The Freund's adjuvant‐injected rat shares a number of features with the arthritis patient, viz the presence of a proliferative synovitis, joint swelling, and cartilage and bone erosion. Naproxen, a prostaglandin synthetase inhibitor which is an effective antiinflammatory agent in laboratory animals and humans, was evaluated as an inhibitor of connective tissue destruction in this model by use of radiologic and histopathologic analyses. Sixteen days after rats were injected with Freund's complete adjuvant, marked joint swelling was noted. On day 17, vehicle or naproxen, 7 mg/kg/day, was administered orally. Twenty‐eight days later, vehicle‐treated animals demonstrated the following pathologic changes in their hindpaws: swelling, cartilage loss, large amounts of pannus within the joint spaces, osteoporosis, bone erosions, periosteal new bone formation, heterotopic ossification, and bony ankylosis. Rats treated 28 days with naproxen had significantly milder disease than the vehicle controls. The incidence of severe juxtaarticular bone destruction was 10/10 in the vehicle controls versus 2/10 of the drug‐treated group (P < 0.01). A comparable reduction in cartilage erosion, incidence of pannus, and new bone formation was noted in the drug‐treated group. These effects may relate to an inhibition of prostaglandin biosynthesis; prostaglandins have been shown to: 1) stimulate collagenase secretion from macrophages, 2) stimulate bone resorption in vivo and in vitro, and 3) diminish proteoglycan synthesis in cartilage.
A technique for the induction of contact sensitivity in the cynomolgus monkey
is described. Seventy percent of the monkeys gave a positive reaction when skin-tested
18 days after sensitization with dinitrochlorobenzene. When re-tested on day 27, both the
number of reactors and the intensity of the reactions had increased. Histological examinations
showed perivascular leukocytic infiltration with an increased proportion of mononuclear
cells, typical of a delayed hypersensitive reaction.
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