Polymorphism of the N-acetyltransferase (NAT2), smoking and the potential risk of periodontal disease

Periodontal disease is a common multifactorial process that leads to bone d estruction and tooth loss. Interactions of environmental and genetic factor s 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 b e 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 periodonta l disease based on radiographic (bone destruction) and clinical criteria (p robing depth, attachment loss) and the number of teeth. In all subjects gen otyping for mutations on NAT2 was performed by means of PCR and RFLP analys is. In the less-affected group genotyping showed a fraction of predicted sl ow and rapid acetylators (53.6% and 46.4%, respectively) corresponding to t he normal distribution in Caucasians. Severely affected patients were predo minantly slow acetylators, the odds ratios being between 2.38 and 5.02 for the NAT2-related risk depending on the outcome parameters chosen. Adjustmen t for age had no influence on these findings. Our data indicate that the sl ow acetylator phenotype is associated with a higher risk of periodontitis, especially with respect to the severity of the disease. Possible implicatio ns with respect to the risk associated with smoking are discussed.