|Support type:||Scholarships in Brazil - Scientific Initiation|
|Effective date (Start):||October 01, 2011|
|Effective date (End):||July 31, 2012|
|Field of knowledge:||Health Sciences - Dentistry - Periodontology|
|Principal researcher:||Luciana Saraiva|
|Grantee:||Nathane de Araujo Mantovani|
|Home Institution:||Faculdade de Odontologia (FO). Universidade de São Paulo (USP). São Paulo , SP, Brazil|
Aggressive periodontitis (AP) is a disease with specific clinical and laboratory findings. The role of microbiota in the etiology of AP has been studied and specificity can exist in different forms. Studies with AP show that the Aggregatibacter actinomycetemcomitans (Aa) is implicated as the primary agent of this disease, especially in its localized form (LAP), although it can also be found in patients with chronic periodontitis and periodontally healthy individuals. The Aa has a variety of virulence factors that have the potential to affect the immune system and promote periodontal inflammation, but little is known about the factors responsible for the establishment of the AP. The six serotypes of Aa are: a, b and c (more frequent), d and e. Serotype b is more associated with AP, although there are differences in the distribution of serotypes among different populations. Sera from patients with LAP often exhibits high levels of immunoglobulin G (IgG) to the antigens of Aa (Leukotoxin, OMPs and LPS). Although the Aa have this strong relationship with the AP, its detection frequency tends to decrease after 21 years with the increase of other pathogens such as Porphyromonas gingivalis (Pg), Prevotella intermedia (Pi), Tanerella forsythia (Tf) among others. Some authors, analyzing the microbiological profile of untreated subjects with LAP, showed that the species were more numerous and prevalent Tf and Pg, suggesting that Aa appears to be associated with the establishment of the LAP, but other bacterial species as Pg, Tf, Pi, T. denticola among others, seems to play a key role in the progression of this disease. The prevention and control of the AP is a challenge. Non-surgical treatment only seems to be less effective in patients with AP. The effectiveness of antibiotics as adjuncts to non-surgical treatment has also been investigated, usually showing improved clinical outcomes. But there are few studies with long-term results following clinical trials of systemic antibiotics in young patients with AP. In relation to new treatment modalities, the role of antibodies to Aa in AP is not well defined. The protective effect of antibodies in periodontal infections has been discussed since the serum levels of IgG to Aa or Pg in stable patients with periodontitis were higher than those with active periodontitis. Characterization of the humoral response in infectious diseases might occur by responding to antigens from whole cells, but analysis of isolated antigens could indicate their involvement in the disease process and the biological functions of antibodies. Thus, this knowledge could provide new strategies for the prevention and / or control of the AP. The identification and functional characterization of surface exposed proteins are prerequisite for the development of an effective vaccine potential. As far as we are aware, there are no studies that evaluate the humoral response in patients with AP and its possible association with insertion loss of additional post-treatment, seeking to elucidate the formation of antibodies have protective action or not in relation to the insertion loss.