Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 Testosterone: an overview of biosynthesis, transport, metabolism and non-genomic actions
- 2 The androgen receptor: molecular biology
- 3 Androgen receptor: pathophysiology
- 4 Behavioural correlates of testosterone
- 5 The role of testosterone in spermatogenesis
- 6 Androgens and hair: a biological paradox
- 7 Androgens and bone metabolism
- 8 Testosterone effects on the skeletal muscle
- 9 Androgens and erythropoiesis
- 10 Testosterone and cardiovascular diseases
- 11 Testosterone and erection
- 12 Testosterone and the prostate
- 13 Clinical uses of testosterone in hypogonadism and other conditions
- 14 Pharmacology of testosterone preparations
- 15 Androgen therapy in non-gonadal disease
- 16 Androgens in male senescence
- 17 The pathobiology of androgens in women
- 18 Clinical use of 5α-reductase inhibitors
- 19 Dehydroepiandrosterone (DHEA) and androstenedione
- 20 Selective androgen receptor modulators (SARMs)
- 21 Methodology for measuring testosterone, DHT and SHBG in a clinical setting
- 22 Synthesis and pharmacological profiling of new orally active steroidal androgens
- 23 Hormonal male contraception: the essential role of testosterone
- 24 Abuse of androgens and detection of illegal use
- Subject Index
7 - Androgens and bone metabolism
Published online by Cambridge University Press: 18 January 2010
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 Testosterone: an overview of biosynthesis, transport, metabolism and non-genomic actions
- 2 The androgen receptor: molecular biology
- 3 Androgen receptor: pathophysiology
- 4 Behavioural correlates of testosterone
- 5 The role of testosterone in spermatogenesis
- 6 Androgens and hair: a biological paradox
- 7 Androgens and bone metabolism
- 8 Testosterone effects on the skeletal muscle
- 9 Androgens and erythropoiesis
- 10 Testosterone and cardiovascular diseases
- 11 Testosterone and erection
- 12 Testosterone and the prostate
- 13 Clinical uses of testosterone in hypogonadism and other conditions
- 14 Pharmacology of testosterone preparations
- 15 Androgen therapy in non-gonadal disease
- 16 Androgens in male senescence
- 17 The pathobiology of androgens in women
- 18 Clinical use of 5α-reductase inhibitors
- 19 Dehydroepiandrosterone (DHEA) and androstenedione
- 20 Selective androgen receptor modulators (SARMs)
- 21 Methodology for measuring testosterone, DHT and SHBG in a clinical setting
- 22 Synthesis and pharmacological profiling of new orally active steroidal androgens
- 23 Hormonal male contraception: the essential role of testosterone
- 24 Abuse of androgens and detection of illegal use
- Subject Index
Summary
Introduction
Osteoporosis and fractures represent a major public health problem, not only in women but also in men. It has been estimated that at the age of 50 years, men have a risk of approximately 12–15% of suffering an osteoporotic fracture in later life, most commonly of the vertebra, hip or forearm (Melton and Chrischilles 1992; Nguyen et al. 1996). At the age of 60 years, the risk for a non-traumatic fracture rises to 25% (Nguyen et al. 1996). In the United States, about 150,000 hip fractures occur in men each year (Poor et al. 1995). Because of their higher peak bone mass, men present with hip, vertebral body, or forearm fractures about 10 years later than women. Hip fractures in men result in a 30% mortality rate at one year after fracture versus a rate of 17% in women (Campion and Maricic 2003). Hypogonadism, i.e. androgen deficiency, has been identified as an independent risk factor for suchincidences (Jackson et al. 1992). The role of androgens in bone metabolism and the effects of androgen therapy on bone tissue in hypogonadal men will be examined in this chapter.
Mechanisms of androgen action in bone tissue
In vitro studies
Growth and resorption of bone tissue are mediated by osteoblasts and osteoclasts, respectively. Both types of cells exert mutual influence on each other and equilibrium between the activity of both cell lines maintains net bone mass during constant renewal and turnover, while decreased osteoblast activity as well as enhanced osteoclast activity will result in loss of bone mass.
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- Chapter
- Information
- TestosteroneAction, Deficiency, Substitution, pp. 233 - 254Publisher: Cambridge University PressPrint publication year: 2004
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