s10.chronic periodontitis aggressive periodontitis(2009)

8/13/2019 s10.Chronic Periodontitis Aggressive Periodontitis(2009)

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PERIODONTALDISEASES

Dr. Wesam AzarBDS, 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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The most common type

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Chronic Periodontitis

an infectious disease resulting in inflammationwithin the supporting tissues of the teeth,

progressive attachment loss, and bone loss.

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Adult periodontitis

Chronic adult periodontitis

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Previous Classification

Can occur in children & adolescents inresponse to chronic plaque and calculus

accumulation

Characteristics

Most prevalent in Adults, but can occur in children andadolescents.

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 ofrapid progression


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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 cigarettesmoking and emotional stress

Characteristics

Clinical features

Inflammatory changes in themarginal gingiva

Presence of periodontal pockets

Loss of clinical attachment

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Radiographic features

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Evidence of bone loss


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Microbiology

a specific group of microorganisms including

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Porphyromonasgingivalis

Tannerellaforsythia

Treponemadenticola

DiagnosisClinical and radiographic Features

Supra and subgingival plaque accumulation.

Gingival inflammation.

Pocket formation.

Attachment loss.

Bone loss.


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Distribution

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bone loss may occur on one surface of atooth while other surfaces maintain normalattachment levels

In the same dentition some teeth have severdestruction while other teeth are free of signof attachment loss

Site-Specific Disease

Distribution

Localized periodontitis:

less than 30% of the sites assessed in the mouthdemonstrate attachment loss and bone loss

Generalized periodontitis:

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

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Pattern of Bone Loss

Vertical (angular)

when attachment and bone loss on one toothsurface is greater than that on an adjacentsurface (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 attachmentloss

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 resultof tooth movement

Teeth have become loose

sensitive to heat, cold, or both

Gingival tenderness or itchiness

presence of areas of food impaction may addto the patients discomfort

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Progression

Slow rate of progression may be modified bysystemic or environmental and behavioralfactors

Chronic periodontitis does not progress at anequal 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 tothe tooth sites affected and the chronology of

the disease process25

Progression Models

The asynchronous, multiple-burstmodelperiodontal destruction occurs around affected teethduring defined periods of life

bursts of activity are interspersed with periods ofinactivity or remission

The chronology of these bursts of disease isasynchronous for individual teeth or groups of teeth

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Prevalence

Increases in prevalence and severity with age

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Age-associated, not an age-related

Most prevalent form of periodontitis

Generally affecting both genders equally

Incidence of Periodontitis

Longitudinal study of periodontitis on 480 teaworkers 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 plaque-retentive factors

prognosis is generally good

severe periodontitis Furcation involvement

increasing clinical mobility

patients who are noncompliant with oral hygienepractices

prognosis may be downgraded to fair to poor.

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Treatment

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Phase I therapy

Pt motivation & OHI

Scaling and root planing

Correction of potential local, systemic and

environmental factors

Treatment Plan Flow Chart

Improved CAL, PD < 5mm

Maintenance

Reconstructive therapyCrowns, implants, bridges, permanent RPDs

Maintenance

Sites with angular bone defectsRegeneration therapy

Sites with horizontal bone lossResective therapy

Persistent deep PD

Re-evaluationImproved patient compliance

maintenance-improve OH

Re-evaluationPatient not compliant

Phase I Therapy

Periodontitis Patient


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Treatment

Before Tt After Tt

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a disease of the periodontium occurring in an otherwise healthy

adolescent which is characterized by a rapid loss of alveolar boneabout more than one tooth of the permanent dentition. The amountof destruction manifested is not commensurate with the amount of

local irritants.

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Aggressive Periodontitis


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Previous Classification

Prepubertal Periodontitis (PPP)

Localized Juvenile Periodontitis

Localised Early-onset Periodontitis

Generalized Juvenile Periodontitis &

Rapidly Progressive PeriodontitisGeneralised Early-onset Periodontitis

Now all called Aggressive Periodontitis

Problems With Old Classification

Systemic diseases predisposing toPrepubertal periodontitis.

Overlap between different disease entities.

Too much dependence on age.

