Abstract
The recent demonstration of estrogen receptors in bone derived cells has stimulated the study of direct effects of sex steroids on bone. We have shown direct stimulation of proliferation by 17β-estradiol (E 2) of ROS 17/2.8 rat osteogenic osteosarcoma cells, and other bone-derived cells in culture, as well as sex-specific stimulation of diaphyseal bone in vivo by estrogen and testosterone, using [ 3H]thymidine incorporation into DNA and stimulation of the specific activity of creatine kinase as markers. ROS 17/2.8 cells were used as models of osteoblast-like cells to study the reciprocal modulation of stimulation of bone cell proliferation by sequential treatment by sex steroid and calciotrophic hormones. Pretreatment with 1,25(OH) 2D 3 and PTH augmented stimulation by E 2, while pretreatment with PGE 2 followed by E 2 resulted in no additional stimulation. Reciprocally, pretreatment with E 2 significantly reduced the response to PGE 2 while showing an insignificant effect on the response to the other hormones. Gonadectomized Wistar-derived rats provided a useful model system for study of post-menopausal osteoporosis. In diaphyseal bone, [ 3H]thymidine incorporation and creatine kinase activity decreased 4 weeks after gonadectomy. At that time, a single i.p. injection of E 2 females, and testosterone in males, resulted in a highly significant increase in both these parameters within 24 h.
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