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Aim: To update the competences and learning outcomes and their evaluation, educational methods and education quality assurance for the training of contemporary specialists in periodontology, including the impact of the 2018 Classification of Periodontal and Peri‐implant Diseases and Conditions (2018 Classification hereafter) and the European Federation of Periodontology (EFP) Clinical Practice Guidelines (CPGs). Methods: Evidence was gathered through scientific databases and by searching for European policies on higher education. In addition, two surveys were designed and sent to program directors and graduates. Results: Program directors reported that curricula were periodically adapted to incorporate advances in diagnosis, classification, treatment guidelines and clinical techniques, including the 2018 Classification and the EFP CPGs. Graduates evaluated their overall training positively, although satisfaction was limited for training in mucogingival and surgical procedures related to dental implants. Traditional educational methods, such as didactic lectures, are still commonly employed, but they are now often associated with more interactive methods such as case‐based seminars and problem‐based and simulation‐based learning. The evaluation of competences/learning outcomes should employ multiple methods of assessment. Conclusion: An update of competences and learning outcomes of specialist training in periodontology is proposed, including knowledge and practical application of the 2018 Classification and CPGs. Harmonizing specialist training in periodontology is a critical issue at the European level. [ABSTRACT FROM AUTHOR]

Aim: 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). [ABSTRACT FROM AUTHOR]

Aim: To examine the adjunctive effect of a Lactobacillus reuteri probiotic (ATCC PTA 5289 & DSM 17938) on the re‐instrumentation of residual pockets. Materials and Methods: This randomized, double‐blind, placebo‐controlled study included 39 previously non‐surgically treated periodontitis patients. A re‐instrumentation was carried out, and probiotic and/or placebo drops were applied according to the study protocoll. Patients afterwards received lozenges to use 2×/day for 12 weeks. Probing pocket depth (PPD), recession, bleeding on probing and plaque levels were analysed, next to the microbiological impact. Results: No effects of the probiotic drops could be found. However, after 24 weeks, the overall PPD in the probiotic lozenges group (2.64 ± 0.33 mm) was significantly lower compared to the control lozenges (2.92 ± 0.42 mm). This difference was even more pronounced in moderate (4–6 mm) and deep (≥7 mm) pockets. In the probiotic lozenges group, there were also significantly more pockets converting from ≥4 mm at baseline to ≤3 mm at 24 weeks (67 ± 18% versus 54 ± 17%) and less sites in need for surgery (4 ± 4% versus 8 ± 6%). However, the probiotic products did not influence the microbiological counts of the periodontopathogens. Conclusion: The adjunctive consumption of L. reuteri lozenges after re‐instrumentation improved the PPD reduction, without an impact on pocket colonization with periodontopathogens. [ABSTRACT FROM AUTHOR]

Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self-esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio-economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. Aim To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. Methods One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. Results & Conclusions There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor ( VDR), Fc gamma receptor IIA ( Fc-γ RIIA) and Interleukin 10 ( IL10) genes. For caries, genes involved in enamel formation ( AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics ( AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end-products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub-optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases. [ABSTRACT FROM AUTHOR]