摘要：Objectives. We investigated the relationship between secondhand smoke and periodontal disease in nonsmokers. Methods. We undertook a cross-sectional analysis of the Atherosclerosis Risk in Communities study with 2739 lifetime nonsmokers aged 53–74 years, unexposed to other sources of tobacco, who received a complete periodontal examination at visit 4. Exposure was reported as average hours per week in close contact with a smoker in the preceding year. We defined severe periodontitis as 5 or more periodontal sites with probing pocket depth of 5 millimeters or more and clinical attachment levels of 3 millimeters or more in those sites. Other outcomes were extent of periodontal probing depths of 4 millimeters or more and extent of clinical attachment levels of 3 millimeters or more. Results. In a binary logistic regression model, adjusted odds of severe periodontitis for those exposed to secondhand smoke 1 to 25 hours per week increased 29% (95% confidence interval = 1.0, 1.7); for those exposed to secondhand smoke 26 hours per week, the odds were twice as high (95% confidence interval = 1.2, 3.4) as for those who were unexposed. Conclusions. Exposure to secondhand smoke and severe periodontitis among nonsmokers had a dose-dependent relationship. Periodontitis is a chronic condition characterized by inflammation of the supporting tissues of the teeth, resulting in breakdown of the connective tissue attaching the teeth to the alveolar bone and eventually to irreversible loss of that bone. Diagnosis is based on signs of destruction of the connective tissues attaching the tooth root to alveolar bone, which is assessed clinically by measuring attachment level. Attachment level is determined by combined parameters of probing depth and gingival recession at numerous sites in the mouth. Ideally, measurements are made at 6 sites per tooth in a full-mouth assessment of 28 teeth. Periodontitis is a leading cause of tooth loss and an important entity in its own right. Also, the underlying infection and complex host immune-modulatory and inflammatory responses that destroy periodontal tissues contribute to several systemic conditions. 1 Systematic reviews of the evidence have supported a relationship between periodontitis and cardiovascular disease 2 , 3 and type 2 diabetes. 4 In 2004, the US Surgeon General concluded that the scientific evidence was sufficient to infer a causal relationship between tobacco smoking and periodontitis. 5 The etiologic fraction, that is, the fraction of severe periodontal disease cases in which cigarette smoking exposure plays an etiologic role, 6 has been estimated to be 52.8%. 7 This percentage indicates that approximately one half of periodontitis cases could be prevented if cigarette smoking were eliminated, with most of that reduction occurring among people who quit smoking, rather than among nonsmokers exposed to secondhand smoke. In the US dentate adult population, prevalence of periodontitis, defined as 2 or more sites with clinical attachment loss of at least 4 millimeters and 1 or more sites with probing depth of 4 millimeters or deeper, was estimated to be 3.6%. 8 The extent of attachment loss and prevalence of the disease increases dramatically with age. Nonsmokers exposed to secondhand smoke are recognized to be at increased risk of periodontitis. On reviewing updated evidence on involuntary exposure to tobacco smoke, the US Surgeon General concluded in 2006 that there is no risk-free level of exposure to secondhand smoke. 9 To date, only 2 studies have examined the association of secondhand smoke exposure and periodontal disease in adults. One analyzed data from the 3rd National Health and Nutrition Examination Survey (NHANES III) and found that the odds of periodontitis for exposed adults who had never actively smoked were 1.6 times (95% confidence interval [CI] = 1.3, 2.0) as much as those of unexposed adults. 10 The second study, of 273 predominantly male Japanese workers, reported higher odds of periodontal disease in passive smokers relative to nonsmokers (odds ratio [OR] = 2.9; 95% CI = 1.1, 7.8). 11 Although these findings are informative, some caution is required in their interpretation. Estimates of effect size vary considerably depending on case definition, extent and severity of periodontal disease, and measurement protocol. 12 Both studies used a partial-mouth measurement protocol limited to sites in 2 quadrants. Compared with full-mouth examinations, half-mouth protocols have severely underestimated the prevalence of periodontitis and produced biased findings, especially in populations with low prevalence of severe disease. 13 – 15 Whether such bias alters the presence and strength of a relationship between secondhand smoke and periodontal disease is not known. To address this limitation, we used a rigorous protocol, examining 6 sites per tooth in a full-mouth survey, and applied a stringent case definition of periodontitis to ensure that we correctly identified all cases that met the case definition. The specific study aim was to determine whether exposure to secondhand smoke was associated with periodontal disease in lifetime nonsmokers of cigarettes who were unexposed to other sources of tobacco or nicotine. We hypothesized that nonsmokers exposed to secondhand smoke would have greater odds of severe periodontitis and greater extent of periodontal disease than those who were unexposed.
