Articular damage in arthritis and its control.
Erosion of joint surfaces in arthritic conditions is always associated with the degradation of the two principal matrix macromolecules of cartilage, proteoglycan and collagen. The major enzymes thought to be involved in articular catabolism have not been isolated, purified, and their properties studied, but precise spatial and temporal activities are still imperfectly understood. We are beginning to understand some aspects of cellular function in the control of catabolic enzyme function. Recent studies on molecular, cellular, and tissue mechanisms in this process are discussed here. 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.
D000818:Animals; D001168:Arthritis / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D002403:Cathepsins / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007596:Joints / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D008081:Liposomes; D010712:Phosphatidic Acids / Q000627:therapeutic use; D010713:Phosphatidylcholines / Q000627:therapeutic use; D011509:Proteoglycans / Q000378:metabolism; D013256:Steroids / Q000627:therapeutic use; D013582:Synovial Fluid / Q000201:enzymology
D008081:Liposomes; D010712:Phosphatidic Acids; D010713:Phosphatidylcholines; D011509:Proteoglycans; D013256:Steroids; D003094:Collagen; D002403:Cathepsins