Abstract

Osteoarthritis (OA), a degenerative joint disease, increases in prevalence with age, and affects majority of individuals over the age of 65. OA frequently affects several joints including the hands, knees, hips and spine, and is a leading cause of impaired mobility in the elderly. The major clinical symptoms include chronic pain, joint instability, stiffness and radiographic joint space narrowing (Felson, 2006; Goldring & Goldring, 2007). During OA development, articular chondrocytes undergo hypertrophy leading to extracellular matrix degradation, articular cartilage breakdown and osteophyte formation in the margins of the articular cartilage (Felson, 2006; Goldring & Goldrig, 2007). The precise signaling pathways which are involved in the degradation of cartilage matrix and development of OA are poorly understood and there are currently no effective interventions to decelerate the progression of OA or retard the irreversible degradation of cartilage except for total joint replacement surgery (Krasnokutsky et al., 2007). In this chapter, we will summarize important molecular mechanisms related to OA pathogenesis and provide new insights into potential molecular targets for the prevention and treatment of OA.

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