Scientists at Johns Hopkins have turned their view of osteoarthritis (OA) inside out. Literally. Instead of seeing the painful degenerative disease as a problem primarily of the cartilage that cushions joints, they now have evidence that the bone underneath the cartilage is also a key player and exacerbates the damage. In a proof-of-concept experiment, they found that blocking the action of a critical bone regulation protein in mice halts progression of the disease.
The prevailing theory on the development of OA focuses on joint cartilage, suggesting that unstable mechanical pressure on the joints leads to more and more harm to the cartilage - and pain to the patient - until the only treatment option left is total knee or hip replacement. The new theory, reported May 19 in Nature Medicine, suggests that initial harm to the cartilage causes the bone underneath it to behave improperly by building surplus bone. The extra bone stretches the cartilage above and speeds its decline.
“If there is something wrong with the leg of your chair and you try to fix it by replacing the cushion, you haven’t solved the problem,” says Xu Cao, Ph.D., director of the Center for Musculoskeletal Research in the Department of Orthopaedic Surgery at the Johns Hopkins University School of Medicine. “We think that the problem in OA is not just the cartilage ‘cushion,’ but the bone underneath,” he adds.
Joints are formed at the intersection of two bones. To prevent the grinding and wearing down of the ends of the bones, they are capped with a thin layer of cartilage, which not only provides a smooth surface for joint rotation but also absorbs some of the weight and mechanical strain placed on the joint. The degeneration of this protective layer causes extreme pain leading to limited mobility.