ArticleAnimal models and experimental medicine2026
Time- and dose-related pathological changes in knee osteoarthritis rat model induced by monosodium iodoacetate.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Adipose-derived mesenchymal stem cell injection into the KI10 acupoint mitigates cartilage damage in KOA rats through PGE2-mediated α7nAChR/NF-κB pathway.Animal models and experimental medicine · 2026Article
- Curcuminoids Phospholipid Attenuates Osteoarthritis and Protects Cartilage in a Monosodium Iodoacetate-Induced Rat Model.Nutrients · 2026Article
- Electroacupuncture alleviates osteoarthritis and is associated with changes in gut microbiota and steroid biosynthesis-related metabolites.Frontiers in molecular biosciences · 2026Article
- Time- and dose-related pathological changes in knee osteoarthritis rat model induced by monosodium iodoacetate.Animal models and experimental medicine · 2026Article
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Abstract
Knee osteoarthritis (KOA) is a chronic degenerative disease. Monosodium iodoacetate (MIA) induction is the most commonly used therapeutic effect evaluation and mechanism of action research model; we observed a lack of standardization and uniformity in current model building methods, which led us to conduct this study.
backgroundThe aim was to investigate the time- and dose-related changes in the behavioral and pathological characteristics in the MIA-induced KOA model rat.
methodsMIA (40, 50, and 60 mg/mL) was injected into the left joint of male Sprague-Dawley rats. After 2 weeks, the changes in the KOA rat model were observed by behavioral evaluation, imaging-level evaluation, and histological-level evaluation. The changes were also compared after 40-mg/mL MIA injection for 2 and 6 weeks.
resultsMIA-induced bone surface defects, osteophyte hyperplasia around the articular rim, increased subchondral bone density, thinning of the sparse trabecular bone, structural disorder, and local clustering were observed. The degree of injury gradually increased with the increase in MIA concentration. After 6 weeks, subchondral bone density and sparse trabecular bone increased in the KOA model.
conclusionsThe severity of the model also increased significantly with the changes in dose and time. In dose-dependent experiments, this study revealed that 40 mg/mL was the optimal dose to induce significant pathological changes without causing undue discomfort or death in animals. This dose may induce pathological changes stably and is suitable for long-term observation.
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