Association between involuntary smoking and salivary markers related to periodontitis: a 2-year longitudinal study.
BACKGROUND
Insufficient data exist regarding the longitudinal influence of involuntary smoking on periodontitis progression. This study examined the relationship between involuntary smoking and periodontitis progression and the effects of involuntary smoking on salivary inflammatory and microbiologic markers related to periodontitis.


METHODS
Participants were recruited during annual health checkups in 2003 and 2005. In 2005, 200 of 273 (73%) Japanese employees examined at baseline underwent periodontal measurements, including clinical attachment level (CAL) and probing depth (PD). Periodontitis progression was identified when a subject displayed one or more teeth with an increase > or = 2.0 mm in CAL and PD during the 2 years. Salivary marker levels, including cotinine, were determined by enzyme assay, including enzyme-linked immunosorbent assay. The proportions of six periodontal pathogens in saliva were assessed using real-time polymerase chain reaction methodology. Based on receiver-operating characteristic analysis, non-, involuntary, and active smokers were defined as subjects exhibiting salivary cotinine levels of 0, 1 to 7, and > or = 8 ng/ml, respectively.


RESULTS
By simple logistic regression analysis, age, alcohol consumption, smoking, breakfast habits, and working hours were related to the risk for significant periodontitis progression. Multiple logistic regression analysis revealed significantly higher periodontitis odds ratios (OR) in involuntary (OR = 2.23; 95% confidence interval [CI]: 1.03 to 4.83) and active (OR = 2.27; 95% CI: 1.02 to 5.04) smokers relative to non-smokers following adjustment for covariates. Levels of salivary markers, including albumin, aspartate aminotransferase, and lactoferrin, were significantly elevated in involuntary smokers relative to non-smokers. In contrast, the percentages of periodontal pathogens did not differ between the smoking groups, with the exception of Prevotella nigrescens, which displayed significantly lower levels in involuntary smokers compared to non-smokers.


CONCLUSIONS
Involuntary smoking increased the inflammatory response and was associated with a greater risk for periodontitis progression.
Nishida
Nobuko
N
Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Yamamoto
Yumiko
Y
Tanaka
Muneo
M
Kataoka
Kosuke
K
Kuboniwa
Masae
M
Nakayama
Kunio
K
Morimoto
Kanehisa
K
Shizukuishi
Satoshi
S
D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000418:Albumins / Q000032:analysis; D000428:Alcohol Drinking; D001219:Aspartate Aminotransferases / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D003367:Cotinine / Q000032:analysis; D018450:Disease Progression; D005247:Feeding Behavior; D005260:Female; D006801:Humans; D007202:Indicators and Reagents / Q000032:analysis; D007781:Lactoferrin / Q000032:analysis; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000503:physiopathology; D010514:Periodontal Pocket / Q000503:physiopathology; D010518:Periodontitis / Q000503:physiopathology*; D045242:Prevotella nigrescens / Q000302:isolation & purification; D012307:Risk Factors; D012463:Saliva / Q000737:chemistry* / Q000382:microbiology; D012907:Smoking / Q000378:metabolism; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014937:Work; D055815:Young Adult
D000418:Albumins; D015415:Biomarkers; D007202:Indicators and Reagents; D014028:Tobacco Smoke Pollution; D001219:Aspartate Aminotransferases; D007781:Lactoferrin; D003367:Cotinine