Association between TNF-α, TGF-β1, IL-10, IL-6 and IFN-γ gene polymorphisms and generalized aggressive periodontitis

Objective: The aim of this study was to investigate links among cytokine genetic variants and generalized aggressive periodontitis (GAgP). Methods: Thirty-five patients with generalized aggressive periodontitis and 85 healthy controls without periodontitis were included in the study. Probing depth (PD), clinical attachment loss (CAL), plaque index (PI), and gingival index (GI) were recorded as clinical parameters. Polymorphisms of IL-6, IL-10, IFN-γ, TGF-ß1 and TNF-α gene were analysed using the polymerase chain reaction sequence-specific primer method (PCR-SSP). Results: No significant differences were observed for IL-6, IL-10, IFN-γ, and TGF-ß1 cytokine polymorphisms, from the genotype distribution and allele frequency, between GAgP and healthy control groups. In contrast, significant differences were observed in the TNF-α gene polymorphism between GAgP and healthy control groups (P = 0.002). Conclusion: Our data suggest that TNF-α (-308) may be associated with the development of generalized aggressive periodontitis. These results should be replicated in a larger and more diverse population of patients diagnosed with generalized aggressive periodontitis to determine of these findings are generalizable. Generalized aggressive periodontitis (GAgP) is characterized by severe and rapid periodontal attachment loss and bone destruction in young and otherwise healthy individuals.1 To explain the severity of periodontal tissue destruction, various studies have concentrated on the specific bacterial etiology associated with GAgP2,3 or on a modified host defense mechanisms in response to specific bacterial plaque.4,5 In addition, previous studies have investigated factors that may increase host susceptibility to tissue destruction in GAgP; including genetic factors5,6 and high levels of inflammatory mediators and cytokines.4,7,8 Cytokines play a major role in a number of biological activities including proliferation, development, homeostasis, regeneration, repair and inflammation.7 Synthesis profiles of cytokines can be considered as ORIGINAL RESEARCH © 2010 CIM Clin Invest Med • Vol 33, no 2, April 2010 E85. either T helper cell type 1 (Th1) responses, promoting cell-mediated immunity and interleukin-2 (IL-2) and interferon gamma (IFN-γ), or Th-2 responses, promoting humoral immunity (IL-4, IL-5, IL-6, IL-10) and Th-3 subset characterized by the transforming growth factor beta (TGF-ß).9 Polymorphisms likely to occur in regulatory regions of cytokine genes may not only increase susceptibility to some infectious diseases, but also influence the course and prognosis of the disease.9 Many studies have evaluated the putative relevance of cytokine gene polymorphism in the pathogenesis of periodontal disease4,8,10; however, the effect of genetic factors in the pathogenesis of periodontal disease remains unclear. The purpose of our study was to compare the relative frequencies of the cytokine genotypes (IL-6, IL10, TNF-α, TGF-ß, IFN-γ) in subjects with and without GAgP.