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Bone. 2013 Jun;54(2):230-6. doi: 10.1016/j.bone.2013.01.025. Epub 2013 Jan 23.

Osteocytes remove and replace perilacunar mineral during reproductive cycles.

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  • 1Section of Endocrinology and Metabolism, Department of Internal Medicine, Yale University School of Medicine, TAC S131, PO Box 208020, New Haven, CT 06520-8020, USA. john.wysolmerski@yale.edu

Abstract

Lactation is associated with an increased demand for calcium and is accompanied by a remarkable cycle of bone loss and recovery that helps to supply calcium and phosphorus for milk production. Bone loss is the result of increased bone resorption that is due, in part, to increased levels of PTHrP and decreased levels of estrogen. However, the regulation of bone turnover during this time is not fully understood. In the 1960s and 1970s many observations were made to suggest that osteocytes could resorb bone and increase the size of their lacunae. This concept became known as osteocytic osteolysis and studies suggested that it occurred in response to parathyroid hormone and/or an increased systemic demand for calcium. However, this concept fell out of favor in the late 1970s when it was established that osteoclasts were the principal bone-resorbing cells. Given that lactation is associated with increased PTHrP levels and negative calcium balance, we recently examined whether osteocytes contribute to bone loss during this time. Our findings suggest that osteocytes can remodel their perilacunar and pericanalicular matrix and that they participate in the liberation of skeletal calcium stores during reproductive cycles. These findings raise new questions about the role of osteocytes in coordinating bone and mineral metabolism during lactation as well as the recovery of bone mass after weaning. It is also interesting to consider whether osteocyte lacunar and canalicular remodeling contribute more broadly to the maintenance of skeletal and mineral homeostasis.

Copyright © 2013 Elsevier Inc. All rights reserved.

PMID:
23352996
[PubMed - indexed for MEDLINE]
PMCID:
PMC3624069
Free PMC Article
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