In the first study of its kind, researchers at Brown University have discovered that the lack of a protein called lubricin results in early wear of joints.
Lubricin acts as a “boundary lubricant” that reduces the friction between opposing layers of cartilage inside joints. Dr. Gregory Jay, an associate professor of emergency medicine and engineering at Brown, has been studying lubricin’s role in joint function for 20 years.
In 2005 Dr. Jay led a study to identify a process to measure the loss of lubrication in the joints. They started with rabbits with injured knees. They examined synovial fluid that was drawn from the rabbits knee cartilage and measured the lubricin. They found that within 3 weeks the lubricin had completely disappeared.
This was followed by evaluating synovial fluid drawn from the injured knees of patients in an emergency room. This procedure is common for relieving swelling that accompanies the knee injury. The results were that those people with knee injuries had substantially less lubrication than people with healthy knees.
These findings dealt with joint injuries, which is a common precursor to osteoarthritis. But how does this relate to rheumatoid arthritis (RA). RA is an autoimmune reaction against the body’s own tissues which results in inflammation, pain and loss of function. Analysis of the synovial fluid of RA patients revealed that there was no lubricating ability. This indicates that the reduction in lubricating ability is a common feature of acute and chronic inflammatory arthritic conditions.
Now he has led a team that has determined that friction in the joints due to the absence of lubricin results in wear and damage to joints.
This conclusion was a result of research in which the team studied the cartilage from the knees of mice that were bred not to produce the protein. They found that at birth the mice had smooth cartilage. But after 2 weeks the cartilage in the mice’s joints began to show signs of wear. The damage, an early sign of joint disease, was clearly seen when viewed through a microscope.
Having determined a cause and effect relationship the team continued their research by looking at the structure of lubricin to determine how in works in the joint. They viewed lubricin protein under an atomic force microscope. What they found were many rows of interlocking fibers. This protein mesh had the ability to repel a microscopic probe with water and electrical charges. This clearly demonstrated how lubricin acts as a buffer in keeping opposing layers of cartilage apart.
Dr. Jay believes that a potential treatment for preventing wear in joints for arthritis sufferers and athletes can be developed. It is possible that lubricin, or a similar protein, could be injected into hips, knees, and other joints that already demonstrate symptoms of joint disease and injury as a preventive to further deterioration. Ultimately, this treatment might nearly eliminate the need for joint replacement surgery.