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.
Periodontal surgery: If it is a localised problem and if the case is non-response to non-surgical treatment despite the oral hygiene being consistently excellent. This could involve an open flap debridement with or without regenerative procedures, with the aim of gaining access and visibility to root and furcation areas so that a thorough instrumentation and debridement can be carried out. Regenerative surgical therapy currently available include the use of bone replacement grafts, barrier membranes or guided tissue regeneration (GTR), biologic modifiers like growth and differentiation factors (GDF), and extracellular matrix proteins like enamel matrix proteins (EMD). There is however, a great variation in periodontal gains reported in the literature available, signifying that results are not entirely predictable. Maintenance
Periodontal treatment may help to stabilise the disease, but it does not change ones susceptibility to the disease. Given the high susceptibility for disease progression of the individual with AgP, there is a higher risk of disease recurrence. It is thus necessary to attend frequent review appointments at the dentist to ensure there is no relapse of the disease, and that the periodontal health is maintained after active periodontal therapy. == References ==