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Bone homeostasis requires precise balance between deposition of new bone by osteoblasts and resorption of old bone by osteoclasts.
In this issue of the Journal of Clinical Investigation, Brendan Boyce and colleagues at the University of Rochester evaluated the role of TNF receptor-associated receptor 3 (TRAF3) in promoting osteoclast formation.
Mice lacking TRAF3 in osteoclast precursor cells had mild osteoporosis that was associated with increased osteoclast formation.
The authors found that chloroquine treatment increased TRAF3 in osteoclast precursor cells and limited osteoclast generation.
Furthermore, treatment of mouse models of osteoporosis with chloroquine inhibited osteoclast formation.
These studies suggest that therapies aimed at increasing TRAF3 in osteoclast precursor cells may limit bone loss for those with bone diseases.
Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our Bones / Orthopedics category page for the latest news on this subject.
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Journal of Clinical Investigation. "In murine osteoporosis, choloroquine reduces formation of bone resorbing cells." Medical News Today. MediLexicon, Intl., 11 Dec. 2013. Web.
18 Apr. 2014. <http://www.medicalnewstoday.com/releases/269924>
Journal of Clinical Investigation. (2013, December 11). "In murine osteoporosis, choloroquine reduces formation of bone resorbing cells." Medical News Today. Retrieved from
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