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


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
Issue number5066
StatePublished - 1992

ASJC Scopus subject areas

  • General

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