Model of Monoiodoacetate-Induced Osteoarthritis in Laboratory Animals

The development of an adequate biomodel of a pathological condition, comparable to the observed clinical case, remains an urgent problem. In order to study the analgesic and anti-inflammatory activity of potential pharmacological substances, it is important to develop inflammation models with signs of cartilage tissue degeneration and pain induced by inflammation. This extends the capabilities of modern approaches. In this work, a model of arthritis induced by monoiodoacetate (MIA) (Sigma-Aldrich, USA) was carried out on rats. To that end, 3 mg of MIA in 50 μl of sterile saline solution was administered intra-articularly into the right knee joint. The model was verified using standard therapy with non-steroidal anti-inflammatory drugs (meloxicam, ibuprofen), which were administered daily from day 3 to day 14 after MIA. Inflammation and behavioral changes associated with pain were assessed on days 3, 7, and 14. On days 8 and 15, the rats were euthanized, and biological material (blood and right knee joint) was collected for histological analysis. The concentration of IL-1β in the synovial fluid was measured on days 8 and 15 after MIA administration to the knee joint of the rats. A single administration of ibuprofen had a pronounced analgesic activity, preventing disability and not weakening the grip strength of the paw into which MIA was administered. At the same time, the selective inhibitor of cyclooxygenase meloxicam was only capable of reducing mechanical hypersensitivity in a von Frey test. Therefore, the effects of a single and course administration were highly similar in terms of the level of influence in pain tests. However, regular administration of cyclooxygenase inhibitors reduced joint inflammation more effectively than a single dose. Meloxicam showed a higher efficiency than ibuprofen in reducing joint inflammation. The results are shown after histological analysis of the knee joint injected with MIA. Thus, a model of osteoarthritis induced by MIA in laboratory animals was developed and characterized.