Cartilage destruction in murine antigen induced arthritis is characterized by enhanced degradation of proteoglycans and inhibition of chondrocyte proteoglycan synthesis. Within this model common NSAIDs only suppress joint swelling, and to some extent granulocyte infiltration, but leave the process of cartilage destruction undisturbed. Evidence is now accumulating that the vast amount of activated granulocytes in the joint space are of minor importance, and that interleukin-1 (IL-1) is the key mediator in this process. Treatment of mice with neutralizing antibodies against IL-1 resulted in relief of chondrocyte proteoglycan synthesis inhibition and prevented matrix destruction. This indicates that it makes sense to focus future therapy on elimination of IL-1.