the balance among the factors
that maintain physiologic tooth position are disturbed by periodontal disease.
It should be differentiated from physiologic migration or drifting. Due to proximal
and occlusal wear the tooth moves occlusally and mesially throughout life, this
shortens the arch by around 0.6cm from midline to third molar by the age of 40.
This is called physiologic migration.When it occurs in the occlusal direction it is
termed extrusion.
it may be present as extrusion,facial flaring,rotation diastema and drifting of
affected teeth, mostly show combined form.
Causes:
1. Weakened periodontal support
2. Pressure from granulation tissue
3. Trauma from occlusion
4. Tongue thrusting
TRAUMA FROM OCCLUSION:
Definition: When occlusal forces exceed the adaptive capacity of the tissues, tissue injury results. The resultant injury is termed TFO.
Clinical features:
Radiographic features:
Widening of PDL space
Lamina dura thickened
Vertical/ angular bony destruction
Radioluscence & condensation of alveolar bone
Buttressing bone
Root resorption
Methods of determination:
Fremitus test:
It is the measurement of the vibratory pattern of the teeth when the teeth are placed in the contacting positions and movements are made.
To measure fremitus, dampened ungloved index finger is placed along the buccal and labial surfaces of maxillary teeth (or the tooth in question) & the
patient is asked to tap the teeth together in maximum intercuspation (CO) & grind systematically in the lateral excursive movements (lateral fremitus).
Vibrations are perceived. It is easier to detect fremitus in the maxillary teeth than the mandibular teeth.
By Ingreval
Class I fremitus: Mild vibrations or movements detected
Class II fremitus: Easily palpable vibrations but no movements detected
Class III fremitus: Movements visible with naked eye
Fremitus
Fremitus means the palpable vibration or movement, in dentistry it refers to the vibratory patterns of the teeth.
Procedure
Seat the patient up right and head stabilized against headrest index finger is firmly placed over the cervical third each maxillary tooth in succession
starting with most posterior tooth on one side and moving around the arch patient is requested to click the posterior tooth.
Record by tooth number where vibration is felt and the teeth where actual movement is noted
Significance
Tooth with fremitus has excess contact, premature contact.
Well distributed posterior contact
Coupled contacts between opposing teeth
Smooth excursive movement without interfere
TOOTH MOBILITY:
The movement of a tooth in its socket as a result of an externally applied force. Tooth mobility is seen as one
of the measures useful in evaluatinvalue depends on the observerss skill and experience.
Causes:
g the health of the periodontal tissues (Prichard, 1979). The most common clinical method used to examine
tooth mobility is to press the tooth in a horizontal or vertical direction with a finger, or with the handle of the
blunt ends of two metal instruments (Prichard, 1979). This method is imprecise and its Local Factors:
Bone loss/loss of tooth support (periodontitis, TFO, endodontic problems)
Hypofuction
Periapical pathology, cysts or tumors
After periodontal therapy [Nyman & Lindhe (1976), Persson (1981)]
Orthodontic forces; heavy fuctional loads (from prosthetic appliances)
Parafunctional habits (bruxism, clenching)
Pathologies (tumours, cysts, osteomyelitis)
Traumatic injuries to dentoalveolar unit
Tooth morphology
Systemic causes:
Age: progressively increases
Sex & Race: females>males; Negroes more
Menstrual cycle: Friedman (1972) observed increased horizontal tooth mobility during 4 th week of menstrual
cycle.
Oral contraceptives (Dorothy, 1981)
Stress
Nutritional deficiency
Pregnancy (Mobility increases from 2nd to 8th month progressively)
Circadian rhythm (more during early morning & progressively decreases)
The clinical importance of increased tooth mobility is frequently overestimated. It has clearly been shown
in animal experiments that, if plaque-induced inflammation is controlled, increased tooth mobility has no
effect on the level of the connective tissue attachment (Ericson and Lindhe, 1977). Hypermobility of tooth
does not necessarily mean that it has a poor prognosis, and the mobility frequently persists after
successful periodontal treatment (Lindhe and Nyman, 1975, 1984). Nevertheless, increasing tooth mobility
over time should alert the clinician to a possible deterioration of periodontal support, and such teeth
require careful evaluation for loss of clinical attachment.
All teeth have a slight degree of physiologic mobility, which varies for different teeth
and at different times of the day. Mobility is greatest on arising in the morning and
progressively decreases. During the waking hours, mobility is reduced by chewing
and swallowing forces, which intrude the teeth in the sockets.
