supra-physiologic testosterone therapy increases BMD at

the hip while maintaining BMD at the spine in female-to-male transsexuals. The effects of

testosterone may be the result of testosterone hormone directly acting on the bone or indirectly

through aromatization to oestradiol. Lower RANKL levels coupled with unchanged OPG levels

results in an increased OPG/RANKL ratio, which may be beneficial to the bone by inhibiting

osteoclastogenesis. Oestrogen is regarded as the dominant sex steroid hormone in maintaining bone mineral

density (BMD) in males and females. Oestrogen therapy in postmenopausal women prevents

bone loss (Wells et al., 2002), increases BMD (Lindsay & Thome, 1990) and prevents

fractures (Women’s Health Initiative, 2002). Oestradiol rather than testosterone in men

correlates more strongly with BMD (Greendale et al., 1997; Khosla et al., 1998; Amin et al.,

2000; Szulc et al., 2003) and is a stronger determinant of peak bone mass (Khosla et al.,

2001). Men who have either defective aromatase (Bilezikian et al., 1998) or oestrogen

receptor (Smith et al., 1994) develop severe osteoporosis, which further supports the notion

that oestradiol is the more dominant sex steroid in preserving bone density.

Previously, testosterone was considered the more dominant sex steroid in men. With ageing,

men experience declining levels of testosterone (Morley et al., 1997) and decreasing BMD

(Meier et al., 1984; Jones et al., 1994; Fatayerji et al., 1999; Melton et al., 2000).

Testosterone treatment of elderly men with hypogonadism increases BMD (Katznelson et

al., 1996; Behre et al., 1997, 1999; Snyder et al., 1999; Amory et al., 2004). However, a

study of elderly men rendered hypogonadal with GnRH agonists demonstrated that men

receiving oestrogen had significantly lower bone turnover than men receiving testosterone

(Falahati-Nini et al., 2000). Thus, it is unclear whether the beneficial effects of testosterone

on bone physiology are the direct effect of testosterone or an indirect effect by the

aromatization of testosterone to oestradiol, either peripherally or locally by osteoblasts

(Shozu & Simpson, 1998).

In the present study, we evaluated the effect of supra-physiologic testosterone administration

on BMD and markers of bone turnover in female-to-male (FTM) transsexuals. FTM

transsexuals are biologic females who take testosterone in order to change their phenotype to

the male gender (Tangpricha et al., 2003). Our initial hypothesis was that testosterone would

not be sparing of BMD because oestradiol levels would decline secondary to the

antigonadotropic effects of testosterone. We measured BMD at the hip and spine annually

over a period of 2 years in addition to levels of sex hormones and markers of bone turnover.

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Dear Dhia

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The traditional answer to the effects of steroidal hormones on bone growth is that estrogens cause closing of the growth plate (epiphyseal plate) while androgens do not. An open plate allows continued growth of the long bones while a closed plate halts growth.

Thank you for your answer @Ben W Snyder

Thank you for your answer @Tausif Raza

Testosterone is metabolized by the cytochrome P450 aromatase enzyme complex into 17β-estradiol, and increasing evidence indicates that at least part of the effect of androgens on bone is mediated by their aromatization to estrogens.Low testosterone can result in loss of bone density, increasing risk of fracture. The following below links may help you.

Article A concise review of testosterone and bone health

Testosterone possesses strong androgenic and anabolic effects that are important for both women and men, despite that men produce significantly more testosterone than women. For example, bone growth and maintenance are significantly influenced by testosterone.

you can get information from this papaer.