The osteocyte

Tate, Melissa L. Knothe; Adamson, Josée R; Tami, Andrea; Bauer, Thomas W.

doi:10.1016/s1357-2725(03)00241-3

Cited by 289 publications

(127 citation statements)

References 16 publications

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“…Osteocytes, found dispersed throughout the bone matrix, are terminally differentiated cells that have much lower bone forming activity than osteoblasts, but constitute over 90% of adult bone cells 74. Despite their relative inactivity compared with osteoblasts, osteocytes play a central role in the determination and maintenance of bone structure 75 – 79.…”

Section: Differentiation and Local Regulation Of Bone Cellsmentioning

confidence: 99%

The cell biology of bone metabolism

et al. 2008

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Contrary to the commonly held misconception, bone is a relatively dynamic organ that undergoes significant turnover as compared to other organs in the body. This review details how complex intercellular signalling, between the osteoprogenitor cells and mature osteoblasts, osteocytes and osteoclasts, regulates and balances activities of bone cells during remodelling and growth. Both systemic, as well as local autocrine and paracrine factors are discussed. A number of recent important advances in cell biology of bone have led to a new paradigm in understanding of the subject. In this regard, the interaction between the immune system and bone cells is of particular interest, leading to the emergence of a new discipline termed osteoimmunology. The role of lymphocytes and a number of key cytokines in the regulation of osteoclastogenesis and osteoblast function is critically examined. The intracellular signalling regulating key cellular pathways involved in cell differentiation and activity are outlined. The emerging evidence of osteocytes as mechanosensors as well as regulators of mineralisation is discussed.

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Section: Differentiation and Local Regulation Of Bone Cellsmentioning

confidence: 99%

The cell biology of bone metabolism

et al. 2008

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“…(1) An extensive network of dendritic processes encased in canaliculi extends from osteocytes to allow for intracellular and extracellular communication and transport of nutrients and small molecules. (5) Studies suggest that osteocytes directly remodel the surrounding perilacunar and canalicular matrix, resorbing bone to maintain skeletal and mineral ion homeostasis. (6,7) Although PTH/PTHrP has been shown to regulate perilacunar remodeling, the roles of 1,25D and FGF23 have not been studied.…”

Section: Introductionmentioning

confidence: 99%

Hormonal Regulation of Osteocyte Perilacunar and Canalicular Remodeling in the Hyp Mouse Model of X-Linked Hypophosphatemia

Tokarz

Martins

Petit

et al. 2017

Journal of Bone and Mineral Research

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Osteocytes remodel their surrounding perilacunar matrix and canalicular network to maintain skeletal homeostasis. Perilacunar/canalicular remodeling is also thought to play a role in determining bone quality. X-linked hypophosphatemia (XLH) is characterized by elevated serum fibroblast growth factor 23 (FGF23) levels, resulting in hypophosphatemia and decreased production of 1,25 dihydroxyvitamin D (1,25D). In addition to rickets and osteomalacia, long bones from mice with XLH (Hyp) have impaired whole-bone biomechanical integrity accompanied by increased osteocyte apoptosis. To address whether perilacunar/canalicular remodeling is altered in Hyp mice, histomorphometric analyses of tibia and 3D intravital microscopic analyses of calvaria were performed. These studies demonstrate that Hyp mice have larger osteocyte lacunae in both the tibia and calvaria, accompanied by enhanced osteocyte mRNA and protein expression of matrix metalloproteinase 13 (MMP13) and genes classically used by osteoclasts to resorb bone, such as cathepsin K (CTSK). Hyp mice also exhibit impaired canalicular organization, with a decrease in number and branching of canaliculi extending from tibial and calvarial lacunae. To determine whether improving mineral ion and hormone homeostasis attenuates the lacunocanalicular phenotype, Hyp mice were treated with 1,25D or FGF23 blocking antibody (FGF23Ab). Both therapies were shown to decrease osteocyte lacunar size and to improve canalicular organization in tibia and calvaria. 1,25D treatment of Hyp mice normalizes osteocyte expression of MMP13 and classic osteoclast markers, while FGF23Ab decreases expression of MMP13 and selected osteoclast markers. Taken together, these studies point to regulation of perilacunar/canalicular remodeling by physiologic stimuli including hypophosphatemia and 1,25D.

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“…Several diseased states have been associated with alterations in osteocyte dendricity. A decrease in interconnectivity has been observed in osteoporotic and osteoarthritic bone, while osteomalacic bone exhibits an increased interconnectivity which is chaotic 4, 5. We detected an increase in the number and length of dendrites in MLO‐Y4 osteocytes cells treated with increasing concentrations of metal ions.…”

Section: Discussionmentioning

confidence: 55%

“…Osteocyte cell death and alterations in dendritic morphology and connectivity play a role in osteonecrosis of the femoral head, especially following chronic steroid treatment 3. Decreased osteocyte dendritic connectivity is also found in osteoporosis and osteoarthritis, while osteomalacic bone exhibits an increased, but chaotic connectivity,4, 5 highlighting the importance of dendricity in pathophysiological conditions.…”

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confidence: 99%

Osteocyte physiology and response to fluid shear stress are impaired following exposure to cobalt and chromium: Implications for bone health following joint replacement

et al. 2016

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The effects of metal ion exposure on osteocytes, the most abundant cell type in bone and responsible for coordinating bone remodeling, remain unclear. However, several studies have previously shown that exposure to cobalt (Co2+) and chromium (Cr3+), at concentrations equivalent to those found clinically, affect osteoblast and osteoclast survival and function. In this study, we tested the hypothesis that metal ions would similarly impair the normal physiology of osteocytes. The survival, dendritic morphology, and response to fluid shear stress of the mature osteocyte‐like cell‐line MLO‐Y4 following exposure to clinically relevant concentrations and combinations of Co and Cr ions were measured in 2D‐culture. Exposure of MLO‐Y4 cells to metal ions reduced cell number, increased dendrites per cell and increased dendrite length. We found that combinations of metal ions had a greater effect than the individual ions alone, and that Co2+ had a predominate effect on changes to cell numbers and dendrites. Combined metal ion exposure blunted the responses of the MLO‐Y4 cells to fluid shear stress, including reducing the intracellular calcium responses and modulation of genes for the osteocyte markers Cx43 and Gp38, and the signaling molecules RANKL and Dkk‐1. Finally, we demonstrated that in the late osteoblasts/early osteocytes cell line MLO‐A5 that Co2+ exposure had no effect on mineralization, but Cr3+ treatment inhibited mineralization in a dose‐dependent manner, without affecting cell viability. Taken together, these data indicate that metal exposure can directly affect osteocyte physiology, with potential implications for bone health including osseointegration of cementless components, and periprosthetic bone remodeling. © 2016 The Authors. Journal of Orthopaedic Research Published by Wiley Periodicals, Inc. on behalf of Orthopaedic Research Society. J Orthop Res 35:1716–1723, 2017.

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The osteocyte

Cited by 289 publications

References 16 publications

The cell biology of bone metabolism

The cell biology of bone metabolism

Hormonal Regulation of Osteocyte Perilacunar and Canalicular Remodeling in the Hyp Mouse Model of X-Linked Hypophosphatemia

Osteocyte physiology and response to fluid shear stress are impaired following exposure to cobalt and chromium: Implications for bone health following joint replacement

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