Evolution of the pathogenesis of postmenopausal bone loss.
At a time when the investigation of bone diseases appears to be on the threshold of a new era, it is appropriate to pause and contemplate past and present thinking on the etiology of postmenopausal osteoporosis. This brief review traces the evolution of ideas on the nature of the pathogenesis of this disease from Albright's hypoosteoblastic hypothesis through other hypotheses that include disturbance in osteoclasia, negative calcium balance, disturbance of calcium homeostatic control mechanisms, increased skeletal sensitivity to parathyroid hormone, deficiency of calcitriol and calcitonin, altered activities of growth factors and cytokines, alterations in the local regulation of osteoclastogenesis, and changes in mechanical usage set points.
Kalu
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DN
Department of Physiology, University of Texas Health Science Center, San Antonio 78284-7756, USA.
D001862:Bone Resorption / Q000503:physiopathology; D002118:Calcium / Q000378:metabolism; D005260:Female; D006410:Hematopoiesis / Q000502:physiology; D006801:Humans; D010006:Osteoblasts / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D015663:Osteoporosis, Postmenopausal / Q000209:etiology* / Q000503:physiopathology; D010281:Parathyroid Hormone / Q000502:physiology; D012307:Risk Factors
D010281:Parathyroid Hormone; D002118:Calcium