aggresive periodontitis

NIDHI

B.D.S FINAL YEAR

AGGRESSIVE PERIODONTITIS

CONTENTS INTRODUCTION

HISTORY


DIFFERENCE BETWEEN CHRONIC AND AGGRESSIVEPERIODONTITIS

CLINICAL FEATURES

LOCALIZED AGGRESSIVE PERIODONTITIS

GENERALIZED AGGRESSIVE PERIODONTITIS

DIFFERENCE BETWEEN LAP & GAP RISK FACTORS

o MICROBIOLOGIC FACTORS

o IMMUNOLOGIC FACTORS

o GENETIC FACTORS

o ENVIRONMENTAL FACTORS

CONCLUSION

REFERENCES

INTRODUCTION

Periodontitis is defined as an inflammatory disease of the supporting tissue of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both.

HISTORY 1923, Gottlieb -- Case of epidemic influenza “Diffuse atrophy of the alveolar bone”

Loss of collagen fibers in the periodontal ligament

Replacement by loose connective tissue Extensive bone resorption, Resulting in a widened periodontal

ligament space. The gingiva apparently was not involved.

In 1938 Wannenmacher described incisor-first molar involvement and called the disease Parodontitis marginalis progressiva.

Finally in 1967, Chaput and colleagues and by Butler in 1969 introduce the term Juvenile Peridontitis.

In 1989 the World Workshop in Clinical Periodontics categorized this disease as ‘Localized Juvenile Periodontitis’ (LJP)

Most recently , it is named as Aggressive Periodontitis.

AGGRESSIVE

PERIODONTITIS

Aggressive periodontitis (AgP) comprises a group of rare, often severe, rapidly progressive forms of periodontitis often characterized by an early age of clinical manifestation and a distinctive tendency for cases to aggregate in families.

(Clinical Periodontology and Implant Dentistry 4th edition)

Aggressive periodontitis describes three of the formerly classified as “early-onset periodontitis”

They are: LOCALIZED AGGRESSIVE PERIODONTITIS

GENERALIZED AGGRESSIVE PERIODONTITIS

RAPIDLY PROGRESSIVE PERIODONTITIS

CHRONIC PERIODONTITIS


AGE More prevalent in adults but may be present in children & adolescents

Circumpubertal onset in LAP & under 30 years of age in GAP

RATE OF PROGGRESSION

Slow rate of progression Rapid rate of progression with pronounced episodic events of attachment and bone loss

MICROBIAL AETIOLOGY

Consist of both aerobic & anaerobic gram positive & gram negative microorganisms

Key microorganisms are Aggregatibacteractinomyctemcomitans & Prevotella intermedia

IMMUNOLOGICAL AETIOLOGY

No abnormalities detected Hyper responsive macrophage phenotype & phocyte abnormalities

CHRONIC PERIODONTIS AGGRESSIVE PERIODONTITIS

DISTRIBUTION Localized when less than 30% of sites involvedGeneralized when more than 30% of sites are affected

Localized when 1st molar & incisors & no more than two permanent teeth are involvedGeneralized when at least 3 permanent teeth other than 1st molar & incisor are involved

LOCAL FACTORS Presence of local factors directly relates to the amount of destruction present

Presence of local factors does not commensurate with the amount of destruction present

FAMILIAL AGGREGATION

Lacks strong evidence of correlation between particular genes and periodontitis

Evidence of strong familial aggregation

FEATURES OF AGGRESSIVE

PERIODONTITIS

(by lang et al. in 1999)

PRIMARY FEATURES

Non contributory medical history

Rapid attachment loss and bone loss

Familial aggregation

SECONDARY FEATURES

Amount of microbial deposits does not commensurate with the severity of periodontal tissue destruction

Elevated proportions of aggregatibacteractinomycetemcomitans (Aa)

Hyper responsive macrophage phenotype with exaggerated response to bacterial endotoxin

Phagocyte abnormalities


LOCALIZED AGGRESSIVE PERIODONTITIS

(previously classified as Localized Juvenile

Periodontitis)

GENERALIZED AGGRESSIVE

PERIODONTITIS

(previously classified as Generalized Juvenile

Periodontitis)

LOCALIZED AGGRESSIVE

PERIODONTITIS

Clinically, it is characterized as having "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” .

