Lanyon L, Skerry T
Department of Veterinary Basic Sciences, The Royal Veterinary College, London, United Kingdom.
J Bone Miner Res. 2001 Nov;16(11):1937-47. doi: 10.1359/jbmr.2001.16.11.1937.
There is substantial evidence that bones' ability to withstand functional loading without damage depends on the processes of bone modeling and remodeling, which are responsible for establishing and maintaining bone architecture, being influenced by a feedback mechanism related to the control of functional strains. It is probably useful to consider the diminished ability to maintain bone strength in postmenopausal osteoporosis as a failure of this mechanism. Acceptance of this approach would not only increase understanding of the etiology of postmenopausal osteoporosis but also significantly influence the ways in which it is investigated and treated. This would not mean that the many other factors affecting bone mass and bone cell activity will be ignored, but rather these factors will be put in perspective. Research to prevent or treat osteoporosis could be directed usefully to understanding how osteoblasts, lining cells, and osteocytes respond to mechanically derived information and how these responses are converted into stimuli controlling structurally appropriate modeling and remodeling. Evidence suggesting that early strain-related responses of bone cells in males and females involve the estrogen receptor (ER) could explain decreased effectiveness of this pathway when ER levels are low.
有大量证据表明,骨骼承受功能负荷而不损伤的能力取决于骨塑形和重塑过程,这些过程负责建立和维持骨骼结构,并受与功能应变控制相关的反馈机制影响。将绝经后骨质疏松症中维持骨强度能力的下降视为这种机制的失效可能是有用的。接受这种方法不仅会增加对绝经后骨质疏松症病因的理解,还会显著影响其研究和治疗方式。这并不意味着影响骨量和骨细胞活性的许多其他因素将被忽视,而是这些因素将被正确看待。预防或治疗骨质疏松症的研究可以有益地指向了解成骨细胞、衬里细胞和骨细胞如何对机械衍生信息作出反应,以及这些反应如何转化为控制结构适当的塑形和重塑的刺激。有证据表明,男性和女性骨细胞早期与应变相关的反应涉及雌激素受体(ER),这可以解释当ER水平较低时该途径的有效性降低。