Relation of androgens to bone tissue in healthy men

Bone density is determined both by peak bone mass achieved during skeletal development and the subsequent amount of maintenance and resorption of bone tissue. Androgens affect both processes and thus are a pivotal determinant of bone mass in men. Trabecular and cortical bone density increase dramatically during puberty, both in girls and boys (Krabbe et al. 1984), but peak cortical bone density is about 25% higher in healthy men compared to women, an observation which has been linked to higher testosterone levels present in males (Riggs et al. 2002). Bone density is maintained at a relatively stable level in younger men, then starts to decline slowly at the age of 30 to 35 years in healthy men (Fig. 7.2, Scopacasa etal. 2002; Zitzmann etal. 2002). The age-related bone loss is putatively associated with declining testosterone levels, a process partly leading to late-onset hypogonadism, but is not uniformly present. Thus, reports on sex steroid levels within the normal

Age (years)

Fig. 7.2 Model of bone density in relation to age and testosterone levels. Data from 156 newly diagnosed untreated hypogonadal men (62 men with primary and 94 men with secondary hypogonadism) and 224 healthy controls aged 18 to 91 years. Bone density was assessed by phalangeal ultrasound. The surface was created according to non-linear regression models (third-degree association of age to bone density and logarithmic association of testosterone levels to bone density). The hypogonadal range is indicated in dark grey.

Age (years)

Fig. 7.2 Model of bone density in relation to age and testosterone levels. Data from 156 newly diagnosed untreated hypogonadal men (62 men with primary and 94 men with secondary hypogonadism) and 224 healthy controls aged 18 to 91 years. Bone density was assessed by phalangeal ultrasound. The surface was created according to non-linear regression models (third-degree association of age to bone density and logarithmic association of testosterone levels to bone density). The hypogonadal range is indicated in dark grey.

range and bone density vary concerning the importance of estradiol or testosterone concentrations within the normal range. Nevertheless, significant contributions of both sex steroids to bone density of older men have been frequently reported (Cetin etal. 2001; Greendale et al. 1997; Khosla etal. 2001; Rudman etal. 1994; van den Beld et al. 2000; van Pottelbergh et al. 2003). It can be assumed that age-related processes which are at best indirectly related to testosterone levels (e.g. inactivity, reduced muscle mass, increasing PTH concentrations) (Riggs et al. 2002) as well as androgen concentrations themselves exert influence on bone density (Zitzmann et al. 2002). While the latter gain importance when the threshold between eu-and hypogonadism is considered, differences in androgenic influence are much less overt when fluctuations within the normal range are investigated (Fig. 7.2). Variations of bone density in eugonadal men in relation to androgenic activity are, within an environment of more or less saturated androgen receptors, rather influenced by the CAG repeat polymorphism of the androgen receptor gene than by testosterone levels themselves. Men with longer CAG repeats, which are associated with decreased androgen effects, exhibit lower bone mass and also a more rapid age-related decline of bone density than healthy men with shorter repeats (Zitzmann etal. 2001, also see Chapter 3).

While studies on bone density in eugonadal men are of some value in elucidating the relationship between androgens and bone tissue, they have no clinical consequence, quite in contrast to observations in hypogonadal men and the effects of androgen treatments on bone density in such patients, which will be discussed below.

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