It has also been found that a low T-helper to T-suppressor ratio is found in aggressive periodontitis which may alter local immune regulation. Monocytes respond to bacterial and inflammatory stimuli with very high levels of local release inflammatory mediators and induce hyper-inflammatory reaction with activation of tissue degrading matrix-metalloproteinases. These is also evidence they produce increased amounts IL-1α and IL-1β which cause osteoclastic bone resorption. These amounts are greatly reduced following treatment.Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis. A persons genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. However, for the disease process to initiate the person must be exposed to the presence of periodontal pathogens and potentially also various environmental factors. Smoking is a generalized risk factor for generalized forms of aggressive periodontitis. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers. Features
According to the 1999 International Workshop for the Classification of Periodontal Diseases, aggressive periodontitis was defined according to 3 primary features, in contrast to chronic periodontitis. These features are common for both localized and generalized form of disease. Primary features
Patients are clinically healthy.Patients do not have any underlying systemic disease that would contribute to aggressive periodontitis.
A significant reduction in the aggregatibacter actinomycetemcomitans count following PDT suggests that the use of PDT in conjunction with conventional non-surgical periodontal treatment can potentially result in a more effective treatment. Considering the global issue of antibiotic resistance, further development and research in PDT successes may prove to present it an ideal adjunct to conventional non-surgical periodontal therapy, as compared to the use of systemic antibiotics. Re-examination/Response to Therapy
This stage of treatment involves the reassessment of the individuals compliance (i.e. level of oral hygiene) and the tissue response to the treatment. This is carried out 10–12 weeks following RSD. If the disease is stabilised, the treatment progresses on to the maintenance stage. In the case where the disease is not stabilised, the cause of failure should be considered, and the treatment progresses on to the stage of definitive therapy, if the cause is correctable. Definitive Therapy
Further RSD at sites which require treatment
Use of Locally Delivered Antimicrobials (LDA) as an adjunct to non-surgical periodontal treatment: For use in deep pockets which fail to respond to repeated non-surgical treatment in patients with adequate oral hygiene. Currently, the available LDA include tetracycline, minocycline, chlorhexidine gluconate and doxycycline, with the mode of delivery being in the form of fibers, chips, polymers and trays. There has yet to be much research into the effects of LDA in AgP, but current studies report an insignificant difference to the adjunctive effect of systemic antibiotics.