The Effect of Endplate Lesions on Lumbar Disc Degeneration and the Mitigating Potential of Traction Intervention: a Finite Element Analysis

This study aims to simulate the process of disc degeneration induced by endplate lesions, quantify the effect of lesion type and severity on disc biomechanical response, and explore the potential of traction intervention in mitigating degenerative changes. A finite element model of the lumbar disc was constructed based on cell-activity coupled mechano-electrochemical mixture theory. Nutrient concentrations, cell density, glycosaminoglycan (GAG) content, water content, and tissue deformation within the disc were predicted under different endplate lesions (endplate calcification and Schmorl's nodes). The impact of traction loadings (100 N, 200 N, and 300 N) on the disc was investigated. The results showed that endplate lesion worsened nutrient concentrations, triggering cell death, which over time led to decreased GAG content, ultimately resulting in tissue shrinkage and a reduction in water content. With increasing endplate lesion severity, GAG content, water content, and volume ratio decreased, while disc height loss and disc radial deformation increased. Moreover, traction intervention increased the minimum glucose concentration, reduced the relative critical volume, and enhanced GAG content in a load-dependent linear manner (R2 > 0.93). This study characterizes the process of disc degeneration induced by endplate lesions, highlighting the significance of endplate integrity in maintaining disc health. A dose-response relationship exists between the severity of endplate lesions and the degree of disc degeneration, with endplate calcification appearing more detrimental than Schmorl's nodes. Furthermore, traction intervention may be effective in mitigating the progression of endplate lesion-induced disc degeneration.