It is well accepted that aging is one of the most prominent risk factors for the initiation and progression of osteoarthritis. One of the most pronounced age-related changes in chondrocytes is the exhibition of a senescent phenotype, which is the result of several factors including the accumulation of reactive oxygen species and advanced glycation end products. Compared with a normal chondrocyte, senescent chondrocytes exhibit an impaired ability to respond to many mechanical and inflammatory insults to the articular cartilage. Furthermore, protein secretion is altered in aging chondrocytes, demonstrated by a decrease in anabolic activity and increased production of proinflammatory cytokines and matrix-degrading enzymes. Together, these events may make the articular cartilage matrix more susceptible to damage and lead to the onset of osteoarthritis. A better understanding of the mechanisms underlying age-related chondrocyte pathophysiology may be critical for the development of novel therapeutic interventions for progressive joint diseases.