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Interleukin‐1 Gene Polymorphisms and Chronic Periodontitis in Adult Whites: A Systematic Review and Meta‐Analysis

Background: Interleukin‐1 (IL‐1) gene polymorphisms have been associated with increased levels of inflammatory mediators and several inflammatory diseases. Periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissues and bone that support the teeth, affect...

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Published in:Journal of periodontology (1970) 2012-11, Vol.83 (11), p.1407-1419
Main Authors: Karimbux, Nadeem Y., Saraiya, Veeral M., Elangovan, Satheesh, Allareddy, Veerasathpurush, Kinnunen, Taru, Kornman, Kenneth S., Duff, Gordon W.
Format: Article
Language:English
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Summary:Background: Interleukin‐1 (IL‐1) gene polymorphisms have been associated with increased levels of inflammatory mediators and several inflammatory diseases. Periodontitis is a bacterially induced chronic inflammatory disease that destroys the connective tissues and bone that support the teeth, affects substantial numbers of adults, and has been implicated as a contributing factor in systemic diseases. IL‐1 gene polymorphisms, most prominently IL1A (−889), IL1A (+4845), and IL1B (+3954), have been associated with chronic periodontitis (CP) in whites. Since the first report, ≥125 studies have examined IL‐1 gene variation in relation to periodontal disease. These studies have produced mixed findings in diverse periodontal phenotypes and in different ethnic groups. One previous meta‐analysis has been published on this topic and supported an association between IL‐1 genes and periodontitis, but considerable doubt remains about the patient populations in which the association may be of clinical relevance. Methods: A systematic review and meta‐analysis was conducted in an attempt to clarify whether IL‐1 gene variants were associated with well‐defined clinical phenotypes of CP in white patients. Study inclusion criteria focused on the analytic framework originally proposed for the IL‐1 genetic effect in which overexpression of inflammatory mediators is hypothesized to result in more severe periodontitis in response to a bacterial challenge. Results: Twenty‐seven studies were included in the qualitative analysis. Nineteen studies yielded significant associations between carriage of the minor IL‐1 alleles and periodontitis. The meta‐analysis, based on 13 qualifying studies, found significant effects for the two individual gene variations (IL1A odds ratio [OR] = 1.48; IL1B OR = 1.54) and for a composite genotype that combines minor alleles at each locus (OR = 1.51). Statistically significant heterogeneity was found that could not be explained, but there was no indication of publication bias. Conclusion: This review and meta‐analysis show that IL1A and IL1B genetic variations are significant contributors to CP in whites.
ISSN:0022-3492
1943-3670
DOI:10.1902/jop.2012.110655