Osteocytes and Estrogen Deficiency

Purpose of Review 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. Recent Findings 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.

Automated summary

Postmenopausal osteoporosis is not only characterized by bone loss due to decreased estrogen levels, but also by alterations in mechanosensitive osteocytes. Research shows that estrogen deficiency affects the osteocyte mechanical and microenvironment, leading to impaired mechanobiological responses and exacerbating osteocyte regulation of osteoclasts. Understanding these changes is crucial for developing targeted therapies to inhibit resorption and secondary mineralization in osteoporosis.