All SFE techniques provided sufficient graft volume for implant treatment. All techniques provoke a partially transient swelling of the Schneiderian membrane. All techniques resulted in a decrease in graft volume after 6 weeks; however, no significant differences were obtained between treatments. Furthermore, no statistical significant correlation between the post-operative swelling of the Schneiderian membrane and reduction in graft volume at 6 weeks could be obtained.

L-PRF Block may be a suitable technique to augment deficient alveolar ridges.

Subgingival debridement is the part of nonsurgical therapy which aims to remove the biofilm without intentionally removing the cementum or subgingival calculus. The objective of this review was to describe the end point of this therapy, the different methods used and how often it should be carried out. The literature shows that several methods are currently available for subgingival debridement, namely hand instrumentation, (ultra)sonic instrumentation, laser, photodynamic therapy and air‐polishing. None of these methods seems superior to any other regarding clinical benefits or microbiological differences. However, less treatment discomfort is reported using laser, photodynamic therapy or air‐polishing compared with hand‐ and/or (ultra)sonic instrumentation. Subgingival debridement can be carried out when, during supportive periodontal therapy, pockets of 5 mm or deeper are detected.

Purpose:The Leucocyte and Platelet Rich Fibrin Block (L-PRF Block) is a composite graft that combine a xenograft that is acting as a scaffold with L-PRF membranes that serve as a bioactive nodule with osteoinductive capacity. This study evaluated the properties of the L-PRF Block and its components in terms of release of growth factors, cellular content and structure. Methods:The concentration of transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor (VEGF), platelet-derived growth factor-AB (PDGF-AB) and bone morphogenetic protein-1 (BMP-1) released by a L-PRF membrane (mb) and a L-PRF Block were examined with ELISA for 5 time intervals (0-4h, 4h-1day, 1-3d, 3-7d, 7-14d). Those levels in L-PRF exudate and Liquid Fibrinogen were also evaluated. The cellular content of the Liquid Fibrinogen, L-PRF membrane and exudate was calculated. The L-PRF Block was also analysed by means of a microCT scan and scanning electron microscopy (SEM).Results: TGF-β1 was the most released growth factor after 14 days, followed by PDGF-AB, VEGF, and BMP-1. All L-PRF blocks constantly release the four growth factors up to 14 days. L-PRF membrane and Liquid Fibrinogen presented high concentration of leucocytes and platelets. The microCT and SEM images revealed the bone substitute particles surrounded by platelets and leucocytes, embedded in a dens fibrin network. Conclusions:The L-PRF Block consists of deproteinized bovine bone mineral particles surrounded by platelets, leucocytes and embedded in a fibrin network that releases growth factors up to 14 days.

No abstract

Background Furcation involvement and attachment loss are major predictors of tooth loss. The aim of this study was to describe specific designs for papilla preservation flaps (PPFs) and minimally invasive surgery to be used in compromised molars and report proof‐of‐principle data with 3 to 16‐year follow‐up in severely compromised molars due to the presence of combined furcation and intrabony defects. Methods Forty‐nine subjects with furcated molars and deep intrabony defects were treated with PPFs, application of periodontal regenerative devices. Improvement as a consequence of therapy was defined as tooth retention, reduction in horizontal and vertical furcation involvement, decrease in probing depths, and increases in clinical attachment level. Subjects were maintained with regular supportive periodontal care. Results At 1 year, 100% of maxillary and 92% of mandibular molars showed improvements. Improvements were not observed in molars with baseline hypermobility: two mandibular molars with hypermobility were extracted at the 1‐year follow‐up. Improvement in vertical sub‐classification was observed in 87.5% of maxillary and in 84.6% of mandibular molars. One‐year improvements could be maintained over the 3 to 16‐year follow‐up. Conclusions PPFs and periodontal regeneration can be applied and provide clinical benefits to severely compromised molars due to the combined presence of furcation involvement and deep intrabony defects. These results were obtained in cases with an interdental peak of bone and gingival margin coronal to the furcation entrance in well‐maintained and compliant subjects. Randomized controlled clinical trials with medium‐ to long‐term follow‐up are needed to confirm these findings.

