Pathological Characteristics of Monosodium Iodoacetate-Induced Osteoarthritis in Rats
10.1007/s13770-023-00520-5
- Author:
Minji KWON
1
;
Dongyeon NAM
;
Junesun KIM
Author Information
1. Rehabilitation Science Program, Department of Health Science, Graduate School, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea
- Publication Type:ORIGINAL ARTICLE
- From:
Tissue Engineering and Regenerative Medicine
2023;20(3):435-446
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND:This study aimed to identify pain-related behavior and pathological characteristics of the knee joint in rats with monosodium iodoacetate (MIA)-induced osteoarthritis (OA).
METHODS:Knee joint inflammation was induced by intra-articular injection of MIA (4 mg/50 lL, n = 14) in 6-weekold male rats. Knee joint diameter, weight-bearing percentage on the hind limb during walking, the knee bending score, and paw withdrawal to mechanical stimuli were measured to evaluate edema and pain-related behavior for 28 d after MIA injection. Histological changes in the knee joints were evaluated using safranin O fast green staining on days 1, 3, 5, 7, 14, and 28 after OA induction (n = 3, respectively). Changes in bone structure and bone mineral density (BMD) were examined 14 and 28 d after OA (n = 3, respectively) using micro-computed tomography (CT).
RESULTS:The knee joint diameter and knee bending scores of the ipsilateral joint significantly increased 1 d after MIA injection, and the increased knee joint diameter and knee bending score persisted for 28 d. Weight-bearing during walking and paw withdrawal threshold (PWT) decreased from 1 and 5 d, respectively, and were maintained up to 28 d after MIA. Cartilage destruction started on day 1, and Mankin scores for bone destruction significantly increased for 14 d, as shown by micro-CT imaging.
CONCLUSION:The present study demonstrated that histopathological structural changes in the knee joint due to inflammation started soon after MIA injection, which induced OA pain from inflammation-related acute pain to spontaneous and evoked associated chronic pain.
