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

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

21 Jan 2005

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.

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: 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@....

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

http://www.medicalnewstoday.com/medicalnews.php?newsid=19100