Relationship between -889 C/T polymorphism in interleukin-1A gene and risk of chronic periodontitis: Evidence from a meta-analysis with new published findings

Med Oral Patol Oral Cir Bucal. 2017 Jan 1;22(1):e7-e14. doi: 10.4317/medoral.21233.

Abstract

Background: Periodontitis results from an inflammatory response caused by accumulative microorganisms in periodontal sites. Several factors are involved in pathogenesis of periodontitis, for example the -889 C/T polymorphism in interleukin-1A gene. This study aimed to evaluate the relationship between this polymorphism and risk of development of chronic periodontitis by a meta-analysis based in new published findings.

Material and methods: Thereunto a review in literature was performed in the electronic biomedical and education databases (Cochrane Library, Google Scholar, MEDLINE and PubMed) to studies published before August 2, 2015, the abstracts were evaluated and the data extraction performed by two calibrated examiners. The calculations of the meta-analysis were obtained through statistical software Review Manager version 5.2 with calculation of Odds Ratio (OR), heterogeneity (I²) and Funnel plots with P < 0.05.

Results: In overall, twenty-one case/control studies were selected with 2,174 patients with chronic periodontitis and 1, 756 controls. The meta-analysis showed T allele was associated with chronic periodontitis (OR = 1.22, 95% CI: 1.09, 1.36, P = 0.0004) with decreased value to heterogeneity (I² = 15%, P = 0.28). TT genotype was associated to patients with chronic periodontitis (OR = 1.40, 95% CI: 1.07, 1.83, P = 0.01). No publication bias was found in this meta-analysis by asymmetry in Funnel plots.

Conclusions: This meta-analysis with 2,174 patients with chronic periodontitis and 1, 756 controls evidenced the -889 C/T polymorphism is associated to risk of development of chronic periodontitis with no significant value to heterogeneity to allelic evaluation.

Publication types

  • Meta-Analysis
  • Review

MeSH terms

  • Chronic Periodontitis / genetics*
  • Humans
  • Interleukin-1alpha / genetics*
  • Polymorphism, Genetic*
  • Risk Factors

Substances

  • IL1A protein, human
  • Interleukin-1alpha