With a little help from its friends, RANKL drives bone loss

Main Category: Bones / Orthopedics
Article Date: 21 Jan 2005 - 4:00 PDT


Inflammation and the loss of calcium in bone are complications of rheumatoid arthritis and gum disease. The cell ultimately responsible for bone breakdown is the osteoclast, which is under the influence of a molecule known as RANKL.

However our understanding of what triggers RANKL expression and its full effects on the osteoclast remains limited.

Steven Teitelbaum and colleagues from Washington University now demonstrate, in mice, that tumor necrosis factor (TNF) induces bone marrow stromal cells to produce RANKL via an interleukin receptor-1 (IL-1)-dependent mechanism, which drives osteoclast production and subsequent bone breakdown.

Furthermore, they show that IL-4 is able to block TNF and IL-1-induced RANKL signaling. The administration of IL-4 and/or the targeting of TNF, IL-1 or RANKL with appropriate drugs represent potential avenues of therapeutic development for diseases characterized by inflammation and loss of bone density.

The study will appear online on January 20 in advance of print publication in the February 1 edition of the Journal of Clinical Investigation.

TITLE: IL-1 mediates TNF-induced osteoclastogenesis.

AUTHOR CONTACT: Steven L. Teitelbaum
Department of Pathology and Immunology. Washington University School of Medicine, St. Louis, Missouri, USA.
Phone: 314-454-8463; Fax: 314-454-5505; E-mail: teitelbs@wustl.edu.

View the PDF of this article at: https://www.the-jci.org/press/23394.pdf

From 5:00PM USA EST Thursday January 20, 2005 a PDF of this article will be available at: http://www.jci.org/papbyrecent.shtml
JCI table of contents, January 20 2005
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Researchers identify pathway that jumpstarts the autoimmune response in lupus
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With a little help from its friends, RANKL drives bone loss
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Brooke Grindlinger
press_releases@the-jci.org
Journal of Clinical Investigation

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