The role of estradiol as testosterone metabolite in bone metabolism

Aromatization of testosterone to estradiol is a pivotal event concerning effects of sex steroids on bone metabolism. Estrogen receptors (ER) have been localized in human osteoblasts (Eriksen etal. 1988; Komm etal. 1988), osteoclasts (Oursler etal. 1991; 1994) and osteocytes (Braidman etal. 2000; Tomkinson etal. 1998). The

ERa- variant is predominant, but also the ERß-type and heterodimers have been described (Kuiper et al. 1996; Petterson et al. 1997). Respective knock-out mouse models (aERKO, ßERKO and double-ERKO) have demonstrated decreased bone-growth, especially for those animals lacking the ERa (Couse etal. 1999; Vidal etal. 2000). Correspondingly, human males with mutations in the ERa or aromatase genes do not achieve normal bone density, despite normal or increased levels of serum testosterone (Bilezikian et al. 1998; Carani et al. 1997; Grumbach 2000; Morishima etal. 1995; Smith etal. 1994). Moreover, as the continual rise in serum estradiol levels during puberty probably causes epiphyseal closure in both sexes, young adult males who are unable to respond to estradiol or who are deficient of this hormone (Grumbach 2000; Smith et al. 1994) have open epiphyses, whereas men with testicular feminization due to mutations of AR achieve epiphyseal closure. Nevertheless, due to the missing intrinsic androgen effects, these patients also exhibit decreased bone density (Bertelloni etal. 1998; Marcus etal. 2000; Zachman et al. 1986). As a consequence, estradiol substitution in aromatase-deficient men can normalize bone density (Bilezikian etal. 1998; Carani etal. 1997; Rochira etal. 2000; 2002).

Moreover, ER polymorphisms that permit normal, but nevertheless significantly graduated effects of estradiol, also cause variations in bone density, both in women and men (Albagha et al. 2001; Becherini et al. 2000; Ho et al. 2000; Langdahl etal. 2000; Patel etal. 2000; Sowers etal. 1999; van Pottelbergh etal. 2003). The menopausal bone loss in women which can be inhibited by estrogen substitution is quite in agreement with these reports (Riggs et al. 2002). In conjunction with observations of estradiol-related effects on bone metabolism (see above), these animal studies and clinical reports provide compelling evidence that estrogens have a major role in bone metabolism.

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