Isolating the tightly linked processes is key to the development of improved osteoporosis treatments, as reported in JCI.

Scientists from St. Vincent’s Institute, Melbourne, have identified one way to separate bone formation from bone destruction in mice. They found that oncostatin M (OSM) is produced by osteoblasts and osteocytes in mouse bone and that it has distinct effects when acting through two different receptors: OSM receptor (OSMR) and leukemia inhibitory factor receptor (LIFR). 

Bone formation is tightly coupled to bone destruction, the researchers point out. Thus those looking to develop new approaches to build bone in individuals with osteoporosis need to identify ways to separate the two processes.

The current study appears in The Journal of Clinical Investigation in a paper titled “Oncostatin M promotes bone formation independently of resorption when signaling through leukemia inhibitory factor receptor in mice.” The authors explain that when OSM bound OSMR, it stimulated the production of cells that destroy bone. Consistent with this, mice lacking OSMR were found to have increased bone density.

When OSM bound LIFR, however, it blocked production of a protein that inhibits bone formation. Importantly, OSM acting via LIFR did not stimulate the production of cells that destroy bone.

Based on these results, the authors suggest the existance of a novel pathway by which bone formation can be stimulated independently of bone destruction. They also believe that these findings could provide new insights into OSMR and LIFR signaling that are relevant to other medical conditions including cardiovascular and neurodegenerative diseases as well as cancer.

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