Association between involuntary smoking and salivary markers related to periodontitis: a 2-year longitudinal study.

Association between involuntary smoking and salivary markers related to periodontitis: a 2-year longitudinal study.
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DOI:
10.1902/jop.2008.080149
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发表时间:
2008-12
影响因子:
4.3
通讯作者:
N. Nishida;Yumiko Yamamoto;Muneo Tanaka;K. Kataoka;M. Kuboniwa;K. Nakayama;K. Morimoto;S. Shizukuishi
N. Nishida;Yumiko Yamamoto;Muneo Tanaka;K. Kataoka;M. Kuboniwa;K. Nakayama;K. Morimoto;S. Shizukuishi
中科院分区:
医学2区
文献类型:
--
作者:
N. Nishida;Yumiko Yamamoto;Muneo Tanaka;K. Kataoka;M. Kuboniwa;K. Nakayama;K. Morimoto;S. Shizukuishi

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背景:关于非自愿吸烟对牙周炎进展的纵向影响的数据不足。本研究探讨了非自愿吸烟与牙周炎进展之间的关系,以及非自愿吸烟对牙周炎相关唾液炎症和微生物标志物的影响。方法在2003年和2005年的年度健康体检中招募参与者。在2005年,200(73%)的273名日本员工在基线检查进行牙周测量,包括临床附着水平(CAL)和探测深度(PD)。当受试者在2年内有一颗或多颗牙齿的CAL和PD增加≥ 2.0 mm时,确定牙周炎进展。唾液标志物水平,包括可替宁,通过酶测定,包括酶联免疫吸附测定。采用实时荧光定量聚合酶链反应方法检测唾液中6种牙周致病菌的比例。根据受试者操作特征分析,非吸烟者、非自愿吸烟者和主动吸烟者分别定义为唾液可替宁水平为0、1 - 7和≥ 8 ng/ml的受试者。结果经单因素Logistic回归分析,年龄、饮酒、吸烟、早餐习惯和工作时间与牙周炎显著进展的风险相关。多元Logistic回归分析显示,在调整协变量后,非自愿吸烟者(OR = 2.23; 95%置信区间[CI]:1.03至4.83)和活动性吸烟者(OR = 2.27; 95% CI:1.02至5.04)的牙周炎比值比(OR)显著高于非吸烟者。唾液标志物水平,包括白蛋白,天冬氨酸转氨酶和乳铁蛋白,在非自愿吸烟者相对于非吸烟者显著升高。相比之下,牙周病原体的百分比在吸烟组之间没有差异,除了Prevotella nigrescens,与非吸烟者相比,非自愿吸烟者的水平显着降低。结论非自愿吸烟增加炎症反应,并与牙周炎进展的风险更大。
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. CONCLUSION Involuntary smoking increased the inflammatory response and was associated with a greater risk for periodontitis progression.