Single-rooted teeth have more mobility than multi-rooted teeth; incisors have the
most mobility. Mobility is principally in a horizontal direction.
Tooth mobility occurs in the following two stages:-
1) In the initial stage the tooth moves within the confines of the periodontal ligament
(PDL). This is associated with viscoelastic distortion of the PDL and redistribution of
the periodontal fluids, interbundle content, and fiberes. This initial movement occurs
with forces of about 100g and is about 0.05 to 0.10mm (50-100m).
2) The secondary stage occurs gradually and entails elastic deformation of the
alveolar bone in response to increased horizontal forces.
When a force such as that applied to teeth in occlusion is discontinued, the teeth
return to their original position.
Furcation involvement
Definition: Furcation involvement is the invasion of bifurcation and trifurcation of teeth by
periodontal disease.
Method to check for furcation involvement: A curved probe called Nabers probe is used.
Classification:
Based on horizontal measurement of bone loss, Glickmans classification, 1953
Grade I: Incipient involvement which is felt as a catch with the probe.
Grade II: There is partial loss of bone. Here the probe penetrates partially but does not pass
through and through. There maybe involvement from both sides but these are not connected
since some amount of bone is still remaining. This is called cul de sac which means dead
end.
Grade III: The bone loss is through and through.
Grade IV: Along with through and through bone loss there is gingival recession leading to the
furcation area becoming clinically visible.
Seiberts Classification:
Class I: loss of facio- lingual width, with normal apico- coronal height
112
Furcation -
radiographs at different
angles
Reduced radiodensity in Furcation
furcation involvment
Marked bone loss adjacent to
single molar root
Periodontal abscess
Radiolucency along lateral
aspect of tooth
Periodontal
113 abscess
Intraoral radiographic survey
It requires full mouth intra-oral radiographic series 14 periapical films; 4 bite wings.
Panoramic radiographs are a simple and convenient view of the dental arch and
surrounding structures. They are helpful in detecting developmental anomalies,
pathologic lesion of teeth and jaws, fractures and dental screening examination of large
groups.
RADIOGRAPHIC EXAMINATION:
The use of radiographic imaging as an aid in diagnosis and treatment of periodontal
disease is widely accepted.
B] Extra-oral radiographs
Orthopantomogram and other extraoral views
II] Digital:
Specialized techniques:
Digital subtraction radiography (DSR)
When two images of same object are registered and the image intensities of corresponding
pixels are subtracted, a uniform difference image will be obtained. If a change of follow-up
image has occurred, it will show up as a brighter area when the change represents the gain and
as a darker area when the change represents loss. Subtraction images allow detection of
mineral changes of as little as 5 %.
Tuned aperture computed tomography (TACT)
TACT is built on basic principles of tomosynthesis by shifting and combining a set of basis
projections, arbitrary slices through the object can be brought into focus. Each radiograph is
taken from different angle relative to the object and the receptor. It is shown to improve the
ability of observers to detect osseous defects around implants.
Computed Tomography (CT)
CT provides exquisite 3-D views, however, its ability to show very small details remains limited.
The application of CT imaging for periodontal diagnosis appears to have an unfavorable cost-
benefit ratio.
Computer-assisted densitometric image analysis (CADIA)
Video camera measures the light transmitted through a radiograph, and the signals from the
camera are converted into gray-scale images. The camera is interfaced with an image
processor and a computer that allows storage and mathematical manipulation of the images
LABORATORY INVESTIGATIONS
Haemoglobin: Differentiate WBC count
Males:14-18gm/dl
Females:12-16gm/dl polymorphs: 55 70%
RBC count: (adult)
Males: 4.6-6.2 49 65% (children)
millions/cumm lymphocytes: 29 40%
Females: 4.2-5.4 (adult)
millions/cumm
30 60% (children)
WBC count: Eosnophil: 1 6%
6000-11000 /cumm
Platelet Count: Monocytes 2 10%
1,50,000-4,00,000/cumm Basophils 0 1%
ESR
men: 4 -10 mm/hr Glucose levels
Women: 8 20 mm/hr Fasting levels: 60-100
mg/dl
Post prandial: <140
Test Description Normal values Disease with
increased values
Bleeding Time Dukes method and Ivys method. < 8 minutes Purpura, von Willebrand
Dukes: Puncture finger tip/ ear lobe and Disease
measure the time until the bleeding stops.
Clotting Time Wrights capillary tube method and Lee and <10 minutes Deficiency of any
Whites method. Wrights: Puncture finger tip procoagulant factor
and collect blood in a capillary tube. At
intervals break the tube and check for a
thread joining the two ends, this is the clot.
