COX-2, NO, and cartilage damage and repair

Curr Rheumatol Rep. 2000 Dec;2(6):447-53. doi: 10.1007/s11926-000-0019-5.


The production of nitric oxide (NO) and prostaglandin E2 (PGE(2)) is increased in human osteoarthritis-affected cartilage. These and other inflammatory mediators are spontaneously released by OA cartilage explants ex vivo. The excessive production of nitric oxide inhibits matrix synthesis, and promotes its degradation. Furthermore, by reacting with oxidants such as superoxide anion, nitric oxide promotes cellular injury, and renders the chondrocyte susceptible to cytokine-induced apoptosis. PGE(2) exerts both anabolic and catabolic effects on chondrocytes, depending on the microenvironment and physiological condition. Thus, NO and PGE(2), produced by activated chondrocytes in diseased cartilage, may modulate disease rogression in osteoarthritis, and should therefore be considered potential targets for therapeutic intervention

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cartilage, Articular / metabolism*
  • Cyclooxygenase 2
  • Dinoprostone / biosynthesis*
  • Female
  • Homeostasis
  • Humans
  • Isoenzymes / biosynthesis*
  • Male
  • Membrane Proteins
  • Nitric Oxide / biosynthesis*
  • Osteoarthritis / complications
  • Osteoarthritis / physiopathology*
  • Osteochondritis / complications
  • Osteochondritis / metabolism
  • Prostaglandin-Endoperoxide Synthases / biosynthesis*
  • Regeneration / physiology*
  • Sensitivity and Specificity


  • Isoenzymes
  • Membrane Proteins
  • Nitric Oxide
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone