This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Contact me when this article is cited  Related Content  • Similar articles in this journal

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

We were fascinated by the reduction in fracture risk with statin therapy reported by the Geelong Osteoporosis Study (odds ratio, 0.40; adjusted odds ratio, 0.45).¹ These striking results are in concordance with 3 other published observational studies that found fracture risk reductions of similar magnitudes associated with statin exposure.^2-4 However, they are in conflict with the results of a randomized clinical trial that found no association between pravastatin use and fracture risk.⁵ The explanation offered for the difference between these results is heterogeneity of effect on bone morphogenic protein-2 production between statins, and this contention is supported by in vitro data showing that pravastatin does not have the same effect as other statins on this biological marker.⁶ This intriguing hypothesis and its role in the divergence between the observational results and the pravastatin clinical trial results could be supported by presenting a subgroup analysis of effect according to specific statin, . . . [Full Text of this Article]