We are analyzing https://link.springer.com/article/10.1007/s00223-013-9774-y.

Title:
Osteocyte-Driven Bone Remodeling | Calcified Tissue International
Description:
Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts. The discovery that the inhibitor of bone formation sclerostin is primarily expressed in osteocytes in bone and downregulated by anabolic stimuli provided a mechanism by which osteocytes influence the activity of osteoblasts. Advances of the last few years provided experimental evidence demonstrating that osteocytes also participate in the recruitment of osteoclasts and the initiation of bone remodeling. Apoptotic osteocytes trigger yet-to-be-identified signals that attract osteoclast precursors to specific areas of bone, which in turn differentiate to mature, bone-resorbing osteoclasts. Osteocytes are also the source of molecules that regulate the generation and activity of osteoclasts, such as OPG and RANKL; and genetic manipulations of the mouse genome leading to loss or gain of function or to altered expression of either molecule in osteocytes markedly affect bone resorption. This review highlights these investigations and discusses how the novel concept of osteocyte-driven bone resorption and formation impacts our understanding of the mechanisms by which current therapies control bone remodeling.
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Keywords {🔍}

bone, pubmed, google, scholar, article, cas, osteocyte, bellido, central, osteocytes, res, miner, cell, apoptosis, plotkin, sclerostin, signaling, remodeling, manolagas, mechanical, formation, biol, parfitt, estrogen, weinstein, control, mice, obrien, chem, osteoblasts, loss, jilka, clin, receptor, noble, tissue, osteoclasts, resorption, chapter, osteoblast, pth, van, sost, allen, han, privacy, cookies, function, content, teresita,

Topics {✒️}

caveolin-1/extracellular signal–regulated kinase month download article/chapter wnt/lrp5 receptor-independent activation antagonizing wnt/beta-catenin signaling osteocyte wnt/beta-catenin signaling osteocyte-driven bone remodeling osteocyte-driven bone resorption osteocytic perilacunar/canalicular remodeling gap junction–independent action e11/gp38 selective expression wnt/beta-catenin signaling active pro-osteoclastogenic signaling ß-catenin survival pathways wnt/β-catenin signaling estrogen receptor α-mediated van bezooijen rl fatigue-loaded bone involves osteocyte-expressed negative regulator full article pdf metalloproteinase mt1-mmp bonewald lf attract osteoclast precursors privacy choices/manage cookies β-catenin signaling aguirre ji armstrong vj beta-catenin-dependent van buchem disease inhibits bone formation periosteal bone formation intra-cortical remodeling precedes osteoclast recruitment nontargeted bone remodeling local wnt signaling jilka rl review highlights winkler dg rankl subcellular trafficking circulating sclerostin levels shear stress inhibits biphasic osteocyte survival distinct osteocyte populations src/erk pathway pth receptor signaling bone remodeling regulation abrupt estrogen withdrawal article bellido increased bone density anabolic stimuli provided uncommitted osteoblast progenitors

Questions {❓}

Verborgt O, Tatton NA, Majeska RJ, Schaffler MB (2002) Spatial distribution of Bax and Bcl-2 in osteocytes after bone fatigue: complementary roles in bone remodeling regulation?

Schema {🗺️}

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         description:Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts. The discovery that the inhibitor of bone formation sclerostin is primarily expressed in osteocytes in bone and downregulated by anabolic stimuli provided a mechanism by which osteocytes influence the activity of osteoblasts. Advances of the last few years provided experimental evidence demonstrating that osteocytes also participate in the recruitment of osteoclasts and the initiation of bone remodeling. Apoptotic osteocytes trigger yet-to-be-identified signals that attract osteoclast precursors to specific areas of bone, which in turn differentiate to mature, bone-resorbing osteoclasts. Osteocytes are also the source of molecules that regulate the generation and activity of osteoclasts, such as OPG and RANKL; and genetic manipulations of the mouse genome leading to loss or gain of function or to altered expression of either molecule in osteocytes markedly affect bone resorption. This review highlights these investigations and discusses how the novel concept of osteocyte-driven bone resorption and formation impacts our understanding of the mechanisms by which current therapies control bone remodeling.
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      headline:Osteocyte-Driven Bone Remodeling
      description:Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts. The discovery that the inhibitor of bone formation sclerostin is primarily expressed in osteocytes in bone and downregulated by anabolic stimuli provided a mechanism by which osteocytes influence the activity of osteoblasts. Advances of the last few years provided experimental evidence demonstrating that osteocytes also participate in the recruitment of osteoclasts and the initiation of bone remodeling. Apoptotic osteocytes trigger yet-to-be-identified signals that attract osteoclast precursors to specific areas of bone, which in turn differentiate to mature, bone-resorbing osteoclasts. Osteocytes are also the source of molecules that regulate the generation and activity of osteoclasts, such as OPG and RANKL; and genetic manipulations of the mouse genome leading to loss or gain of function or to altered expression of either molecule in osteocytes markedly affect bone resorption. This review highlights these investigations and discusses how the novel concept of osteocyte-driven bone resorption and formation impacts our understanding of the mechanisms by which current therapies control bone remodeling.
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         Sost
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