BACKGROUND: The individual susceptibility to periodontal disease is probably the result of an interaction of multiple genetic and environmental influences. Polymorphism of the N-acetyltransferase (NAT 2) modifies the individual susceptibility to toxicity from certain therapeutic drugs or heterocyclic amines including substances from cigarette smoke. Subjects are to be classified as 'slow' or 'rapid' acetylators according to how fast their bodies metabolise such xenobiotics. Differences in their ability to detoxify these substances may contribute to an increased risk for periodontitis in subjects exposed to cigarette smoke or other xenobiotics. OBJECTIVE: The purpose of this study was to assess whether the NAT2 genotype is a risk factor for periodontal disease in Caucasian patients suffering from adult periodontitis. MATERIAL AND METHODS: 154 Caucasian subjects were assigned to one of the 3 groups: no, moderate, and severe periodontal disease based on bone and attachment loss. In all subjects, genotyping for mutations on the N-acetyltransferase (NAT2) gene was performed by means of PCR and RFLP analysis. RESULTS: Comparison of frequency distribution of NAT2 acetylation types between the most diseased group and not or moderately affected subjects showed a tendency to over-representation of slow acetylators with severe disease. When using bone loss as measure of periodontitis, this over-representation shows a significant association with the disease (odds ratio=2.13, p=0.025). In the logistic regression analysis, adjusted for age and smoking, NAT2 slow phenotype was significantly associated with the severity of bone loss, the odds ratio being 2.09 (95% C.I. 1.02-4.26, p=0.043). In a case-control analysis (controlled for smoking, gender and age) mean bone loss showed a significant difference between the 2 NAT2-type groups (Mann-Whitney test p=0.041). CONCLUSION: The data suggest that the slow acetylator phenotype may be associated with a higher risk of periodontitis, especially in smokers. Possible explanations regarding the mechanism are discussed; however, such attempts are highly speculative at this time.
BACKGROUND: The individual susceptibility to periodontal disease is probably the result of an interaction of multiple genetic and environmental influences. Polymorphism of the N-acetyltransferase (NAT 2) modifies the individual susceptibility to toxicity from certain therapeutic drugs or heterocyclic amines including substances from cigarette smoke. Subjects are to be classified as 'slow' or 'rapid' acetylators according to how fast their bodies metabolise such xenobiotics. Differences in their ability to detoxify these substances may contribute to an increased risk for periodontitis in subjects exposed to cigarette smoke or other xenobiotics. OBJECTIVE: The purpose of this study was to assess whether the NAT2 genotype is a risk factor for periodontal disease in Caucasian patients suffering from adult periodontitis. MATERIAL AND METHODS: 154 Caucasian subjects were assigned to one of the 3 groups: no, moderate, and severe periodontal disease based on bone and attachment loss. In all subjects, genotyping for mutations on the N-acetyltransferase (NAT2) gene was performed by means of PCR and RFLP analysis. RESULTS: Comparison of frequency distribution of NAT2 acetylation types between the most diseased group and not or moderately affected subjects showed a tendency to over-representation of slow acetylators with severe disease. When using bone loss as measure of periodontitis, this over-representation shows a significant association with the disease (odds ratio=2.13, p=0.025). In the logistic regression analysis, adjusted for age and smoking, NAT2 slow phenotype was significantly associated with the severity of bone loss, the odds ratio being 2.09 (95% C.I. 1.02-4.26, p=0.043). In a case-control analysis (controlled for smoking, gender and age) mean bone loss showed a significant difference between the 2 NAT2-type groups (Mann-Whitney test p=0.041). CONCLUSION: The data suggest that the slow acetylator phenotype may be associated with a higher risk of periodontitis, especially in smokers. Possible explanations regarding the mechanism are discussed; however, such attempts are highly speculative at this time.