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Altered Ovarian Function Affects Skeletal Homeostasis Independent of the Action of Follicle-Stimulating Hormone

Calcium Research Laboratory and Department of Medicine (J.G., R.S., D.M., D.G.), McGill University Health Centre and McGill University, Montreal, Quebec, Canada H3A 1A1; Molecular Reproduction Research Laboratory (R.T.-P., Y.Y., M.R.S.), Clinical Research Institute of Montreal, Montreal, Quebec, Canada H2W IR7; and Lady Davis Institute for Medical Research and Department of Medicine (A.C.K.), Jewish General Hospital and McGill University, Montreal, Quebec, Canada H3T IE2

Address all correspondence and requests for reprints to: Dr. David Goltzman, Calcium Research Laboratory, McGill University Health Centre, 687 Pine Avenue West, Room H4.67, Montreal, Quebec, Canada H3A 1A1. E-mail: david.goltzman{at}mcgill.ca.

Osteoporosis is a leading public health problem. Although a major cause in women is thought to be a decline in estrogen, it has recently been proposed that FSH or follitropin is required for osteoporotic bone loss. We examined the FSH receptor null mouse (FORKO mouse) to determine whether altered ovarian function could induce bone loss independent of FSH action. By 3 months of age, FORKO mice developed age-dependent declines in bone mineral density and trabecular bone volume of the lumbar spine and femur, which could be partly reversed by ovarian transplantation. Bilateral ovariectomy reduced elevated circulating testosterone levels in FORKO mice and decreased bone mass to levels indistinguishable from those in ovariectomized wild-type controls. Androgen receptor blockade and especially aromatase inhibition each produced bone volume reductions in the FORKO mouse. The results indicate that ovarian secretory products, notably estrogen, and peripheral conversion of ovarian androgen to estrogen can alter bone homeostasis independent of any bone resorptive action of FSH.