A hypothesis for the local control of osteoclast function by Ca2+, nitric oxide and free radicals |
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Authors: | A. S. M. Towhidul Alam Christopher L. -H. Huang David R. Blake Mone Zaidi |
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Affiliation: | (1) Department of Cellular and Molecular Sciences, St. George's Hospital Medical School, SW17 0RE London, UK;(2) The Physiological Laboratory, University of Cambridge, CB2 3EG Cambridge, UK;(3) Bone and Joint Research Unit, The London Hospital Medical College, EC1 2AD London, UK |
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Abstract: | Several important conclusions have recently emerged fromin vitro studies on the resorptive cell of bone, the osteoclast. First, it has been established that osteoclast function is modulated locally, by changes in the local concentration of Ca2+ caused by hydroxyapatite dissolution. It is thought that activation by Ca2+ of a surface membrane Ca2+ receptor mediates these effects, hence providing a feedback control. Second, a number of molecules produced locally by the endothelial cell, with which the osteoclast is in intimate contact, have been found to affect bone resorption profoundly. For instance, the autocoid nitric oxide strongly inhibits bone resorption. Finally, reactive oxygen species have been found to aid bone resorption and enhance osteoclastic activity directly. Here, we will attempt to integrate these control mechanisms into a unified hypothesis for the local control of bone resorption. |
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Keywords: | osteoclast Ca2+ receptor peroxide nitric oxide |
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