Influence of genetic polymorphisms in the colonization/recolonization patterns in chronic periodontitis patients

Abstract

Periodontal diseases have a complex etiology, involving the interactions of multiple genes controlling the host response to infecting microorganisms. Adult twin studies have suggested a relation between genetic background and periodontitis risk. Population variations on host´s infection response control genes can explain a great proportion of the differential clinical presentation of periodontitis. The ecologic changes of subgingival biofilm leading to increased proportions of Gram (-) rods of the so called red and orange complex are correlated to worsening of the clinical parameters of periodontitis and treatment failure. Recent genome-wide association studies have identified Single Nucleotide Polymorphisms (SNP) associated to an increased risk of infection by red and orange complex microorganism and the putative periodontal pathogen A. actinomycetemcomitans. In this context, the purpose of this study is to investigate the involvement of SNP in the differential pre and post treatment subgingival biofilm profile and to correlate the later with clinical parameters and immunological markers of periodontitis. The study design consider two different population samples: (1) a longitudinal one of 75 chronic periodontitis patients and 50 healthy controls, who will receive cause-related treatment as needed and followed by a period of one year. Subgingival biofilm samples of these volunteers will be collected at baseline, 6 and 12 months; and (2) a cross-sectional sample of 197 chronic periodontitis patients, 193 gingivitis patients and 218 healthy individuals. Affected gingival tissue samples of the chronic periodontitis patients scheduled for surgical treatment will be collected to quantify the expression profiles of immunological markers. The subgingival biofilm samples will be characterized by DNA-DNA hybridization checkerboard for 40 species and quantitative Real Time PCR for 12 species, both pathogenic and commensal. The participants will be genotypified for the SNP of interest and the microbiological, clinical and immunological data will be analyzed to establish correlations between the risk alleles and the response variables. The data analysis will consider a case/control design, using both the "classic" healthy control group and the "resistant" phenotype group of gingivitis-affected individuals. This alternative approach maximizes the possibilities of finding true correlations between genetic profiles and the study variables. Such knowledge might allow the development of diagnostic, preventive and therapeutic strategies in order to improve the clinical management of periodontal diseases. (AU)