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Background: Polymorphisms within the interleukin-1 cluster are known to be associated with adult periodontal disease. However, interactions of genetic with other risk factors, especially smoking, remain questionable. The aim of this cross-sectional study was to evaluate the genetic influence on periodontal variables in relation to environmental factors. Methods: One-hundred fifty-four (154) Caucasian subjects were clinically and radiographically assessed for their periodontal status, their smoking history recorded, and their allelic pattern of IL-1α, IL-1β, and IL-1RN polymorphisms determined by genotyping. Results: In assessing periodontitis with mean probing depth, mean attachment loss, or mean bone loss, no differences were found in allele frequencies or combined allotypes between subjects with mild or moderate versus those with severe signs of periodontitis. However, the extent of attachment loss defined as percentage of sites >4 mm was significantly associated with the composite genotype of IL-1α/1β in smokers (odds ratio [OR] = 4.00; 95% confidence interval [Cl] 1.03 to 16.70; P = 0.02). No differences were found in genotype negative subjects irrespective of their smoking status. They had nearly identical attachment loss as genotype positive non-smokers. Similar non-significant results were found with respect to extent of bone loss. An increased risk of more extended attachment loss was observed also in individuals carrying mutations of the combined genotype IL-1α/IL-1RN, again showing enhanced risk only in genotype-positive and smoking subjects. Conclusions: The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive. [ABSTRACT FROM AUTHOR]

Polymorphisms influencing the binding affinity between the Fcγ receptors and IgG of different subclasses are thought to be of importance in the individual susceptibility to infections with Gram-negative bacteria contributing to periodontal disease. One hundred and fifty-four Caucasian subjects were clinically and radiographically examined for their periodontal status and genotyped for their allelic pattern of Fcγ/Rlla, Fcγ/RIIla, and Fcγ/lllb polymorphism. In assessing periodontitis according to mean probing depth and attachment loss, no differences were found in allele frequencies or combined allotypes between the subjects with mild or moderate and those with severe signs of periodontitis. However, the extent and severity of bone loss were significantly associated with the genotype of the receptor Fcγ/RIIla. An increased risk of severe bone destruction was observed in individuals carrying the Fcγ/RIIla-VV genotype (OR = 5.3; 95% CI 1.4-26.2). Fcγ/RIIIb is in linkage disequilibrium with Fcγ/RIIla. Hence it is also related to periodontal disease. There is no indication of an association between the polymorphism of Fcγ/Rlla and periodontitis. The results are evidence that the Fcγ/RIIla genotype coding for the high affinity receptor imposes an additional risk of bone loss as does the Fcγ/RIIIb genotype coding for the low affinity receptor. Genes and Immunity (2001) 2, 258-262. [ABSTRACT FROM AUTHOR]

Periodontal disease is a common multifactorial process that leads to bone destruction and tooth loss. Interactions of environmental and genetic factors determine the extent and severity of periodontal disease. Smoking is one of the risk factors for periodontal disease, and the risk may be influenced by the polymorphism of N-acetyltransferase (NAT2) via metabolism of smoke-derived xenobiotics. We therefore hypothesized that a NAT2 genotype would be a risk factor for periodontal disease. A total of 154 Caucasian subjects were assigned to one of two groups (1) no or mild and (2) severe periodontal disease based on radiographic (bone destruction) and clinical criteria (probing depth, attachment loss) and the number of teeth. In all subjects genotyping for mutations on NAT2 was performed by means of PCR and RFLP analysis. In the less-affected group genotyping showed a fraction of predicted slow and rapid acetylators (53.6% and 46.4%, respectively) corresponding to the normal distribution in Caucasians. Severely affected patients were predominantly slow acetylators, the odds ratios being between 2.38 and 5.02 for the NAT2-related risk depending on the outcome parameters chosen. Adjustment for age had no influence on these findings. Our data indicate that the slow acetylator phenotype is associated with a higher risk of periodontitis, especially with respect to the severity of the disease. Possible implications with respect to the risk associated with smoking are discussed. [ABSTRACT FROM AUTHOR]