Osteoporosis

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OSTEOPOROSIS

Osteoporosis

Osteoporosis

Objective

Osteoporosis is a major public health issue. It is an age related disease that affects an estimated 10 millionAmericans.1 Another 34 million Americans are at risk for osteoporosis because of a low bone mass.1 By the year 2050, the number of Americans older than 65 years is expected to double, reaching 69 million.2 Therefore, the impact of osteoporosis is expected to increase dramatically in the United States in the coming decades. Eighty percent of patients with osteoporosis are women.1 the risk for osteoporosis increases after menopause, with 1 in 5 white postmenopausal women affected.3 Whites are the racial group for which the most data on osteoporosis are available, but other racial and ethnic groups also are at risk.[1]

Introduction

Osteoporosis currently is defined as a skeletal disorder characterized by compromised bone strength, predisposing to fractures.2Bone strength reflects both bone density and bone quality. Bone density usually is assessed by noninvasive means using various measures of bone mineral density (BMD, i.e., the grams of mineral per area or volume). Bone quality reflects bone architecture (strength, connectivity), turnover (i.e., replacement), accumulated damage (e.g., micro fractures), and mineralization.2 Bone quality usually is not assessed in clinical practice because it currently involves a bone biopsy, which is an invasive method. The incidence of fractures is an indirect measure of bone quality. The U.S. Food and Drug Administration (FDA) now requires data demonstrating a favorable impact on fracture incidence for approval of drugs to prevent or treat osteoporosis, although an impact on BMD sufficed for drug approval years ago.

Bone undergoes a continuous remodeling process (i.e., replacement)involving resumption of old bone by osteoclasts and formation of new bone by osteoblasts.3 The activity of osteoclastsand osteoblasts ordinarily is balanced and regulated by physical factors and hormonal influences. Osteoporosis is characterized ban imbalance between orthoclase and osteopath activity and a rate of bone resumption that exceeds the rate of bone formation, resulting in bone loss and skeletal fragility.

Discussion

Postmenopausal osteoporosis is the result of estrogen deficiency, which results in up-regulation of several cytokines and excessive bone resumption. Various bone mineral density (BMD) testing methods are available, but the World Health Organization based the diagnosis of postmenopausal osteoporosis on the presence of a BMD T-score that is 2.5 standard deviations or greater below the mean for young women as assessed by dual-energy X-ray absorptiometry (DXA) at the hip, spine, and midbrains. Ensuring adequate calcium and vitamin D intake is the cornerstone of any regimen aimed at preventing or treating postmenopausal osteoporosis. Other no pharmacologic measures address modifiable risk factors for the disease and include exercise, smoking cessation, reducing consumption of caffeine and alcohol, and avoiding medications known to decrease bone mass. Postmenopausal osteoporosis is the result of estrogen deficiency and excessive bone resumption. Ensuring intake combined with lifestyle changes to address modifiable risk factors for the disease may help in the prevention and treatment of this condition[2].

Osteoporosis may be primary or secondary to an identifiable cause (i.e., a drug, disease, or condition). Most cases of osteoporosis are primary, especially in ...
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