Nitric oxide and arthritis

MARÍA S. DI GENARO

Advances in Chemistry and Biology of Nitric Oxide

Research Signpost

Lugar: Kerala, India; Año: 2007; p. 179 - 206

Inflammatory joint diseases include various forms of arthritis such as rheumatoid arthritis (RA), septic arthritis, reactive arthritis (ReA) and osteoarthritis (OA). RA is an autoimmune disease that is characterised by persistent joint inflammation, which results in chronic tissue destruction. ReA, in contract with septic arthritis, is a sterile chronic arthritis that develops after gastrointestinal or genitourinary infection. OA is characterised by progressive cartilage destruction. Nitric oxide (NO), produced by inducible nitric oxide synthase (iNOS), has been shown to be involved in various inflammatory arthritis in a complex manner. Expression of iNOS is induced following exposure to pro-inflammatory cytokines and bacterial products. Synovium and cartilage are important sources of NO production in patients with inflammatory arthritis. Once synthesised, iNOS generates large amounts of NO. A vast amount of evidence implicates NO as mediator of inflammation and/or tissue destruction in arthritic disorders. However, some recent studies support the concept of NO as an important immunoregulator molecule. Thus, NO induces a population of regulatory T cells (Treg), and these Treg efficiently suppress several arthritic responses. The current chapter presents an overview of the dual role of NO in arthritis as cytotoxic effector and immunoregulator. Molecular mechanisms of NO action will be discussed.