Abstract

1.1 Osteoporosis and peak bone mass Osteoporosis is a skeletal disease characterized by low bone mass and the deterioration of the micro architecture of bone tissue resulting in bone fragility and susceptibility to fractures (Gordon, 2003). According to the World Health Organization, osteoporosis is estimated to affect approximately 200 million women worldwide (Kanis, 2007) with the burden of osteoporosis being felt both personally and economically. Although the prevalence of fractures is higher is women, the mortality rate related to fragility fractures is higher in men (Center et al. 1999; Hasserius et al., 2003). Moreover, the annual cost of treating fractures in the United States is projected to increase to $25 billion in 2025 from $17 billion in 2005 (Burge et al., 2005). Achieving peak bone mass (PBM) during adolescence and the subsequent rate of bone loss are major determinants of bone mass later in life (Hansen et al., 1991). The amount of bone mass achieved early in life has been shown to predict the level of bone mass and the incidence of fracture later in life suggesting that a primary risk factor for the development of osteoporosis is the inability to attain high PBM (Hansen et al., 1991; Heaney et al., 2000). PBM is generally defined as the highest level of bone mass achieved as a result of normal growth and seems to be established, for most sites of the skeleton, by late adolescence (Matkovic et al., 1994). Previous studies (Bonjour et al., 1991; Bailey et al., 1996) have demonstrated the period between 9-20 years of age to be critical in building peak bone mass as 90% of total body bone mineral content (BMC) is accrued by the age of 16 (Elgan et al., 2003; Stager et al., 2006), with the remaining 5-10% of total body bone mass achieved in the third decade (Cadogan et al, 1998). In fact, the most rapid bone mineral accumulation occurs approximately 1 year after the age of peak linear growth (Bailey et al., 1996); around the time of menarche for females (Cadogan et al., 1998). With considerable increases in bone mass occurring during puberty, maximizing PBM during this time is often advocated as the best way to delay age-related bone loss and prevent osteoporotic fractures (Fulkerson et al., 2004; Molgaard et al., 1999; Valimaki et al., 1994). It appears, therefore, as though there is a critical period, a ‘window of opportunity’ (MacKelvie et al., 2002), in which we can influence the amount of bone mass we attain. However, bone development is the product of complex interactions between genetic and environmental factors including diet, hormonal influences, and mechanical stimuli (Gordon, 2003; Steelman & Zeitler, 2001). Permanent deficits in PBM are the result of any process that

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