Finite element analysis of the effect of morphological differences in endplate defects on biomechanics of lumbar intervertebral discs

Abstract

BACKGROUND: Endplate defects are one of the important causative factors of lumbar degeneration, and their morphological characteristics may significantly affect the local mechanical environment of the spine. However, the effects of their different morphologic defects on the biomechanical properties of the lumbar spine have not been fully elucidated. OBJECTIVE: To investigate the effects of focal marginal defects, focal central defects, and angular defects on the stress distribution of lumbar endplates, intervertebral discs, and small joints, and to reveal their underlying biomechanical mechanisms. METHODS: Lumbar CT images were obtained from a healthy 36-year-old male volunteer, and a complete endplate model of the L4-L5 segment was reconstructed. Three typical endplate defect models (focal marginal defect, focal central defect, and angular defect) were constructed based on the classification of vertebral endplate defects in clinical imaging studies. By applying dynamic loads and corresponding moments to simulate physiological spinal muscle loads and typical motion loads, such as stance, forward flexion, backward extension, lateral bending, and rotation, the biomechanical stress distribution characteristics and peak changes in the vertebral cartilage endplates, intervertebral disc annulus fibrosus, nucleus pulposus, and facet joints during physiological spinal movements were evaluated. The effects of different defect types on the biomechanical stability of the lumbar spine were explored. RESULTS AND CONCLUSION: (1) Different defect types significantly altered the stress transmission pathways of the endplate and adjacent structures; marginal defects mainly affected the lateral annulus fibrosus stress distribution, while central defects significantly changed load bearing during extension. (2) There was obvious stress gradient concentration at the defect edges, suggesting potential microdamage risk. (3) Angular endplate defects produced significant stress concentration under dynamic loads, possibly being one of the high-risk factors leading to segmental instability and accelerated degeneration. (4) The experimental results provide biomechanical evidence for the involvement of endplate defects in intervertebral disc degeneration and facet joint damage, and have important guiding value for early clinical identification of high-risk defect types and formulation of targeted prevention strategies.

1. Introduction

Factors associated with the progression of intervertebral disc degeneration include aging, insufficient nutrient supply to disc cells, and higher mechanical stress. Biomechanical evidence suggests that initial damage or structural defects in the annulus fibrosus or endplate can lead to disc degeneration [1-3]. Recent studies have focused on vertebral endplate degeneration and structural defects, which may play an important role in the pathogenesis of disc degeneration [4-6].

The vertebral endplate, as the interface tissue between the vertebral trabecular bone and the intervertebral disc, is crucial for maintaining the morphological and functional integrity of both structures [7-8]. It helps balance loads between the disc and vertebral body, maintains normal hydrostatic pressure in the nucleus pulposus by resisting water loss under load, and regulates nutrient metabolite transport between the disc and vertebral body [9]. The motion segment or functional spinal unit consists of two adjacent vertebrae, the intervertebral disc, and all adjacent ligaments. The vertebral endplate is a relatively thin, porous structure that cannot withstand compressive stress over the long term and is prone to fracture and structural defects, making it a 'weak link' in the lumbar spine [10].

Clinical imaging techniques such as computed tomography and MRI can detect subtle changes in endplate structure, especially MRI, which can also reveal subchondral bone marrow changes associated with endplate defects (i.e., abnormalities, fractures, damage, interruptions, or discontinuities in the structural endplate morphology) [11-12]. Structural endplate damage leads to lower intradiscal pressure in the affected spinal motion segment and adjacent nucleus pulposus, causing the annulus fibrosus to bear [text truncated]