Investigation of acute and chronic injury mechanisms of the deltoid ligament: insights from finite element analysis and animal study

BACKGROUND: The deltoid ligament (DL) is the primary stabilizer of the medial ankle, but its injury mechanisms remain poorly understood. This study aimed to investigate the injury risk and mechanisms of individual DL bundles under both acute and chronic conditions to inform prevention and treatment strategies. METHODS: A validated finite element model of the human foot was used to examine peak stresses in DL bundles under four acute loading scenarios. Chronic loading was simulated by applying gait loads after transecting the lateral ligaments, and the resulting DL stresses were compared with those of the intact model. Additionally, thirty-nine rats were assigned to three groups: a lateral ligament rupture group (LR, n = 13), a tibialis posterior tendon rupture group (TPR, n = 13), and a sham group (n = 13). After 6 weeks of treadmill running, the mechanical properties and histological characteristics of the DL, along with ankle joint morphology and articular stresses, were evaluated to further verify the hypothesized mechanisms of chronic injury. RESULTS: Under acute loadings, the tibiocalcaneal ligament (TCL), anterior tibiotalar ligament (ATTL), and deep posterior tibiotalar ligament (dPTTL) showed the highest stress under pronation-external rotation loading. Lateral ligament rupture increased DL stress during gait. After 6 weeks of treadmill running, the LR and TPR groups showed roughened articular surfaces with osteophyte formation, increased articular stress, decreased talar bone volume fraction, lower failure load and stiffness ratios of the DL (p < 0.01), reduced fluorescence intensity of COL1, and elevated levels of COL3, MMP-2 and IL-1β compared with the sham group (p < 0.01). CONCLUSION: The TCL, ATTL, and dPTTL bundles are particularly susceptible to acute injury, with pronation-external rotation posing the greatest risk. Chronic degeneration of the DL occurs following rupture of the lateral ligament or tibialis posterior tendon, with a more pronounced effect after lateral ligament rupture.