Association between passive and active smoking evaluated by salivary cotinine and periodontitis

被引:49
作者
Yamamoto, Y
Nishida, N
Tanaka, M
Hayashi, N
Matsuse, R
Nakayama, K
Morimoto, K
Shizukuishi, S
机构
[1] Osaka Univ, Grad Sch Dent, Dept Prevent Dent, Suita, Osaka 5650871, Japan
[2] Japan Fdn Aging & Hlth, Kyoto, Japan
[3] Kyoto Med Sci Lab Inc, Kyoto, Japan
[4] Osaka Univ, Grad Sch Med, Dept Social & Environm Med, Suita, Osaka 5650871, Japan
关键词
active smoking; cotinine; passive smoking; periodontitis; saliva;
D O I
10.1111/j.1600-051X.2005.00819.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Aim: This study attempted to determine the relationship between passive and active smoking on the basis of salivary cotinine levels and periodontitis severity. Methods: Japanese workers (n = 273) were surveyed via an oral examination, a self-administered questionnaire and collection of whole saliva. Probing pocket depth (PPD) and clinical attachment level (CAL) served as periodontal parameters. Periodontitis was defined as the presence of two or more teeth with PPD >= 3.5 mm and CAL >= 3.5 mm. Salivary cotinine was determined using ELISA. Statistical methods included Wilcoxon's rank-sum test and multiple logistic regression analysis. Results: Based on the results of receiver-operating characteristic plots for cotinine-level classification derived from self-reported smoking status, non-, passive and active smokers were defined as those subjects exhibiting cotinine levels of 0, 1-7 and >= 8 ng/ ml, respectively. Numbers of teeth displaying CAL >= 3.5 mm in passive and active smokers were significantly higher than those in non-smokers. Multiple logistic regression analysis revealed significantly higher periodontitis odds ratios in passive and active smokers relative to non-smokers following adjustment for other lifestyle factors; odds ratios were 2.87 [95% confidence interval (CI); 1.05-7.82] and 4.91 (95% CI; 1.80-13.35), respectively. Conclusion: These findings suggest that passive smoking classified in terms of salivary cotinine level may be an independent periodontitis risk indicator.
引用
收藏
页码:1041 / 1046
页数:6
相关论文
共 26 条
[1]   Association of pediatric dental caries with passive smoking [J].
Aligne, CA ;
Moss, ME ;
Auinger, P ;
Weitzman, M .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 2003, 289 (10) :1258-1264
[2]   Environmental tobacco smoke and periodontal disease in the United States [J].
Arbes, SJ ;
Agustsdóttir, H ;
Slade, GD .
AMERICAN JOURNAL OF PUBLIC HEALTH, 2001, 91 (02) :253-257
[3]  
Armitage G C, 1999, Ann Periodontol, V4, P1, DOI 10.1902/annals.1999.4.1.1
[4]   Cotinine as a biomarker of environmental tobacco smoke exposure [J].
Benowitz, NL .
EPIDEMIOLOGIC REVIEWS, 1996, 18 (02) :188-204
[5]   Local and systemic total antioxidant capacity in periodontitis and health [J].
Brock, GR ;
Butterworth, CJ ;
Matthews, JB ;
Chapple, ILC .
JOURNAL OF CLINICAL PERIODONTOLOGY, 2004, 31 (07) :515-521
[6]  
Chen X, 2000, GLYCOBIOLOGY, V10, P1084
[7]  
Etter JF, 2000, AM J EPIDEMIOL, V151, P251
[8]   A REVIEW OF THE USE OF SALIVA COTININE AS A MARKER OF TOBACCO-SMOKE EXPOSURE [J].
ETZEL, RA .
PREVENTIVE MEDICINE, 1990, 19 (02) :190-197
[9]   Serum cotinine levels, smoking, and periodontal attachment loss [J].
Gonzalez, YM ;
DeNardin, A ;
Grossi, SG ;
Machtei, EE ;
Genco, RJ ;
DeNardin, E .
JOURNAL OF DENTAL RESEARCH, 1996, 75 (02) :796-802
[10]   ZERO-LENGTH CROSSLINKING PROCEDURE WITH THE USE OF ACTIVE ESTERS [J].
GRABAREK, Z ;
GERGELY, J .
ANALYTICAL BIOCHEMISTRY, 1990, 185 (01) :131-135