Although arthritis occurs in many different forms, loss of articular cartilage and joint inflammation are the predominant pathophysiological processes consistently present in this group of diseases. Depending upon the particular arthritide, these two pathologies may take place together or separately. Evidence is accumulating to suggest that NO is produced locally within human osteoarthritic and rheumatoid joints. The articular chondrocytes and, perhaps, infiltrating leukocytes appear to be the major intraarticular sources of NO. All published data agree that biosynthesis of NO increases in animal models of rheumatoid arthritis, and inhibitors of NO synthases show strong prophylactic, anti-inflammatory activity. However, one study suggests that therapeutic activity may be weak. Chondrocytes produce large amounts of NO after exposure to interleukin-1 (IL-1). In rabbit, human and rat, but not bovine, articular cartilage endogenously produced NO inhibits the biosynthesis of matrix proteoglycans. However, studies with bovine articular cartilage further indicate that NO partially protects proteoglycans from degradation in response to IL-1. These data encourage the notion that NO is involved in the pathophysiology of arthritis, but caution that this involvement may be complex.
ASJC Scopus subject areas
- Molecular Biology
- General Biochemistry, Genetics and Molecular Biology