aggressive

AGGRESSIVE PERIODONTITIS

“Infectious, inflammatory disease of thePeridontium with rapid attachment loss and

bone loss in otherwise healthyadolescent with familial aggregation of

diseased individuals.”

DEFINITION OF AGGRESSIVE PERIODONTITIS

CLASSIFICATION

Age of onsetRapid rate of disease progressionThe nature and composition of associated

sub-gingival microflora Alterations in the host’s immune responseFamilial aggregation of diseased individuals

DIFFERENCE BETWEEN AGGRESSIVE AND CHRONIC PERIODONTITIS

Except for the presence of periodontitis, these patients are otherwise clinically healthy

Rapid attachment loss and bone destruction

Absence of large amount of plaque and calculus

Family history is positive

PRIMARY DIAGNOSTIC FEATURES OF AGGRESSIVE PERIODONTITIS

Elevated levels of Actinobacillus actinomycetem-comitans and, in some cases, Porphyromonas gingivalis

Abnormal phagocytes and hyper-responding macrophages

The progression of bone loss may be self-arresting

Disease is more prevalent among the African Americans

SECONDARY FEATURES OF AGGRESSIVE PERIODONTITIS

“LOCALIZED AGGRESSIVE

PERIODONTITIS’’

Clinical features:1. Age of onset at about puberty.2. Affects both the sexes3. Main characteristic

feature affects mainly the

4. Lack of clinical inflammation despite the presence of deep periodontal pockets.

LOCALIZED AGGRESSIVE PERIODONTITIS

11 mm

9 mm

FIRST MOLARS and INCISORS

Clinical features (cont.)5. Plaque that is present forms

thin biofilm on the teeth.6. Plaque contains elevated

levels of : Actinobacillus actinomycetem-comitans (Serotype b) Porphyromonas gingivalis (in some pts)

7. Disease progresses rapidly


Clinical features (cont.)

8. The rate of bone loss is 3 to 4 times faster than in chronic periodontitis.


Other Clinical Findings:

1. Maxillary incisors migrate disto-labially that results in diastema formation.

2. Increasing mobility of the affected teeth

3. Sensitivity of denuded root surfaces to thermal and tactile stimuli


4. Deep, dull radiating pain during mastication.5. Periodontal abscess may form.6. Regional lymph node enlargement may occur.


Following are the possible reasons for localized distribution of lesions:

1. Strong antibody response to infecting agents:

“BURN-OUT PHENOMENA”

Actinobacillus actinomycetem initially colonizes the 1st permenant teeth to erupt.

The host defenses are evaded.


Entry of bacteria into the pocket

Initiation of destruction of periodontal tissues.

In turn, immune defenses are stimulated production of opsonic antibodies enhance clearance of invading bacteria and neutralize leukotoxic activity.

This may prevent colonization at other sites.


2. Action of antagonistic bacteria:

Colonization of periodontal tissues.

Inhibit further colonization of Actinobacillus actinomycetem-comitans.

Localized tissue destruction.


3. Actinobacillus actinomycetem-comitans loses its ability to produce leukotoxin

Progression of the disease may become arrested.

4. Denuded root surfaces

Defect in cementum formation maybe resposible for localization of the lesions.

Hypoplasic or aplasitic cementum.


Radiographic finding:

o Classic diagnostic sign VERTICAL LOSS of alveolar bone around the first molars and incisors.


o Other finding “Arc-shaped” loss of alveolar bone extending from the distal surface of 2nd premolar to the mesial surface of the 2nd molar.

o Bone defects are usually wider than usually seen with chronic periodontitis.

LOCALILIZED AGGRESSIVE PERIODONTITIS

Notice the typical angular (vertical) bone loss and its typical location involving the first molars. Calculus is absent and is not an etiologic factor.

GENERALIZED AGGRESSIVE

PERIODONTITIS

Generalized aggressive periodontitis

“Characterized by generalized interproximal attachment loss affecting at least three

permanent teeth other than first molars and incisors”

Generalized juvenile periodontitis Rapidly progressive periodontitis

Etiology

The amount of plaque seems inconsistent with the amount of periodontal destruction.

Bacteria frequently detected are p.gingivalis, a.actinomycetem-comitans and tannerella forsythia

Clinical featuresUsually affects individuals between

puberty and 35 years (may be older).No Gender discriminationPronounced episodic nature of

destruction followed by stages of quiescence that may last weeks to months or years.

almost all or most of the teeth are affected.

