Increased osteoclast development after estrogen loss: Mediation by interleukin-6

Robert L. Jilka, Giao Hangoc, Giuseppe Girasole, Giovanni Passeri, Daniel C. Williams, John S. Abrams, Brendan Boyce, Hal Broxmeyer, Stavros C. Manolagas

Research output: Contribution to journalArticlepeer-review

1218 Scopus citations

Abstract

Osteoclasts, the cells that resorb bone, develop from hematopoietic precursors of the bone marrow under the control of factors produced in their microenvironment. The cytokine interleukin-6 can promote hematopoiesis and osteoclastogenesis. Interleukin-6 production by bone and marrow stromal cells is suppressed by 17β-estradiol in vitro. In mice, estrogen loss (ovariectomy) increased the number of colony-forming units for granulocytes and macrophages, enhanced osteoclast development in ex vivo cultures of marrow, and increased the number of osteoclasts in trabecular bone. These changes were prevented by 17β-estradiol or an antibody to interleukin-6. Thus, estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.

Original languageEnglish (US)
Pages (from-to)88-91
Number of pages4
JournalScience
Volume257
Issue number5066
DOIs
StatePublished - 1992

ASJC Scopus subject areas

  • General

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