Use of β-Blockers and Risk of Fractures

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Abstract
Studies have suggested that the sympathetic nervous system has a catabolic effect on bones.1-4 In vitro data show that adrenergic agonists stimulate bone resorption in organ culture of mouse calvariae.4 Chemical sympathectomy with guanethidine, a sympathetic neurotoxic agent, impairs bone resorption by inhibiting preosteoclast differentiation and disturbing osteoclast activation in adult rats.1 Additionally, the β-blocker propranolol increased bone formation in ovariectomized female rats.3 These results suggest that β-blockers may overcome loss of bone mass in postmenopausal women.5 Indeed, in a recent observational study including 569 fracture case and 775 control patients, use of β-blockers was associated with a higher bone mineral density at the hip and forearm in women aged 50 years or older, and β-blocker use was associated with a 30% decrease in fracture risk.6
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