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PERIODONTAL DISEASES

Dr. Wesam Azar BDS, MSc JUST

Periodontal Pathology

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How is Periodontitis Measured?

In clinical practice, periodontal disease is assessed by a full mouth clinical examination that includes:

6 point probing depths per tooth on all teeth

Recording of recession, furcation involvement, mobility, bleeding upon probing, Calculation of CAL (gold standard to distinguish periodontitis from gingivitis)

AAP classification 1999

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Chronic Periodontitis
The most common type

an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.

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Previous Classification
Adult periodontitis Chronic adult periodontitis
Can occur in children & adolescents in response to chronic plaque and calculus accumulation

Characteristics

Most prevalent in Adults, but can occur in children and

adolescents.
Amount of destruction is consistent with the presence of local

factors
Associated with variable microbial pattern

Slow to moderate rate of progression, but may have period of

rapid progression

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Characteristics
Can be further classified on the basis of extent and severity Can be associated with local predisposing factors (e.g., tooth-

related or iatrogenic factors)

May be modified by and /or associated with systemic diseases

(e.g., diabetes mellitus, HIV infection)

Can be modified by environmental factors such as cigarette

smoking and emotional stress

Clinical features
Inflammatory changes in the marginal gingiva
Presence of periodontal pockets Loss of clinical attachment

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Radiographic features
Evidence of bone loss

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Microbiology
a specific group of microorganisms including

Porphyromonas gingivalis

Tannerella forsythia

Treponema denticola

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Diagnosis
Clinical and radiographic Features

Supra and subgingival plaque accumulation. Gingival inflammation. Pocket formation. Attachment loss. Bone loss.

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Distribution
Site-Specific Disease

bone loss may occur on one surface of a

tooth while other surfaces maintain normal attachment levels In the same dentition some teeth have sever destruction while other teeth are free of sign of attachment loss
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Distribution
Localized periodontitis:

less than 30% of the sites assessed in the mouth demonstrate attachment loss and bone loss
Generalized periodontitis:

30% or more of the sites assessed in the mouth demonstrate attachment loss and bone loss

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Pattern of Bone Loss

Vertical (angular)

when attachment and bone loss on one tooth surface is greater than that on an adjacent surface (intrabony pocket formation) Horizontal when attachment and bone loss proceeds at a uniform rate on the majority of tooth surfaces (suprabony pockets)
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Disease Severity
Slight (mild) periodontitis:

no more than 1 to 2 mm of clinical attachment loss

Moderate periodontitis

3 to 4 mm of clinical attachment loss

Severe periodontitis

5 mm or more of clinical attachment loss

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Symptoms
Gums bleed when brushing or eating Spaces occur between their teeth as a result

of tooth movement Teeth have become loose sensitive to heat, cold, or both Gingival tenderness or itchiness presence of areas of food impaction may add to the patients discomfort
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Progression
Slow rate of progression may be modified by

systemic or environmental and behavioral factors

Chronic periodontitis does not progress at an equal rate in all affected sites throughout the mouth

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Progression Models
The continuous model
disease progression is slow and continuous affected sites showing a constantly

progressive rate of destruction throughout the duration of the disease

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Progression Models
The random or episodic-burst model
disease progresses by short bursts of

destruction followed by periods of no destruction

pattern of disease is random with respect to

the tooth sites affected and the chronology of the disease process
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Progression Models
The asynchronous, multiple-burst model
periodontal destruction occurs around affected teeth

during defined periods of life

bursts of activity are interspersed with periods of

inactivity or remission
The chronology of these bursts of disease is

asynchronous for individual teeth or groups of teeth

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Prevalence
Most prevalent form of periodontitis

Increases in prevalence and severity with age

Age-associated, not an age-related

Generally affecting both genders equally
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Incidence of Periodontitis
Longitudinal study of periodontitis on 480 tea workers in Sri Lanka (Le et al 1968)

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Risk factors
Local factors Systemic factors Environmental and behavioral factors Genetic predisposition

Prognosis
slight-to-moderate periodontitis
provided the inflammation can be controlled through

good oral hygiene and the removal of local plaqueretentive factors

prognosis is generally good severe periodontitis

Furcation involvement increasing clinical mobility patients who are noncompliant with oral hygiene

practices

prognosis may be downgraded to fair to poor.

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Treatment
Phase I therapy
Pt motivation & OHI Scaling and root planing Correction of potential local, systemic and

environmental factors

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Treatment Plan Flow Chart

Periodontitis Patient Phase I Therapy

Re-evaluation Improved patient compliance

Improved CAL, PD < 5mm Persistent deep PD

Re-evaluation Patient not compliant

maintenance-improve OH

Sites with angular bone defects Regeneration therapy Maintenance Reconstructive therapy Crowns, implants, bridges, permanent RPDs Maintenance

Sites with horizontal bone loss Resective therapy

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Treatment
Before Tt After Tt

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Aggressive Periodontitis

a disease of the periodontium occurring in an otherwise healthy adolescent which is characterized by a rapid loss of alveolar bone about more than one tooth of the permanent dentition. The amount of destruction manifested is not commensurate with the amount of local irritants.

