Primary features Non-contributory Medical history Rapid attachment loss and bone destruction Familial aggregation
SECONDARY FEATURES Microbial deposits inconsistent with severity Elevated proportions of Aggregatibactor actinomycetemcomitans Phagocyte abnormalities Hyper responsive macrophage BURN OUT
Gingival responses Severely , acutely inflamed tissue. Suppuration, Ulcerated and Fiery red. Pink, Free of inflammation with / without stippling.
Localized Aggressive PERIODONTITITS First molar and INCISORS. two teeth apart from them 0.1 to 0.5% prevalence
Clinical features Circumpubertal onset rapid Localized molar/ incisor presentation Robust serum antibody response to infecting agents
OTHER Features Diastema formation Increasing mobility Sensitivity Deep, dull radiating pain during mastication
Reasons of limitation of pd destruction to certain teeth A A evades host response by chemotaxis inhibiting factors, endotoxins, collegenases , leukotoxin. Strong antibody response later on. Antagonist bacteria to AA colonize periodontal tissues AA may loose its leukotoxin producing ability Defect in cementum formation responsible for localization
Radiographic finding Arc- shaped bone loss from distal of second premolar to mesial of second molar
Generalized Aggressive Periodontitis 0.13 % Prevalence 3 teeth or more apart from molars and incisors. Poor serum antibody response to infecting agents
Radiographic findings Severe bone loss 25 to 60 % bone loss
Microbiologic factors No Significant clear association was found between Aggressive and AA Bacterial invasion of connective tissue
Immunologic factors Display functional defects of PMN , monocytes or both Can be due to bacterial infection or may be genetic High amount of Igg2 in response to AA in LAP
Genetic factors Major gene or set of genes play a role Autosomal dominant pattern
Environment factors Smoking has more of an impact on general aggressive compared to localized aggressive