Association between polymorphisms of anti-inflammatory gene alleles and periodontitis risk in a Chinese Han population.

Abstract

Cytokines that mediate the immune responses are important in the pathogenesis of periodontitis. The genetic polymorphisms of IL-10, TNFAIP3 (A20), and NF-κB1 (p105/p50) and their association with the risk of periodontitis were investigated. Venous blood from 102 clinical periodontal healthy participants and 100 patients with periodontitis was collected to genotype the IL-10 (rs1800872), A20 (rs2230926, rs5029937, rs6927127), and NF-κB1 (rs28362491) SNP loci by Sanger technology. Univariable and multivariable logic regression and path analysis model was used to analyze the genotypes and alleles. Single-gene mutations in the A20 (rs2230926, rs5029937, rs6927127) and IL-10 (rs1800872) genes were not associated with the risk of periodontitis. NF-κΒ1 (rs28362491) gene influenced periodontitis susceptibility by affecting CAL. The combined effect of A20 and IL-10 was related to the risk of periodontitis (ORa = 0.123-0.151). One site mutated in the A20 (rs2230926, rs5029937, rs6927127) gene or IL-10 (rs1800872) gene reduced the risk of periodontitis. Single gene polymorphisms in A20 and IL-10 genes were not associated with the risk of periodontitis. NF-κB1 gene polymorphism indirectly affects susceptibility to periodontitis. The combined effect of anti-inflammatory gene polymorphisms (A20 and IL-10) correlated with the decreased risk of periodontitis. This study helps to explore the potential mechanisms underlying the role of anti-inflammatory genes in the progression of periodontal disease and provides a basis for the selection and development of appropriate periodontal treatment strategies based on the genetic profile of the patient.