Mouse model of subtalar post-traumatic osteoarthritis caused by subtalar joint instability

Abstract

Background Common ankle sprains are often accompanied by injury to the subtalar joint, which eventually leads to subtalar joint instability. Because the clinical manifestations for subtalar joint instability are similar to ankle joint injuries, these are often overlooked. This study aimed to establish an animal model of subtalar joint instability to study post-traumatic osteoarthritis of the subtalar joint caused by long-term subtalar joint instability and to provide a reference for future clinical research on chronic subtalar joint instability. Methods In all, 24 C57BL/6 male mice were randomly divided into three groups: Sham, cervical ligament (CL) transection and CL + calcaneofibular ligament (CFL) transection groups. One week after surgical operation, all mice were trained to run in the mouse rotation fatigue machine every day. During this period, a balance beam test was used to evaluate the motor level and coordination ability of the mice before the operation and three days, one week, four weeks, eight weeks, and twelve weeks after operation. Further, post-traumatic osteoarthritis of the subtalar joint was quantified via micro-CT and histological staining. Results The mice in the partial ligament transection group took significantly longer than those in the Sham group to pass through the balance beam and showed an increased number of hindfoot slips. Micro-CT analysis showed that the subtalar bone volume fraction in the CL + CFL transection group and CL transection group was 5.8% and 2.8% higher than that in the Sham group, respectively. Histological staining showed obvious signs of post-traumatic osteoarthritis (PTOA) in the subtalar joint of the ligament transection group. Conclusions The transection of CL and CL + CFL can cause instability of the subtalar joint in mice, resulting in a decrease in motor coordination, and long-term instability of the subtalar joint in mice can cause PTOA of the subtalar joint, which is manifested as destruction and loss of articular cartilage.