Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Polymorphism of the N-acetyltransferase (NAT2), smoking and the potential risk of periodontal disease. 1100 81

Smoking is a major risk of periodontal diseases. At the site of first contact, the gingiva is exposed to aromatic amines and polycyclic hydrocarbons. These are metabolized by the N-acetyltransferases (NAT), leading to local detoxification and/or activation reactions contributing to the risk of periodontal destruction in smokers. The purpose of this study was to detect the expression of N-acetyltransferase isoenzymes NAT1 and NAT2 in periodontal granulation tissue. In 24 specimens obtained from periodontitis patients or control subjects, mRNA encoding for NAT1 and NAT2 was detected by RT-PCR, and proteins were identified by immunohistochemistry. In periodontal granulation tissues, immunoreactivity for NAT1 and NAT2 was detected in infiltrating leukocytes and fibroblasts. In normal gingiva, both enzymes were found in epithelial cells, whereas NAT1 was also detected in endothelial cells. The results suggest that these enzymes may play a role in the defense against xenobiotics and the accelerated progression of periodontal disease in smokers.
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PMID:Expression of N-acetyltransferases in periodontal granulation tissue. 1209 50

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, sex, diabetes, socio-economic 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 polymorphisms of genetic polymorphisms inflicted in the pathogenesis.In a randomly selected population-based study, 1083 subjects were typed for the polymorphisms of the IL-1 genotype, Fcgamma RIIIb receptor gene, myeloperoxidase and N-acetyltransferase (NAT2) and related to their periodontal state. Smoking behavior was assessed including present and past quality and quantity of smoking.There is 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 are gene-environmental interactions as subjects bearing variant genotypes show an enhanced smoking-associated risk of the disease modulated by these genotypes. In non-smokers, the impact of these genetic polymorphisms is mostly negligible.This study provides support for the hypothesis that subjects bearing genetic variants of polymorphically expressed phenotypes are at an increased risk of periodontitis when smoking. Mostly, this may be accomplished via the influence of smoking-related impairment on defense mechanisms rather than on the pathogenic pathways.
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PMID:Impact of genetic polymorphisms on the smoking-related risk of periodontal disease: the population-based study SHIP. 1957 Feb 60