Animal models of rheumatoid arthritis and their relevance to human disease  Krishnaswamy Kannan, Robert A. Ortmann, Donald Kimpel  Pathophysiology  Volume 12, Issue 3, Pages 167-181 (October 2005) DOI: 10.1016/j.pathophys.2005.07.011 Copyright © 2005 Terms and Conditions

Fig. 1 Time kinetics of arthritis development in female Lewis rats injected with SCW antigen. Female Lewis rats were injected with 10s fraction of PGPS by a single i.p. injection and the day of PGPS injection designated as ‘0’ day. Rats were scored for arthritis (arthritis index) daily for the first 10 days, then thrice weekly by a set visual criterion as previously described [30]. A score of 0–4 was assigned to each paw with a theoretical maximum of 16 per mouse as follows: (1) hyperemia and redness with little or no swelling; (2) swelling was confined predominantly to the ankle region; (3) joint swelling was extended to ankle and metatarsal regions and when the swelling area was extensive and more obvious; and (4) maximal paw swelling in both ankle and metatarsal regions and or involving disability in mobility typically manifested by rat dragging the hind paws. The data included in this figure is obtained from two individual rats during a 4 week period. Pathophysiology 2005 12, 167-181DOI: (10.1016/j.pathophys.2005.07.011) Copyright © 2005 Terms and Conditions

Fig. 2 Genetic models of arthritis: IL-1 receptor antagonist gene deletion and K/BxN mice. IL-1ra gene knockout mice on the BALB/c background develop a mild arthritis in the hindpaws (A); compared to littermate controls (B). The arthritis is evident in the mild thickening of the midfoot, and on the medial aspect of the ankle with loss of distinction of the achilles tendon. The IL-1−/− mice also exhibit a distinct “scruffy” appearance to their coat (C); compared to littermate controls (D). When krn mice, which carry the transgene for a specific TCR, are crossed to NOD mice or mice transgenic for the H2g7 of NOD an inflammatory arthritis develops spontaneously (E); which is not present in the littermate controls which lack the TCR transgene (F). Pathophysiology 2005 12, 167-181DOI: (10.1016/j.pathophys.2005.07.011) Copyright © 2005 Terms and Conditions