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SUBJECT: Participants had type 2 diabetes, were on stable medication regimens, had HbA1c levels between 7% and

Purpose: To present a review of available literature on the association of vitamin D and periodontal disease.Materials and Methods: A thorough search of articles was carried out on the databases PUBMED and MEDLINE regarding vitamin D and periodontal disease. The selected literature included cross-sectional, case-control and prospective and retrospective cohort studies. The main aspects of the association evaluated were a) the association of 25(OH)D and 1,25(OH)2D3 with periodontal disease severity, periodontal disease progression and tooth loss, b) the effect of vitamin D supplementation on periodontal health and c) the association of vitamin D receptor polymorphisms with periodontal disease. A brief overview of the biological mechanisms linking periodontal disease with vitamin D was also included.Results and Conclusions: There is conflicting evidence regarding the effects of 25(OH)D on periodontal disease severity, progression and tooth loss, with some studies reporting beneficial effects of higher 25(OH)D serum concentrations on periodontal health and tooth retention, whereas others could not find such an association. Limited evidence also supports a positive association between 1,25(OH)2D3 and periodontal health as well as a trend towards better periodontal health with vitamin D supplementation. Finally, various vitamin D polymorphisms were associated with chronic and aggressive periodontitis, with different outcomes reported for the various ethnic populations assessed. [ABSTRACT FROM AUTHOR]

Aims: Noonan syndrome (NS) is a clinically and genetically heterogeneous condition characterized by distinctive facial features, short stature, and congenital heart defects. The oral manifestations have not been sufficiently described. In an attempt to enrich our understanding regarding the oral manifestations, the aim of the current study was to present the clinical, radiographic, and microbiological findings of eleven subjects with NS syndrome. Methods and Results: A complete intraoral clinical evaluation, a radiographic analysis using panoramic and cephalometric x‐rays, and a supra‐ and sub‐gingival microbiological profiling of 20 periodontal and cariogenic microbiota using the checkerboard DNA‐DNA hybridization technique were performed in a series of 11 NS individuals. Compared to previous reports very few dental findings were present. Gingivitis and carious lesions were present in all subjects and could be related to poor oral hygiene. High‐arched palate and malocclusions such as crossbite, open‐bite, and deep‐bite were very common findings but without a specific pattern. Two findings that have not been reported before included the different shapes of the condyles and the irregular shape of the sella turcica. Conclusion: Due to the elevated prevalence of gingivitis, caries, and malocclusion, a multidisciplinary approach including dental follow‐ups should be the standard care in NS patients. [ABSTRACT FROM AUTHOR]

Periodontitis is considered to be a multifactorial disease. Studies have indicated that part of the clinical variability in periodontitis may be explained by genetic factors. Genes can affect the immunoinflammatory host response to bacterial challenge in the periodontal tissues by means of an overproduction of proinflammatory cytokines, such as interleukin-1 (IL-1). IL-1 plays an important role in the pathogenesis of periodontitis, through its involvement in the regulation of the host's inflammatory response and bone resorption. Therefore, the genes that encode for IL-1 production have recently received most attention as potential predictors of periodontal disease progression. Hence, the relationship between IL-1 genotype and periodontal disease has been investigated by a number of studies. This review article aimed to determine whether IL-1 could be regarded as a genetic marker for periodontitis by reviewing data concerning susceptibility, clinical parameters, and treatment strategies in relation to the IL-1 genotype. The review concluded that there is currently limited evidence to implicate a specific IL-1 genotype as a risk factor for chronic periodontitis in white populations. However, there is limited evidence that genetic variation in the IL-1B polymorphism could be a risk factor for aggressive periodontitis. [ABSTRACT FROM AUTHOR]

Endosseous implants present high survival rates within a 10-year observation time; however, implant failure and biologic complications are not completely avoidable. Although specific bacteria, dental plaque, and environmental factors are associated with peri-implant disease, there are currently no reliable predictors of peri-implantitis occurrence and severity. Disagreement about which clinical measures of peri-implant health are of diagnostic value continues because of the complexity of the disease process. Thus, identification of genes that control or modify aspects of the host response may provide a method to identify individuals at an elevated risk for peri-implant infections. Elevated levels of the inflammatory cytokine interleukin-1 (IL-1) in the crevicular fluid around diseased implants seem to play an important role in the pathogenesis and severity of peri-implantitis. The purpose of this review article was to critically address the genetic associations regarding IL-1 genotype claimed for peri-implant disease and to validate the use of IL-1 genetic susceptibility tests. It was revealed that the diagnostic value of both IL-1 genotyping and genetic tests for peri-implantitis should be reconsidered before altering treatment planning, regimens, and maintenance in implant dentistry. [ABSTRACT FROM AUTHOR]

Background: A variety of systemic diseases and conditions can affect the course of periodontitis or have a negative impact on the periodontal attachment apparatus. Gingival recessions are highly prevalent and often associated with hypersensitivity, the development of caries and non‐carious cervical lesions on the exposed root surface and impaired esthetics. Occlusal forces can result in injury of teeth and periodontal attachment apparatus. Several developmental or acquired conditions associated with teeth or prostheses may predispose to diseases of the periodontium. The aim of this working group was to review and update the 1999 classification with regard to these diseases and conditions, and to develop case definitions and diagnostic considerations. Methods: Discussions were informed by four reviews on 1) periodontal manifestions of systemic diseases and conditions; 2) mucogingival conditions around natural teeth; 3) traumatic occlusal forces and occlusal trauma; and 4) dental prostheses and tooth related factors. This consensus report is based on the results of these reviews and on expert opinion of the participants. Results: Key findings included the following: 1) there are mainly rare systemic conditions (such as Papillon‐Lefevre Syndrome, leucocyte adhesion deficiency, and others) with a major effect on the course of periodontitis and more common conditions (such as diabetes mellitus) with variable effects, as well as conditions affecting the periodontal apparatus independently of dental plaque biofilm‐induced inflammation (such as neoplastic diseases); 2) diabetes‐associated periodontitis should not be regarded as a distinct diagnosis, but diabetes should be recognized as an important modifying factor and included in a clinical diagnosis of periodontitis as a descriptor; 3) likewise, tobacco smoking – now considered a dependence to nicotine and a chronic relapsing medical disorder with major adverse effects on the periodontal supporting tissues – is an important modifier to be included in a clinical diagnosis of periodontitis as a descriptor; 4) the importance of the gingival phenotype, encompassing gingival thickness and width in the context of mucogingival conditions, is recognized and a novel classification for gingival recessions is introduced; 5) there is no evidence that traumatic occlusal forces lead to periodontal attachment loss, non‐carious cervical lesions, or gingival recessions; 6) traumatic occlusal forces lead to adaptive mobility in teeth with normal support, whereas they lead to progressive mobility in teeth with reduced support, usually requiring splinting; 7) the term biologic width is replaced by supracrestal tissue attachment consisting of junctional epithelium and supracrestal connective tissue; 8) infringement of restorative margins within the supracrestal connective tissue attachment is associated with inflammation and/or loss of periodontal supporting tissue. However, it is not evident whether the negative effects on the periodontium are caused by dental plaque biofilm, trauma, toxicity of dental materials or a combination of these factors; 9) tooth anatomical factors are related to dental plaque biofilm‐induced gingival inflammation and loss of periodontal supporting tissues. Conclusion: An updated classification of the periodontal manifestations and conditions affecting the course of periodontitis and the periodontal attachment apparatus, as well as of developmental and acquired conditions, is introduced. Case definitions and diagnostic considerations are also presented. [ABSTRACT FROM AUTHOR]