Background. Periodontitis is a kind of chronic infectious disease, affecting the health of billions of people. In recent years, a number of studies have shown that multiple immune gene polymorphisms are associated with the susceptibility to periodontitis, among which TLR-2 plays a critical role in periodontitis. But most of the studies reported TLR-2 gene polymorphism and susceptibility to periodontitis are not consistent. Therefore, we included all eligible studies in our study for further meta-analysis. Methods. We used electronic databases, including CNKI, PubMed, EMBASE, and Web of Science databases, and relevant research published through June, 2020. Selecting studies involved case-control trials. For all eligibility studies, odds ratios (ORs) and 95% confidence intervals (95% CI) are provided or can be calculated from the study data. The size of the combined effect was calculated using STATA 15.0. Results. Our meta-analysis included 14 articles representing 18 case-control studies with a total of 3873 cases and 3438 control subjects. Significant association was found between periodontitis and TLR-2 rs1898830 polymorphism under the allelic model (A allele vs. G allele: p=0.014, OR=1.208, 95% CI: 1.039-1.406), recessive model (GG vs. GA+AA: p=0.028, OR=0.755, 95% CI: 0.588-0.970), and codominant model (GG VS. AA: p=0.014, OR=0.681, 95% CI: 0.501-0.925). In subgroup analysis, TLR-2 rs5743708 polymorphism was associated with periodontitis risk in Asians under an allelic model (G allele vs. A allele: p=0.017, OR=12.064, 95% CI: 1.570-92.688), dominant model (GA+AA vs.GG: p=0.016, OR=0.08, 95% CI: 0.010-0.620), and codominant model (GA VS. GG: p=0.016, OR=1.026, 95% CI: 0.821-1.282). Conclusion. The TLR-2 rs1898830, rs5743708 polymorphism may be associated with susceptibility to periodontitis. In the future, genome-wide approaches and large-scale, multiethnic case-control trials are still needed.
The aim of this study was to explore the possible associations between single nucleotide polymorphisms (SNPs) and DNA methylation levels of seven genes in the inflammatory response pathway with susceptibility to chronic periodontitis (CP) among the Uighur population of the Xinjiang Autonomous Region of China. Methods: A total of 444 eligible subjects (279 CP patients and 165 healthy controls) were enrolled in the study. Genomic DNA was obtained from gingival tissue for genotyping eight SNPs and performing methylation measurements of seven genes. Results: SNP rs2070745 in the formyl peptide receptor 1 (FPR1) gene achieved statistical significance in a standard allelic association analysis for CP ( p = 0.02). The frequency of the rs2070745 minor allele G was higher in the cases than in controls (0.367 vs. 0.291). Additionally, rs2070745 was significantly associated with CP under the dominant genetic model ( p = 0.03). Using logistic regression analysis, rs2070745 was found to be consistently associated with CP under the additive dominant model, and this association remained significant after covariates were taken into account [odds ratio (OR) = 1.49 (1.09-2.05), p = 0.014; OR = 1.58 (1.04-2.40), p = 0.031, respectively]. No significant gene-gene interactions were identified. Although we did not find a polymorphism in interleukin 6 (IL6) associated with CP in our study, the methylation level of a CpG island region located within the promoter region of IL6 was significantly less in CP patients compared with controls ( p < 0.05). Conclusions: The genetic polymorphism rs2070745 in FPR1 and the methylation level of the promoter region of IL6 might be associated with CP in the Uighur population of China.
The ever-increasing global prevalence of obesity has trended towards a younger age. The ecological characteristics and changes of the oral and gut microbial community during childhood are poorly understood.In this study, we analyzed the salivary and fecal microbiota of 30 children with obesity and 30 normal weight children aged 3-5 years via third-generation long-range DNA sequencing,with the aim of understanding the structure of childhood microbiota and identifying specific oral and gut microbial lineages and genera in children that may be associated with obesity.The results revealed significant variation in alpha diversity indices among the four groups (Chao1: P < 0.001; observed species: P < 0.001; Shannon < 0.001). Principal coordinate analysis (PCoA) and nonmetric multidimensional scaling (NMDS) revealed significant differences in oral and gut microbial community structure between obesity and controls. The Firmicutes/Bacteroidetes (F/B) abundance ratios of oral and intestinal flora among children with obesity were higher than those of controls. The most abundant phyla and genera found in oral and intestinal flora were Firmicutes, Proteobacteria, Bacteroidetes, Neisseria, Bacteroides, Faecalibacterium, Streptococcus, Prevotella and so on. Linear discriminant analysis effect size (LEfSe) revealed higher proportions of Filifactor (LDA= 3.98; P < 0.05) and Butyrivibrio (LDA = 2.54; P < 0.001) in the oral microbiota of children with obesity, while the fecal microbiota of children with obesity were more enriched with Faecalibacterium (LDA = 5.02; P < 0.001), Tyzzerella (LDA=3.25; P < 0.01), Klebsiella (LDA = 4.31; P < 0.05),which could be considered as dominant bacterial biomarkers for obesity groups.A total of 148 functional bacterial pathways were found to significantly differ in the oral and gut microbiota among controls and obesity using PICRUSt 2. Most predicted functional pathways were clustered in biosynthesis. In conclusion, This work suggests there were significant differences in oral and gut microbiota in controls and obesity groups, microbiota dysbiosis in childhood might have significant effect on the development of obesity.
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