McNamara Laoise M
Mechanobiology and Medical Device Research Group, Biomedical Engineering, College of Science and Engineering, National University of Ireland, Galway, Ireland.
Centre for Research in Medical Devices (CÚRAM), National University of Ireland, Galway, Ireland.
Curr Osteoporos Rep. 2021 Dec;19(6):592-603. doi: 10.1007/s11914-021-00702-x. Epub 2021 Nov 26.
Postmenopausal osteoporosis reduces circulating estrogen levels, which leads to osteoclast resorption, bone loss, and fracture. This review addresses emerging evidence that osteoporosis is not simply a disease of bone loss but that mechanosensitive osteocytes that regulate both osteoclasts and osteoblasts are also impacted by estrogen deficiency.
At the onset of estrogen deficiency, the osteocyte mechanical environment is altered, which coincides with temporal changes in bone tissue composition. The osteocyte microenvironment is also altered, apoptosis is more prevalent, and hypermineralization occurs. The mechanobiological responses of osteocytes are impaired under estrogen deficiency, which exacerbates osteocyte paracrine regulation of osteoclasts. Recent research reveals changes in osteocytes during estrogen deficiency that may play a critical role in the etiology of the disease. A paradigm change for osteoporosis therapy requires an advanced understanding of such changes to establish the efficacy of osteocyte-targeted therapies to inhibit resorption and secondary mineralization.
绝经后骨质疏松症会降低循环雌激素水平，进而导致破骨细胞吸收、骨质流失和骨折。本综述探讨了新出现的证据，即骨质疏松症不仅仅是一种骨质流失疾病，而且调节破骨细胞和成骨细胞的机械敏感骨细胞也会受到雌激素缺乏的影响。
在雌激素缺乏开始时，骨细胞的力学环境发生改变，这与骨组织成分的时间变化相吻合。骨细胞微环境也发生改变，细胞凋亡更为普遍，并且出现矿化过度。在雌激素缺乏的情况下，骨细胞的机械生物学反应受损，这加剧了骨细胞对破骨细胞的旁分泌调节。最近的研究揭示了雌激素缺乏期间骨细胞的变化，这些变化可能在该疾病的病因中起关键作用。骨质疏松症治疗的范式转变需要深入了解这些变化，以确定针对骨细胞的疗法抑制吸收和继发性矿化的疗效。
