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Aim: Diabetes is a metabolic disease that is becoming increasingly important and widespread all over the world. One of the complications of T2DM is an impaired vascularization. In this master thesis, we have attempted finding an answer on the following question: Is T2DM bone tissue poorly vascularized? What are the factors that cause a possible impaired vascularization in T2DM bone tissue? Materials and methods: Using the PubMed search engine, we selected appropriate information relative to the blood flow in diabetic bone. The following keywords were used to search relevant articles to answer our questions: bone perfusion, bone vascularization, bone vasculature, bone vessel calcification, vessel calcification, vessel stiffening, bone vascular calcification, bone atherosclerosis. Each keyword was also used to search in combination with ‘diabetes type 2’. When diabetes type 2 was not involved in the articles but only diabetes type 1 was found, those articles were excluded. Only articles that reported in vivo studies were judged as appropriate, either animal studies, clinical studies or reviews of the latter. Results: Using the keywords as mentioned above, we obtained 203 results. After applying the exclusion criteria, thus eliminating all articles concerning type 1 diabetes and in vitro studies as well as duplicates, 14 articles (4 animal studies, 8 clinical studies and 2 review articles) remained relevant. Conclusion: In T2DM, evidence is clear that the vascularization is impaired. BMP-2 and OPG are increased in T2DM patients. The BMP-2 level is increased in the endothelial cells, causing vascular calcification by promoting differentiation of VSMCs in cells with an osteoblast-like phenotype. The OPG level is increased in T2DM patients, especially in those with microvascular complications. OPG plays a protective role in bone tissue by inhibition of maturation and activity of osteoclasts. In the vasculature, OPG inhibits atherosclerosis and vascular inflammation and promotes the survival of vascular cells. The increase of OPG in T2DM patients could be explained by the fact that OPG production is upregulated as a protective compensatory mechanism in conditions were vascular calcification is increased. Insulin plays a protective role by improving osteoblast function and bone formation. The vascular calcification in T2DM is associated with a reduced bone health, bone turnover and BMD and an increased bone loss and osteoporotic fractures. More research on the vascularization of T2DM bone is urgently needed.

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BACKGROUND: Nowadays osteoporosis is a worldwide common and well known disease. Bisphosphonates are the gold standard for osteoporotic treatment. An important side effect of this treatment is the osteonecrosis of the jaw. This study aims at analyzing the current literature concerning osseointegration and survival of dental implants. METHODS: The PubMed, the electronic database of the US National Library of medicine, was screened for English language literature published during the period January 2010-September 2015 using the following Mesh terms: bisphosphate and osteoporosis, mechanism, (fracture) healing, and osseointegration of dental implants. Keywords and filters were inserted into the PubMed database. RESULTS: Nineteen papers including 8 reviews, 3 retrospective studies, 3 randomized controlled trials, 2 prospective studies, 1 single blind controlled trial and 1 clinical trial were selected. The results of this analysis indicate that intravenous bisphosphonate administration harbors a risk for dental implant failure. At the same time, several reports indicate that oral bisphosphonate administration also carries a risk for osteopathology. Results about impact of oral BP therapy on dental implant failure are still contradictory. CONCLUSION: The decision regarding implant placements in patients with bisphosphonate therapy depends on various factors such as the duration of drug exposure, drug type, dosage (continuous or intermittent), delivery route (oral versus IV), patient age, dental/periodontal status and underlying health condition. Risk analysis should be made individually and patients should be informed concerning potential complications and treatment alternatives. Presence of serious bone disease and exposure to high bisphosphate doses contraindicate implant therapy.