Sugiyama T, Kim Y T, Oda H
Department of Orthopaedic Surgery, Saitama Medical University, 38 Morohongo, Moroyama, Saitama, 350-0495, Japan,
Osteoporos Int. 2015 Feb;26(2):443-7. doi: 10.1007/s00198-014-2923-y. Epub 2014 Oct 7.
The skeleton normally responds to mechanical environment to maintain the resulting elastic deformation (strain) of bone, while increased bone strength by an osteoporosis drug results in decreased bone strain. Thus, it can be hypothesized that the effect of osteoporosis therapy is limited by natural homeostatic system in the skeleton. This logic is consistent with the fact that there exists a powerful effect that returns bone mass to its pre-treatment level after the withdrawal of treatment with osteoporosis agents. The present hypothesis provides a new significant insight into the mechanisms by which osteoporosis drugs improve bone fragility. Here we briefly discuss the effects of teriparatide, romosozumab, and odanacatib on bones in animals and humans.
骨骼通常会对机械环境做出反应，以维持由此产生的骨弹性变形（应变），而骨质疏松症药物增加骨强度会导致骨应变降低。因此，可以推测骨质疏松症治疗的效果受到骨骼中自然稳态系统的限制。这一逻辑与以下事实一致：停用骨质疏松症药物后，存在一种强大的作用会使骨量恢复到治疗前水平。目前的假设为骨质疏松症药物改善骨脆性的机制提供了新的重要见解。在此，我们简要讨论特立帕肽、罗莫单抗和奥达卡替对动物和人类骨骼的影响。
