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Prevention of osteoporosis

E Michael Lewiecki, MD
Section Editors
Clifford J Rosen, MD
Kenneth E Schmader, MD
Deputy Editor
Jean E Mulder, MD


Osteoporosis is a common disease that is characterized by low bone mass, microarchitectural disruption, and skeletal fragility, resulting in an increased risk of fragility fracture. Osteoporosis affects more than 75 million people in the United States, Europe, and Japan [1]. In the year 2000, there were approximately 9 million osteoporotic fractures worldwide [2].

Prevention of low bone mass and fractures using nonpharmacologic and pharmacologic therapies will be discussed here. The prevention of glucocorticoid-induced osteoporosis and the treatment of established osteoporosis are reviewed separately. (See "Prevention and treatment of glucocorticoid-induced osteoporosis" and "Overview of the management of osteoporosis in postmenopausal women" and "Treatment of osteoporosis in men".)


A clinical diagnosis of osteoporosis may be made in the presence of a fragility fracture, particularly at the spine, hip, wrist, humerus, rib, and pelvis, without measurement of bone mineral density (BMD). Fragility fractures are those occurring from a fall from a standing height or less, without major trauma such as a motor vehicle accident. Certain skeletal locations, including the skull, cervical spine, hands, and feet, are not associated with fragility fractures. Stress fractures are also not considered fragility fractures, as they are due to repetitive injury. (See "Overview of stress fractures".)

In the absence of a fragility fracture, BMD assessment by dual-energy x-ray absorptiometry (DXA) is the gold standard to diagnose osteoporosis, according to the classification of World Health Organization (WHO) [3]. BMD that is 2.5 standard deviations (SD) or more below the mean BMD of a young-adult reference population, which is a T-score of -2.5 or less, qualifies for a diagnosis of osteoporosis, provided that other causes of low BMD have been ruled out. Low bone mass (osteopenia) is defined as a T-score between -1.0 to -2.5. Individuals with T-scores of ≤-2.5 have the highest risk of fracture. However, there are more fractures in patients with a T-score between -1.0 and -2.5 because there are so many more patients in this category [4]. (See "Clinical manifestations, diagnosis, and evaluation of osteoporosis in postmenopausal women" and "Clinical manifestations, diagnosis, and evaluation of osteoporosis in men" and "Osteoporotic fracture risk assessment", section on 'Assessment of fracture risk'.)


Bone strength reflects the integration of bone mineral density (BMD) and other properties of bone that are collectively called "bone quality" [5]. BMD in adults is determined by peak bone mass and the subsequent rate of bone loss. As BMD measured by dual-energy x-ray absorptiometry (DXA) decreases, fracture risk increases as a continuum, with no "fracture threshold." In one analysis, for every one standard deviation (SD) decrease in BMD at the hip, there was a 2.6-fold increase in the risk of hip fracture [6]. Thus, the prevention of low bone mass is directed to maximizing peak bone mass and minimizing the rate of bone loss, with the ultimate goals of maintaining bone strength and preventing fractures. Since most fractures occur with some impact on the bone, preventing falls is another important aspect of preventing fractures, especially in frail patients. (See "Falls: Prevention in community-dwelling older persons".)

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Literature review current through: Nov 2017. | This topic last updated: Mar 26, 2017.
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