Reaction between Osteoclasts and Osteocytes When They Encounter Each Other at the Bone Resorption Surface during Bone Modeling
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Keywords:
Osteocyte
Bone remodeling
Bone cell
Bone matrix
Bone remodeling period
Bone histomorphometry
Bone Formation
Accumulation of microdamage in bone leads to the reduced strength of our skeleton. In health, bone adapts to the prevailing mechanical needs of the organism and is also capable of self-repair, sensing, removing and replacing damaged or mechanically insufficient volumes of bone. In disease and old age these characteristics are reduced. In order to undertake both of the processes of functional adaptation and repair the bone resorbing and forming cells must be very accurately targeted to areas of physiological need. The mechanism by which cells are precisely targeted to areas requiring repair is both clinically relevant and poorly understood. The osteocyte has been assumed to play a role in sensing damage and signaling for its removal, due largely to its abundance throughout the mineralized bone matrix. However, until recently there has been little evidence that osteocyte function is modified in the vicinity of the microdamage. Here I outline the possibility that the targeted removal of bone containing microcracks might involve signals derived from the apoptotic death of the osteocyte. I shall discuss data that support or refute this view and will consider the possible molecular mechanisms by which controlled cell death might contribute to the signals for repair in the light of work involving cells in bone and other tissue systems.
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Osteocyte
Bone remodeling period
Bone remodeling
Sclerostin
Bone cell
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Osteocyte
Bone remodeling
Bone remodeling period
Sclerostin
Bone cell
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Osteocytes are stellate-shaped or dendritic cells that represent the most abundant cell type in bone. As mechanosensory cells,osteocytes participate in bone remodeling by producing some factors which regulate the activities of osteoblasts and osteoclasts. Apoptosis of osteocyte is at least the part of the pathogen-esis of osteoporosis. Moreover, the protein products from osteocyte including sclerostin, fibroblast growth factor 23(FGF23),dentin matrix protein1 (DMP1) and so on,play important roles in maintaining the normal bone metabolism. So there is close relationship between osteocyte and bone metabolism. Further research on apopto-sis of osteocyte and its protein products may provide novel ways and targets for preventing and treating bone metabolic diseases.
Key words:
Osteocyte; Apoptosis; Osteoporosis; Mechanical strain
Osteocyte
Sclerostin
Bone remodeling
DMP1
Bone matrix
Bone cell
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Osteocyte
Bone cell
Bone matrix
Bone remodeling
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Osteocytes make up 90–95% of the cellular content of bone and form a rich dendritic network with a vastly greater surface area than either osteoblasts or osteoclasts. Osteocytes are well positioned to play a role in bone homeostasis by interacting directly with the matrix; however, the ability for these cells to modify bone matrix remains incompletely understood. With techniques for examining the nano- and microstructure of bone matrix components including hydroxyapatite and type I collagen becoming more widespread, there is great potential to uncover novel roles for the osteocyte in maintaining bone quality. In this review, we begin with an overview of osteocyte biology and the lacunar–canalicular system. Next, we describe recent findings from in vitro models of osteocytes, focusing on the transitions in cellular phenotype as they mature. Finally, we describe historical and current research on matrix alteration by osteocytes in vivo , focusing on the exciting potential for osteocytes to directly form, degrade, and modify the mineral and collagen in their surrounding matrix.
Osteocyte
Bone matrix
Matrix (chemical analysis)
Bone cell
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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.
Osteocyte
Bone remodeling
Bone cell
Bone remodeling period
Bone matrix
Bone Formation
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Osteocyte
Bone matrix
Bone cell
Bone remodeling
Bystander effect
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Bone remodeling period
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Bone histomorphometry is defined as a quantitative evaluation of bone remodeling. In bone remodeling, bone resorption and bone formation are coupled with scalloped cement lines. Another mechanism of bone formation is minimodeling which bone formation and resorption are independent. The finding of minimodeling appeared in special condition with metabolic bone disease or anabolic agents. We need further study for minimodeling feature and mechanism.
Bone remodeling
Bone histomorphometry
Bone remodeling period
Bone cell
Bone Formation
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Osteocyte
Bone matrix
Matrix (chemical analysis)
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