A novel mouse model for full-thickness articular cartilage defects

Yunru Ge; Huan Liu; Qirui Ding; Haonan Qin; Peng Sun; Yongxin Ren

doi:10.1016/j.injury.2025.112528

A novel mouse model for full-thickness articular cartilage defects

Injury. 2025 Jun 17;56(8):112528. doi: 10.1016/j.injury.2025.112528. Online ahead of print.

Authors

Yunru Ge¹, Huan Liu², Qirui Ding², Haonan Qin², Peng Sun², Yongxin Ren³

Affiliations

¹ Department 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.
² 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.
³ Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029 Jiangsu Province, PR China. Electronic address: renyongxinjsph@163.com.

PMID: 40570648
DOI: 10.1016/j.injury.2025.112528

Abstract

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.

Keywords: Animal model; Articular cartilage defects; Cartilage repair; Full-thickness.