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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Smoking has been associated with diseases of the lung, pulmonary airways and oral cavity. Cytologic, genomic and transcriptomic changes in oral mucosa correlate with oral pre-neoplasia, cancer and inflammation (e.g. periodontitis). Alteration of smoking-related gene expression changes in oral epithelial cells is similar to that in bronchial and nasal epithelial cells. Using a systems toxicology approach, we have previously assessed the impact of cigarette smoke (CS) seen as perturbations of biological processes in human nasal and bronchial organotypic epithelial culture models. Here, we report our further assessment using in vitro human oral organotypic epithelium models. We exposed the buccal and gingival organotypic epithelial tissue cultures to CS at the air-liquid interface. CS exposure was associated with increased secretion of inflammatory mediators, induction of cytochrome P450s activity and overall weak toxicity in both tissues. Using microarray technology, gene-set analysis and a novel computational modeling approach leveraging causal biological network models, we identified CS impact on xenobiotic metabolism-related pathways accompanied by a more subtle alteration in inflammatory processes. Gene-set analysis further indicated that the CS-induced pathways in the in vitro buccal tissue models resembled those in the in vivo buccal biopsies of smokers from a published dataset. These findings support the translatability of systems responses from in vitro to in vivo and demonstrate the applicability of oral organotypical tissue models for an impact assessment of CS on various tissues exposed during smoking, as well as for impact assessment of reduced-risk products.
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PMID:In vitro systems toxicology approach to investigate the effects of repeated cigarette smoke exposure on human buccal and gingival organotypic epithelial tissue cultures. 2504 38

Background. Although the direct cause of chronic periodontitis is bacterial infection, the progression of this disease depends on genetic and environmental factors, and smoking is a known risk factor in the development and severity of the disease. An individual's susceptibility may be influenced by polymorphisms in the glutathione S-transferase genes. These genes encode enzymes that metabolize xenobiotic compounds. The aim of this study was to determine the frequency of GSTM1, GSTT1, and GSTP1 polymorphisms in Mexicans with chronic periodontitis. Methods. 60 Mexicans with chronic periodontitis (30 smokers and 30 nonsmokers) were studied. A peripheral blood sample was taken for subsequent DNA extraction. The genetic material was PCR-amplified followed by restriction fragment length polymorphism with the aim of identifying GST polymorphisms. Results. Polymorphisms in the GSTT1 and GSTP1 genes were not significantly different between the smokers and nonsmokers. However, there were significant differences (P = 0.05) between groups in polymorphisms in the GSTM1 gene. The patients with chronic periodontitis have a higher frequency of null and mutant polymorphisms in GSTM1, GSTT1, and GSTP1 compared with historical data from a healthy Mexican population. Conclusions. The presence of these polymorphisms may be a risk factor for the development of chronic periodontitis.
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PMID:Polymorphisms in Glutathione S-Transferase M1, T1, and P1 in Patients with Chronic Periodontitis: A Pilot Study. 2735 Sep 70