Influences of Nutrition Supply and Pathways on the Degenerative Patterns in Human Intervertebral Disc

Abstract

Study design: Investigation of the effects of the impairment of different nutritional pathways on the intervertebral disc degeneration patterns in terms of spatial distributions of cell density, glycosaminoglycan content, and water content.

Objective: The aim of this study was to test the hypothesis that impairment of different nutritional pathways would result in different degenerative patterns in human discs.

Summary of background data: Impairment of nutritional pathways has been found to affect cell viability in the disc. However, details on how impairment of different nutritional pathways affects the disc degeneration patterns are unknown.

Methods: A 3D finite element model was used for this study. This finite element method was based on the cell-activity coupled mechano-electrochemical theory for cartilaginous tissues. Impairment of the nutritional pathways was simulated by lowering the nutrition level at the disc boundaries. Effects of the impartment of cartilaginous endplate-nucleus pulposus (CEP-NP) pathway only (Case 1), annulus fibrosus (AF) pathway only (Case 2), and both pathways (Case 3) on disc degeneration patterns were studied.

Results: The predicted critical levels of nutrition for Case 1, Case 2, and Case 3 were around 30%, 20%, and 50% of the reference values, respectively. Below this critical level, the disc degeneration would occur. Disc degeneration appeared mainly in the NP for Case 1, in the outer AF for Case 2, and in both the NP and inner to middle AF for Case 3. For Cases 1 and 3, the loss of water content was primarily located in the mid-axial plane, which is consistent with the horizontal gray band seen in some T2-weighted magnetic resonance imaging (MRI). For the disc geometry used in this study, it was predicted that there existed a high-intensity zone (for Case 3), as seen in some T2-weighted MRI images.

Conclusion: Impairment of different nutrition pathways results in different degenerative patterns.

Level of evidence: N/A.

Figure 1

(A) Geometry and size of the disc from human lumbar spine (L2–3, male, non-degenerated) and (B) Schematic of the right–upper quarter of the disc used in the simulations. The cell density in the healthy disc was assumed to be 4000 cells/mm³ in NP and 9000 cells/mm³ in AF.

Figure 2

Three-dimensional distributions of normalized cell density at steady state after nutrient concentrations on CEP-NP boundary decreased to 30%, 20%, 10%, and 0% of the corresponding reference values.

Figure 3

Three-dimensional distributions of normalized cell density at steady state after nutrient concentrations on AF periphery decreased to 20%, 15%, 10%, and 0% of the corresponding reference values.

Figure 4

Three-dimensional distributions of normalized cell density at steady state after nutrient concentrations on both NP and AF boundaries decreased to 50%, 40%, 30%, 20% and 10% of the corresponding reference values.

Figure 5

(A) Percent of the affected regions (relative to the whole disc volume) where cell death is greater than 10% of the corresponding value at healthy state for Case 1 (black line), Case 2 (red line), and Case 3 (blue line). (B) Changes in normalized cell density (averaged over the whole disc volume) for Case 1 (black line), Case 2 (red line), and Case 3 (blue line). All the results presented in this figure were values at steady state.

Figure 6

Comparison of the GAG content distributions (A) in the healthy disc with reference values of nutrition level, (B) in Case 1 where nutrition level was decreased in CEP-NP pathway only, (C) in Case 2 where nutrition level was decreased in AF pathway only, and (D) in Case 3 where nutrition level was reduced in both pathways. The results shown in (B-D) are GAG distributions at 10 years after cell density reached steady state as nutrition level reduced to 15% of the reference values.

Figure 7

Comparison of the water content distributions on the disc mid-axial plane (A) in the healthy disc with reference values of nutrition level, (B) in Case 1 where nutrition level was decreased in CEP-NP pathway only, (C) in Case 2 where nutrition level was decreased in AF pathway only, and (D) in Case 3 where nutrition level was decreased in both pathways. The high water content zone is clearly shown in the posterior region in the disc for Case 3. The results shown in (B-D) are water content distributions at 10 years after cell density reached steady state as nutrition level reduced to 15% of the corresponding reference values.

Figure 8

Comparison of the water content distributions on the mid-sagittal plane (A) in the healthy disc with reference values of nutrition level, (B) in Case 1 where nutritional level was decreased in CEP-NP pathway only, (C) in Case 2 where nutrition level was decreased in AF pathway only, and (D) in Case 3 where nutrition level was decreased in both pathways. The results shown in (B–D) are water content distributions at 10 years after cell density reached steady state as nutrition level reduced to 15% of the corresponding reference values.