Pathogenesis, prevention, and treatment of osteoporosis

Half of women who develop osteoporosis will sustain some form of osteoporotic fracture. Fracture incidence is directly related to bone density, which is determined by peak adult bone mass and the amount of postmenopausal bone loss. Peak adult bone mass is, to a large extent, genetically determined, but hormonal factors (time since menopause, number of pregnancies, and previous oral contraceptive use) are the prime determinants of bone density after menopause. Time elapsed since menopause, rather than chronological age, determines skeletal composition; oral contraceptive use and parity appear to have a positive effect on the skeleton. Nonhormonal factors such as body weight and some forms of weight-bearing exercise appear to correlate with bone density at certain skeletal sites. Hormone replacement in the early postmenopausal period is the most effective means of preventing osteoporosis and can have a major impact on the incidence of subsequent fracture. Calcitonin may be used as an alternative when hormonal therapy is contraindicated. Established osteoporosis is difficult to treat because bone density has fallen below the fracture threshold and trabecular elements may have been lost. Antiresorptive agents can be used to prevent further bone loss, and stimulation of new bone formation by use of anabolic steroids or fluoride may increase the overall amount of bone.