TNF-α-308G/A Gene Polymorphism And Risk Of Chronic Periodontitis: A Meta Analysis

Objective Perform a meta-analysis to evaluate the association betweenTNF-α308G/A gene polymorphism and the risk of chronicperiodontitis(CP).Methods Studies on correlation between TNF-α-308G/A genepolymorphism and susceptibility to CP were systematically retrieved fromCochrane library, Embase, Pubmed, Medline, VIP and Wanfang data，CNKI, CBM. Last search was updated in March,2014.The relatedcase-control studies and cohort studies were screened out according to theinclusion criteria and exclusion criteria.Academic level of studies includedin this article was assessed on the basis of the Newcastle-Ottawa Scale(NOS). Meta analysis was carried out using the Review Manager (version5.2.0) and Stata (version12.0). The Q statistic and the I2statistic wereused to assess the degree of heterogeneity among the studies included inthe meta-analysis.A P value greater than0.10for the Q-test and I2≤50%indicated a lack of heterogeneity among studies, so that the pooled ORestimate of each study was calculated by the fixed-effects model.Otherwise,the random-effects model was used.The subgroup analysis and sensitivity analysis were utilized to deal with the heterogeneity.Crude odds ratios(ORs) with95%confidence intervals (95%CI) were used to evaluate thestrength of associations between TNF-α-308G/A gene polymorphism andthe risk of chronic periodontitis(CP).Potential publication bias wasobserved by the Begg’s funnel plot and Egger’s linear regression test.Sensitivity analyses were carried out by limiting the meta-analysis tostudies conforming high quality (score≥7).Results A total of18case-control studies (1420cases,1538controls)were included in this meta analysis.7studies were conducted in Caucasianpopulations,including434cases and452controls;7in Asian populations,including717cases and701controls;8studies focused on severe CP,including424cases and552controls;4studies focused onmild-to-moderate CP, including247cases and313controls;and5studiesreported nosmokers,including284cases and277controls.In the overall population,There was no evidence of significantassociation between TNF-α-308G/A gene polymorphism and the risk ofCP:allele genetic model A vs. G (OR=1.05,95%CI=0.83-1.34, P=0.68),additive genetic model AA vs. GG (OR=1.35,95%CI=0.78-2.34, P=0.28),dominant model AA+AG vs. GG (OR=1.02,95%CI=0.79-1.33, P=0.88),recessive model AA vs. AG+GG (OR=1.42,95%CI=0.82-2.45, P=0.21).There was no evidence of significant association between TNF-α-308G/A gene polymorphism and CP in Caucasian populations:allele genetic model A vs.G(OR=0.97,95%CI=0.73-1.29,P=0.85),additive geneticmodel AA vs.GG(OR=4.70,95%CI=0.95-23.14,P=0.06),dominant modelAA+AG vs.GG(OR=0.92,95%CI=0.68-1.25,P=0.60),recessive model AAvs.AG+GG (OR=2.76,95%CI=0.64-11.84, P=0.17).No association was found between TNF-α-308G/A gene polymorphismand CP among Asians: allele genetic model A vs.G(OR=1.36,95%CI=0.88-2.12,P=0.17),additive genetic model AA vs.GG(OR=1.95,95%CI=0.75-5.08, P=0.17),dominant model AA+AG vs.GG(OR=1.39,95%CI=0.92-2.12, P=0.12),recessive model AA vs.AG+GG(OR=1.85,95%CI=0.71-4.86, P=0.21).There was no significant association between TNF-α-308G/A genepolymorphism and severe CP: allele genetic model A vs.G(OR=0.88,95%CI=0.65-1.18,P=0.39),additive genetic model AA vs.GG(OR=0.57,95%CI=0.18-1.80,P=0.34),dominant model AA+AG vs.GG(OR=0.89,95%CI=0.65-1.23,P=0.48),recessive model AA vs.AG+GG(OR=0.62,95%CI=0.20-1.94, P=0.41).No association was found between TNF-α-308G/A gene polymorphismand mild-to-moderate CP: allele genetic model A vs.G(OR=1.08,95%CI=0.72-1.64,P=0.70),additive genetic model AA vs.GG(OR=1.29,95%CI=0.39-4.34,P=0.68),dominant model AA+AGvs.GG(OR=1.02,95%CI=0.65-1.60,P=0.93),recessive model AA vs.AG+GG(OR=1.91,95%CI=0.46-8.04, P=0.38). No significant result was observed for the association betweenTNF-α-308G/A gene polymorphism and CP for nosmoker: additive geneticmodel A vs.G(OR=1.01,95%CI=0.68-1.48,P=0.98),additive genetic modelAA vs.GG(OR=1.05,95%CI=0.34-3.21,P=0.93),dominant model AA+AGvs.GG(OR=0.99,95%CI=0.65-1.52),P=0.97),recessive model AA vs.AG+GG (OR=1.15,95%CI=0.38-3.51, P=0.80).Conclusions TNF-α-308G/A gene polymorphism may not be a riskfactor of CP. Due to the limited quantity of the included studies; furtherstudies are needed to validate the above conclusion.