Activated Partial Measures efficiency of intrinsic and common < 40 seconds Deficiency of factors III,
Thromboplastin pathways IX, and XI
Time
Laboratory diagnosis
When the dentist detects unusual gingival or periodontal problems that cannot be explained by local causes, the possibility of contributing systemic factors must be explored.
The signs and symptoms of oral manifestations of systemic disease must be clearly understood ad analyzed and discussed with the patients physician.
LABORATORY INVESTIGATIONS
Haemoglobin
Males: 14-18gm/dl; Females: 12-16gm/dl
Significance: if reduced, hampers healing; risk of syncope
RBC count:
Males: 4.6-6.2 millions/cumm
Females: 4.2-5.4 millions/cumm
Decreased: anemia, dietary def., pregnancy, bone marrow failure, hodgkins disease, multiple myeloma, hemoglobinopathies, renal dis., collagen vascular dis.
Increased: COPD, CHD, polycythemia vera
WBC count:
6000-11000 /cumm
Decreased in: reduced defence
Increased in: infections, leukaemia
Platelet Count:
1,50,000-4,00,000/cumm
If less than 1 lakh/cumm: surgery cannot be done
Bleeding time:
Dukes method: < 5 mins
Prolonged: thrombocytopenia, leukaemia, liver disease, drugs(NSAIDs,warfarin, streptokinase, anticoagulants), DIC, collagen vascular dis., connective tissue dis.
Clotting time:
Capillary tube method: 1-7 min
Kruse and Moses method: 2.5-5 mins
Lee and White method: 5-10 mins
Prolonged: Hemophilia, fibrinogen deficiency
Glucose levels
Fasting levels: 60-100 mg/dl
Post prandial: <140 mg/dl
Increased in Diabetes
Significance: nutrient for bacterial growth, reduced healing
In the biofilms, the microorganisms live in a well-organized symbiosis, supplied with nutrients via microchannels through the plaque matrix and inaccessible to
phagocytozing leukocytes, chemical plaque control agents, and antibiotics.
At 1996 World Workshop in Periodontics, it was concluded that human periodontitis is caused mainly by Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis
(exogenous, transmissible pathogens) and Bacteroides forsythus (endogenous, opportunistic pathogen). Recently, Machtei et al (1997) showed that, in deep periodontal
pockets, high levels of B forsythus increase the risk for further loss of periodontal attachment seven-fold. Other species of opportunistic endogenous periopathogens are
Prevotella intermedia and Treponema denticola. The presence and levels of subgingival periopathogens can be evaluated by subgingival sampling, with a sterile curette or
paper point, and DNA probe analyses, conventional anaerobic culture techniques, or chairside tests.
Bacterial culturing
It has been frequently used as the reference method when determining the performance of a new detection method. It is the only current method capable of determining
the invitro antimicrobial susceptibility of periodontal pathogens. It can also provide a quantitative measurement of all major viable microorganisms in the specimen. It
identifies only live microorganisms, therefore strict sampling and transport conditions are essential. Some of the putative pathogens are fastidious and difficult to culture.
The sensitivity of culture methods is rather low. It requires sophisticated equipment, experienced personnel and is relatively time-consuming and expensive.
Direct microscopy
Darkfield or Phase-contrast microscopy has been suggested as an alternative to culture methods on the basis of its ability to directly and rapidly assess the
morphology and motility of bacteria in the sample. However, most of the putative periodontal pathogens (Aa, Pg, Bf, Ec) are nonmotile and therefore cannot be identified.
Immunodiagnostic methods
Immunodiagnostic methods employ antibodies that recognize specific bacterial antigens to detect target microorganism.
Advantages:
Do not require viable bacteria
Less susceptible to variation in sample processing
Less time consuming
Easier to perform (than culture)
Disdvantages:
Accuracy of immunodiagnostic tests depends greatly on the quality of the reagents used
Generally show poorer detection limits than DNA probe and PCR
Expensive
Membrane immunoassay(Evalusite):
It is a commercially developed, antibody-based sandwich enzyme-linked immunosorbent assay fro detection of Aa, Pg, P intermedia. It involves linkage
between the antigen and membrane-bound antibody to form an immunocomplex that is later revealed through a colorimetric reaction. The sample wells are
first coated with antibodies against antigens specific for the target bacterial species. Antibody-antigen reactions are then detected by adding enzyme-linked
antigen-specific antibodies to the sample wells, followed by the addition of enzyme substrate.
