Research Papers

3D Finite Element Analysis of Nutrient Distributions and Cell Viability in the Intervertebral Disc: Effects of Deformation and Degeneration

[+] Author and Article Information
Alicia R. Jackson

Tissue Biomechanics Lab,  Department of Biomedical Engineering, University of Miami, Coral Gables, FL 33146; Department of Orthopaedics,  University of Miami Miller School of Medicine, Miami, FL 33136

Chun-Yuh C. Huang

Stem Cell and Mechanobiology Lab,  Department of Biomedical Engineering, University of Miami, Coral Gables, FL 33146

Mark D. Brown

Department of Orthopaedics,  University of Miami Miller School of Medicine, Miami, FL 33136

Wei Yong Gu1

Tissue Biomechanics Lab,  Department of Biomedical Engineering, University of Miami, Coral Gables, FL 33146; Department of Mechanical and Aerospace Engineering,  University of Miami, Coral Gables, FL 33146 e-mail: wgu@miami.edu


Corresponding author.

J Biomech Eng 133(9), 091006 (Oct 11, 2011) (7 pages) doi:10.1115/1.4004944 History: Received July 12, 2011; Accepted August 22, 2011; Published October 11, 2011; Online October 11, 2011

The intervertebral disc (IVD) receives important nutrients, such as glucose, from surrounding blood vessels. Poor nutritional supply is believed to play a key role in disc degeneration. Several investigators have presented finite element models of the IVD to investigate disc nutrition; however, none has predicted nutrient levels and cell viability in the disc with a realistic 3D geometry and tissue properties coupled to mechanical deformation. Understanding how degeneration and loading affect nutrition and cell viability is necessary for elucidating the mechanisms of disc degeneration and low back pain. The objective of this study was to analyze the effects of disc degeneration and static deformation on glucose distributions and cell viability in the IVD using finite element analysis. A realistic 3D finite element model of the IVD was developed based on mechano-electrochemical mixture theory. In the model, the cellular metabolic activities and viability were related to nutrient concentrations, and transport properties of nutrients were dependent on tissue deformation. The effects of disc degeneration and mechanical compression on glucose concentrations and cell density distributions in the IVD were investigated. To examine effects of disc degeneration, tissue properties were altered to reflect those of degenerated tissue, including reduced water content, fixed charge density, height, and endplate permeability. Two mechanical loading conditions were also investigated: a reference (undeformed) case and a 10% static deformation case. In general, nutrient levels decreased moving away from the nutritional supply at the disc periphery. Minimum glucose levels were at the interface between the nucleus and annulus regions of the disc. Deformation caused a 6.2% decrease in the minimum glucose concentration in the normal IVD, while degeneration resulted in an 80% decrease. Although cell density was not affected in the undeformed normal disc, there was a decrease in cell viability in the degenerated case, in which averaged cell density fell 11% compared with the normal case. This effect was further exacerbated by deformation of the degenerated IVD. Both deformation and disc degeneration altered the glucose distribution in the IVD. For the degenerated case, glucose levels fell below levels necessary for maintaining cell viability, and cell density decreased. This study provides important insight into nutrition-related mechanisms of disc degeneration. Moreover, our model may serve as a powerful tool in the development of new treatments for low back pain.

Copyright © 2011 by American Society of Mechanical Engineers
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Figure 1

(a) Schematic of the intervertebral disc showing the annulus fibrosus (AF), nucleus pulposus (NP), and cartilaginous endplate (CEP) regions; (b) photograph of human L2-L3 disc using for determining disc geometry; (c) mesh of upper right quarter of disc.

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Figure 2

Criteria for cell viability based on threshold levels of glucose. Cell density varies with glucose concentration: when glucose levels fall below 0.5 mM, cell density decreases (i.e., cells begin to die) in a linear fashion until reaching 0.2 mM, when cell density reaches zero (i.e., all cells die).

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Figure 3

Schematic showing (a) reference configuration, without deformation; (b) deformation configuration, with 10% static axial compression

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Figure 4

Glucose distributions and minimum concentrations in the IVD for the four cases investigated: (a) normal disc in reference (i.e., undeformed) configuration; (b) normal disc in deformed configuration; (c) degenerated disc in reference configuration; (d) degenerated disc in deformed configuration

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Figure 5

Normalized cell density in the degenerated disc for (a) reference and (b) deformed cases. Note that the density is for the slice shown in the upper left is shown. Cell density values are normalized by original values (see Table 1).




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