The sensitivity of synthesis of human cartilage matrix to inhibition by IL-1 suggests a mechanism for the development of osteoarthritis.

The damage to articular cartilage, characteristic of arthritic disease, is usually ascribed to increased degradative activity by enzymes or free radicals from locally activated cells. We propose that inhibition of matrix synthesis, and consequential impairment of the natural repair process, may be at least as important in chronic joint disease.