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吸烟与牙周病中白细胞介素-1基因多态性的剂量效应关系。

Dose-effect relation of smoking and the interleukin-1 gene polymorphism in periodontal disease.

作者信息

Meisel P, Schwahn C, Gesch D, Bernhardt O, John U, Kocher T

机构信息

Department of Pharmacology, Ernst Moritz Arndt University Greifswald, Greifswald, Germany.

出版信息

J Periodontol. 2004 Feb;75(2):236-42. doi: 10.1902/jop.2004.75.2.236.

DOI:10.1902/jop.2004.75.2.236
PMID:15068111
Abstract

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.

摘要

背景

牙周炎是一种细菌性炎症性疾病,会导致附着丧失,最终可能导致牙齿脱落。牙周炎存在多因素风险模式,包括细菌感染、吸烟、年龄、性别、糖尿病以及社会经济和遗传因素。吸烟对疾病进程的影响最大,且受所有其他因素的调节。在此,我们报告吸烟与白细胞介素-1(IL-1)基因多态性之间的关系。

方法

在一项基于人群的随机抽样研究中,我们对1085名受试对象进行了IL-1基因分型,检查了他们的牙周状况,并评估了他们的吸烟行为,包括目前和过去的吸烟质量和数量。

结果

以附着丧失和牙齿脱落评估的牙周疾病程度与接触烟草烟雾之间存在显著的剂量效应关系。此外,还存在基因-环境相互作用。在IL-1A -889和IL-1B +3954位点携带至少一个变异等位基因2拷贝(基因型阳性)的受试者,与IL-1基因型阴性的对应者相比,吸烟相关的牙周炎风险更高。以基因型阴性的非吸烟者为参照,逻辑回归得出基因型阳性的非吸烟者、基因型阴性的吸烟者和基因型阳性的吸烟者的比值比分别为0.98(95%置信区间:0.83至1.14)、2.37(1.96至2.87)和4.50(2.30至8.82)。

结论

吸烟与IL-1基因多态性之间存在基因-环境相互作用。携带基因型阳性IL-1等位基因组合的吸烟者患牙周炎风险增加。IL-1基因型对非吸烟者没有影响。

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