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Previous Classification
Prepubertal Periodontitis (PPP) Localized Juvenile Periodontitis

Localised Early-onset Periodontitis Generalized Juvenile Periodontitis & Rapidly Progressive Periodontitis Generalised Early-onset Periodontitis Now all called Aggressive Periodontitis

Problems With Old Classification

Systemic diseases predisposing to

Prepubertal periodontitis. Overlap between different disease entities. Too much dependence on age. Thus changed to the simpler more general term of Aggressive Periodontitis

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Aggressive Periodontitis
Aggressive:

progression of this disease is 3-4 times more rapid and severe, than seen in chronic periodontitis
Periodontitis:

persistent bacterial infection which causes chronic inflammation, resulting in destruction of tooth supporting tissues.

Primary Features

No obvious sign or symptoms of systemic disease Rapid attachment loss and bone destruction Familial aggregation

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Secondary Features
(not always present)

Amounts of microbial deposits are inconsistent with the severity

of periodontal tissue destruction may be elevated

Elevated proportions of Aa and, in some populations, P. gingivalis Phagocyte abnormalities Hyper-responsive macrophage phenotype, including elevated

levels of PGE2 and IL-1 arresting

Progression of attachment loss and bone loss may be self-

Progression

Attachment loss is episodic

Succession of acute destructive phases with intermittent inactive phases

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Distribution
Localized aggressive periodontitis Generalized aggressive periodontitis

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Localized aggressive periodontitis

Circumpubertal onset Robust serum antibody response to infecting

agents Localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors
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Localized aggressive periodontitis

Possible reasons for localization to certain teeth
1.

After initial attack by Aa, adequate immune defenses are stimulated & colonization of other sites may be prevented.
(A strong antibody response to infecting agents is one characteristic of LAP)

2. Bacteria antagonistic to Aa may colonize the periodontal

tissues and inhibit Aa from further colonization of periodontal sites in the mouth
3.

Aa may lose its leukotoxin-producing ability for unknown reasons

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Clinical features of LAP

Lack of clinical inflammation despite the

presence of deep periodontal pockets and advanced bone loss Minimal amount of plaque on the affected teeth & inconsistent with the amount of periodontal destruction present (qualitative composition) Rate of bone loss is about three to four times faster than in chronic periodontitis
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Other Clinical features of LAP

Distolabial migration of the maxillary incisors with

concomitant diastema formation Increasing mobility of the maxillary and mandibular incisors and first molars Sensitivity of denuded root surfaces to thermal and tactile stimuli Deep, dull, radiating pain during mastication, probably caused by irritation of the supporting structures by mobile teeth and impacted food. Periodontal abscesses may form at this stage, and regional lymph node enlargement may occur. Progression of attachment loss and bone loss may be selfarresting
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Radiographic Findings
Vertical loss of alveolar bone around the first

molars and incisors

May include an "arc shaped loss of alveolar

bone extending from distal surface of second premolar to mesial surface of second molar

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Generalized aggressive periodontitis

Usually affecting persons under 30 years of age,

but patients may be older Poor serum antibody response to infecting agents Pronounced episodic nature of the destruction of attachment and alveolar bone Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors.
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Gingival Response in GAP

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Other Clinical Findings

patients with GAP may have systemic

manifestations, such as weight loss, mental depression, and general malaise

GAP may be arrested spontaneously or after therapy, whereas others may continue to progress to tooth loss despite intervention with conventional treatment

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Radiographic Findings
range from severe bone loss associated with

the minimal number of teeth to advanced bone loss affecting the majority of teeth in the dentition

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Prevalence
Generalized aggressive periodontitis (GAP) in untreated periodontal disease conducted in Sri Lanka by Le et al, 8% of the population had rapid progression of periodontal disease, characterized by a yearly loss of attachment of 0.1 to 1.0 mm Localized aggressive periodontitis (LAP) occurs in less than 1% of adolescents. blacks were at much higher risk than whites for all forms of aggressive periodontitis male teenagers were more likely to have GAP than female adolescents
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Host Response
Defective chemotactic response in neutrophils
Hyper-inflammatory state resulting in the

presence of pro-inflammatory cytokines in the serum

Phagocyte and macrophage abnormalities are

minor in the sense that they are usually not associated with infections other than periodontitis.

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Risk factors
Microbiological factors (Aa in 90% of LAP) Immunological factors
human leukocyte

antigens (HLAs), which regulate immune responses have been evaluated as candidate markers for aggressive periodontitis (HLA A9 and B15) PMN and/ or monocyte functional defects

Genetic Factors
gene or genes of major effect exists for aggressive

periodontitis
all individuals are not equally susceptible to aggressive

periodontitis
some immunologic defects associated with aggressive periodontitis

may be inherited

Environmental Factors (smoking)

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Prognosis
Localized aggressive periodontitis
When diagnosed early, treatment result in an

excellent prognosis. If advanced disease occurs, the prognosis can be good if the lesions are treated with debridement, local and systemic antibiotics, and regenerative therapy

Generalized aggressive periodontitis

Patients often have a fair, poor, or questionable

prognosis
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Treatment
Pt motivation & OHI Scaling and root planing Correction of potential local, systemic and

environmental factors Antibiotics Chlorhexidine rinses Evaluation & counseling for other family members
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Aggressive periodontitis

Currently, an ideal antibiotic for the treatment of periodontal diseases does not exist. Although oral bacteria are susceptible to many antibiotics, no single antibiotics at concentrations achieved in body fluids inhibits all putative periodontal pathogens

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Combination Therapy
Periodontal infections contain a wide diversity of

bacteria.
Metronidazole +Amoxycillin or Augmentin. Never use antibiotics alone without adjunctive

mechanical debridement and OHI.

Antibiotics
Tetracyclins (avoid in children) Doxycycline 100mg/day

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