The Effects of Androgen Deficiency on Murine Bone Remodeling and Bone Mineral Density Are Mediated via Cells of the Osteoblastic Lineage

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Abstract
Both estrogens and androgens act on bone marrow stromal/osteo- blastic cells to inhibit the production of local factors that promote osteoclast development. Based on this and the evidence that loss of sex steroids up-regulates not only osteoclastogenesis but also osteoblas- togenesis, we have hypothesized that cells of the osteoblastic lineage are the mediators of the adverse effects of sex steroid deficiency on bone. To test this hypothesis, we used the senescence-accelerated mouse (SAMP6), a model of defective osteoblast development, and examined the effects of orchidectomy on static and dynamic histo- logical features of bone remodeling and on bone mineral density. After orchidectomy in SAMP6 mice, the expected increases in osteoblast precursors, cancellous osteoclasts and osteoblasts, frequency of re- modeling events, trabecular spacing, and rate of bone formation were absent or greatly attenuated. Moreover, whereas bone mineral den- sity decreased in orchidectomized controls, it did not change in SAMP6. Our data indicate that when osteoblast development is de- fective, orchidectomy fails to result in bone loss. This evidence sug- gests that cells of the osteoblastic lineage are essential mediators of the changes in the rate of bone remodeling and loss of bone mass that ensue following loss of androgens. (Endocrinology 138: 4013- 4021, 1997)

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