Laoise M McNamara1,2. 1. Mechanobiology and Medical Device Research Group, Biomedical Engineering, College of Science and Engineering, National University of Ireland, Galway, Ireland. Laoise.McNamara@nuigalway.ie. 2. Centre for Research in Medical Devices (CÚRAM), National University of Ireland, Galway, Ireland. Laoise.McNamara@nuigalway.ie.
Abstract
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.
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.
Authors: Amanda M D Malone; Charles T Anderson; Padmaja Tummala; Ronald Y Kwon; Tyler R Johnston; Tim Stearns; Christopher R Jacobs Journal: Proc Natl Acad Sci U S A Date: 2007-08-02 Impact factor: 11.205
Authors: Yilin Wang; Laoise M McNamara; Mitchell B Schaffler; Sheldon Weinbaum Journal: Proc Natl Acad Sci U S A Date: 2007-09-25 Impact factor: 11.205
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