A new therapeutic target for osteoporosis is identified in a mouse study published online this week in Nature Communications. A receptor found on osteoblasts - the cells that make bone - has been shown to promote bone deposition and adjust imbalances in bone metabolism that are associated with osteoporosis.
Bone is constantly remodelled through synchronized action of bone-forming osteoblasts and bone-degrading osteoclasts; altered function of these cells can lead to bone loss. Current therapies for osteoporosis are mostly focused on antiresorptive agents that block the function of osteoclasts, but these treatments can cause adverse effects. Promoting bone deposition is an obvious and yet poorly explored alternative therapeutic avenue in osteoporosis treatment.
Michael Amling and colleagues describe a new cellular and molecular mechanism of osteoclast-osteoblast interaction, which they find is regulated by the hormone calcitonin. They show that calcitonin blocks the release of a molecule from osteoclasts that binds to S1PR3 receptors on osteoblasts. This reduction in communication between the two types of cells appears to result in decreased bone formation.
The authors then show that a drug called fingolimod, which activates the S1PR3 receptor on osteoblasts, can increase bone formation in mice. Fingolimod is currently used to treat multiple sclerosis; however, the authors caution that the beneficial effects of this drug on unbalanced bone metabolism in mice do not directly translate into clinical applicability. Further research is needed to investigate the possibility of developing new, more effective drugs that target S1PR3 activity.
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