There is also a relatively fast progression of periodontal tissue loss.With an increase in the age of the patient, there may be progression of the disease involving the adjacent teeth and lead to the patient developing GAP. The periodontal tissue also exhibits minimal signs of inflammation clinically and show a robust response with serum antibodies to pathogens.The amount of plaque present is inconsistent with the amount and severity of tissue destruction  but with a high plaque pathogenicity due to the presence of increased levels of bacteria like Aggregatibacter actinomycetemcomitans (A.a) and Porphyromonas Gingivalis (P.g).Secondary features of LAP may also be present including;
diastema formation with disto-labial migration of the incisors
increased mobility of the affected teeth, sensitivity due to exposed root,
deep dull pain that radiates to the jaw
periodontal abscess with lymph node enlargement

Radiographic features
Radiographically, the periodontal lesion often presents with alveolar bone loss in a horizontal  pattern at the interproximal surface of the permanent first molars  and usually horizontal bone pattern of bone loss at the interproximal surface of the incisors as the bone is thinner than at the interproximal surface of the molars.The alveolar bone loss patterns are usually bilateral and similar on both sides and has been referred to as being a mirror-image pattern.In advanced cases the alveolar bone loss may be depicted as a horizontal bone loss pattern radiographically. Generalized aggressive periodontitis
Clinical features
Mostly in individuals under 30 years oldIn GAP, the clinical appearance of the disease resembles chronic periodontitis.
They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue. There are abnormalities associated with phagocytes.Phagocytes are essential in resolving inflammation. The impairment of their phagocytic activity results in persistent inflammation in periodontal tissues. Hyper-responsive macrophage phenotype.Due to the increased responsiveness, the macrophages produce excessive levels of inflammatory mediator and cytokine, such as prostaglandin E2 (PGE2) and interleukin-1β (IL-1B). Their hyperactivity is associated with periodontal tissue destruction and bone loss. Progression of attachment loss and bone loss may be self-arresting.In some patients, the disease may burnout without any cause-related therapy. Caries levels have seen to be lower in cases of aggressive periodontitis.Staging
Cases of aggressive periodontitis have been staged into Stage I, II and III based on the severity of the cases. The staging index was proposed based on clinical features, radiological features and possible risk factors. The proposed index was validated with 10 cases of aggressive periodontitis followed for 10 years. Clinical and radiographic features
Localized aggressive periodontitis
Clinical features
LAP begins around the age of puberty where there is interproximal loss of attachment of the first molar, and or incisors. on at least two permanent teeth (one which is a first molar) and no involvement of more than two teeth other than the first molars and incisors, lack of inflammation and evidence of deep periodontal pocket with advanced bone loss.