Control of Bone Remodeling by the Peripheral Sympathetic Nervous System

Elefteriou, Florent; Campbell, Preston; Ma, Yun

doi:10.1007/s00223-013-9752-4

Cited by 129 publications

(106 citation statements)

References 125 publications

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“…Accordingly, the bone homeostasis regulated by leptin requires the integrity of the hypothalamus, which in turn affects sympathetic activity [18]. Consequently, the sympathetic nervous system represents an important linkage between the brain and bone [18][19][20][21].…”

Section: Bone Homeostasis Regulated By the Central Nervous Systemmentioning

confidence: 99%

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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Section: Bone Homeostasis Regulated By the Central Nervous Systemmentioning

confidence: 99%

Chronic Psychological Stress as a Risk Factor of Osteoporosis

Chen

Adachi

Hayashi

et al. 2015

J UOEH

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“…10 Although early studies suggested that such coordination between osteoclast and osteoblast activity occurred in relative isolation in the basic multicellular unit, it is now clear that several important local accessory cell types influence bone metabolism through their paracrine secretions, 11 and may mediate many of the effects of drugs and cytokines on bone metabolism. These accessory cells include osteocytes, 12 bone marrow stromal cells and osteal macrophages; 13 some less well-delineated influences include those from local endothelial cells, 14 nerve cells 15,16 and cell populations of the bone marrow cavity such as lymphocytes, as discussed below.…”

Section: Multiple Cellular Interactions Regulate Bone Structurementioning

confidence: 99%

Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease

Sims

Quinn

2014

BoneKEy Reports

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Bone remodeling in health and disease is carried out by osteoblasts and osteoclasts, which respectively produce bone matrix and resorb it. Endocrine and paracrine control of these cells can be direct, but they are also exerted indirectly, either by influencing progenitor cell differentiation or by stimulating paracrine signals from local accessory cells including osteocytes (which form a critical communication and regulation network within the bone matrix), macrophages and T lymphocytes. Here we review the osteotropic actions of the interleukin-6 family member cytokine oncostatin M (OSM), which is of particular interest because of its ability to stimulate bone accrual. OSM is produced within the bone microenvironment by cells of both mesenchymal and hematopoietic origin, including osteocytes, osteoblasts, macrophages and T lymphocytes, and can act via two receptor complexes: OSM receptor:gp130 and leukemia inhibitory factor receptor (LIFR):gp130. Although OSM can directly stimulate osteoblast mineralization activity and differentiation, it can also stimulate mesenchymal stem cell osteoblastic commitment at the expense of adipogenesis. In osteocytes, OSM can suppress the production of the bone formation inhibitor sclerostin, an action that is mediated by LIFR:gp130. OSM also stimulates the production of receptor activator of nuclear factor kB ligand by osteoblasts and thereby drives the formation of osteoclasts particularly in pathological conditions. Thus, cellular effects of OSM on bone metabolism include direct and indirect actions mediated by two related receptor/ligand complexes. OSM therefore provides an example of paracrine and endocrine control mechanisms that regulate bone mass by controlling both bone formation and resorption.

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“…These pathways probably significantly regulate fracture healing. Recently, research based on a number of anatomic, pharmacologic, and genetic studies on β2 β-adrenergic receptor (AR) have shown that the sympathetic nervous system (SNS) can link the central nervous system with the skeleton (Castañeda-Corral et al, 2011;Elefteriou et al, 2014). By regulating the SNS and βAR signaling, the SNS can control bone remodeling (Elefteriou et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Analysis of gene expression profiles in healing rat fractures treated with nail and plate fixation

Wang¹,

Li²,

Liu³

2014

Genet. Mol. Res.

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ABSTRACT.To compare fracture healing therapies, the gene expression profiles of rat fracture samples treated with nail and plate fixation were analyzed at 1 day, 3 days, 1 week, 2 weeks, 4 weeks, and 6 weeks after surgery. The gene expression profiles GSE1685, which include 19 samples, were downloaded from the Gene Expression Omnibus database. After preprocessing, the gene expression profiles were subjected to time series analysis using the Short Time-series Expression Miner software, and the significantly differentially expressed gene (DEG) sets were selected. Further, the distributions of those DEG sets on the corresponding chromosomes were identified using the functional classification tool. Finally, the DEGs were subjected to function and pathway enrichment analysis. DEG analysis indicated that the number of DEGs (854 genes) from nail fixation was significantly lower than that of DEGs (1029 genes) from plate fixation. The DEGs were mainly enriched in cell proliferation, cellular localization, and response to wounding functions. Several critical DEGs expressed during the fracture healing process were screened, and 2 common pathways were enriched for the DEGs in the nail fixation and plate fixation. These Gene expression profile comparisonDEGs and pathways may be potential targets or predictive markers during fracture healing.

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Control of Bone Remodeling by the Peripheral Sympathetic Nervous System

Cited by 129 publications

References 125 publications

Chronic Psychological Stress as a Risk Factor of Osteoporosis

Chronic Psychological Stress as a Risk Factor of Osteoporosis

Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease

Analysis of gene expression profiles in healing rat fractures treated with nail and plate fixation

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