Osteocytes are cells buried in the bone matrix. They largely contribute to the regulation of bone remodeling in response to mechanical and microenvironmental changes. Much has been recognized in recent years regarding the role of osteocytes in bone homeostasis. nevertheless their ability to directly contribute to mineral equilibrium has been neglected. In the light of the renewed interest in their biology, we revisited the literature and discuss experimental evidence favoring the hypothesis that osteocytes are able to remove and replace the bone matrix according to the systemic needs of the body. We also reviewed reports against this theory, thus providing current views of what is known so far on the ability of osteocytes to mobilize bone mineral. This re-examination of osteocytic osteolysis might stimulate new interest and open new perspectives in osteocyte biology and in the cellular mechanisms that control bone homeostasis. (C) 2008 Elsevier Inc. All rights reserved.

Do osteocytes contribute to bone mineral homeostasis? Osteocytic osteolysis revisited

TETI, ANNA MARIA;
2009-01-01

Abstract

Osteocytes are cells buried in the bone matrix. They largely contribute to the regulation of bone remodeling in response to mechanical and microenvironmental changes. Much has been recognized in recent years regarding the role of osteocytes in bone homeostasis. nevertheless their ability to directly contribute to mineral equilibrium has been neglected. In the light of the renewed interest in their biology, we revisited the literature and discuss experimental evidence favoring the hypothesis that osteocytes are able to remove and replace the bone matrix according to the systemic needs of the body. We also reviewed reports against this theory, thus providing current views of what is known so far on the ability of osteocytes to mobilize bone mineral. This re-examination of osteocytic osteolysis might stimulate new interest and open new perspectives in osteocyte biology and in the cellular mechanisms that control bone homeostasis. (C) 2008 Elsevier Inc. All rights reserved.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/18317
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