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The osteocyte: key player in regulating bone turnover.

Goldring SR - RMD Open (2015)

Bottom Line: Osteocytes are the most abundant cell type in bone and are distributed throughout the mineralised bone matrix forming an interconnected network that ideally positions them to sense and to respond to local biomechanical and systemic stimuli to regulate bone remodelling and adaptation.The adaptive process is dependent on the coordinated activity of osteoclasts and osteoblasts that form a so called bone multicellular unit that remodels cortical and trabecular bone through a process of osteoclast-mediated bone resorption, followed by a phase of bone formation mediated by osteoblasts.Osteocytes mediate their effects on bone remodelling via both cell-cell interactions with osteoclasts and osteoblasts, but also via signaling through the release of soluble mediators.

View Article: PubMed Central - PubMed

Affiliation: Research Division , Hospital for Special Surgery, Weill Cornell Medical College , New York, New York , USA.

ABSTRACT
Osteocytes are the most abundant cell type in bone and are distributed throughout the mineralised bone matrix forming an interconnected network that ideally positions them to sense and to respond to local biomechanical and systemic stimuli to regulate bone remodelling and adaptation. The adaptive process is dependent on the coordinated activity of osteoclasts and osteoblasts that form a so called bone multicellular unit that remodels cortical and trabecular bone through a process of osteoclast-mediated bone resorption, followed by a phase of bone formation mediated by osteoblasts. Osteocytes mediate their effects on bone remodelling via both cell-cell interactions with osteoclasts and osteoblasts, but also via signaling through the release of soluble mediators. The remodelling process provides a mechanism for adapting the skeleton to local biomechanical factors and systemic hormonal influences and for replacing bone that has undergone damage from repetitive mechanical loading.

No MeSH data available.


Related in: MedlinePlus

Osteocyte-derived sclerostin and Dickkopf-related protein 1 (DKK-1) regulate bone formation. Loading decreases osteocyte-derived sclerostin and DKK-1, which results in activation of the Wnt/β-catenin signaling in osteoblasts and increased bone formation.
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RMDOPEN2015000049F2: Osteocyte-derived sclerostin and Dickkopf-related protein 1 (DKK-1) regulate bone formation. Loading decreases osteocyte-derived sclerostin and DKK-1, which results in activation of the Wnt/β-catenin signaling in osteoblasts and increased bone formation.

Mentions: In addition to OPG and RANKL, osteocytes are the source of a diverse array of products that have the capacity to modulate bone remodelling, including small molecule mediators such as prostanoids, nitric oxide, and nucleotides, as well as a broad spectrum of cytokines and growth factors such as insulin-like growth factor-1 (IGF-1), vascular endothelial cell growth factor (VEGF) and TGF-β.1318–24 Osteocytes also are a major source of fibroblast growth factor 23, which regulates serum phosphorus levels by increasing renal phosphate excretion.25 Recent studies have drawn attention to the role of two osteocyte-derived products, sclerostin and Dickkopf-related protein 1 (DKK-1), in the regulation of bone remodelling. These molecules are potent and specific inhibitors of the Wnt/β-catenin pathway, which plays a major role in the regulation of osteoblast-mediated bone formation.26 Robling and co-workers were the first to show that mechanical loading decreased the expression of sclerostin and DKK-1 in osteocytes. The decrease in the production of these Wnt pathway inhibitors by osteocytes resulted in upregulation of β-catenin signaling in osteoblasts and an associated increase in bone formation27–29 (figure 2). In contrast, unloading resulted in increased expression of sclerostin and DKK-1 and reduction in bone formation. Osteocytes also play a role in mediating the effects of parathyroid hormone (PTH) on bone formation. These effects are in part attributable to PTH-induced suppression of sclerostin by osteocytes.30–32 In addition, there is evidence that PTH-induces increases in RANKL production by osteocytes, indicating a key role of osteocytes in mediating the effects of PTH on osteoclast-mediated bone resorption.33


The osteocyte: key player in regulating bone turnover.

