Migliaccio Silvia, Brama Marina, Fornari Rachele, Greco Emanuela A, Spera Giovanni, Malavolta Nazzarena
Dipartimento di Fisiopatologia Medica, Policlinico Umberto I, Università degli Studi di Roma La Sapienza, 00166 Roma, Italy.
Aging Clin Exp Res. 2007 Jun;19(3 Suppl):5-10.
It is well-known that glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. It is estimated that 30% to 50% of patients receiving chronic glucocorticoid therapy suffer vertebral or hip fractures, which are often asymptomatic. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Glucocorticoids impair osteoblast homeostasis and induce apoptosis of both osteoblasts and osteocytes, leading to suppression of bone formation. Glucocorticoids also favor osteoclastogenesis and, as a consequence, increase bone resorption. The end-point of these alterations is a net decrease in BMD and alterations in bone quality. Bisphosphonates have been approved for both prevention and treatment of GIO. At the present time, anabolic therapeutic agents are still under investigation.
众所周知,糖皮质激素性骨质疏松症(GIO)是继发性骨质疏松症最常见的形式。据估计,接受慢性糖皮质激素治疗的患者中有30%至50%会发生椎体或髋部骨折,而这些骨折通常没有症状。椎体骨折在接触糖皮质激素后早期就会发生,此时骨矿物质密度(BMD)迅速下降。糖皮质激素损害成骨细胞稳态,并诱导成骨细胞和骨细胞凋亡,导致骨形成受到抑制。糖皮质激素还促进破骨细胞生成,结果增加了骨吸收。这些改变的最终结果是BMD净减少和骨质量改变。双膦酸盐已被批准用于预防和治疗GIO。目前,合成代谢治疗药物仍在研究中。