The aim of the study was to evaluate whether the use of a xenograft is not inferior to the use of xenograft and autogenous bone chips in treating dehiscences at implant placement. Materials and Methods: After implant placement, leaving a dehiscence, control sites were treated using a composite graft (autogenous bone chips and xenograft) and at the test sites 100% xenograft was used. Both sites were covered with a resorbable collagen membrane. Dehiscences were measured clinically at implant placement and at re-entry. CBCT was taken immediately after implant placement and after 4 months. Results: In total, 28 GBR procedures were performed in 14 patients. On average, the change in vertical defect height was 2.07 mm (46.7%-test group) and 2.28 mm (50.9%-control group) (p > .05). The horizontal defect width at the implant shoulder change on average 1.85 mm (40.5%-test group) and 1.75 mm (40.9%-control group) (p > .05). On average, a loss in augmentation thickness of 0.45 mm (68.9%-test group) and 0.64 mm (55.5% control group) between implant placement and augmentation and abutment surgery was obtained at the implant shoulder. Conclusion: Both treatment modalities seem to work to a certain extent. At implant shoulder level, the augmentation thickness seems to be disappeared after the healing phase. (NCT03946020).

dental implant, implant treatment, patient compliance, peri-implantitis | INTRODUC TI ONIt is well-established that the maintenance of healthy tissues around implants is one of the key factors in the long-term success of implants. Plaque accumulation induces an inflammatory process that may lead to a progressive destruction of soft and hard tissues and, ultimately, to implant failure. 1-3 The inflammatory process, mucositis, is a marginal inflammation without attachment or bone loss, 4 similar to gingivitis around natural teeth. The inflammatory process associated with the loss of marginal supporting bone around an implant is defined as peri-implantitis. 5,6 One problem with the diagnosis of peri-implant disease is that substantial variation in prevalence has been reported in the same patient population depending on which diagnostic criteria are used. 7The current guidelines for the definition and diagnosis of peri-implant diseases were established in the sixth, seventh, and eighth European Workshops on Periodontology. 6,8,9 The prevalence of peri-implantitis seems to be of the order of 10% at implant level and 20% at patient level during 5-10 years of function. 10 A meta-analysis reported a weighted mean prevalence of peri-implant mucositis of 43% (1196 patients and 4209 implants) and a weighted mean prevalence of peri-implantitis of 22% (2131 patients and 8893 implants).However, the authors stated that the heterogeneity in definition criteria of peri-implantitis could be a confounder.Peri-implantitis has been primarily described as a simple infectious pathologic condition of peri-implant tissues. 1,11 Many local factors, such as implant surface, topology, and bacterial contamination at the implant/abutment junction, and patient factors, such as smoking habit, poor oral hygiene, history or presence of periodontitis, genetics, and excessive alcohol consumption, have also been associated with an increased risk of developing peri-implant diseases. [12][13][14][15][16] The etiology of alveolar bone loss around implants plays a crucial role in the classification of the disease. The most common theories to explain alveolar bone loss are the infection theory and the overload theory. 17 The infection theory states that implants are susceptible to similar types of disease as teeth, the major difference being that the term periodontitis is reserved for teeth and peri-implantitis is reserved for implants. The overload theory has not been clearly determined. Some studies have suggested that Occlusal overload may play a role when associated with plaque accumulation or pre-existing inflammation. 18 A third theory has also been developed, where alveolar bone loss is explained by the synergy of combined factors, such as surgical procedures, prosthodontics, and patient disorders. 17 The difference between primary and secondary peri-implantitis has also been presented. In primary peri-implantitis, bacterial infection is the primary cause of alveolar bone loss, whereas secondary peri-implantitis may originate from other factors. 1...