Estrogen, cytokines, and pathogenesis of postmenopausal osteoporosis

Estrogen, cytokines, and pathogenesis of postmenopausal osteoporosis N RECENT YEARS, our understanding of the role that estrogen deficiency plays in the pathogenesis of postmenopausal osteoporosis and of the mechanism of estrogen action in bone has grown considerably. This is mainly a result of the recognition that estrogen regulates bone remodeling by modulating the production of cytokines and growth factors from bone marrow and bone cells. However, several potential mediators of estrogen effects on bone have been identified, and controversy persists concerning the specific contribution of each candidate factor. In this mini-review, I have provided an overview of the state-of-the-art knowledge regarding this most important research domain. POTENTIAL MEDIATORS OF ESTROGEN EFFECTS IN BONE At present, production of a large number of immune and hematopoietic factors in the bone microenvironment has been documented, and the complex and overlapping effects of these factors on both bone formation and resorption have been identified. Among these factors are interleukin-1 a (IL-la) and p,(’-’) IL-6,(6-8’tumor necrosis factor a (TNF-a) and p(9,’o) macrophage colony stimulating factor (M-CSF),(”,i2) and granulocyte macrophage colony stimulating factor (GM-CSF)(’’,l4) (Table 1). IL-1 and T N F are among the most powerful stimulants of bone resorption known and well recognized inhibitors of bone formation.(’\’,’’) These cytokines promote http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Bone and Mineral Research Wiley

Estrogen, cytokines, and pathogenesis of postmenopausal osteoporosis

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Publisher
Wiley
Copyright
Copyright © 1996 ASBMR
ISSN
0884-0431
eISSN
1523-4681
D.O.I.
10.1002/jbmr.5650110802
Publisher site
See Article on Publisher Site

Abstract

N RECENT YEARS, our understanding of the role that estrogen deficiency plays in the pathogenesis of postmenopausal osteoporosis and of the mechanism of estrogen action in bone has grown considerably. This is mainly a result of the recognition that estrogen regulates bone remodeling by modulating the production of cytokines and growth factors from bone marrow and bone cells. However, several potential mediators of estrogen effects on bone have been identified, and controversy persists concerning the specific contribution of each candidate factor. In this mini-review, I have provided an overview of the state-of-the-art knowledge regarding this most important research domain. POTENTIAL MEDIATORS OF ESTROGEN EFFECTS IN BONE At present, production of a large number of immune and hematopoietic factors in the bone microenvironment has been documented, and the complex and overlapping effects of these factors on both bone formation and resorption have been identified. Among these factors are interleukin-1 a (IL-la) and p,(’-’) IL-6,(6-8’tumor necrosis factor a (TNF-a) and p(9,’o) macrophage colony stimulating factor (M-CSF),(”,i2) and granulocyte macrophage colony stimulating factor (GM-CSF)(’’,l4) (Table 1). IL-1 and T N F are among the most powerful stimulants of bone resorption known and well recognized inhibitors of bone formation.(’\’,’’) These cytokines promote

Journal

Journal of Bone and Mineral ResearchWiley

Published: Aug 1, 1996

References

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