Clinical features:1. Age of onset at about puberty.

2. Affects both the sexes

3. Main characteristic feature affects mainly the FIRST MOLARS and INCISORS

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

5. Plaque that is present forms thin biofilm on the teeth.

6. Plaque contains elevated levels of :Aggregatibacter

actinomycetem-comitans(Serotype b)

Porphyromonas gingivalis(in some pts)

7. Disease progresses rapidly and Plaque that is present forms a thin biofilm on the teeth and rarely mineralizes to form calculus

8. The rate of bone loss is 3 to 4 timesfaster than in chronic

periodontitis.

9. Robust serum antibody response. to infecting agents

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.

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.

Generalized aggressive

periodontitis

“Characterized by generalized interproximal attachment loss affecting at least three

permanent teeth other than first molars and incisors”

FEATURES

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

Poor serum antibody response to infecting agents.

Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors.

Pronounced episodic nature of the destruction of attachment and alveolar bone.

Radiographic features No definitive pattern of distribution. Ranges

from severe bone loss associated with the minimal no. of teeth, to advanced bone loss affecting the majority of teeth in the dentition.

Patients with GAP demonstrate osseous destruction of 25% to 60% during a 9 week period and other sites show no bone loss.

Localized aggressive periodontitis (LAP)

Generalized aggressiveperiodontitis (GAP)

AGE OF ONSET Circumpubertal Under 30 yrs of age but older patients may be affected

DISTRIBUTION Localized 1st molar or incisor presentation with interproximal attachment loss & not involving more than 2 permanent teeth

Generalized interproximal attachment loss affecting at least three permanent teeth other than 1st molars & incisors

SEVERITY Rapid & severe loss of alveolar bone

Episodic in nature

AETIOLOGY Predominantly Aa Predominantly P. gingivalis

IMMUNOLOGICALRESPONSE

Robust serum antibody response to infecting agent

Poor serum antibody response to infecting agent

PRESENCE OF LOCAL FACTORS

There is minimal amount of local factors present on the affected teeth

There is marked plaque & calculus accumulation

FAMILIAL PATTERN

Strong association Unclear association

Localized Aggressive Periodontitis

Generalized Aggressive Periodontitis

GINGIVALINFLAMMATION

Lack of clinical inflammation despite the presence of deep pockets and advanced bone loss

Clinical signs of gingival inflammation are evident

RADIOGRAPHIC APPEARANCE

Vertical or arc-shaped bone loss around 1st molars and incisors

There is generalized extensive destruction or bone loss around involved teeth

Risk factors for aggressive form of

periodontitis

Microbiologic factors

Immunologic factors

Genetic factors

Environmental factors

Microbiologic factors

Presence of Aggregatibacteractinomycetemcomitans (Aa) is a key agent in LAP as it is present in high nos. & the patient has high titre of serum antibodies against Aa.

Virulence factors possessed by Aa, such as leucotoxin, lipopolysaccharide, proteases, collagenases, surface associated material affect the immune response & lead to connective tissue destruction and bone resorption.

Immunologic factors

Defective chemotaxis due to functional defect of PMNs.

Hyper responsive monocytes that increase prostaglandin, IL-1 α IL-1βproduction, which result in one resorption.

Human leucocyte antigen (HLA) A9 & B 15 are recognized as candidate markers of aggressive periodontitis.

Genetic factors

Tendency to occur in families: familial aggregation

Segregation & linkage analysis have shown that presence of specific gene is responsible for neutrophil abnormalities

Transmission through autosomal- dominant mode of inheritance

Environmental factors

Smoking has a significant influence in the progression of generalized aggressive periodontitis. Smokers have greater attachment loss than non smokers.

CONCLUSION Aggressive forms of periodontitis are currently

considered to be multifactorial diseases developing as a result of complex interactions between specific host genes and the environment.

Interactions between the disease process and environmental factors and genetically controlled modifying factors are thought to contribute to determining the specific clinical manifestation of the disease.

For a successful treatment outcome the conventional therapy is to be combined with a wide range of therapeutic procedures to increase the chances of disease resolution.

REFERENCES

CARRANZA’S CLINICAL PERIODONTOLOGY; 10th edition.

J LINDHE; CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY: 4th edition

aggresive periodontitis

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