Department of Orthopedic Surgery, School of Biology and Basic Medical Sciences, Orthopedic Institute, The First Affiliated Hospital, Suzhou Medical College, Soochow University, 899 Pinghai Road, Suzhou, Jiangsu, 215007, People's Republic of China.
School of Physical Education and Sports, Soochow University, 50 Donghuan Road, Suzhou, Jiangsu, 215006, People's Republic of China.
Arthritis Res Ther. 2024 Sep 28;26(1):168. doi: 10.1186/s13075-024-03402-w.
Untreated acute ankle sprains often result in chronic ankle instability (CAI) and can ultimately lead to the development of post-traumatic osteoarthritis (PTOA). At present, a typical animal model of ankle instability in mice is established by transecting the ligaments around the ankle joint. This study aimed to establish a grade I acute ankle sprain animal model by rapid stretching of peri-ankle joint ligaments. Furthermore, we tried to explore the pathophysiological mechanism of ankle osteoarthritis.
In all, 18 male C57BL/6 J mice (7 weeks) were randomly divided into three groups: calcaneofibular ligament (CFL) laxity group, deltoid ligament (DL) laxity group, and SHAM group. One week after the surgical procedure, all mice were trained to run in the mouse rotation fatigue machine daily. The mice were tested on the balance beam before surgery and three days, 4 weeks, 8 weeks, and 12 weeks after surgery. Footprint analyses were performed on each mouse before surgery and 12 weeks after surgery. Micro-CT scanning was then performed to evaluate the degeneration of ankle joints and histological staining was performed to analyze and evaluate PTOA caused by ankle joint instability.
After surgery, the mice in the CFL and DL laxity groups took longer to cross the balance beam and slipped more often than those in the SHAM group (p < 0.05). The step length and width in the CFL and DL laxity groups were significantly shorter and smaller than those in the SHAM group 12 weeks after surgery (p < 0.05). There was a significant increase in the bone volume fraction (BV/TV) in the CFL and DL laxity groups compared with the SHAM group (p < 0.05). Histological staining results suggested obvious signs of PTOA in the CFL and DL laxity groups.
Based on CFL and DL laxity in a mouse ankle instability model, this study suggests that grade I ankle sprain can contribute to chronic ankle instability, impair motor coordination and balance, and eventually lead to PTOA of ankle with significant degeneration of its adjacent joints.
未经治疗的急性踝关节扭伤常导致慢性踝关节不稳定(CAI),最终可导致创伤后骨关节炎(PTOA)的发生。目前,通过切断踝关节周围的韧带在小鼠中建立典型的踝关节不稳定动物模型。本研究旨在通过快速拉伸踝关节周围的韧带来建立 I 级急性踝关节扭伤动物模型。此外,我们试图探讨踝关节骨关节炎的病理生理机制。
共 18 只雄性 C57BL/6J 小鼠(7 周)随机分为三组:跟腓韧带(CFL)松弛组、距腓前韧带(DL)松弛组和 SHAM 组。手术后一周,所有小鼠每天都在小鼠旋转疲劳机上进行训练。所有小鼠在手术前和手术后 3 天、4 周、8 周和 12 周进行平衡梁测试。在手术前和手术后 12 周对每只小鼠进行足迹分析。然后进行微 CT 扫描以评估踝关节的退变,并进行组织学染色以分析和评估由踝关节不稳定引起的 PTOA。
手术后,CFL 和 DL 松弛组的小鼠在平衡梁上的通过时间更长,滑倒次数多于 SHAM 组(p<0.05)。CFL 和 DL 松弛组的步幅和步宽在手术后 12 周明显短于 SHAM 组(p<0.05)。与 SHAM 组相比,CFL 和 DL 松弛组的骨体积分数(BV/TV)明显增加(p<0.05)。组织学染色结果表明 CFL 和 DL 松弛组有明显的 PTOA 迹象。
基于 CFL 和 DL 松弛的小鼠踝关节不稳定模型,本研究表明 I 级踝关节扭伤可导致慢性踝关节不稳定,损害运动协调和平衡,最终导致踝关节 PTOA 及其相邻关节明显退变。