Effects of Smoking and Genotype on the PSR Index of Periodontal Disease in Adults Aged 18–49

International Journal of Environmental Research and Public Health

Deborah E. Polk⁵  Xiaojing Wang⁴  Eleanor Feingold¹  John R. Shaffer¹  Daniel E. Weeks¹  Robert J. Weyant⁵  Richard J. Crout²  Daniel W. McNeil³ 

[1] Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA;Department of Periodontics, School of Dentistry, West Virginia University, Morgantown, WV 26506, USA;Departments of Psychology and Dental Practice and Rural Health, West Virginia University, Morgantown, WV 26506, USA;Center for Craniofacial and Dental Genetics, School of Dental Medicine, University of Pittsburgh, Pittsburgh, PA 15219, USA;Department of Dental Public Health and Information Management, University of Pittsburgh, School of Dental Medicine, Pittsburgh, PA 15261, USA;

关键词: adult;    chronic periodontitis;    genetics;    genomics;    smoking;   

DOI  :  10.3390/ijerph9082839

来源: mdpi

【 摘 要 】

Studies have found both genetic and environmental influences on chronic periodontitis. The purpose of this study was to examine the relationships among previously identified genetic variants, smoking status, and two periodontal disease-related phenotypes (PSR1 and PSR2) in 625 Caucasian adults (aged 18–49 years). The PSR Index was used to classify participants as affected or unaffected under the PSR1 and PSR2 phenotype definitions. Using logistic regression, we found that the form of the relationship varied by single nucleotide polymorphism (SNP): For rs10457525 and rs12630931, the effects of smoking and genotype on risk were additive; whereas for rs10457526 and rs733048, smoking was not independently associated with affected status once genotype was taken into consideration. In contrast, smoking moderated the relationships of rs3870371 and rs733048 with affected status such that former and never smokers with select genotypes were at increased genetic risk. Thus, for several groups, knowledge of genotype may refine the risk prediction over that which can be determined by knowledge of smoking status alone. Future studies should replicate these findings. These findings provide the foundation for the exploration of novel pathways by which periodontitis may occur.

【 授权许可】

CC BY   
© 2012 by the authors; licensee MDPI, Basel, Switzerland.