Impact of smoking on peri‐implant bleeding on probing

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.

Immediate implant placement utilizing vestibular socket therapy versus early implant placement with contour augmentation for rehabilitation of compromised extraction sockets in the esthetic zone: A randomized controlled clinical trial

“…[29][30][31] The present study excluded smoking and former smoking participants, as this is considered a risk factor for successful implant treatment. 32,33 Thin biotype extraction sites were not included, as they were reported to demonstrate a three times higher risk of mid-facial recession and may require soft-tissue augmentation along with implant placement, 34 which would confound the effect of surgical technique and is out of the current trial's scope.…”

“…The mixture of autogenous and xenogeneic bone combined the benefits of both types, as the former has an osteogenic effect with rapid remodeling, while the latter is slowly resorbing and hence provides a stable matrix over a longer period 29–31 . The present study excluded smoking and former smoking participants, as this is considered a risk factor for successful implant treatment 32,33 . Thin biotype extraction sites were not included, as they were reported to demonstrate a three times higher risk of mid‐facial recession and may require soft‐tissue augmentation along with implant placement, 34 which would confound the effect of surgical technique and is out of the current trial's scope.…”

Influence of Smoking on Periodontal and Implant Therapy: A Narrative Review

“…The study thus concluded that the transition from health to mucositis and progression to peri-implantitis takes an alternate pathway in smokers, which includes the further enrichment of the microbiome and a decrease in diversity [ 92 ]. Another cross-sectional study compared the peri-implant microbiota in smokers and nonsmokers and also demonstrated a significantly higher microbial richness in smoker patients around implants affected by peri-implantitis as compared to either healthy implants or implants presenting with mucositis [ 93 ].…”

“…In non-periodontitis subjects, 75% of individuals can share a core microbiome in the healthy peri-implant sulcus in smokers and nonsmokers, with smokers presenting with a more disease-associated core microbiome including a lower bacterial diversity [ 14 , 91 ]. The transition from health to peri-implant mucositis and progression to peri-implantitis in smokers includes further enrichment of the microbiome and a decrease in bacterial diversity [ 92 , 93 ]. In contrast, the shift from health to peri-implant mucositis in nonsmoker patients comprises a significant increase in bacterial diversity [ 92 ].…”

Smoking by altering the peri-implant microbial community structure compromises the responsiveness to treatment

“…Smoking is known to affect the composition and metabolism of the oral microbiome and is considered a major risk factor for periimplantitis or periodontitis (Bizzarro et al, 2013;Moon et al, 2015;Tsigarida et al, 2015;Duan et al, 2017;Pimentel et al, 2018;Torrungruang et al, 2020;Amerio et al, 2022). Our results are consistent with previous studies, showing that even for a clinically healthy peri-implant environment, smoking increases the abundances of putative pathogens such as A. geminatus, E. saphenum, and P. denticola (Abusleme et al, 2013;Bao et al, 2017;Al Kawas et al, 2021) and regulates the functional potential of the peri-implant microbiome (Figure 1), shifting it to a more disease-related, sub-healthy status (Tsigarida et al, 2015).…”