4 research outputs found

    Bisphosphonates and osteomyelitis of the jaw: a pathogenic puzzle.

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    The maxillary and mandibular bones undergo high-turnover remodeling to maintain mechanical competence. Common dental or periodontal diseases can increase local bone turnover. Bisphosphonates (BPs) accumulate almost exclusively in skeletal sites that have active bone remodeling. The maxillary and mandibular bones are preferential sites for accumulation of BPs, which become buried under new layers of bone and remain biologically inactive for a long time. Surgical odontostomatological procedures create open bony wounds that heal quickly and without infection, as a result of activation of osteoclasts and subsequently osteoblasts. Once BPs are removed from the bone via activation of osteoclasts after a tooth extraction or a periodontal procedure, they induce osteoclast apoptosis. This inhibition of osteoclast bone resorption impairs bone wound healing because of decreased production of cytokines derived from the bone matrix, and the bone is exposed to the risk of osteomyelitis and necrosis. The pathogenic relationship between BPs and osteonecrosis of the jaw is unclear, but there is evidence to indicate an association between high-dose BP treatment and exposure to dental infections or oral surgical procedures. A better knowledge of the interactions between BPs and jaw and maxillary bone biology will improve clinical and therapeutic approaches

    The prevention of corticosteroid-induced osteoporosis with nandrolone decantate Bone and Mineral 15, 72-81 (1991)

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    The effects of nandrolone decanoate (ND; 50 mg IM every three weeks) on calcium metabolism and forearm bone density were studied in a randomized trial in 35 women receiving long-term therapy with corticosteroids (CST) for rheumatic disease. The 17 patients who served as controls were on CST therapy for less years and their bone density was higher. Thus a second control group, pair-matched with the active treatment group for age, duration of CST therapy and bone density, was selected retrospectively. At the end of the 18 months' treatment course with ND, forearm bone density was increased by 5.1% (P less than 0.01) but fell by 11.3% (P less than 0.01) and 6.7% respectively in the first and second control group. The patients on ND differed significantly from both control groups in the changes at 6, 12 and 18 months (P less than 0.01). Urinary excretion of hydroxyproline fell significantly in patients receiving ND, whereas the biochemical indices of bone formation did not change (alkaline phosphatase) or increased (osteocalcin; P less than 0.01). In conclusion, nandrolone decanoate therapy may be used in the prevention of CST-induced osteoporosis. It also seems to exert mild inhibition of bone resorption without affecting or even stimulating bone formation
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