Dr Black served as a consultant and received grants from Merck & Co., NIAMS, NPS Pharmaceuticals, and Novartis. All other authors have no conflict of interest.
β-Blocker Use, BMD, and Fractures in the Study of Osteoporotic Fractures
Version of Record online: 6 DEC 2004
Copyright © 2005 ASBMR
Journal of Bone and Mineral Research
Volume 20, Issue 4, pages 613–618, April 2005
How to Cite
Reid, I. R., Gamble, G. D., Grey, A. B., Black, D. M., Ensrud, K. E., Browner, W. S. and Bauer, D. C. (2005), β-Blocker Use, BMD, and Fractures in the Study of Osteoporotic Fractures. J Bone Miner Res, 20: 613–618. doi: 10.1359/JBMR.041202
- Issue online: 4 DEC 2009
- Version of Record online: 6 DEC 2004
- Manuscript Accepted: 22 OCT 2004
- Manuscript Revised: 7 JUL 2004
- Manuscript Received: 29 APR 2004
- central nervous system;
A role for osteoblastic β-adrenoreceptors in bone regulation is suggested by the finding that β-blockers increase bone mass in mice. We studied the association of β-blocker use with BMD and fractures in the Study of Osteoporotic Fractures. β-blocker use and BMD are unrelated in this cohort, and associations with fracture risk are inconsistent.
Introduction: The central nervous system has been shown to regulate bone mass in mice, possibly by way of the β2-adrenoreceptors on osteoblasts. β-blockers have been shown to increase bone mass in mice. Because these agents are widely used therapeutically, it is possible that they may influence fracture epidemiology in humans, and they are a potential therapy for osteoporosis.
Materials and Methods: We have studied the association of β-blocker use with BMD and fracture rates in the Study of Osteoporotic Fractures. β-blocker use was recorded at the fourth visit, in 8412 women, of whom 1099 were users, and these women were followed for 7 years.
Results: Users had significantly higher weight, more thiazide use, more estrogen use, less glucocorticoid use, more statin use, and more hypertension than nonusers, and they smoked less. Total hip BMD at the fourth visit was higher in the β-blocker users (0.746 versus 0.735 g/cm2, p = 0.02), but adjustment for weight alone, or together with these other variables, eliminated this difference (p = 0.62). There was no effect of β-blocker use on loss of hip BMD over a mean follow-up of 4 years (p = 0.48). Os calcis BMD at visit 4 was also higher in those taking β-blockers (0.385 versus 0.375 g/cm2, p = 0.005), but weight adjustment eliminated this difference (p = 0.14). The frequencies of hip or any fracture (since age 50) were similar in users and nonusers (p = 0.80 and p = 0.51, respectively). Over a mean follow-up of 7 years, there were 2167 total fractures, including 431 at the wrist and 585 at the hip. Among β-blocker users, hazards ratios were 0.92 (0.81, 1.05) for any fracture, 0.74 (0.54, 1.01) for wrist fracture, and 0.76 (0.58, 0.99) for hip fracture. Adjustment for weight and other factors previously shown to influence hip fracture incidence in this cohort made little difference to the outcome. When fracture data were analyzed for nonselective and β1-selective agents separately, trends toward fewer fractures were confined to the users of selective β1-blockers.
Conclusions: β-blocker use and BMD are unrelated in this cohort, and associations with fracture risk are inconsistent. Therefore, a history of use of these drugs is not useful in assessing fracture risk, nor do they have a role in osteoporosis management at this time. The relationship between β-blocker use and hip fracture deserves further study.