aggresive periodontitis
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NIDHI
B.D.S FINAL YEAR
AGGRESSIVE PERIODONTITIS
CONTENTS INTRODUCTION
HISTORY
AGGRESSIVE PERIODONTITIS
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
AGGRESSIVE 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
AGGRESSIVE PERIODONTITIS
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
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