Thus changed to the simpler more general termof Aggressive Periodontitis


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Aggressive Periodontitis

Aggressive:

progression of this disease is 3-4 times more rapidand severe, than seen in chronic periodontitis

Periodontitis:persistent bacterial infection which causes chronicinflammation, 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 severityof periodontal tissue destruction

Elevated proportions ofAa and, in some populations, P. gingivalismay be elevated

Phagocyte abnormalities

Hyper-responsive macrophage phenotype, including elevatedlevels of PGE2 and IL-1

Progression of attachment loss and bone loss may be self-arresting

Progression

Attachment loss is episodic

Succession of acute destructive phases withintermittent inactive phases

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Distribution

Localized aggressive periodontitis

Generalized aggressive periodontitis

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Localized aggressiveperiodontitis

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Circumpubertal onset

Robust serum antibody response to infectingagents

Localized first molar/incisor presentation withinterproximal attachment loss on at least twopermanent teeth, one of which is a first molar,and involving no more than two teeth other thanfirst molars and incisors


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Possible reasons for localization to certain teeth1. After initial attack byAa, adequate immune defenses are

stimulated & colonization of other sites may beprevented.

(A strong antibody response to infecting agents is one characteristic

of LAP)

2. Bacteria antagonistic toAa may colonize the periodontaltissues and inhibitAa from further colonization of

periodontal sites in the mouth

3. Aa may lose its leukotoxin-producing ability for unknownreasons

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Clinical features of LAP

Lack of clinical inflammation despite thepresence of deep periodontal pockets andadvanced bone loss

Minimal amount of plaque on the affected

teeth & inconsistent with the amount ofperiodontal destruction present (qualitativecomposition)

Rate of bone loss is about three to four timesfaster than in chronic periodontitis

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Distolabial migration of the maxillary incisors withconcomitant diastema formation

Increasing mobility of the maxillary and mandibular incisorsand first molars

Sensitivity of denuded root surfaces to thermal and tactilestimuli

Deep, dull, radiating pain during mastication, probablycaused by irritation of the supporting structures by mobileteeth and impacted food.

Periodontal abscesses may form at this stage, and regionallymph node enlargement may occur.

Progression of attachment loss and bone loss may be self-arresting

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Other Clinical features of LAP

Radiographic Findings

Vertical loss of alveolar bone around the firstmolars and incisors

May include an "arc shaped loss of alveolar

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

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Generalized aggressive

periodontitis

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Usually affecting persons under 30 years of age,but patients may be older

Poor serum antibody response to infectingagents

Pronounced episodic nature of the destruction ofattachment and alveolar bone

Generalized interproximal attachment loss

affecting at least three permanent teeth otherthan first molars and incisors.

Gingival Response in GAP

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Other Clinical Findings

patients with GAP may have systemicmanifestations, such as weight loss, mentaldepression, and general malaise

GAP may be arrested spontaneously or aftertherapy, whereas others may continue to

progress to tooth loss despite interventionwith conventional treatment

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Radiographic Findings

range from severe bone loss associated withthe minimal number of teeth to advancedbone loss affecting the majority of teeth inthe dentition

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Prevalence

Generalized aggressive periodontitis (GAP) in

untreated periodontal disease conducted in Sri Lankaby Le et al, 8% of the population had rapidprogression of periodontal disease, characterized bya yearly loss of attachment of 0.1 to 1.0 mm

Localized aggressive periodontitis (LAP) occurs inless than 1% of adolescents.

blacks were at much higher risk than whites for allforms of aggressive periodontitis

male teenagers were more likely to have GAP thanfemale adolescents

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Host Response

Defective chemotactic response in neutrophils

Hyper-inflammatory state resulting in thepresence of pro-inflammatory cytokines in theserum

Phagocyte and macrophage abnormalities areminor in the sense that they are usually notassociated with infections other thanperiodontitis.


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Risk factors

Microbiological factors (Aa in 90% of LAP)

Immunological factors human leukocyte antigens (HLAs), which regulate immuneresponses have been evaluated as candidate markers for aggressiveperiodontitis (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 periodontitismay be inherited

Environmental Factors (smoking)

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Prognosis


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 andenvironmental factors

Antibiotics

Chlorhexidine rinses

Evaluation & counseling for other familymembers

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Aggressive periodontitis

Currently, an ideal antibiotic for thetreatment of periodontal diseases

does not exist. Although oral bacteriaare susceptible to many antibiotics, no

single antibiotics at concentrationsachieved in body fluids inhibits allputative periodontal pathogens


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Combination Therapy

Periodontal infections contain a wide diversity ofbacteria.

Metronidazole +Amoxycillin or Augmentin.

Never use antibiotics alone without adjunctivemechanical debridement and OHI.

Antibiotics

Tetracyclins (avoid in children)

Doxycycline 100mg/day

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s10.chronic periodontitis aggressive periodontitis(2009)

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