IGHG2 and FCGRs Polymorphisms in Patients with Generalized Aggressive Periodontitis

摘要

Generalized aggressive periodontitis (GAP) is an inflammatory disease characterized by the rapid periodontal tissue destruction initiated by bacterial infections. Interactions between FcY Receptors (FCGRs) and IgG-opsonized bacteria play a major rolein host immune defense, which may predispose to the development of GAP. We investigated genetic effects of functional polymorphisms of the FCGRs, IGHG2 genes, and the FCGRs haplotypes on GAP. Four polymorphisms, FCGR2A Hisl31Arg, FCGR3A PhelSSVal, FCGR3B, and IGHG2, were genotyped by using polymerase chain reaction-allele specific primers in 93 GAP patients and in 142 healthy controls. The genotype and allele frequencies of FCGR2A HisBlArg, FCG/Z3A PhelSSVal, FCGR3B, and IGHG2 polymorphisms did not showsignificant differences between the GAP patients and the controls. Frequency of individuals carrying both FCGR3A 158*Val and FCGR3B *2 alleles were higher in the patients than in the controls (40.9% vs 30.3%). In the never-smoker group FCGR3B*2 carrierfrequency was significantly higher in the GAP patients than in the controls (70.8% vs 54.7%; odds ratio [OR] = 2.0, 95% confidence interval [CI] = 1.02-3.98, p = 0.044). And individuals having both FCGR3A 158*Val and FCGR3B*2 alleles were significantly more prevalent in the patients than in the controls (46.2% vs 25.6%; OR = 2.5, 95% CI = 1.25-4.96, p = 0.008). Haplotype frequencies of FCGR2A, FCGR3A, and FCGR3B were not found to be different between the patients and the controls. These results suggestthat each of FCGR2A, 3A, 3B, and IGHG2 polymorphisms alone was not sufficient for the development of GAP, but that combined genes of FCGR3B *2 and FCGR3A. 158*Val were associated with never-smoker GAP patients, in particular.