Background Due to complex morphology and limited access, the cleaning of the furcation area is extremely challenging. Therefore, novel therapeutic approaches need to be tested to potentially overcome debridement limitations. The aim of the present prospective 12-month study was to compare clinical and microbiological effects following erythritol air-polishing versus conventional mechanical debridement of furcation defects in a cohort of periodontal maintenance patients. Methods Twenty patients with grade II mandibular molar furcation defects volunteered to enroll in this single-centre, examiner masked, randomized controlled trial. In a split-mouth study design, two furcation sites in each patient were randomly assigned to either receive subgingival debridement using erythritol air-polishing (test) or conventional ultrasonic/curette debridement (control) at baseline, and at 3, 6, 9 and 12 months. Probing depth, clinical attachment level and bleeding on probing were recorded at 3-month intervals. Subgingival microbiological samples obtained at baseline, 6 and 12 months were analyzed using checkerboard DNA–DNA hybridization. Discomfort from treatment was scored at 12 months using a visual analogue scale. The differences between treatments, and time-points, were tested using multilevel analysis (mixed effect models and robust variance estimates). Results A significant reduction in probing depth took place following both treatments (p < 0.001). Control sites experienced a significant mean gain in clinical attachment level of 0.5 mm (± 0.2) (p = 0.004), whereas a non-significant gain of 0.4 mm (± 0.3) was observed at test sites (p = 0.119). At 6 months, a significant between-treatment difference of 0.8 mm (± 0.4) was observed in favor of the control (p = 0.032). No significant between-treatment differences were observed in microbial load or composition. Notably, at 12 months patients experienced significantly less discomfort following air-polishing compared with control (p = 0.001). Conclusions The 12-month observations indicate that erythritol air-polishing and conventional mechanical debridement both support clinical improvements. A significant between-treatment difference in clinical attachment level was, however, detected in favour of control debridement at 6 months. In terms of patient comfort, erythritol air-polishing is superior. Trial Registration: The clinical trial was retrospectively registered in ClinicalTrial.gov with registration NCT04493398 (07/28/2020).

AimTo evaluate the effect of smoking at patient, tooth, and site level following non‐surgical and surgical periodontal therapy.Material and MethodsEighty chronic periodontitis patients, 40 smokers and 40 non‐smokers, were recruited to this single‐arm clinical trial. Smoking status was validated by measuring serum cotinine levels. Periodontal examinations were performed at baseline (T0) and 3 months following non‐surgical and surgical periodontal therapy (T1). At T0 and T1, subgingival plaque samples were collected from the deepest periodontal pocket in each patient and analysed using checkerboard DNA–DNA hybridization. Probing depth (PD) ≥ 5 mm with bleeding on probing (BoP) was defined as the primary outcome. Unadjusted and adjusted logistic regression analyses, corrected for clustered observations within patients and teeth, were conducted comparing smokers with non‐smokers.ResultsClinical parameters significantly improved in both groups (p < 0.001). An association was revealed between smoking and PD ≥ 5 mm with BoP (OR= 1.90, CI: 1.14, 3.15, p = 0.013), especially for plaque‐positive sites (OR= 4.14, CI: 2.16, 7.96, p < 0.001). A significant reduction of red complex microbiota was observed for non‐smokers only (p = 0.010).ConclusionSmokers respond less favourably to non‐surgical and surgical periodontal therapy compared with non‐smokers, in particular at plaque‐positive sites.

AimTo evaluate the effect of cigarette smoking on periodontal health at patient, tooth, and site levels following supportive therapy.Materials and MethodsEighty chronic periodontitis patients, 40 smokers and 40 non‐smokers, were recruited to a single‐arm clinical trial. Periodontal examinations were performed at baseline (T0), 3 months following active periodontal therapy (T1), and 12 months following supportive periodontal therapy (T2). Smoking status was validated measuring serum cotinine levels. Probing depth (PD) ≥ 5 mm with bleeding on probing (BoP) was defined as the primary outcome. Logistic regression analyses adjusted for clustered observations of patients, teeth, and sites and mixed effects models were employed to analyse the data.ResultsAll clinical parameters improved from T0 to T2 (p < 0.001), whereas PD, bleeding index (BI), and plaque index (PI) increased from T1 to T2 in smokers and non‐smokers (p < 0.001). An overall negative effect of smoking was revealed at T2 (OR = 2.78, CI: 1.49, 5.18, p < 0.001), with the most pronounced effect at maxillary single‐rooted teeth (OR = 5.08, CI: 2.01, 12.78, p < 0.001). At the patient level, less variation in treatment outcome was detected within smokers (ICC = 0.137) compared with non‐smokers (ICC = 0.051).ConclusionSmoking has a negative effect on periodontal health following 12 months of supportive therapy, in particular at maxillary single‐rooted teeth.

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.