Review of pathogenesis of adjuvant arthritis and its relation to rheumatoid arthritis (Abstract)
Induced arthritis in rats has been utilized as an experimental model of rheumatoid arthritis and/or Reiter’s syndrome for more than two decades. It seems to be the best available model of human inflammatory joint diseases. In addition to the usual technique of inducing this disease in rats by complete Freund’s adjuvant it has recently been observed that a similar type of polyarthritis can be induced in rats with incomplete Freund’s adjuvant (IFA) plus (a) bacterial cell wall structures (usually made up of a disaccaride and an hexapeptide) (b) Type II collagen (c) a synthetic compound, MDP, (muramyl-dipeptide) or (d) a totally unrelated compound, a alkadimamine (molecular weight 714). It has also recently been shown that antibodies to Type II collagen appear in 40% of rats injected with Type II collagen in IFA. Furthermore, antibodies to both Type I and Type II collagen will soon be reported in traditional adjuvant arthritis. This animal disease can be inhibited or minimized by the early administration of immunosuppressive agents, or antiviral agents such as interferon. Later modifications of these forms of arthritis occur when anti-inflammatory compounds such as corticosteroids, butazoladine or a number of NSAIDs are given soon before the arthritis is to appear. There is pathological evidence that the latter compounds reduce the inflammatory synovitis and bony proliferation by about 50% when administered at sufficient dosage levels.