Flow cytometry/Cytofluorography:
It is for rapid identification of oral bacteria and involves labeling bacterial cells from a patient plaque sample with both species-specific antibody and a second
fluorecscein conjugated antibody. The suspension is then introduced into the flow cytometer, which separates the bacterial cells into an almost single-cell
suspension by means of a laminar flow through a narrow tube. The sophistication and cost involved in this procedure precludes its wide usage.
ELISA:
It is similar to other radioimmunoassay in principle, but an enzymatically derived color reaction is substituted as the label in place of radioisotope. The intensity
of colour depends on the concentration of the antigen and is usually read photometrically for optimal quantification. It has been used to detect
periodontopathogens.
Latex agglutination:
It is a very simple immunological assay based on the binding of protein to latex. Latex beads are coated with species-specific antibody, and when these beads
come in contact with the microbial cell surface antigens or antigen extracts, cross-linking occurs; its agglutination or clumping is visible usually in 2-5 mins.
Because of their simplicity and rapidity, these assay have great potential for chairside detection or periodontopathogens.
.
Enzymatic methods
BANA test
B forsythus, Pg, Treponema denticola and capnocytophaga species share a common enzymatic profile, since all have in common trypsin-like enzyme. The
activity of this enztme can be measured with the hydrolysis of the colour substrate N-bezoyl-dl-arginine-2-naphthylamide (BANA). When the hydrolysis takes
place, it releases the chromophore, -naphthylamide, which turns orange red when a drop of fast granet is added to the solution.
Diagnostic kits have been developed using this reaction (e.g. Perioscan).
BANA test can serve as a marker of disease activity. Loesche et al showed that shallow pockets exhibited only 10% positive BANA reactions, while deep
pockets (>7mm) exhibited 80-90% positive BANA tests. Beck et al used BANA as a risk indicator for periodontal attachment loss.
However, it detects a very limited number of pathogens.
DNA probes:
DNA probes entail segments of single-stranded nucleic acid, labeled with an enzyme or radioisotope that can locate and bind to their complementary nucleic
acid sequences with low cross-reactivity to target organisms. The assay can rapidly test for multiple bacteria, including Aa, Pg, B intermedius, C rectus, E
corrodens, F nucleatum, and T denticola.
As the GCF migrates from the host microcirculation, through inflamed tissues, and into periodontal pocket, it acquires mediators involved
in the destructive host response and by-products of local tissue metabolism as well as PMNLs, microorganisms, and their products from
the periodontal pocket. The following four mediators in GCF have been investigated extensively for their potential application in
diagnosis of active periodontal disease and prediction of further loss of periodontal support:
Prostaglandin E2 (PGE2)
-glucouronidase (G)
Neutrophil elastase (NE)
Aspartate aminotransferase (AST)
Prostaglandin E2 (PGE2)
It is a proinflammatory metabolite of arachidonic acid.
Released from: macrophages, PMNLs, fibroblasts
Effects:
Vasodilation/increased vascular permeability
Enhanced responsiveness of receptors to painful stimuli
Release of collagenase by inflammatory cells
Activation of osteoclasts
Recruitment of inflammatory cells
Studies:
In a study by Offenbacher et al (1986), crevicualr fluid levels of PGE2 were three times more in subjects with aggressive periodontitis
(who experience rapid disease progression) than those with chronic periodontitis.
In another study by Offenbacher et al (1986), GCF from sites with active periodontal disease contained a mean PGE2 concentration of
305.6g/ml, while inactive sites contained about 65.7g/ml of PGE2.
. Chronic Periodontitis
a) Localized
b) Generalized
III. Aggressive Periodontitis
a) Localized
b) Generalized
IV. Periodontitis as a manifestation of systemic diseases.
A) Associated with hematological. disorders.
