Progress in understanding rheumatoid (RA) and inflammatory arthritis has been limited in part because there has been no widely accepted animal model of naturally occurring human disease and because the clinical syndrome of RA may reflect the expression of multiple etiologies. We have considered that inflammatory joint disease may be induced and/or exacerbated by food related antigens. To facilitate our investigations, we studied inflammatory synovitis in rabbits induced by oral exposure to environmental antigens. In our preliminary experiments, we examined 9 Florida White, 30 New Zealand White, and 9 Old English rabbits. They were nourished with normal rabbit chow supplemented with either water or cow's milk beginning at age 7 to 26 weeks and observed for 81 to 204 days. Animals were then sacrificed. Histological sections of the knees were examined and graded in a blinded fashion for synovial cell hyperplasia, inflammation, and lymphoplasmocytic infiltration. In addition, serum levels of IgG antimilk, IgG antibovine serum albumin, IgG anticasein, and IgG-C3 complexes were quantified. We found no abnormalities among Florida White rabbits but observed histological synovitis in 53% of the milk fed New Zealand White (9/17), 40% of the water fed Old English (2/5), and all of the milk fed Old English rabbits (4/4) (p = 0.05, milk fed vs water fed animals). Milk fed animals had significantly (p less than 0.0005) greater levels of antibodies and complexes than water fed animals. Our data suggest that environmental antigens may be arthritogenic for some rabbit strains. These observations may provide an important model for the study of inflammatory joint disease analogous to oral, environmental antigen exposure in man.
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