Mammalian bones respond to gonadal steroids (GS) via intracellular and/or membranal receptors binding. Rat and mice bones in vivo and their derived cell cultures in vitro respond sex-specifically by stimulating the specific activity of creatine kinase (CK). Similar results were obtained in cultured human male or female-derived bone cells (Obs). Female Obs responded only to estradiol-17β (E2), phytoestrogens and the estrogen mimetic anti-idiotypic antibody 1D5 (1D5), whereas male Obs responded only to dihydrotestosterone (DHT) by stimulating CK, 1α, 25 vitamin D hydroxylase mRNA (1OHase) expression and 1,25(OH)2D3 production. Rat epiphyseal cartilage in vivo and in vitro responded to both classes of hormones. The sex-specific response of Obs was modified by manipulating the endocrine environment in early development like gonadectomy, neonatally androgenization of female rats and androgen- receptor deficiency in male rats (Tfm). Rat bone marrow (BM) transplanted under the renal capsule formed bone responding to GS according to the donor gender. Rat demineralized tooth matrix particles (DTM) implanted under the skin induced bone formation responding to GS according to the host gender. Cultured femoral rat BM differentiated into Obs responding to GS according to the donor gender, modified after gonadectomy. Human Obs responded to GS via both genomic (CK) and non-genomic (intracellular Ca++ concentration) binding. Male Obs although not responding to estrogenic compounds, expressed estrogen receptors suggesting involvement of post-receptor mechanism (s). The less-differentiated epiphyseal cartilage cells and the de-differentiated Obs after gonadectomy lost sex-specific responses. In conclusion Obs and bones respond sex-specifically to GS in a yet unknown mechanism.
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