1) Acquired neutropenia
2) Leukemias
3) Other
B) Associated with genetic disorders
1. Familial and cyclic Neutropenia
2. Down syndrome
3. Leukocyte adhesion deficiency syndromes
4. Papillon - Lefevre syndrome
5. Chediak Higashi syndrome
6. Histiocytosis syndrome
7. Glycogen storage disease
8. Infantile genetic agranulocytosis
9. Cohen syndrome
10. Ehlers Danlos syndrome (Types IV and VIII)
11. Hypophosphatasia
12. Other
V. Necrotising Periodontal Diseases
a) Necrotising ulcerative gingivitis
b) Necrotising ulcerative periodontitis
VI. Abscesses of the periodontium
a) Gingival abscess
b) Periodontal abscess
c) Periocoronal abscess
VII Periodontitis assoicated with endodontic lesions
A. Combined periodontal endodontic lesions
VIII. Developmental or Acquired Deformities and conditions
A. Localized tooth related factors that modify or predispose to plaque induced gingival disease / periodontitis
1. Tooth anatomic factors
2. Dental restorations / appliances
3. Root fractures
4. Cervical root resorption and cemental tears
B. Mucogingival deformities and conditions around teeth
1. gingival / soft tissue recession
a. facial or lingual surfaces
b. interproximal (papillary)
2. lack of keratinized gingiva
3. decreased vestibular depth
4. aberrant frenum / muscle position
5. gingival excess
a. pseudopocket
b. inconsistent gingival margin
c. excessive gingival display
d. gingival enlargement (see section I, parts A3 and B4)
abnormal color
C. Mucogingival deformities and conditions on edentulous ridges
1. vertictal and / or horizontal ridge deficiency
2. lack of gingiva / keratinized tissue
3. gingiva / soft tissue enlargement
4. aberrant frenum / muscle position
5. decreased vestibular depth
6. abnormal color
D. Occlusal trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
Clinically healthy gingiva
Pale pink
Stippled
Thin margins
Firm and resilient
DIAGNOSIS OF GINGIVITIS
Clinical signs
Redness
Swelling (due to increased vascular permeability; Lindhe
& Rylander, 1975)
Bleeding on probing (objective sign)
Exudate
Severity of gingivitis
Le & Silness Gingival index (1963)
GINGIVITIS
CLINICAL PRESENTATION
Most common form of periodontal disease
PD: 1-3 mm
Clinical signs of inflammation
Plaque usually present; calculus often seen
Precedes periodontitis but does not always lead to
periodontitis
Reversible
RADIOGRAPHIC PRESENTATION
No bone loss seen
DIAGNOSIS OF PERIODONTITIS
Local factors
Age of onset
Family history
Clinical attachment loss
Rate/Duration of destruction/symptoms
Radiographic evidence of destruction
Nature and composition of microbial flora
Alteration in host immune response
CHRONIC PERIODONTITIS
CLINICAL PRESENTATION:
Pocket depth >3mm
BOP, suppuration, other signs of active disease
Fremitus/tooth mobility
Furcation invasion
RADIOGRAPHIC PRESENTATION:
Horizontal to angular bone loss
RADIOGRAPHIC PRESENTATION:
Bone loss localized to the distal of the deciduous first
molar
Localized form <30% of sites involved
Generalized form >30% of sites involved
CLINICAL PRESENTATION:
Little or no inflammation of gingiva
Usually amenable to standard periodontal therapy with
appropriate antibiotics
Seen after eruption of primary teeth
RADIOGRAPHIC PRESENTATION:
Bone loss localized to the distal of the deciduous first
molar
GENERALIZED AGGRESSIVE PERIODONTITIS
[PREPUBERTAL PERIODONTITIS]
CLINICAL PRESENTATION:
Extreme gingival inflammation
Rapid bony destruction
Often accompanied by sever functional defects of
neutrophils and monocytes
Otitis media and URTI also found
In some cases more sever lesions are refractory to
antibiotics
RADIOGRAPHIC PRESENTATION:
Generalized bone loss
ABSCESSES OF THE PERIODONTIUM
GINGIVAL ABSCESS
Is a localized purulent infection that involves marginal gingiva or interdental
papilla.
Confined to marginal tissues
Previously non-diseased site
Impaction of foreign material
Short history of onset
PERICORONAL ABSCESS
Localized purulent infection within the tissues surrounding a partially erupted
tooth.
PERIODONTAL ABSCESS
A periodontal abscess is a localized accumulation of pus within the gingival
wall of a periodontal pocket.
History of onset, progression, previous periodontal therapy
Continuity with gingival margin
Vitality of tooth
Presence/ absence of caries
Radiographic examination
Necrotizing Ulcerative Periodontitis (NUP)
CLINICAL PRESENTATION:
Usually observed in individuals with HIV;
immunosuppression; or severe malnutrition
Generalized or localized rapid soft and hard tissue
destruction
Bone sequestration, denudation
Teeth may become mobile
Spontaneous, usually nocturnal, gingival bleeding
Fetid breath
Intense, deep-seated pain
May be preceded by necrotizing ulcerative gingivitis
Periodontitis associated with endodontic lesions