Perrotta I, Cristofaro M G, Amantea M, Russo E, De Fazio S, Zuccalà V, Conforti F, Amorosi A, Donato G, Tripepi S, Giudice M
Department of Ecology, University of Calabria, Arcavacata di Rende, Cosenza, Italy.
Ultrastruct Pathol. 2010 Aug;34(4):207-13. doi: 10.3109/01913121003729806.
Osteonecrosis of the jaw is a severe bone disorder traditionally associated with periodontal disease, local malignancy, chemotherapy, glucocorticoid therapy, or trauma. Recently a growing number of publications reported the occurrence of osteonecrosis of the jaw in patients undergoing treatment with bisphosphonates. The mechanism by which bisphosphonates might contribute to the development of osteonecrosis of the jaw is far from being fully elucidated. Suppression of bone turnover, infection, tissue hypoxia and cellular toxicity were proposed as possible mechanisms by which bisphosphonates may exert adverse effects on bone metabolism. Here, we studied 25 consecutive patients treated with bisphosphonates for osteoporosis or tumoral pathologies. We provide good evidence of hyperactive osteoclastic bone resorption and suggest a direct cytotoxic effect of bisphosphonates on bone tissue through induction of osteocyte cell death. We also demonstrate that bisphosphonates only have limited adverse effects on bone vascular network.
颌骨坏死是一种严重的骨疾病，传统上与牙周病、局部恶性肿瘤、化疗、糖皮质激素治疗或创伤有关。最近，越来越多的出版物报道了接受双膦酸盐治疗的患者发生颌骨坏死。双膦酸盐可能导致颌骨坏死的机制远未完全阐明。骨转换抑制、感染、组织缺氧和细胞毒性被认为是双膦酸盐可能对骨代谢产生不利影响的潜在机制。在此，我们研究了连续25例接受双膦酸盐治疗骨质疏松症或肿瘤性疾病的患者。我们提供了破骨细胞性骨吸收活跃的有力证据，并提示双膦酸盐通过诱导骨细胞死亡对骨组织产生直接细胞毒性作用。我们还证明双膦酸盐对骨血管网络的不良影响有限。
