Astrand Jörgen, Aspenberg Per
Department of Orthopaedics, Lund University Hospital, Lund, Sweden.
BMC Musculoskelet Disord. 2002 Aug 7;3:19. doi: 10.1186/1471-2474-3-19.
Avascular necrosis of bone (osteonecrosis) can cause structural failure and subsequent deformation, leading to joint dysfunction and pain. Structural failure is the result of resorption of necrotic bone during revascularization, before new bone has formed or consolidated enough for loadbearing. Bone resorption can be reduced by bisphosphonates. If resorption of the necrotic bone could be reduced during the revascularization phase until sufficient new bone has formed, it would appear that structural failure could be avoided.
To test whether resorption of necrotic bone can be prevented, structural grafts were subjected to new bone ingrowth during systemic bisphosphonate treatment in a rat model.
In rats treated with alendronate the necrotic bone was not resorbed, whereas it was almost entirely resorbed in the controls.
Systemic alendronate treatment prevents resorption of necrotic bone during revascularization. In patients with osteonecrosis, bisphosphonates may therefore prevent collapse of the necrotic bone.
骨缺血性坏死(骨坏死)可导致结构破坏及随后的变形,进而引起关节功能障碍和疼痛。结构破坏是在血管再生过程中,坏死骨在新骨形成或巩固到足以承受负荷之前被吸收的结果。双膦酸盐可减少骨吸收。如果在血管再生阶段坏死骨的吸收能够减少,直至形成足够的新骨,那么似乎可以避免结构破坏。
为了测试是否能够防止坏死骨的吸收,在大鼠模型中,于全身应用双膦酸盐治疗期间,对结构性移植物进行新骨长入实验。
用阿仑膦酸钠治疗的大鼠,坏死骨未被吸收,而在对照组中几乎完全被吸收。
全身应用阿仑膦酸钠治疗可防止血管再生过程中坏死骨的吸收。因此,对于骨坏死患者,双膦酸盐可能会防止坏死骨塌陷。