Poor serum antibody response to infecting bacteria.

Tissue response

Episodic nature of disease produces Two gingival response.

1. Destructive phase2. Non-destructive phase

Destructive phase:Tissue appears severely inflamed, ulcerated &

fiery red.Bleeding with or without stimulation.Suppuration.Active attachment & bone loss.

Non-destructive phase:

Tissues appear pink with some stippling.Lack of inflammation.Probing will reveal deep pockets.Bone & attachment levels relatively stable.

Associated Systemic manifestations

Some patients with GAP may exhibit:Weight lossMental depression, general malaise

Systemic conditions may predispose client to GAP, these include:Chronic neutrophil defects, leukocyte

adherence deficiencyFunctional defects of PMNs, monocytes or

both impaired chemotaxis & phagocytosis

Radiographic evaluation

Radiographic evaluation can range from :

Severe bone loss affecting minimal number of teeth -OR-

Majority of teeth affected by advanced bone loss

Case no.1A 11 year old boy diagnosed as generalized

aggressive periodontitis

Radiographic presentation:

Case no 2.A case of 31 year old female with LAP over

14 years

Radiographic status after full mouth disinfection therapy and surgical

regenrarive procedures.(impressive regenration at the mandibular first

molars)

RISK FACTORS FOR AGGRESSIVE

PERIODONTITIS.

RISK FACTORS:There are mainly four recognized risk factors

for aggressive periodontitis:

Microbiological factorsImmunological factorsGenetic factorsEnvironmental factors

MICROBIOLOGICAL FACTORS:

A. actinomycetemcomitans:These are short, facultative anaerobic gram

negative rods.Virulence factors associated with

A.actinomycetemcomitans: Leukotoxins Endotoxins Collegenase Chemotactic inhibition factors

Studies show… A.actinomycetemcomitans is found in high

frequency with lesions associated with LAP.

Sites with rapid progression show elevated levels of this bacteria.

Patients with cliniclly manifested LAP show elevated levels of A.actinomycetemcomitans.

Treatment shows reduction in sub-ginival load of this bacteria.

Other microbiological factors include:Porphyromonas gingivalisCapnocytophaga sputigenaPrevotella intermediaMycoplasma speciesSpirochetes

IMMUNOLOGICAL FACTORS:Functional defects of PMNs and monocytes Impairment of the chemotactic attraction

of the PMNs to the site of infection Ultimately

leading to reduced phagocytosis.

Functional neutrophil defects may be induced by bacterial infection or it may be genetic in origin.

GENETIC FACTORS:

Familial clustering of the neutrophil abnormalities suggest that defects my be inherited.

Several studies show that response to periodontal pathogens is under genetic control.

ENVIRONMENTAL FACTORS:Amount and duration of Smoking.Smokers with GAP usually have more no. of

teeth affected.

TREATMENT FOR LOCALIZED AGGRESSIVE PERIODONTITIS:

Extraction of involved teeth (depends on severity of tissue loss)

Periodontal therapy:Plaque control

instructionDebridement with or

without flap surgeryIrrigation with CHX,

home rinsing with CHXBone grafts, root

resections, hemisections

Antibiotic therapy:Adjunctive therapy often

required to eliminate A.a. from tissues

Tetracycline (250 mg qid for 2 weeks)

Metronidazole combined with amoxicillin

Doxycycline

The earlier the condition is diagnosed, the sooner treatment can begin – outcome often more predictable

TREATMENT FOR GENERALIZED AGGRESSIVE PERIODONTITIS:

Careful monitoring of younger clients with GAP b/c rate of disease progression is often faster

Maintenance every 3 weeks or less is recommended if disease in active phase

Periodontal therapy:Debridement in combination with antibiotic

therapy, strict plaque control, CHX irrigation & rinsing

Periodontal surgery

Antibiotic therapy:Highly recommended that microbial

diagnostic & susceptibility testing be done

Combination therapies include:Metronidazole/amoxicillinAmoxicillin/doxycyclineClindamycin

PERIODONTAL SURGERY

1. PRE-SURGICAL BONY DEFECT

2. FLAP INCISION ACCESSES BONE

3. IF NECESSARY, BONE IS CONTOURED

4. IN SOME CASES THE BONE WILL BE REBUILT WITH A BONE GRAFT.

5. GUM IS SUTURED.

6. GUM HEALED INTO NEW POSITION.

THANK YOU!!!

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