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J Korean Med Assoc > Volume 49(1); 2006 > Article
Shin: Pharmacological Therapy for Postmenopausal Osteoporosis


Osteoporosis, now defined as a disease characterized by a low bone mass and a microarchitectural deterioration of bone tissue leading to an enhanced bone fragility and fracture risk, is a major public health problem, affecting 200 million individuals worldwide. Optimal treatment and prevention of osteoporosis require modification of risk factors, particularly smoking cessation, adequate physical activity, and attention to diet, in addition to pharmacologic intervention. A number of pharmacologic options are now available to health care providers. The estrogens and raloxifene both prevent bone loss in postmenopausal women, and the estrogens probably also decrease the risk of first fracture. There is a good evidence that raloxifene prevents further fractures in postmenopausal women who already have had fractures and some evidence that estrogen does as well. Bisphosphonate alendronate prevents bone loss and reduces fractures in healthy and osteoporotic postmenopausal women, and in osteoporotic men as well. Risedronate is more potent and has fewer upper gastrointestinal side effects than alendronate, and reduces the incidence of fractures in osteoporotic women. An intermittent use of potent bisphosphonate zoledronate also increases bone mineral density and may become an alternative in the prevention and treatment of osteoporosis. Calcitonin increases bone mineral density in early postmenopausal women and men with idiopathic osteoporosis, and also reduces the risk of new fractures in osteoporotic women. All of the agents discussed above prevent bone resorption, whereas teriparatide increases bone formation and is effective in the treatment of osteoporotic women and men. Bisphosphonates are also effective in the treatment of secondary osteoporosis associated with the use of glucocorticoids to treat inflammation or prevent rejection after transplantation. New avenues for targeting osteoporosis will emerge as our knowledge of the regulatory mechanisms of bone remodelling increases, although issues of tissue specificity may remain to be solved.


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Figure 1
Changes in bone mineral density in the subjects participated in the PROOF study
Figure 2
Changes in bone mineral density in the VERT study
* p < 0.05 vs. placebo
Figure 3
Changes in bone mineral density in the subjects taking alendronate (● 5mg alendronate, ■ 10mg alendronate, ◆ Discontinuation group; alendronate 20mg for 2 years → 5mg 5 years → placebo 5 years)
Figure 4
Cumulative fracture incidence in the subjects participated in the MORE study
Figure 5
Mechanism of action of parathyroid hormone
Figure 6
Reduction of fracture rate in response to parathyroid hormone therapy
Figure 7
Mechanism of action of strontium ranelate


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