Experimentally dissociating the overuse mechanisms of endplate fracture lesions and Schmorl's node injuries using the porcine cervical spine model.

Background: Compared to the documented overuse mechanisms of endplate fracture lesions, the cause of Schmorl's node injuries remains unknown, despite existing hypotheses. Therefore, this study aimed to examine and dissociate the overuse injury mechanisms of these spinal pathologies.

Methods: Forty-eight porcine cervical spinal units were included. Spinal units were randomly assigned to groups that differed by initial condition (control, sham, chemical fragility, structural void) and loading posture (flexed, neutral). Chemical fragility and structural void groups involved a verified 49% reduction in localized infra-endplate trabecular bone strength and removal of central trabecular bone, respectively. All experimental groups were exposed to cyclic compression loading that was normalized to 30% of the predicted tolerance until failure occurred. The cycles to failure were examined using a general linear model and the distribution of injury types were examined using chi-squared statistics.

Findings: The incidence of fracture lesions and Schmorl's nodes was 31(65%) and 17(35%), respectively. Schmorl's nodes were exclusive to chemical fragility and structural void groups and 88% occurred in the caudal joint endplate (p = 0.004). In contrast, 100% of control and sham spinal units sustained fracture lesions, with 100% occurring in the cranial joint endplate (p < 0.001). Spinal units tolerated 665 fewer cycles when cyclically loaded in flexed postures compared to neutral (p = 0.015). Furthermore, the chemical fragility and structural void groups tolerated 5318 fewer cycles compared to the control and sham groups (p < 0.001).

Interpretation: These findings demonstrate that Schmorl's node and fracture lesion injuries can result from pre-existing differences in the structural integrity of trabecular bone supporting the central endplate.