Journal of periodontology · 2004
Dose-effect relation of smoking and the interleukin-1 gene polymorphism in periodontal disease.
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Meisel P, Schwahn C, Gesch D, Bernhardt O, John U, Kocher T
Аннотация
BACKGROUND: Periodontitis is a bacterial inflammatory disease leading to attachment loss with the consequence of tooth loss. There exists a multifactorial risk pattern including bacterial challenge, smoking, age, gender, diabetes, and socioeconomic and genetic factors. Smoking has the highest impact on the course of the disease modulated by all the other factors. Here, we report the relationship between smoking and the genetic polymorphism of interleukin-1 (IL-1).
METHODS: In a randomly selected population-based study, we genotyped 1,085 test persons for the IL-1 genotype, examined their periodontal status, and assessed their smoking behavior including present and past quality and quantity of smoking.
RESULTS: There was a significant dose-effect relationship between the exposure to tobacco smoke and the extent of periodontal disease assessed as attachment loss and tooth loss. Moreover, there was a gene-environmental interaction. Subjects bearing at least one copy of the variant allele 2 at positions IL-1A -889 and IL-1B +3954 (genotype positive) had an enhanced smoking-associated periodontitis risk as compared to their IL-1 genotype-negative counterparts. With genotype-negative non-smokers as a reference, logistic regression resulted in odds ratios of 0.98 (95% confidence interval: 0.83 to 1.14), 2.37 (1.96 to 2.87), and 4.50 (2.30 to 8.82) for genotype-positive non-smokers, genotype-negative smokers, and genotype-positive smokers, respectively.
CONCLUSIONS: There is a gene-environmental interaction between smoking and the IL-1 genetic polymorphism. Smokers bearing the genotype-positive IL-1 allele combination have an increased risk of periodontitis. The IL-1 genotype has no influence in non-smokers.
METHODS: In a randomly selected population-based study, we genotyped 1,085 test persons for the IL-1 genotype, examined their periodontal status, and assessed their smoking behavior including present and past quality and quantity of smoking.
RESULTS: There was a significant dose-effect relationship between the exposure to tobacco smoke and the extent of periodontal disease assessed as attachment loss and tooth loss. Moreover, there was a gene-environmental interaction. Subjects bearing at least one copy of the variant allele 2 at positions IL-1A -889 and IL-1B +3954 (genotype positive) had an enhanced smoking-associated periodontitis risk as compared to their IL-1 genotype-negative counterparts. With genotype-negative non-smokers as a reference, logistic regression resulted in odds ratios of 0.98 (95% confidence interval: 0.83 to 1.14), 2.37 (1.96 to 2.87), and 4.50 (2.30 to 8.82) for genotype-positive non-smokers, genotype-negative smokers, and genotype-positive smokers, respectively.
CONCLUSIONS: There is a gene-environmental interaction between smoking and the IL-1 genetic polymorphism. Smokers bearing the genotype-positive IL-1 allele combination have an increased risk of periodontitis. The IL-1 genotype has no influence in non-smokers.