医学
探血
佩里
牙科
植入
混淆
流血
单变量分析
微生物群
牙种植体
种植周围炎
内科学
多元分析
牙周炎
外科
生物信息学
生物
作者
Ettore Amerio,Gonzalo Blasi,Cristina Vallés,Vanessa Blanc,Gerard Àlvarez,Alexandre Arredondo,José Nart,Alberto Monje
摘要
Abstract Background Studies around natural dentition demonstrated that smoking can reduce the tendency of inflamed tissue to bleed upon probing after controlling for possible confounders. In addition, previous research suggested that smokers may present alterations of the peri‐implant microbiome. Aim This study aimed at investigating the impact of smoking on: (1) peri‐implant bleeding on probing (BOP; primary objective); (2) the association between BOP/bone loss and BOP/visible gingival inflammation; (3) peri‐implant microbiome. Methods Partially edentulous patients with implants restored with a single crowns were included in this study. Subjects were either smokers (≥1 cigarettes per day) or nonsmokers (never smokers). The primary outcome of this cross‐sectional study was BOP and secondary outcomes included: Probing pocket depth (PPD), Modified gingival Index (mGI) and Progressive Marginal Bone Loss. In addition, microbial profiles of the subjects were assessed through sequencing of the 16S rRNA gene. Univariate and multilevel multivariate analyses by means of Generalized Estimating Equations were conducted to analyze the association between smoking and peri‐implant BOP. Results Overall, 27 nonsmokers and 27 smokers were included and 96.3% and 77.78% of patients presented peri‐implant BOP in the nonsmoker and smoker group, respectively ( p = 0.046). Smoking was inversely associated with BOP in the multivariate multilevel analysis (OR = 0.356; 95% CI: 0.193–0.660; p = 0.001) whereas a positive correlation was demonstrated for mGI > 0 (OR = 3.289; 95% CI: 2.014–5.371; p < 0.001); PPD (OR = 1.692; 95% CI: 0.263–0.883; p = 0.039) and gender (OR = 2.323; 95% CI: 1.310–4.120 p = 0.004). A decrease of BOP sensitivity in detecting visible gingival inflammation (mGI > 0) was observed in smokers. Besides, taxonomic and changes in diversity regarding the peri‐implant microbiota were detected comparing the two groups. Significantly higher richness of the microbiota was demonstrated in the smoker group when implants affected by peri‐implantitis were compared to either healthy implants or implants presenting mucositis. Conclusions Smoking is a potential modifier of BOP and peri‐implant microbiota.
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