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Telomere Erosion and Senescence in Human Articular Cartilage Chondrocytes

^a Iowa City Veterans Administration Medical Center and University of Iowa Department of Orthopaedics, Iowa City

James A. Martin, Department of Orthopaedic Surgery, Biochemistry Laboratory, 1182 ML, The University of Iowa, Iowa City, IA 52242 E-mail: james-martin{at}uiowa.edu.

Decision Editor: John A. Faulkner, PhD

Aging and the degeneration of articular cartilage in osteoarthritis are distinct processes, but a strong association exists between age and the incidence and prevalence of osteoarthritis. We hypothesized that this association is due to in vivo replicative senescence, which causes age-related declines in the ability of chondrocytes to maintain articular cartilage. For this hypothesis to be tested, senescence-associated markers were measured in human articular chondrocytes from donors ranging in age from 1 to 87 years. These measures included in situ staining for senescence-associated ß-galactosidase activity, ³H-thymidine incorporation assays for mitotic activity, and Southern blots for telomere length determinations. We found that senescence-associated ß-galactosidase activity increased with age, whereas both mitotic activity and mean telomere length declined. These findings indicate that chondrocyte replicative senescence occurs in vivo and support the hypothesis that the association between osteoarthritis and aging is due in part to replicative senescence. The data also imply that transplantation procedures performed to restore damaged articular surfaces could be limited by the inability of older chondrocytes to form new cartilage after transplantation.

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