Matsumoto Tadami, Kitamura Kenji, Ichiseki Touru, Kaneuji Ayumi, Sugimori Tanzo
Kanazawa Medical University, Department of Orthopedic Surgery.
Clin Calcium. 2007 Jun;17(6):887-91.
The increasing incidence of steroid-induced osteonecrosis of the femoral head is a recent and emerging problem. In-depth pathogenesis, however, has not been well understood. We focused on oxidative stress, which was reported to be involved in many diseases, and conducted animal studies to investigate it. Our results from the rabbit model of steroid-induced osteonecrosis demonstrated that administration of steroids caused oxidative damage in bones, and the administration of glutathione reduced the incidence of osteonecrosis. We were also the first to have successfully induced osteonecrosis in rats by administering buthionine sulfoximine (BSO) . The results indicated the involvement of oxidative stress in the development of osteonecrosis and may contribute to elucidating the underlying mechanisms and prevention of the pathogenesis of steroid-induced osteonecrosis.
类固醇诱导的股骨头坏死发病率不断上升是一个新出现的问题。然而，其深层发病机制尚未得到充分理解。我们聚焦于氧化应激，据报道氧化应激与多种疾病有关，并开展了动物研究以进行调查。我们在类固醇诱导的股骨头坏死兔模型中的研究结果表明，给予类固醇会导致骨骼发生氧化损伤，而给予谷胱甘肽可降低骨坏死的发生率。我们也是首个通过给予丁硫氨酸亚砜胺（BSO）成功在大鼠中诱导出骨坏死的。结果表明氧化应激参与了骨坏死的发生发展，可能有助于阐明类固醇诱导的骨坏死发病机制的潜在机制及预防方法。
