Faculty of Medicine and Dentistry, Department of Clinical Dentistry, University of Bergen, Bergen, Norway.
J Periodontal Res. 2017 Aug;52(4):713-724. doi: 10.1111/jre.12438. Epub 2017 Mar 17.
Periodontal health is mediated by suppressing microorganisms inducing a local inflammatory host response. Smoking may impair this process. This study compares gingival crevicular fluid levels of inflammatory and bone remodeling markers in heavy smokers and non-smokers following active and supportive periodontal therapy in patients with chronic periodontitis.
Gingival crevicular fluid and subgingival plaque were collected from the deepest periodontal pocket in 50 patients, 25 smokers and 25 non-smokers, at baseline (T0), following active (T1) and 12 mo of supportive periodontal therapy (T2). Smoking status was validated measuring serum cotinine levels. Gingival crevicular fluid levels of 27 inflammatory and two bone remodeling markers were analyzed using multiplex and singleplex micro-bed immunoassays, and subgingival plaque samples using checkerboard DNA-DNA hybridization. Amounts of markers in smokers and non-smokers were compared calculating the effect size.
Expression of inflammatory and bone-remodeling markers in smokers demonstrated an overall reduced effect size at T0 and T2 (p < 0.001). In particular, proinflammatory markers (p < 0.001), chemokines (p = 0.007) and growth factors (p = 0.003) at T0, osteoprotegerin (p = 0.003) at T1, proinflammatory markers (p = 0.019) and chemokines (p = 0.005) at T2. At T2, interleukin-8 was detected in significantly higher levels in smokers. Ten different markers in non-smokers and none in smokers responded to periodontal therapy (p < 0.05). An overall negative association was revealed between smoking and subgroups of markers at sites presenting ≥ 10 red complex periodontal microbial species.
Except for an upregulation of interleukin-8, smokers exhibited reduced gingival crevicular fluid levels of several inflammatory markers at baseline and following active and supportive periodontal therapy. Only inflammatory responses in non-smokers adapted to periodontal therapy. Apparently, there seems to be an immunosuppressant effect of smoking regulating the local inflammatory response and bone remodeling markers captured in gingival crevicular fluid following periodontal therapy.
牙周健康受抑制诱导局部炎症反应的微生物的影响。吸烟可能会损害这一过程。本研究比较了慢性牙周炎患者在接受积极和支持性牙周治疗后,重度吸烟者和不吸烟者的龈沟液中炎症和骨改建标志物的水平。
在基线(T0)、积极治疗后(T1)和支持性牙周治疗 12 个月(T2)时,从 50 名患者(25 名吸烟者和 25 名不吸烟者)最深的牙周袋中收集龈沟液和龈下菌斑。通过测量血清可替宁水平来验证吸烟状况。使用多重和单重微床免疫分析检测龈沟液中 27 种炎症和两种骨改建标志物的水平,使用棋盘式 DNA-DNA 杂交检测龈下菌斑样本。计算效应量比较吸烟者和不吸烟者的标志物含量。
吸烟者的炎症和骨改建标志物表达在 T0 和 T2 时总体呈现较小的效应量(p<0.001)。特别是在 T0 时的促炎标志物(p<0.001)、趋化因子(p=0.007)和生长因子(p=0.003),在 T1 时的护骨素(p=0.003),在 T2 时的促炎标志物(p=0.019)和趋化因子(p=0.005)。在 T2 时,吸烟者龈沟液中检测到白细胞介素-8 的水平明显升高。非吸烟者中有 10 种不同的标志物对牙周治疗有反应,而吸烟者没有(p<0.05)。在存在≥10 种红色复合体牙周微生物的位点,吸烟与标志物亚组之间呈现总体负相关。
除了白细胞介素-8 的上调外,吸烟者在基线和积极及支持性牙周治疗后,龈沟液中几种炎症标志物的水平均较低。只有非吸烟者的炎症反应适应了牙周治疗。显然,吸烟可能存在一种免疫抑制作用,调节了牙周治疗后龈沟液中局部炎症反应和骨改建标志物。