Elsevier

Journal of Biomechanics

Volume 42, Issue 3, 9 February 2009, Pages 341-348
Journal of Biomechanics

Influence of single-level lumbar degenerative disc disease on the behavior of the adjacent segments—A finite element model study

https://doi.org/10.1016/j.jbiomech.2008.11.024Get rights and content

Abstract

The current study investigated mechanical predictors for the development of adjacent disc degeneration. A 3-D finite element model of a lumbar spine was modified to simulate two grades of degeneration at the L4–L5 disc. Degeneration was modeled by changes in geometry and material properties. All models were subjected to follower preloads of 800 N and moment loads in the three principal directions of motion using a hybrid protocol. Degeneration caused changes in the loading and motion patterns of the segments above and below the degenerated disc. At the level (L3–L4) above the degenerated disc, the motion increased due to moderate degeneration by 21% under lateral bending, 26% under axial rotation and 28% under flexion/extension. At the level (L5-S1) below the degenerated disc, motion increased only during lateral bending by 20% due to moderate degeneration. Both the L3–L4 and L5-S1 segment showed a monotonic increase in both the maximum von Mises stress and shear stress in the annulus as degeneration progressed for all loading directions, expect extension at L3–L4. The most significant increase in stress was observed at the L5-S1 level during axial rotation with nearly a ten-fold increase in the maximum shear stress and 103% increase in the maximum von Mises stress. The L5-S1 segment also showed a progressive increase in facet contact force for all loading directions with degeneration. Nucleus pressure did not increase significantly for any loading direction at either the caudal or cephalic adjacent segment. Results suggest that single-level degeneration can increase the risk for injury at the adjacent levels.

Introduction

Degenerative disc disease (DDD) is a progressive condition that alters the biochemistry and morphology of the intervertebral disc (IVD) eventually affecting its ability to support and transfer loads. Observation of the macroscopic patterns of the disease suggests that further deterioration of the disc is significantly related to the number of degenerated discs and ageing (Elfering et al., 2002; Waris et al., 2007). Why IVDs adjacent to a degenerated level have a higher prevalence of developing the disease remains unknown. Abnormal mechanical loads and/or motion patterns have been traditionally linked to degenerative changes of the spine and a risk for injury (Adams et al., 2000; Stokes and Iatridis, 2004). Understanding how DDD alters the biomechanics of the spine is of clinical significance, due to its association with chronic lower back pain, sciatica, and adult onset scoliosis (Kjaer et al., 2006).

With degeneration, the nucleus dehydrates and transitions from a fluid-like behavior to a solid-like behavior making it harder to distinguish it from the annulus fibrosus (Iatridis et al., 1997). The progressive loss of hydration leads to a decrease in the disc height and high localized stress peaks in the annulus (Adams et al., 1996; Frobin et al., 2001). Abnormal mechanics in terms of magnitude and asymmetry of motion, transverse or sagittal translation, location of the instantaneous axis of rotation, patterns of coupled motion and load bearing at the neural arch and facet joints have been reported with DDD (Seligman et al., 1984; Mimura et al., 1994; Fujiwara et al., 2000; Lund et al., 2002; Pollintine et al., 2004). Despite numerous studies on the mechanics of the degenerated disc, limited data exists on how the condition affects the adjacent caudal and cephalic segments, thus contributing to the progression of disc degeneration.

The goal of this study was to quantitatively describe how DDD at a single level alters the loading and motion patterns of the adjacent discs by means of a three-dimensional finite element model (FEM) of the lumbar spine subjected to physiological loading conditions. We hypothesized that progressive degeneration at a single-level would cause the adjacent cephalic and caudal segments to undergo,

  • (1)

    an increase in rotational motion in the three principal axes of motion,

  • (2)

    an increase in the maximum shear stress and von Mises stress of the annulus ground substance,

  • (3)

    an increase in facet contact forces and,

  • (4)

    an increase in nucleus pressure.

Section snippets

Non-linear three-dimensional FEM of a healthy lumbar spine

A FEM of the lumbar spine was previously developed by our research team (Renner et al., 2007). The vertebral body cancellous bone, cortical bone and posterior elements were modeled with a linear isotropic elastic law (Table 1). The annulus was modeled as a fiber-reinforced composite material. The annulus ground substance was modeled by Mooney–Rivlin hyper-elastic elements. Three layers of fibers were embedded in the annulus at an angle of inclination of ±30° with the horizontal plane. The

Results

The predicted response of the FEM of the healthy spine compared favorably with values obtained in-vitro. The segmental range of motion during FLEX/EXT bending loads with 800 N of follower preload and without preload, fell within one standard deviation of the in-vitro results at all levels except L3–L4 and L4–L5 (Fig. 1). In-vitro values of segmental motion during LB and AR were only available under no preload conditions. The predicted segmental range of motion during LB loads for all levels fell

Discussion

A three-dimensional non-linear FEM of the lumbar spine with degeneration at the L4–L5 disc level has been developed. Two different grades of disc degeneration were modeled by changing both the geometry and associated material properties. Adjacent level effects were tested using a hybrid protocol as per the recommendations of Panjabi (2007). Models were subjected to compressive preloads of physiological magnitude using the follower load technique (Patwardhan et al., 1999).

Some of the FEM results

Conflict of interest statement

The authors do not have any financial and personal relationships with other people or organizations to disclose that could inappropriately influence and/or bias the work.

Acknowledgements

The authors would like to thank Susan M. Renner, Ph.D., for providing the in-vitro data. This study was funded in part by the National Institute of Health (NIH AR48152-02).

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