Contribution of Interleukin-10-592 (-590, -597) C>A Polymorphisms to Periodontitis Susceptibility: An Updated Meta-Analysis Based on 18 Case-Control Studies

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.

Evaluation of IL6, IL10 and VDR alleles distribution in an Italian large sample of subjects affected by chronic periodontal disease

“…17,18 Four recent meta-analysis reached similar conclusion supporting IL10 polymorphisms as possible biomarkers for PD. 19–22…”

“…17,18 Four recent metaanalysis reached similar conclusion supporting IL10 polymorphisms as possible biomarkers for PD. [19][20][21][22] The effect of VDR appeared less consistent among different populations. 23,24 Although increasing number of papers reported association between genetic polymorphisms and PD, the way for their use for diagnostic or prognostic purposes appeared full of obstacles.…”

Next-Generation Examination, Diagnosis, and Personalized Medicine in Periodontal Disease

“…In early studies, candidate genes involved in host immunity, inflammation, and tissue remodeling were selected as targets, and their single nucleotide polymorphisms (SNPs) were associated with periodontitis. A number of candidate gene studies showed that IL1A, IL1B, IL4, IL6, IL10, TNFA, FcγR, VDR, TLR2, TLR4, and MMP1 [ 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 ] were the main genes associated with periodontal disease. In particular, the IL-1 gene cluster has been analyzed since the early days of studies on periodontal genetics, and SNPs in the IL-1 genes were proposed to be used for genotyping periodontal patients [ 70 , 71 , 72 , 73 ].…”

Interleukin Gene Variability and Periodontal Bacteria in Patients with Generalized Aggressive Form of Periodontitis

“…The candidate genes for AgP include, among others, IL-1 and its receptor antagonist ( IL-1RN ), IL-6 and its receptor ( IL-6R ), IL-10 , IL-17A , and IL-18 . As individual case-control studies in various populations reported controversial results, meta-analyses focused on variants in the mentioned genes were performed and their relation to localized, generalized, or both AgP was predicted [ 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ]. Studies investigating combinations of polymorphisms within specific haplotypes and host genotypes with microbial profiles might provide important information on the pathogenesis of this complex disease [ 31 ].…”