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Updated: Jul 10, 2026
The Monoiodoacetate Model of Osteoarthritis Pain in the Mouse
Published on: May 16, 2016
Up-regulation of peripheral and central CGRP expression combined with subchondral bone remodeling in rat MIA-induced
Liqin Xu1, Henghua Jiang1, Qijun Xu2
1State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, 430079 Wuhan, Hubei, China.
Background:
Temporomandibular joint osteoarthritis (TMJOA) is a pathological condition marked by subchondral bone remodeling. Osteoarthritis can lead to TMJ pain, nevertheless, the relationship between nociceptive mechanisms and subchondral bone in TMJOA still unclear.
Methods:
In the present investigation, a rat TMJOA model was established via intra-articular administration of monosodium iodoacetate (MIA). Following the induction of MIA-triggered TMJOA, tissue samples were collected from the TMJ condyle, trigeminal system components including ganglion (TG) and nucleus caudalis (TNC), and hippocampal formation. Micro-computed tomography (Micro-CT) was employed to evaluate subchondral bone degeneration in the TMJ, while tartrate-resistant acid phosphatase (TRAP) staining was conducted to measure the activity of osteoclasts in the subchondral bone. Furthermore, immunofluorescence (IF) staining was performed to detect the expression of calcitonin gene related peptide (CGRP) in the TMJ subchondral bone. Afterwards, immunohistochemistry (IHC) was used to detect the expression of CGRP in the TG, TNC and hippocampus tissues. The experimental results were expressed as mean ± Standard Error of the Mean (SEM) values and two-way Analysis of Variance (ANOVA) with Student-Newman-Keuls post hoc testing was employed for statistical comparisons, adopting a significance threshold of p < 0.05.
Results:
Compared with the control group, Micro-CT results revealed progressive condylar degeneration over time. Consistently, MIA-induced TMJOA rats demonstrated a pronounced accumulation of TRAP-positive osteoclasts in the subchondral bone. The expression of CGRP in the TMJ subchondral bone, TG, TNC and hippocampus tissues was also obviously increased in MIA-induced TMJOA rats.
Conclusions:
MIA-induced rat TMJOA pain could be attributed to the augmented exprssion of CGRP in the TMJ subchondral bone, TG, TNC and hippocampus tissues. An elevated level of CGRP stimulated nociception which was implicated in the development of peripheral and central sensitization in TMJOA pain.
