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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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Localized aggressive periodontitis
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
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 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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