Dataset Information

Interleukin-1? rs1143627 polymorphism with susceptibility to periodontal disease.

ABSTRACT: Association between interleukin-1 beta (IL-1?) rs1143627 polymorphism and periodontal disease susceptibility was inconsistent; hence we performed this meta-analysis to explore the precise correlation between them. The degree of association was appraised through calculating pooled odds ratio (OR) and its 95% confidence interval (CI). The databases known as PubMed, Embase, and Chinese National Knowledge Infrastructure were searched up to October 26, 2016. A total of 8 eligible case-control studies were finally included, which involved 229 aggressive periodontitis patients, 382 chronic periodontitis patients, and 555 healthy controls. All the five genetic models revealed a non-significant association between IL-1? rs1143627 polymorphism and periodontal disease susceptibility (TT vs. CC: OR = 1.22, 95% CI = 0.80-1.87; CT+TT vs. CC: OR = 0.66, 95% CI = 0.44-1.01; TT vs. CT + CC: OR = 1.19, 95% CI = 0.81-1.74; T vs. C: OR = 0.92, 95% CI = 0.81-1.12; CT vs. CC: OR = 0.92, 95% CI = 0.69-1.23). Sensitivity analyses indicated that the results were robust and the subgroup analyses reached similar conclusions. IL-1? rs1143627 polymorphism is not related to periodontal disease susceptibility in the overall population based on the current evidence, but further studies are required in more large scale sample size with risk factor adjusted.

SUBMITTER: Huang W

PROVIDER: S-EPMC5458217 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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Interleukin-1β rs1143627 polymorphism with susceptibility to periodontal disease.

Huang Wei W He Bing-Yang BY Shao Jun J Jia Xiao-Wei XW Yuan Ya-Di YD

Oncotarget 20170501 19

Association between interleukin-1 beta (IL-1β) rs1143627 polymorphism and periodontal disease susceptibility was inconsistent; hence we performed this meta-analysis to explore the precise correlation between them. The degree of association was appraised through calculating pooled odds ratio (OR) and its 95% confidence interval (CI). The databases known as PubMed, Embase, and Chinese National Knowledge Infrastructure were searched up to October 26, 2016. A total of 8 eligible case-control studies ...[more]

PMID: 28404906

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Project description:BackgroundInterleukin (IL)-35 is a novel anti-inflammatory cytokine that is produced by regulatory T cells. IL-35 mediates immunological functions and plays a protective role in several diseases such as asthma and rheumatoid arthritis. However, the role of IL-35 in gingivitis and periodontitis remains unclear. The aim of this study was to systematically review the literature and collecting the available evidence regarding the role of IL-35 in pathogenesis of periodontal disease.MethodsA systematic search of electronic databases including MEDLINE, Google Scholar, Cochrane Library, Web of Science, and Scopus was conducted in November 2020 to identify studies addressing the Interleukin-35 pathobiology in periodontal disease. The identified studies were subjected to pre-identified inclusion criteria. The retrived papers were assessed by the authours independently and consensus was reached in cases where disagreement occurred. Articles written in languages other than English, case reports, letters to editors, conference abstracts, theses, and dissertations were excluded from the review.ResultsA total of 176 possibly relevant articles were identified through the search strategy. Finally, 15 papers which met the criteria of eligibility were included in this review by consensus. The included articles were classified based on their design and level of evidence.Three subclinical study, ten cross sectional investigation and two randomized clinical trials constituted the final set of studies in this review. At preclinical level, Il-35 showed inhibitory characteristics regarding alveolar bone resorption of animal periodontitis models. The results of observatory human studies confirmed the presence of high levels of IL-35 in saliva, GCF, serum, and gingival biopsies of patients suffering from inflammatory periodontal disease. Moreover, two included clinical trials showed that non-surgical periodontal therapy could downregulate IL-35 production in chronic periodontitis patients.ConclusionInterleukin-35 has an undeniable role in pathobiology of inflammatory periodontal disease. Further well-controlled studies are needed to better elucidate the functional pattern of IL-35 in pathogeneisis of gingival and periodontal disease.

Dataset Information

Interleukin-1? rs1143627 polymorphism with susceptibility to periodontal disease.

Publications

Interleukin-1β rs1143627 polymorphism with susceptibility to periodontal disease.

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