Effects of Smoking on Salivary Biomarker Levels in Periodontitis Progression

Objectives: Changes in the host-microbe interactions involved in periodontal destruction in smokers are poorly understood. The objective of this study was to investigate the effects of passive and active smoking on salivary inflammatory and microbiological parameters in periodontitis progression. Methods: Clinical attachment level (CAL) and periodontal pocket depth (PPD) were measured during annual health check-ups of Japanese employees in 2003 and 2005. In 2005, 203 of 273 (74%) employees examined at baseline completed periodontal measurements. For assessment of periodontitis progression, change in periodontal status was used if one site or more displayed an increase of ≥2 mm of CAL and PPD over 2 years. Salivary marker levels were determined by enzyme assay including ELISA. Populations of six periodontal pathogens in saliva were assessed employing real-time PCR methodology. Non-, passive and active smokers were defined as subjects exhibiting salivary cotinine levels of 0, 1-7 and ≥8 ng/ml, respectively; 57, 73 and 73 subjects were classified as non-, passive and active smokers, respectively. Statistical methods included post hoc test and Mann-Whitney U test. Results: Levels of salivary markers including albumin, aspartate aminotransferase and lactoferrin were elevated significantly in passive smokers relative to non-smokers (p<0.05); in contrast, the percentages of Prevotella nigrescens exhibited significantly lower level in passive and active smokers than in non-smokers (p<0.05). Percentage of Porphyromonas gingivalis tended to be higher in active smokers than in non-smokers. Subjects with periodontitis progression showed significantly higher levels of salivary markers including PGE₂, MMP-8, lactoferrin and Prevotella intermedia in comparison to subjects without periodontitis progression (p<0.05). Conclusions: Passive smoking may elevate inflammatory response and active smoking might promote periodontal infection in involvement of periodontitis progression. This work was supported by Health and Labour Science Research Grants, and Japan Foundation for Aging and Health.