A team of orthopaedic researchers has found definitive, genetic proof of how the most common form of arthritis destroys joint cartilage in nearly 21 million aging Americans, according to a study published online Sept. 2 in the Journal of Bone and Mineral Research.
The findings serve as an important foundation for the design of new treatments for osteoarthritis (OA), researchers said.
OA gradually destroys all cartilage in joints while forming scar tissue and painful bony growths. Advanced cases bring deformity and severe pain as patients loose the protective cushion between bones in weight-bearing joints like knees and hips. Until the late 1980s, OA was regarded as part of growing old. Since then, studies have revealed that biochemical changes contribute to the disease that might be reversed by drugs. Current medications, NSAIDs and Cox 2 inhibitors, are used to reduce symptoms in patients with mild cases, and joint replacement surgery for severe cases. Few options exist for those in between.
Going into the current study, little was known about the cellular and molecular events that cause cartilage to break down in osteoarthritic joints. Past studies had suggested that higher levels of a key signaling protein, beta-catenin, were connected to osteoarthritis, but there was no direct evidence to confirm it, or to suggest its role. The current study provides both.
Researchers genetically engineered adult mice to have high levels of beta-catenin, and saw that they lost most of their articular cartilage, the protective layer that covers the ends of bones within joints. The mice also developed the same bony growths and microfractures seen in the joints of human OA patients. A companion experiment on human cartilage cells taken from patients with severe arthritis also confirmed that their beta-catenin levels were much higher than normal.
"We have created study the first model in a living animal that shows exactly how osteoarthritis causes damage," said Di Chen, M.D., Ph.D., associate professor in the Department of Orthopaedics at the University of Rochester Medical Center, and lead author of the study. "That of course puts us in position to interfere with the processes that contribute to the damage in a new and powerful way."
http://www.sciencedaily.com/releases/2008/09/080902122838.htm