作者: Robert S. Weinstein , Robert L. Jilka , A. Michael Parfitt , Stavros C. Manolagas
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摘要: Both estrogens and androgens act on bone marrow stromal/osteoblastic cells to inhibit the production of local factors that promote osteoclast development. Based this evidence loss sex steroids up-regulates not only osteoclastogenesis but also osteoblastogenesis, we have hypothesized osteoblastic lineage are mediators adverse effects steroid deficiency bone. To test hypothesis, used senescence-accelerated mouse (SAMP6), a model defective osteoblast development, examined orchidectomy static dynamic histological features remodeling mineral density. After in SAMP6 mice, expected increases precursors, cancellous osteoclasts osteoblasts, frequency events, trabecular spacing, rate formation were absent or greatly attenuated. Moreover, whereas density decreased orchidectomized controls, it did change SAMP6. Our data indicate when development is defective, fails result loss. This suggests essential changes mass ensue following androgens.