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Am Fam Physician. 2006;74(7):1202-1203

Osteoporosis is characterized by low bone mass and increased bone fragility. The disease causes an estimated 1.5 million fractures in the United States each year, usually in the vertebrae, hip, and wrist. Osteoporosis commonly is undiagnosed until a fracture occurs. Primary and secondary prevention of osteoporosis has the potential to significantly reduce fracture-related morbidity and mortality in at-risk patients. Mauck and Clarke reviewed current diagnostic, screening, prevention, and treatment recommendations for osteoporosis.

A fracture caused by a fall from a standing height or lower is called a low-impact fracture, and a spontaneous or atraumatic fracture is called a fragility fracture. The occurrence of either fracture type is diagnostic for osteoporosis. Osteoporosis also is present if the lumbar spine or hip bone mineral density (BMD) is 2.5 standard deviations or more below the young adult reference mean. Measuring BMD with central dual-energy x-ray absorptiometry (DEXA) is recommended.

Tobacco use, low body weight, previous oral corticosteroid use, premature menopause, and a history in a first-degree relative are known to increase the risk of osteoporosis. Major organizations disagree about the relative importance of these risk factors, who should be screened, and how often screening should occur. The National Osteoporosis Foundation, U.S. Preventive Services Task Force, and Institute for Clinical Systems Improvement recommend routinely screening women who are 65 years or older. However, these guidelines should not replace clinical judgment. There is no evidence to support routinely testing postmenopausal women for secondary causes of osteoporosis. Experts advocate such testing for men and perimenopausal women with osteoporosis because secondary causes (see accompanying table) are present in 30 to 60 percent of these patients.

Glucocorticoid use
Perimenopausal women
Low estrogen levels
Glucocorticoid use
Anticonvulsant therapy

In general, nonpharmacologic interventions should not be used as stand-alone therapy for patients with osteoporosis. Calcium and vitamin D supplementation and weight-bearing exercise produce modest increases in BMD but have little or no effect on fracture risk. In randomized trials involving older patients, a comprehensive risk factor assessment and interventions (e.g., physical therapy, environmental modification) reduced the risk of falls.

Medications for osteoporosis include bisphosphonates, raloxifene (Evista), calcitonin (Miacalcin), estrogen, and teriparatide (Forteo). There is strong evidence from clinical trials that oral bisphosphonates (i.e., alendronate [Fosamax], risedronate [Actonel], and ibandronate [Boniva]) reduce the risk of vertebral and hip fractures, making them the mainstays of therapy. Although raloxifene and estrogen (used alone or in combination with progesterone) also prevent fractures, they increase the risk of venous thromboembolism. Calcitonin may reduce pain associated with vertebral fractures, but it is less effective than bisphosphonates. Teriparatide, a recombinant parathyroid hormone analogue that is administered subcutaneously, has multiple adverse effects including hypercalcemia, and its use has been limited to patients at high risk of fractures.

The authors conclude that there is a lack of evidence to guide follow-up BMD testing for patients receiving treatment for osteoporosis. Because of variations in mechanical precision and technician expertise, a follow-up measurement on a different DEXA machine or at an interval of less than two years may falsely indicate treatment failure. Therefore, repeating the DEXA every two to five years is recommended for most patients. Although multiple biochemical markers of bone turnover can indicate a response to therapy after as little as three months, none are currently accurate or reliable enough to be recommended for use in clinical practice.

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Copyright © 2006 by the American Academy of Family Physicians.

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