Abstract
More than a decade ago, receptor activator of nuclear factor-κB ligand (RANKL) was identified as the key molecule mediating osteoclast development, activity, and survival.1 Since osteoporosis results, in part, from increased osteoclastic bone resorption, the inhibition of RANKL activity has been an obvious therapeutic target. In this issue of the Journal, two articles2,3 report pivotal studies that reflect more than 10 years of drug development and that establish the efficacy of a human monoclonal antibody to RANKL, denosumab, in reducing fractures. Cummings et al.2 enrolled 7868 postmenopausal women with osteoporosis and randomly assigned them to receive either 60 . . .
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