Osteoporosis is a disease of the skeleton marked by low bone mass and microarchitectural degeneration of bone tissue, with a subsequent increase in fracture risk.1,2 In the United States, 10 million people are estimated to have osteoporosis and almost 34 million more are believed to have osteopenia (low bone mass), placing them at risk of developing osteoporosis.3 Studies suggest that over 2 million osteoporosis-related fractures occur in the United States annually, with an estimated cost of $17 billion.4,5 Some speculate that the prevalence of these bone metabolism disorders may be on the rise, in part, due to a decrease in the overall routine utilization of hormone replacement therapy (HRT) for most postmenopausal women. In 2002, the Women's Health Initiative (WHI) was published suggesting that the risks of long-term estrogen plus progestin supplementation outweighed any benefits (namely, the FDA-approved prevention of osteoporosis).5 Also, while osteoporosis is less prevalent in men than women, men account for almost 30% of low bone mass related (fragility) fractures.4
The human adult skeleton is essentially comprised of two types of bone: cortical (80%) and trabecular (20%). Cortical bone forms the exterior portion, while trabecular bone forms the porous interior, as well as at the ends of long bones, vertebrae and distal forearms. Throughout life, bone undergoes remodeling, a process where old, damaged bone is routinely removed and replaced by new bone.6 The resorption (removal) phase is conducted by osteoclasts utilizing proteolytic enzymes to dissolve a targeted area. This is closely followed by the formation (replacement) phase, as osteoblasts utilize calcium and phosphorous, among other ions, to lay down newly formed bone tissue. This process normally tends to favor bone formation over resorption until the age of 30 years, when bone reaches its peak mass and formation and resorption become balanced.7 Osteopenia, and ultimately osteoporosis, is the result of an uncoupling of this balance in favor of osteoclast-driven resorption.6,8,9 Modalities of prevention and treatment of osteoporosis typically target osteoblastic or osteoclastic function, either directly or indirectly.
Osteoporosis is routinely asymptomatic. In some cases, osteoporosis may present as shortened stature (kyphosis, or humpbacked; lordosis, or bent backward), bone pain or most frequently as a fracture of the vertebra, hip, or forearm.5 Therefore, it is critical to provide screening to those patients at risk (Table 46-1).8,9 The diagnosis of osteoporosis is characteristically made by evaluating bone mineral density (BMD) via dual energy x-ray absorptiometry (DXA). A BMD is recorded as a T-score, which is the difference between a patient's bone mineral density (g/cm2) and the expected BMD of a sex-matched young healthy adult.1 The World Health Organization (WHO) uses specific T-score ranges to assist in the diagnosis of osteopenia and osteoporosis (Table 46-2).1
TABLE 46-1 Common Risk Factors for Osteoporosis