Inflammatory Joint Disease: Clinical, Histological, and Molecular Parameters of Acute and Chronic Inflammation and Tissue Destruction

Peptidoglycan-polysaccharide complexes from Group A streptococcal cell walls (SCW) induce a biphasic inflammatory response in rats that resembles rheumatoid arthritis (RA) in humans (1–3). Initiation of synovitis is dependent on the dissemination, deposition, and persistence of the SCW in the synovium. The subsequent infiltration of leukocytes into the synovial tissue coincides with the development of an acute inflammatory response. The clinical acute phase is transient and as the erythema and swelling subside, mononuclear cells are recruited into the synovial tissue as the chronic, erosive arthritis evolves. Similar to RA, susceptibility to the development of SCW-arthritis is gender-biased (4) and under genetic control with neuroendocrine and hormonal influences (5–7). Moreover, the mechanisms responsible for the development of SCW-arthritis are susceptible to regulation by pharmacologic agents and biological response modifiers and as such, this model is considered a valid preclinical model of RA.