Goldring SR - RMD Open (2015)

Osteocyte-derived sclerostin and Dickkopf-related protein 1 (DKK-1) regulate bone formation. Loading decreases osteocyte-derived sclerostin and DKK-1, which results in activation of the Wnt/β-catenin signaling in osteoblasts and increased bone formation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4632148&req=5

RMDOPEN2015000049F2: Osteocyte-derived sclerostin and Dickkopf-related protein 1 (DKK-1) regulate bone formation. Loading decreases osteocyte-derived sclerostin and DKK-1, which results in activation of the Wnt/β-catenin signaling in osteoblasts and increased bone formation.
Mentions: In addition to OPG and RANKL, osteocytes are the source of a diverse array of products that have the capacity to modulate bone remodelling, including small molecule mediators such as prostanoids, nitric oxide, and nucleotides, as well as a broad spectrum of cytokines and growth factors such as insulin-like growth factor-1 (IGF-1), vascular endothelial cell growth factor (VEGF) and TGF-β.1318–24 Osteocytes also are a major source of fibroblast growth factor 23, which regulates serum phosphorus levels by increasing renal phosphate excretion.25 Recent studies have drawn attention to the role of two osteocyte-derived products, sclerostin and Dickkopf-related protein 1 (DKK-1), in the regulation of bone remodelling. These molecules are potent and specific inhibitors of the Wnt/β-catenin pathway, which plays a major role in the regulation of osteoblast-mediated bone formation.26 Robling and co-workers were the first to show that mechanical loading decreased the expression of sclerostin and DKK-1 in osteocytes. The decrease in the production of these Wnt pathway inhibitors by osteocytes resulted in upregulation of β-catenin signaling in osteoblasts and an associated increase in bone formation27–29 (figure 2). In contrast, unloading resulted in increased expression of sclerostin and DKK-1 and reduction in bone formation. Osteocytes also play a role in mediating the effects of parathyroid hormone (PTH) on bone formation. These effects are in part attributable to PTH-induced suppression of sclerostin by osteocytes.30–32 In addition, there is evidence that PTH-induces increases in RANKL production by osteocytes, indicating a key role of osteocytes in mediating the effects of PTH on osteoclast-mediated bone resorption.33

Bottom Line: Osteocytes are the most abundant cell type in bone and are distributed throughout the mineralised bone matrix forming an interconnected network that ideally positions them to sense and to respond to local biomechanical and systemic stimuli to regulate bone remodelling and adaptation.The adaptive process is dependent on the coordinated activity of osteoclasts and osteoblasts that form a so called bone multicellular unit that remodels cortical and trabecular bone through a process of osteoclast-mediated bone resorption, followed by a phase of bone formation mediated by osteoblasts.Osteocytes mediate their effects on bone remodelling via both cell-cell interactions with osteoclasts and osteoblasts, but also via signaling through the release of soluble mediators.

View Article: PubMed Central - PubMed

Affiliation: Research Division , Hospital for Special Surgery, Weill Cornell Medical College , New York, New York , USA.

ABSTRACT
Osteocytes are the most abundant cell type in bone and are distributed throughout the mineralised bone matrix forming an interconnected network that ideally positions them to sense and to respond to local biomechanical and systemic stimuli to regulate bone remodelling and adaptation. The adaptive process is dependent on the coordinated activity of osteoclasts and osteoblasts that form a so called bone multicellular unit that remodels cortical and trabecular bone through a process of osteoclast-mediated bone resorption, followed by a phase of bone formation mediated by osteoblasts. Osteocytes mediate their effects on bone remodelling via both cell-cell interactions with osteoclasts and osteoblasts, but also via signaling through the release of soluble mediators. The remodelling process provides a mechanism for adapting the skeleton to local biomechanical factors and systemic hormonal influences and for replacing bone that has undergone damage from repetitive mechanical loading.

No MeSH data available.


Related in: MedlinePlus