Abstract
INTRODUCTION: The association between interleukin-10- (IL-10-) 592 (-590, -597) C>A polymorphisms and susceptibility to chronic or aggressive periodontitis (CP or AgP) is conflicting. This meta-analysis is aimed at quantitatively estimating the association. MATERIALS AND METHODS: PubMed, Embase, Web of Science, and WANFAN were searched for studies performed prior to January 31, 2018, to collect data for our research. Meta-analysis was performed using RevMan 5.3 or STATA 14.0. RESULTS: In total, 18 studies that met our criteria were included. Overall or HWE subgroup analysis of individuals with this polymorphism revealed that in terms of CP susceptibility, there was a significant difference between case groups and control groups in the A allele versus C allele model (OR = 1.38, 95% CI = 1.17-1.64 or OR = 1.38, 95% CI = 1.12-1.70), in the AA versus CC+CA model (OR = 1.49, 95% CI =1.06-2.10 or OR = 1.42, 95% CI = 1.13-1.78), and in the CC versus CA+AA model (OR = 0.69, 95% CI = 0.51-0.92 or OR = 0.68, 95% CI = 0.49-0.93); subgroup analysis based on a nonsmoking population also displayed significance in the A allele versus C allele model (OR = 1.43, 95% CI = 1.15-1.79) and CC versus CA+AA model (OR = 0.62, 95% CI = 0.44-0.87). For this polymorphisms and AgP susceptibility, our analyses revealed a significant association in both the A allele versus C allele model (OR = 1.29, 95% CI = 1.01-1.63) and the AA versus CC+CA model (OR = 1.93, 95% CI = 1.30-2.89); subgroup analysis based on Caucasian or nonsmoking populations showed significant differences in the AA versus CC+CA model (OR = 6.29, 95% CI = 1.78-22.21 or OR = 3.24, 95% CI = 1.59-6.61). CONCLUSIONS: IL-10-592 (-590, -597) A allele and the associated AA genotype may be risk factors for the onset of CP or AgP-particularly for the AA genotype and the increased risk of AgP in Caucasian or nonsmoking populations. Conversely, the CC genotype may act as a protective factor against the onset of CP.