Effect of etodolac on type-II collagen-induced arthritis in mice

Abstract

We tested the effect of etodolac on the development of type-II collagen-induced arthritis in DBA/1J mice. It was administered orally once daily for 35 days after the primary immunization with type-II collagen. Etodolac (10 mg/kg) significantly inhibited the development of signs of arthritis on day 28 to day 35. Indomethacin (1 mg/kg) also significantly inhibited it on day 29 to day 34. Radiographic examination showed that etodolac (10 mg/kg) significantly prevented the development of osteopenia, bone erosion and new bone formation of the joints on day 35, while indomethacin (1 mg/kg) significantly prevented only the development of bone erosion. Histopathological examination showed that both etodolac (10 mg/kg) and indomethacin (1 mg/kg) significantly prevented the development of synovitis, erosion of cartilage of the joints and bone destruction of the limbs on day 35. Etodolac and indomethacin did not affect the serum level of anti-type-II collagen antibodies. These results suggest that etodolac and indomethacin suppress type-II collagen-induced arthritis without affecting humoral immune responses.

The effect of etodolac on experimental temporomandibular joint osteoarthritis in dogs

“…Similar results have been found in other studies of the effects of etodolac on osteoarthritis in animal limbs (Wooley et al, 1987;Inoue et al, 1993;Johnston and Budsberg, 1997;Budsberg et al, 1999;Mathews, 2000). The mechanism of this drug's action is believed to involve inhibition of COX-2 activity (Gervais et al, 1984;Lynch and Brogden, 1986;Humber, 1987).…”

“…Etodolac suppresses osteoarthritis induced experimentally in limbs of mice (Wooley et al, 1987). High doses of etodolac are more effective than lower doses (Inoue et al, 1993). Effects of etodolac on TMJ osteoarthritis have not yet been assessed in (previously reported) experimental studies.…”

Utility of animal models for identification of potential therapeutics for rheumatoid arthritis

“…The AIA model was commonly used to evaluate corticosteroids, NSAIDs and selective cyclo-oxygenase-2 (COX-2) inhibitors; these classes of agent showed therapeutic efficacy in this model. The NSAID indomethacin also showed therapeutic efficacy when tested in the rat and mouse CIA models 36 62 65 70 – 72. It is important to note that NSAIDs are effective in treating the pain associated with arthritis, but these drugs do not inhibit progression of joint damage, despite demonstrating efficacy in the rodent models of arthritis.…”

Suppression of Adjuvant-Induced Arthritic Bone Destruction by Cyclooxygenase-2 Selective Agents With and Without Inhibitory Potency Against Carbonic Anhydrase II

“…Accumulated evidence has also shown the bonesparing effects of COX-2 inhibitors using mouse and rat models in vitro and in vivo. (10,34,(44)(45)(46)(47) Because both COX-2 and CAII show 80-90% homologies in nucleotides and amino acids among mice, rats, and humans, (48)(49)(50) these results may be applicable to humans. For the clinical application of COX-2 selective agents as a treatment of bone resorptive disorders including RA, however, we should be cautious not only with cardiovascular events above, but also with possible inhibition of bone repair and ingrowth that has recently been reported in animal models when administered for a long period of time.…”