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Updated: Sep 18, 2025
Development and Evaluation of a Rat Model of Full-Thickness Cartilage Defects
Published on: May 19, 2023
A novel mouse model for full-thickness articular cartilage defects
Yunru Ge1, Huan Liu2, Qirui Ding2
1Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029 Jiangsu Province, PR China; Department of Orthopedics, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an City 223300 Jiangsu Province, PR China; Department of Orthopedics, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Northern Jiangsu Institute of Clinical Medicine, Nanjing Medical University, Huai'an City 223300 Jiangsu Province, PR China.
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This study reported the development of a novel mouse model for full-thickness articular cartilage defects. A total of 120 C57BL/6 mice were assigned to a sham group and three defect groups. The defect groups included D0.1, D0.2, and D0.3 groups, with 0.1, 0.2, and 0.3 mm wide full-thickness defects in the femoral trochlear grooves, respectively. The reproducibility and consistency of full-thickness defects and cartilage repair were evaluated by histological examination. The mRNA and protein expression levels of cAMP response element binding protein (CREB), phosphorylated CREB (p-CREB), parathyroid receptor 1 (PTH1R), Sonic hedgehog (Shh), Smoothened (Smo), and Gli 1 were assessed by immunohistochemistry and qRT-PCR. The results showed that the full-thickness defects displayed good reproducibility and consistency. Injury widths of 0.1 and 0.2 mm presented superior repair abilities than 0.3 mm (p < 0.05). During cartilage repair, the expression levels of PTH1R, CREB, p-CREB, Shh, Smo, and Gli 1 in the three defect groups were significantly higher than in the sham group (p < 0.05). In addition, the PTH/PTHrP and Hh signaling pathways were activated. In conclusion, we successfully established a novel mouse model for full-thickness articular cartilage defects, which enables deeper exploration of the biological mechanisms involved in cartilage repair in mice.
