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Research Article Free access | 10.1172/JCI1039

Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow. Evidence for autonomy from factors released during bone resorption.

R L Jilka, K Takahashi, M Munshi, D C Williams, P K Roberson, and S C Manolagas

Division of Endocrinology and Metabolism, the University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

Find articles by Jilka, R. in: PubMed | Google Scholar

Division of Endocrinology and Metabolism, the University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

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Division of Endocrinology and Metabolism, the University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

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Division of Endocrinology and Metabolism, the University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

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Division of Endocrinology and Metabolism, the University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

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Division of Endocrinology and Metabolism, the University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

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Published May 1, 1998 - More info

Published in Volume 101, Issue 9 on May 1, 1998
J Clin Invest. 1998;101(9):1942–1950. https://doi.org/10.1172/JCI1039.
© 1998 The American Society for Clinical Investigation
Published May 1, 1998 - Version history
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Abstract

Loss of sex steroids causes an increase in both the resorption and formation of bone, with the former exceeding the latter. Based on evidence that the increased bone resorption after estrogen loss is due to an increase in osteoclastogenesis, we hypothesized that estrogen loss also stimulates osteoblastogenesis. We report that the number of mesenchymal osteoblast progenitors in the murine bone marrow was increased two- to threefold between 2 and 8 wk after ovariectomy and returned to control levels by 16 wk. Circulating osteocalcin, as well as osteoclastogenesis and the rate of bone loss, followed a very similar temporal pattern. Inhibition of bone resorption by administration of the bisphosphonate alendronate led to a decrease of the absolute number of osteoblast progenitors; however, it did not influence the stimulating effect of ovariectomy on osteoblastogenesis or osteoclastogenesis. These observations indicate that the increased bone formation that follows loss of estrogen can be explained, at least in part, by an increase in osteoblastogenesis. Moreover, they strongly suggest that unlike normal bone remodeling, whereby osteoblast development is stimulated by factors released from the bone matrix during osteoclastic resorption, estrogen deficiency unleashes signals that can stimulate the differentiation of osteoblast progenitors in a fashion that is autonomous from the need created by bone resorption, and therefore, inappropriate.

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Related comments

  • Response to Baylink and colleagues
    Robert L. Jilka, Ph.D.
  • Concerns about the conclusions of Jilka et al.
    David J. Baylink, M.D.

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