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01-01-2015 | Osteoarthritis | Book Chapter | Article

1. Pathogenesis of Osteoarthritis

Author: PhD Mohit Kapoor

Publisher: Springer International Publishing

Abstract

  • Osteoarthritis (OA) is one of the most chronic health disorders in the western world and becomes particularly common with advanced age. The joints most commonly affected by OA include the knees, hips, ankle, elbow, shoulder, hand, wrist and spine.
  • Risk factors that may increase the risk of developing OA are age, gender, joint injury or overuse caused by physical labour or sports, obesity, joint alignment, and heredity.
  • Symptoms of OA may appear well after disease onset. Such symptoms include joint pain, limitation of motion, stiffness after inactivity, tenderness, crepitus, and joint enlargement.
  • While previously characterized as a disease of progressive articular cartilage degradation, OA pathophysiology involves all of the tissues that form the synovial joint which are the subchondral and metaphyseal bone, synovium, ligaments, joint capsules, and the muscles acting across the joint. Subchondral bone remodelling, osteophyte formation, synovial inflammation, ligamentous laxity (loose ligaments), and the weakening of periarticular muscles exemplify several joint structure alterations observed.
  • Chondrocytes, the only cell types present in the articular cartilage, are responsible for maintaining an equilibrium between the anabolic and catabolic activities in the extracellular matrix (ECM).
  • The trigger of OA is unclear; however, it may begin with tissue damage from mechanical injury, infiltration of inflammatory mediators from the synovium into the cartilage, or defects in cartilage metabolism/homeostasis. Chondrocytes attempt to repair cartilage damage/degradation by increasing the production of ECM macromolecules. As degeneration continues, catabolic mechanisms overpower the anabolic capabilities of chondrocytes and the homeostatic balance is tipped resulting in progressed cartilage breakdown.

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