The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
β-Blocker Use, BMD, and Fractures in the Study of Osteoporotic Fractures
Open accessAbstract
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.
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“Leptin deficiency or resistance is associated with high BMD in mice despite the fact that gonadal function is diminished (103).”
From Pathogenesis of osteoporosis: concepts, conflicts, and prospects (2005) · cites this paper as [103]
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Leptin Inhibits Bone Formation through a Hypothalamic Relay
Ducy, P., Amling, M., Takeda, S., Priemel, M., Schilling, A. F., Beil, F. T., Shen, J., Vinson, C., Rueger, J. M., & Karsenty, G. (2000) · Cell · doi:10.1016/s0092-8674(00)81558-5 · Cited by 2,077
Leptin Regulates Bone Formation via the Sympathetic Nervous System
Takeda, S., Elefteriou, F., Levasseur, R., Liu, X., Zhao, L., Parker, K. L., Armstrong, D., Ducy, P., & Karsenty, G. (2002) · Cell · doi:10.1016/s0092-8674(02)01049-8 · Cited by 1,735
Cauley, J. A. (2003) · JAMA · doi:10.1001/jama.290.13.1729 · Cited by 1,229
Pasco, J. A., Henry, M. J., Sanders, K. M., Kotowicz, M. A., Seeman, E., & Nicholson, G. C. (2004) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.0301214 · Cited by 260
Effects of neonatal sympathectomy and capsaicin treatment on bone remodeling in rats
Hill, E. L., Turner, R. T., & Elde, R. (1991) · Neuroscience · doi:10.1016/0306-4522(91)90094-5 · Cited by 187
Reid, I. R., Ames, R. W., Orr‐Walker, B., Clearwater, J. M., Horne, A. M., Evans, M. C., Murray, M. A. F., McNeil, A. R., & Gamble, G. D. (2000) · The American Journal of Medicine · doi:10.1016/s0002-9343(00)00510-6 · Cited by 179
Self-citationMoore, R. E. B., Smith, C. K., Bailey, C. S., Voelkel, E. F., & Tashjian, A. H. (1993) · Bone and Mineral · doi:10.1016/s0169-6009(08)80105-5 · Cited by 175
Cherruau, M., Facchinetti, P., Baroukh, B., & Jl, S. (1999) · Bone · doi:10.1016/s8756-3282(99)00211-2 · Cited by 144
Takeuchi, T., Tsuboi, T., Arai, M., & Togari, A. (2001) · Biochemical Pharmacology · doi:10.1016/s0006-2952(00)00591-8 · Cited by 139
Intermittent Use of Nitrates Increases Bone Mineral Density: The Study of Osteoporotic Fractures
Jamal, S. A., Browner, W. S., Bauer, D. C., & Cummings, S. R. (1998) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.1998.13.11.1755 · Cited by 131
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Pathogenesis of osteoporosis: concepts, conflicts, and prospects
Raisz, L. G. (2005) · Journal of Clinical Investigation · doi:10.1172/jci27071 · Cited by 1,779
Relationships between fat and bone
Reid, I. R. (2008) · Osteoporosis International · doi:10.1007/s00198-007-0492-z · Cited by 475
Self-citationReid, I. R. (2010) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2010.06.027 · Cited by 368
Self-citationImpact of the Autonomic Nervous System on the Skeleton
Elefteriou, F. (2018) · Physiological Reviews · doi:10.1152/physrev.00014.2017 · Cited by 248
A paradigm of integrative physiology, the crosstalk between bone and energy metabolisms
Confavreux, C. B., Levine, R. L., & Karsenty, G. (2009) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2009.04.004 · Cited by 246
Metadata
- Authors
- Reid, I. R., Gamble, G. D., Grey, A. B., Black, D. M., Ensrud, K. E., Browner, W. S., & Bauer, D. C.
- Affiliations
- University of Auckland (NZ)
- Department of Medicine, University of Auckland, Auckland, New Zealand
- University of California, San Francisco (US)
- University of Minnesota (US)
- Corresponding author
- Reid, Ian R
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-04-01
- Volume
- 20
- Issue
- 4
- Pages
- 613-618
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- OpenAlex
- W2046327104
- Cited by
- 156
- References
- 19
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 6 · 2018: 7 · 2017: 2 · 2016: 5 · 2015: 9 · 2014: 3 · 2013: 13 · 2012: 14
- FWCI
- 17.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Journal of Bone and Mineral Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service
- Health Research Council of New Zealand
- National Institute on Aging (AG05394, AG-05407)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR035584, AR35583, AR-35584, AR 35582, R01AR035582, R01AR035583)
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Menopause: Health Impacts and Treatments
- Keywords
- beta-blockers, bone mineral density, osteoporotic fractures, hip fracture, wrist fractures, bone mass regulation, Study of Osteoporotic Fractures, women, thiazide diuretics, glucocorticoids, estrogen use, statins, hypertension, osteoporosis treatment, fracture risk factors
- MeSH terms
- Adrenergic beta-Antagonists, Aged, Bone and Bones, Female, Fractures, Spontaneous, Humans, Osteoporosis, Bone Density, Risk Assessment
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