login

Increased Osteoclast Development After Estrogen Loss: Mediation by Interleukin-6

SciencePublished 3 July 1992
Robert L. Jilka, Giao Hangoc, Giuseppe Girasole, Giovanni Passeri, Daniel C. Williams, John S. Abrams
Citations1,458
SJR quartileQ1
SJR score10.42
SNIP6.62

TL;DR

Estrogen loss results in an interleukin-6-mediated stimulation of osteoclastogenesis, which suggests a mechanism for the increased bone resorption in postmenopausal osteoporosis.

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 17 beta-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 17 beta-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.

Keywords

MedicineBiochemistry, Genetics and Molecular Biology