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.