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 pa
st 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 hypothe
sis through other hypotheses that include disturbance in osteoclasia,
negative calcium balance, disturbance of calcium homeostatic control m
echanisms, increased skeletal sensitivity to parathyroid hormone, defi
ciency of calcitriol and calcitonin, altered activities of growth fact
ors and cytokines, alterations in the local regulation of osteoclastog
enesis, and changes in mechanical usage set points.