Aim. Periodontitis is an inflammatory disease that affects the teeth supporting structures, triggered by periodontal pathogens, and is influenced by environmental and genetic factors. Genes encoding molecules related to the immune response, such as cytokine, are the main candidates for polymorphisms analysis and may be possibly associated with this pathology. A G/C promoter polymorphism on the IL6 gene has been shown to affect basal IL-6 levels. The aim of this study was to investigate the association between the IL6 c.-174G>C polymorphism and periodontitis in individuals from Vitória da Conquista, Bahia, Brazil. Material and Methods. Three hundred and thirty individuals (134 cases, 196 controls) were genotyped for the IL6 c.-174G>C by MS-PCR technique. Concentrations of salivary IL-6 were determined by ELISA method. Results. The IL6 c.-174G>C polymorphism was associated with periodontitis when comparing the distribution of genotypes between patients with periodontitis and control subjects. The GC genotype appeared as a protective factor for periodontitis. Results showed increased levels of salivary IL-6 in periodontitis patients. Nevertheless, there was no relationship between the concentrations of IL-6 and genotypes when comparing the case and control groups. Conclusions. Our data indicate an association between IL6 c.-174G>C polymorphism and periodontitis and showed that IL-6 may be considered an important marker for periodontitis. 1. Introduction Periodontal disease is an inflammatory condition brought about by the interaction between microorganisms that compose supragingival and subgingival biofilms and the host inflammatory response [1]. Some of these microorganisms have been shown to be responsible for the periodontal disease initiation and progression, and the red complex, which includes Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, is considered the most important pathogens in periodontal disease [2, 3]. The inflammation progression induces the production of persistent inflammatory signals by the cells of periodontal tissues. Such persistent signals, represented by the proinflammatory cytokines, for example, interleukin-1 (IL-1), interleukin-2 (IL-2), and tumor necrosis factor-alpha (TNF-α), stimulate the production of secondary mediators which in turn amplify the inflammatory cascade. This continuing amplification process results in the increased production of proteases and osteoclastic signals that lead to connective tissue and bone destruction [4, 5]. Although the host immune response is caused by bacterial
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