transiently enhance bone mass (Lee et al., 1996; Matkovic et al., 2005). These effects disappear during or after cessation of increased calcium intake; final bone mass, measured in randomized trials of calcium supplementation during this period, did not differ between controls and calcium-supplemented individuals (Matkovic et al., 2005). However, this period of bone accretion determines adult bone mass, which, in turn, is a significant predictor of fracture risk late in life.
After puberty and throughout most of adulthood, bone formation and resorption are balanced. During this period, bone mass is consolidated, and calcium requirements are relatively stable. Peak bone mass, the maximum amount of bone that can be accumulated, is reached in early adulthood (Bonjour et al., 1994). The ability to attain peak bone mass is affected by genetic background and by lifestyle factors such as physical activity and total calcium intake. Specific skeletal sites have been found to reach peak bone mass at different ages, and bone mineral accretion has been reported to continue slowly into the third decade of life (Recker et al., 1992). Bone is a dynamic tissue, and a number of clinical studies suggest that increasing bone mass early in life has a transient effect, but does not confer protection against later bone loss and osteoporosis (Gafni and Baron, 2007). The calcium content of bone at maturity is approximately 1,200 g in women and 1,400 g in men (Ilich and Kerstetter, 2000; Anderson, 2001). In men, this level remains relatively constant until the onset of age-related bone loss later in life. In women, the level remains relatively constant until the onset of menopause. Although bone mass generally remains at a plateau during reproductive years, some studies have suggested that mean bone mass gradually reaches a plateau and then declines slowly with age.
Age-related bone loss, in both men and women, results when bone remodeling becomes uncoupled and bone resorption exceeds bone formation. However, the pathogenesis of bone loss is a multi-faceted process. The roles and interactions of various hormonal, genetic, and other factors in bone loss and risk for decreased bone health are not yet clear. Moreover, the ability of increased calcium intake to overcome the effects of bone loss related to menopause or normal aging continues to be debated.
In postmenopausal women, estrogen loss increases the rate of bone remodeling, characterized by an imbalance between osteoclast and osteoblast activity, resulting in irreversible bone loss (Riggs et al., 1998; Seeman, 2003). Estrogen loss can further accelerate bone loss through its effect on