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Journal of Dental Research, Vol. 82, No. 3, 189-193 (2003)
DOI: 10.1177/154405910308200308

The Interleukin-1 Polymorphism, Smoking, and the Risk of Periodontal Disease in the Population-based SHIP Study

P. Meisel1,*, A. Siegemund1, R. Grimm2, F.H. Herrmann2, U. John3, C. Schwahn4 and T. Kocher4

1 Departments of Pharmacology,
2 Genetics,
3 Epidemiology, and
4 Periodontology, Ernst Moritz Arndt University, F-Loeffler-Str. 23d, D-17487 Greifswald, Germany;


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  		Figure 1. Odds ratio (on a log scale) for the risk associated with the IL-1 genotype to belong to subjects with extent of attachment loss within the range indicated on the abscissa; reference group consisted of subjects with attachment loss within the first quartile. * OR = 1.83 (95% C.I. 1.07-3.14; p = 0.029). (A) Smokers (who have ever smoked, N = 495, including pipe and cigar smokers); {chi}2 for trend = 5.46 (p = 0.019). (B) Subjects who have never smoked (N = 515).

 

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  		Figure 2. Interaction plot for number of teeth, effects of IL-1 genotype and smoking (error bars, 95% confidence interval), including all subjects with a complete data set (N = 1085). Open bars: non-smokers (N = 508 genotype-negative, N = 286 genotype-positive). Filled bars: current smokers (N = 182 genotype-negative, N = 109 genotype-positive). ANOVA: genotype p = 0.006, smoking p < 0.0001, genotype * smoking p = 0.084. (ANOVA for former and current smokers: genotype p = 0.023, not shown.)

 

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