NIH Radio

Right Click to Download MP3 File

Brief Description:

A new study demonstrates that a chemical mediator in the blood plays a key role in maintaining the balance between the build-up and breakdown of bones in the body. This mediator, which acts on cells that degrade bone, may provide a new target for scientists developing therapies and preventions for bone-degenerating diseases such as osteoporosis and rheumatoid arthritis.

Transcript:

Balintfy: Bones are very dynamic, constantly growing and breaking down.

Germain: People think about them as relatively hard, static structures, but at the micro scale, at the small scale where biologists and, you know, doctors think about it, bone is undergoing remodeling at a fairly high rate.

Balintfy: Dr. Ronald Germain, an immunologist at the National Institute of Allergy and Infectious Diseases, explains the process.

Germain: You have a set of cells that build up bone that are called osteoblasts, and then you have these other cells that we’ve worked on that break down bone called osteoclasts, and it’s the proper balance of the two that give you what appears to be stable bone structure.

Balintfy: In people with bone-destructive disorders such as osteoporosis, however, osteoclast activity outpaces osteoblast activity, leading to a loss of bone density. Dr. Germain says osteoclasts come from a type of white blood cell.

Germain: The way this works is with those white cells that are recruited from the blood after circulating in the bone matrix, because bone is not dead, it’s live, and they get certain signals that cause them to attach to the surface, and if the right set of signals are there besides those attraction signals, then they actually aggregate, fuse together, and make big giant cell, which is the mature osteoclast that can begin to destroy the bone.

Balintfy: While most current therapies for bone-degrading diseases target mature osteoclasts, Dr. Germain explains that a rheumatologist who treats people with bone diseases, Dr. Masaru Ishii from Osaka, Japan, became interested in understanding what signals control immature osteoclasts, precursor cells that might otherwise go back into the bloodstream. Dr. Ishii worked with Dr. Germain’s lab to determine if a specific chemical mediator controlled immature osteoclast migration in live mice.

Germain: And what we discovered is there’s this lipid, this fatty molecule that’s at high concentration in the blood, and when it interacts with a receptor, a receiving apparatus, a sensing apparatus on these precursor cells, it tells them to come back into the blood stream, don’t hang out on the bone’s surface, and don’t make a mature osteoclast, and therefore, more of that signal decreases bone destruction.

Balintfy: According to Drs. Germain and Ishii, these findings, combined with previous data, indicate that it may be possible to use combined therapies that target immature osteoclast migration and mature osteoclast function to treat and prevent certain bone disorders. For more on this study, and the report published online in Nature, visit www.niaid.nih.gov. This is Joe Balintfy, National Institutes of Health, Bethesda, Maryland.