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Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/73504

Type: Journal article
Title: Osteocyte regulation of bone mineral: a little give and take
Author: Atkins, Gerald James
Findlay, David Malcolm
Citation: Osteoporosis International, 2012; 23(8):2067-2079
Publisher: Springer London Ltd
Issue Date: 2012
ISSN: 0937-941X
School/Discipline: School of Medicine : Orthopaedics and Trauma
Statement of
Responsibility: 
G. J. Atkins, D. M. Findlay
Abstract: Osteocytes actively participate in almost every phase of mineral handling by bone. They regulate the mineralisation of osteoid during bone formation, and they are also a major RANKL-producing cell. Osteocytes are thus able to liberate bone mineral by regulating osteoclast differentiation and activity in response to a range of stimuli, including bone matrix damage, bone disuse and mechanical unloading, oestrogen deficiency, high-dose glucocorticoid and chemotherapeutic agents. At least some of these activities may be regulated by the osteocyte-secreted product, sclerostin. There is also mounting evidence that in addition to regulating phosphate homeostasis systemically, osteocytes contribute directly to calcium homeostasis in the mature skeleton. Osteocyte cell death and the local loss of control of bone mineralisation may be the cause of focal hypermineralisation of bone and osteopetrosis, as seen in aging and pathology. The sheer number of osteocytes in bone means that 'a little give and take' in terms of regulation of bone mineral content translates into a powerful whole organism effect.
Keywords: Mineralization; Osteocyte; RANKL; Sclerostin
Rights: © International Osteoporosis Foundation and National Osteoporosis Foundation 2012
RMID: 0020121492
DOI: 10.1007/s00198-012-1915-z
Appears in Collections:Orthopaedics and Trauma Publications
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