Erosion of joint surfaces in arthritic conditions is always associated with the degradation of the 2 principal matrix macromolecules of cartilage, proteoglycan and collagen. The major enzymes thought to be involved in articular catabolism have now been isolated, purified, and their properties studied, but precise spatial and temporal activities are still imperfectly understood. Some aspects of cellular function in the control of catabolic enzyme function are beginning to be understood. Recent studies on molecular, cellular and tissue mechanisms in this process are discussed. Of particular interest is a possible natural control mechanism involving a recently discovered inhibitor of collagenase. A newly developed pharmacologic method of inflammation control utilizes the properties of liposomes in the closed environment of the joint cavity. Very low doses of modified steroids encapsulated within liposomes are capable of substantially reducing inflammation in experimentally arthritic animals and may be applicable to man.