β-Adrenergic Blockers Reduce the Risk of Fracture Partly by Increasing Bone Mineral Density: Geelong Osteoporosis Study

Pasco, Julie A.; Henry, Margaret J.; Sanders, Kerrie M.; Kotowicz, Mark A.; Seeman, Ego; Nicholson, Geoffrey C.

doi:10.1359/jbmr.0301214

Cited by 243 publications

(147 citation statements)

References 39 publications

(57 reference statements)

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“…Although favorable associations between b-blocker use and bone mineral density or fracture risk were reported in the majority of the human studies [5,27,30,32], some studies found no effect or unfavorable associations [28,29]. It is possible that badrenergic receptor antagonists exert biphasic effects, favorable and deleterious, on the skeletal system not only in rats, but also in humans, depending on the dose or individual susceptibility.…”

Section: Discussionmentioning

confidence: 99%

Effects of propranolol on the development of glucocorticoid-induced osteoporosis in male rats

Folwarczna

Pytlik

Śliwiński

et al. 2011

Pharmacological Reports

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Abstract:Glucocorticoid-induced osteoporosis is the most frequently occurring type of secondary osteoporosis. Antagonists of b-adrenergic receptors are now considered to be potential drugs under investigation for osteoporosis. The aim of the present study was to investigate the effects of propranolol, a nonselective b-receptor antagonist, on the skeletal system of mature male rats and on the development of bone changes induced by glucocorticoid (prednisolone) administration. The experiments were performed on 24-week-old male Wistar rats. The effects of prednisolone 21-hemisuccinate sodium salt (7 mg/kg, sc daily) or/and propranolol hydrochloride (10 mg/kg, ip daily) administered for 4 weeks on the skeletal system were studied. Bone and bone mineral mass in the tibia, femur and L-4 vertebra, length and diameter of the long bones, mechanical properties of tibial metaphysis, femoral diaphysis and femoral neck, bone histomorphometric parameters and turnover markers in serum were determined. Prednisolone-induced unfavorable skeletal changes led to disorders in bone mechanical properties. Propranolol not only did not improve bone parameters, but even caused deleterious effects on the skeletal system. Concurrent administration of propranolol with prednisolone did not counteract the changes induced by prednisolone. The results of this study may help to understand the equivocal results of human studies on the effects of b-blockers on the skeletal system. It is possible that the drugs exert biphasic effects on the skeletal system, both favorable and deleterious, depending on the dose or individual susceptibility.

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Section: Discussionmentioning

confidence: 99%

Effects of propranolol on the development of glucocorticoid-induced osteoporosis in male rats

Folwarczna

Pytlik

Śliwiński

et al. 2011

Pharmacological Reports

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“…Administration of β-blockers inhibits bone resorption, stimulates bone formation, and increases trabecular bone volume. A significant decline in the incidence of hip fractures in patients treated with β-blockers has also been reported [24,25]. Bone homeostasis is also modulated by the hypothalamus through the HPA axis.…”

Section: Bone Homeostasis Regulated By the Central Nervous Systemmentioning

confidence: 96%

Chronic Psychological Stress as a Risk Factor of Osteoporosis

Chen

Adachi

Hayashi

et al. 2015

J UOEH

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: Osteoporosis, the most common metabolic skeletal disease, is characterized by decreased bone mass and deteriorated bone quality, leading to increased fracture risk. With the aging of the population, osteoporotic fracture is an important public health issue. Organisms are constantly exposed to various stressful stimuli that affect physiological processes. Recent studies showed that chronic psychological stress is a risk factor for osteoporosis by various signaling pathways. The purpose of this article is to review the recent progress of the association between chronic psychological stress and osteoporosis. Increasing evidence confirms the physiological importance of the central nervous system, especially the hypothalamus, in the regulation of bone metabolism. Both animal and human studies indicate that chronic psychological stress induces a decrease of bone mass and deterioration of bone quality by influencing the hypothalamic-pituitary-adrenocortical (HPA) axis, sympathetic nervous system, and other endocrine, immune factors. Active mastication, proven to be an effective stress-coping behavior, can attenuate stress-induced neuroendocrine responses and ameliorate stress-induced bone loss. Therefore, active mastication may represent a useful approach in preventing and/or treating chronic stress-associated osteoporosis. We also discuss several potential mechanisms involved in the interaction between chronic stress, mastication and osteoporosis. Chronic stress activates the HPA axis and sympathetic nervous system, suppresses the secretion of gonadal hormone and growth hormone, and increases inflammatory cytokines, eventually leading to bone loss by inhibiting bone formation and stimulating bone resorption.

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“…On the other hand, the positive effects of beta blockers are not always detectable. In humans, a series of studies showed that beta blockers promote positive, (17)(18)(19)(20) negative, (21) or no effects (22)(23)(24) on bone mass.…”

Section: Introductionmentioning

confidence: 99%

Double disruption of α2A- and α2C -adrenoceptors results in sympathetic hyperactivity and high-bone-mass phenotype

Fonseca

Jorgetti

Costa

et al. 2010

Journal of Bone and Mineral Research

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Evidence demonstrates that sympathetic nervous system (SNS) activation causes osteopenia via b 2 -adrenoceptor (b2-AR) signaling. Here we show that female mice with chronic sympathetic hyperactivity owing to double knockout of adrenoceptors that negatively regulate norepinephrine release, a 2A -AR and a 2C -AR (a 2A /a 2C -ARKO), present an unexpected and generalized phenotype of high bone mass with decreased bone resorption and increased formation. In a 2A /a 2C -ARKO versus wild-type (WT) mice, micro-computed tomographic (mCT) analysis showed increased, better connected, and more plate-shaped trabeculae in the femur and vertebra and increased cortical thickness in the vertebra, whereas biomechanical analysis showed increased tibial and femoral strength. Tibial mRNA expression of tartrate-resistant acid phosphatase (TRACP) and receptor activator of NF-kB (RANK), which are osteoclast-related factors, was lower in knockout (KO) mice. Plasma leptin and brain mRNA levels of cocaine amphetamine-regulated transcript (CART), which are factors that centrally affect bone turnover, and serum levels of estradiol were similar between mice strains. Tibial b 2 -AR mRNA expression also was similar in KO and WT littermates, whereas a 2A -, a 2B -and a 2C -AR mRNAs were detected in the tibia of WT mice and in osteoblast-like MC3T3-E1 cells. By immunohistochemistry, we detected a 2A -, a 2B -, a 2C -and b 2 -ARs in osteoblasts, osteoclasts, and chondrocytes of 18.5-day-old mouse fetuses and 35-day-old mice. Finally, we showed that isolated osteoclasts in culture are responsive to the selective a 2 -AR agonist clonidine and to the nonspecific a-AR antagonist phentolamine. These findings suggest that b 2 -AR is not the single adrenoceptor involved in bone turnover regulation and show that a 2 -AR signaling also may mediate the SNS actions in the skeleton. ß

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β-Adrenergic Blockers Reduce the Risk of Fracture Partly by Increasing Bone Mineral Density: Geelong Osteoporosis Study

Cited by 243 publications

References 39 publications

Effects of propranolol on the development of glucocorticoid-induced osteoporosis in male rats

Effects of propranolol on the development of glucocorticoid-induced osteoporosis in male rats

Chronic Psychological Stress as a Risk Factor of Osteoporosis

Double disruption of α2A- and α2C -adrenoceptors results in sympathetic hyperactivity and high-bone-mass phenotype

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