Aging phenomena and osteoarthritis: cause or coincidence? Claude P. Brown memorial lecture.
Osteoarthritis is an ubiquitous disease, primarily occurring in older individuals. Any attempt to explain the disease in terms of biologic aging must first define the basic pathology of the disease, accurately classify the clinicopathologic variants of the disease, and develop a scientific approach to the recognition of the pathologic physiology of any known precursor states. This epidemiologic information must insure comparability between populations of patients or animals under study, since significant differences in susceptibility among groups do exist. Cumulative environmental influences on joints do have pathophysiologic consequences but require careful study to isolate cause and effect from coincidental occurrences. Musculoskeletal aging itself is a complex process including both post-synthetic changes in the extracellular matrix macromolecules and alteration of phenotypic expression by the connective tissue cells themselves. In contrast to older assertions that chondrocytes are terminally differentiated cells incapable of replication, evidence has accumulated that chondrocytes proliferate in vivo and in vitro under appropriate conditions. Studies in several laboratories have confirmed that articular chondrocytes from aged animals both proliferate and synthesize macromolecules in a fashion similar to comparable cells extracted from young animals. Further studies are necessary before osteoarthritis can be definitively separated into aging-dependent and aging-independent categories.
D000375:Aging; D002356:Cartilage / Q000473:pathology / Q000503:physiopathology; D003094:Collagen / Q000378:metabolism; D006801:Humans; D007596:Joints / Q000473:pathology / Q000503:physiopathology; D010003:Osteoarthritis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D011509:Proteoglycans / Q000378:metabolism
D011509:Proteoglycans; D003094:Collagen