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The painful and potentially immobilizing condition of rheumatoid arthritis (RA) begins most often in a single joint and then, within a few years, spreads throughout other joints in the body. This autoimmune disease destroys the cartilage padding between bones and causes painful inflammation in joints along with limitations in mobility.


Elena Neumann (a molecular biologist) explains that a specific type of fibroblasts known as rheumatoid arthritis synovial fibroblasts (RASFs), are responsible for much of the cartilage damage exhibited in RA. These cells are in the fluid within joints of people with RA and secrete enzymes that lead to cartilage decomposition. Wondering if the RAFs might contribute to the spread of RA from joint to joint, Neumann and colleagues implanted human cartilage under the skin of genetically engineered mice; these mice do not reject tissues from other species. Cartilage containing the RASFs was implanted into one flank of each of the mice and normal cartilage was implanted in the other flank.


After 60 days, the RASF cells had invaded and damaged cartilage throughout the bodies of most of the mice. High concentrations of RASFs were found in the spleen and circulating blood from over half the mice contained RASFs. The researchers are proposing that these damaging fibroblasts move from joint to joint in people with RA by migrating through the bloodstream.


As a result of these studies, pharmacological interventions to halt the spread of RA may be possible. Medications would be developed to prevent the RASFs from spreading from joint to joint and slow, or even halt, the progression of RA. Interestingly, James Woods, a microbiologist at Midwestern University in Downers Grove, Illinois suggests that RASFs might be genetically engineered to heal the joints they invade, as opposed to damaging them.


Source: Kean S. Arthritis on the move. ScienceNow Daily News. November 9, 2009. Available at Accessed November 15, 2009.


Submitted by: Robin Pattillo, PhD, RN, News Editor