Longitudinal study of the association between smoking as a periodontitis risk and salivary biomarkers related to periodontitis

• Published in: Journal of periodontology (1970) Vol. 78; no. 5; p. 859
• Main Authors: Kibayashi, Miyuki, Tanaka, Muneo, Nishida, Nobuko, Kuboniwa, Masae, Kataoka, Kosuke, Nagata, Hideki, Nakayama, Kunio, Morimoto, Kanehisa, Shizukuishi, Satoshi
• Format: Journal Article
• Language: English
• Published: United States 01.05.2007
• Subjects: Adolescent; Adult; Albumins - metabolism; Alkaline Phosphatase - metabolism; Aspartate Aminotransferases - metabolism; Bacteroidaceae - isolation & purification; Biomarkers - metabolism; Dental Health Surveys; Dinoprostone - metabolism; Disease Progression; Female; Humans; Japan; L-Lactate Dehydrogenase - metabolism; Lactoferrin - metabolism; Life Style; Logistic Models; Longitudinal Studies; Male; Middle Aged; Periodontitis - etiology; Periodontitis - metabolism; Periodontitis - microbiology; Population Surveillance; Regression Analysis; Risk Factors; Saliva - metabolism; Sex Factors; Smoking - adverse effects; Smoking - metabolism; Japan
• DOI: 10.1902/jop.2007.060292
• ISSN: 0022-3492

Insufficient data exist regarding the long-term influence of lifestyle factors including smoking on periodontal health. The objective of this study was to examine the prospective association between smoking and periodontal disease progression and the effects of smoking on salivary biomarkers related to periodontitis. Probing depth (PD) was measured at health checkups of workers in 1999 and 2003; additionally, lifestyle information was obtained through a questionnaire. In 2003, 219 of 256 (86%) workers examined at baseline completed PD measurements; saliva samples were also collected. Change in PD was used for assessment of periodontitis progression when three or more sites displayed an increase of >or=2 mm over 4 years. Salivary biomarker levels were determined by real-time polymerase chain reaction and enzyme assay. Statistical methods included bivariate and multivariate regression analyses. In the multiple logistic model, in which lifestyle-related factors served as independent variables, significant variables were current smoking and hours of sleep; respective odds ratios were 2.3 and 2.1. Additionally, 38.5% of periodontal disease progression was attributable to current smoking. Moreover, pack-years of smoking showed a dose-response relationship with disease progression. Levels of salivary markers including prostaglandin E(2), lactoferrin, albumin, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase were significantly lower in current smokers than in non-current smokers. However, no meaningful differences in the proportions of six periodontal pathogens were observed between current and non-current smokers. Smoking exerted the greatest influence on periodontitis risk among lifestyle factors. Smoking may suppress the host-defense system, which may promote periodontal disease progression.