Analysis of serum IgG response against OMP29 and whole cell of A. actinomycetemcomitans of different serotypes and against whole cell of P. gingivalis and T. forsythia in patients with aggressive periodontitis

Abstract

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 the specificity can exist in different forms. Studies with AP show that the Aggregatibacter actinomycetemcomitans (Aa) is implicated as the principal 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 the AP, although there are differences in the distribution of these serotypes among different populations. Regarding the outer membrane protein of Aa, the top six have been identified - Omp100, Omp64, Omp39, Omp29, Omp18 and Omp16. The sequence of each Omp protein showed homology with some virulence factors of other pathogenic bacteria. It is important to elucidate the physiological functions of these Omps and its potential as virulence factors of Aa, because these proteins can be recognized by antibodies in the serum of patients with AP. The serum of patients with LAP often displays high levels of immunoglobulin G (IgG) to the antigens of Aa (leukotoxin, LPS and Omps). It was also showed that the Omps of Aa, especially Omp29, reacts strongly with the serum of patients with AP. While the Aa has this strong relationship with the AP, its frequency of detection 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 microbial profile of subjects with untreated LAP showed that Tf and Pg were the most prevalent and numerous species, suggesting that Aa be associated with the establishment of the LAP, but other species such as Pg, Tf, Pi, T. denticola among others, appear to have a key role in the progression of this disease. The prevention and control of 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, generally showing improved clinical outcomes. But there are few studies with long-term results following clinical trials of systemic antibiotics in young individuals with AP. For further treatment, the role of antibodies to Aa in AP is not well defined. The association of virulence with Omps may suggest that burnout could predict disease onset and/or its progression. The protective effect of antibodies in periodontal infections has been discussed since the serum levels of IgG to Pg or Aa in stable patients with periodontitis were higher than those with active periodontitis. The characterization of the humoral response in infectious diseases could occur by the response to antigens of whole cells, but analysis of the antigens isolated could indicate its involvement in the disease process and the biological functions of antibodies. Thus, this knowledge could provide new strategies for prevention and/or control of AP. Identification and functional characterization of outer membrane proteins are prerequisite for developing of a potentially effective vaccine. As far as we know, there are no studies that assess the humoral response in patients with AP and their relationship with a probable additional attachment loss after treatment elucidating the formation of antibodies has or has not protective action with regard to clinical attachment loss. (AU)