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Interleukin‐1 Genetic Association With Periodontitis in Clinical Practice
Author(s) -
McDevitt Michael J.,
Wang HwaYing,
Knobelman Carol,
Newman Michael G.,
di Giovine Francesco S.,
Timms Janice,
Duff Gordon W.,
Kornman Kenneth S.
Publication year - 2000
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2000.71.2.156
Subject(s) - periodontitis , medicine , genotype , odds ratio , tooth loss , haplotype , gastroenterology , logistic regression , population , clinical attachment loss , immunology , dentistry , biology , genetics , gene , oral health , environmental health
Background: Periodontitis is a bacterial disease modified by multiple risk factors. The pro‐inflammatory cytokine interleukin‐1 (IL‐1) is a key regulator of the host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption. It has been reported that variations in the IL‐1 gene cluster on chromosome 2 are associated with increased susceptibility to severe adult periodontitis. Methods: The present study evaluated the association between a composite IL‐1 genotype, including allele 2 at each of two loci (IL‐1A +4845 plus IL‐1B +3954), and a broad spectrum of periodontally healthy to diseased patients in a population that is typically encountered in a dental practice setting. Ninety patients, non‐smokers or former smokers with less than 10 pack‐year (pk/yr) history, were recruited from a private dental practice. The major outcome variable was bone loss determined by computerized linear measurements of radiographs. Genotypes were analyzed from finger‐stick blood samples using previously reported methods. Results: Multivariate logistic regression models demonstrated that patient age, former smoking history, and the IL‐1 genotype were significantly associated with severity of adult periodontitis. For nonsmokers or former light smokers (<5 pk/yr), IL‐1 genotype positives were at increased odds ratio of having moderate to severe periodontal disease of 3.75 (95% CI: 1.04‐13.50) to 5.27 (95% CI: 1.23‐22.70), depending on ethnicity, compared to IL‐1 genotype negatives. Former moderate smokers (>5 pk/yr and <10 pk/yr) who were IL‐1 genotype negative were at increased odds ratio of having moderate to severe periodontal disease of 7.43 (95% CI: 1.20‐46.20) compared to non‐smokers or former light smokers who were IL‐1 genotype negative. In addition, past smoking history was also a significant effect modifier as demonstrated by the statistically significant interaction between past smoking history status and IL‐1 genotype status. Conclusions: This study demonstrates that the composite IL‐1 genotype is significantly associated with the severity of adult periodontitis. It also confirmed that both IL‐1 genotyping and smoking history provide objective risk factors for periodontal disease in a private practice environment. J Periodontol 2000;71:156‐163.