Cartilage is to blame after all. Once believed to be an innocent bystander in cases of rheumatoid arthritis, researchers in Melbourne, Australia, find that cartilage plays an active role in the destruction of joints.
As reported by Allan Gill of Medical Press, a team of researchers from the Walter and Eliza Hall Institute made the discovery while investigating the role of the protein SOCS3 in controlling inflammation. Arthritis causes pain and inflammation in joints and, over time, destroys the cartilage that lubricates and cushions the joints. Bones can even be remodeled by rheumatoid arthritis which leads to disfigurement and increased pain.
For a long time doctors thought that cartilage was a victim of a patient’s overzealous immune system. Then Tommy Liu, M.D., and his colleagues found that cartilage “participates in the production of inflammation-signaling chemicals and contributes to its own destruction, ” he said.
Liu’s study investigated how the molecules—known as suppressors of cytokine signaling (SOCS3) molecules—control the flow of chemical messages within and between cells. They also regulate inflammation in rheumatoid arthritis. When the researchers created a model that lacked SOCS3 molecules in the cartilage, they found that tissue degradation increased.
“Without SOCS3, cartilage cells produced enzymes that drove tissue degradation and increased inflammation by releasing signaling molecules that triggered an increased autoimmune response, ” Liu said. “We also found that cartilage could produce a protein called RANKL that triggers bone remodeling.”
Liu’s study revealed the fact that cartilage, itself, plays an active role in the progression of rheumatoid arthritis. There is no cure for the disease and few treatments are effective in slowing the progress of the ailment. But Liu is hopeful. “Targeting the action of these inflammatory chemical messages could boost the efficacy of current treatments, ” he said.
