Soft‐Tissue Phenotype as a Risk Indicator of Peri‐Implantitis and Peri‐Implant Soft‐Tissue Dehiscence—A Cross‐Sectional Study

ABSTRACT Aim To investigate the association, as well as to characterize the associated panel of pro‐ and anti‐inflammatory markers, between the different components of the peri‐implant phenotype and the presence of peri‐implantitis/peri‐implant soft‐tissue dehiscence (PISTD). Materials and Methods A total of 324 implants in 112 patients were included. The following components of the peri‐implant phenotype were clinically measured through the use of a manual periodontal probe or a digital calliper: keratinized mucosa width (PIKM‐W), mucosal thickness (MT), attached mucosa (AM) and vestibulum depth (VD). The presence of peri‐implantitis and PISTD was assessed through clinical and radiographic examination. Mixed‐models logistic regression analyses were performed to analyse the association between peri‐implant phenotype and the presence of peri‐implantitis or PISTD, adjusting for relevant confounders. Multiplex immunoassays were employed to evaluate the peri‐implant crevicular fluid levels of a panel of pro‐ and anti‐inflammatory markers. Results Peri‐implant health, peri‐implant mucositis and peri‐implantitis were diagnosed in 36.6%, 21.4% and 42% of the patients (classified according to their worst implant) and 35.2%, 34.3%, and 30.5% of the implants, respectively. In the multi‐level multiple regression model, the absence of PIKM‐W (odds ratio [OR] = 9.24; 95% CI: 2.73–31.28), the absence of attached mucosa (OR = 19.58; 95% CI: 6.12–62.56) and a reduced (<4 mm) vestibulum depth (OR = 2.61; 95% CI: 1.05–6.48) were associated with peri‐implantitis. Similarly, the absence of PIKM‐W (OR = 6.32; 95% CI: 1.67–23.83), a thin (<2 mm) mucosa (OR = 157.75; 95% CI: 14.06–1769.9) and a reduced vestibulum depth (OR = 3.32; 95% CI: 1.02–10.84) were associated with the presence of PISTD. Implants with PIKM‐W = 0 mm showed statistically significantly higher levels of interferon‐γ in both regular (≥2 maintenance/year) and irregular (<2 maintenance/year) compliers ( p = 0.046 and p = 0.012). In irregular compliers, the absence of PIKM‐W was also associated with statistically significantly higher levels of interleukin (IL)‐1β and IL‐21 ( p = 0.016, p = 0.046). These associations were independent of the effect of relevant confounders (e.g., plaque, compliance with maintenance, etc.). Conclusions Within their limits, the present findings indicate that (a) peri‐implant soft‐tissue phenotype appears to be associated with the presence of peri‐implantitis and PISTD, and (b) in the absence of PIKM‐W, the inflammatory response seems to be dysregulated and the soft‐tissue remodelling up‐regulated.