Abstract
Capturing patient- or condition-specific intervertebral disk (IVD) properties in finite element models is outmost important in order to explore how biomechanical and biophysical processes may interact in spine diseases. However, disk degenerative changes are often modeled through equations similar to those employed for healthy organs, which might not be valid. As for the simulated effects of degenerative changes, they likely depend on specific disk geometries. Accordingly, we explored the ability of continuum tissue models to simulate disk degenerative changes. We further used the results in order to assess the interplay between these simulated changes and particular IVD morphologies, in relation to disk cell nutrition, a potentially important factor in disk tissue regulation. A protocol to derive patient-specific computational models from clinical images was applied to different spine specimens. In vitro, IVD creep tests were used to optimize poro-hyperelastic input material parameters in these models, in function of the IVD degeneration grade. The use of condition-specific tissue model parameters in the specimen-specific geometrical models was validated against independent kinematic measurements in vitro. Then, models were coupled to a transport-cell viability model in order to assess the respective effects of tissue degeneration and disk geometry on cell viability. While classic disk poro-mechanical models failed in representing known degenerative changes, additional simulation of tissue damage allowed model validation and gave degeneration-dependent material properties related to osmotic pressure and water loss, and to increased fibrosis. Surprisingly, nutrition-induced cell death was independent of the grade-dependent material properties, but was favored by increased diffusion distances in large IVDs. Our results suggest that in situ geometrical screening of IVD morphology might help to anticipate particular mechanisms of disk degeneration.
Highlights
Changes in the optimal biophysics of the intervertebral disk (IVD) are thought to be one of the major causes of degeneration, in contrast to the normal aging processes (Smith et al, 2011)
The IVD is the largest avascular organ in humans and the metabolism of the relatively few disk cells has to ensure the maintenance of a large amount of extracellular matrix (ECM), while it mainly relies on proper diffusion of metabolites from and to the periphery of the disk
nucleus pulposus (NP) damaged shear modulus, calculated from Eq 8 increased with degeneration while annulus fibrosus (AF) damaged shear modulus showed a decrease from grade 3 to grade 4 (Figure 4A), in agreement with the increase of AF damage
Summary
Changes in the optimal biophysics of the intervertebral disk (IVD) are thought to be one of the major causes of degeneration, in contrast to the normal aging processes (Smith et al, 2011). The IVD is the largest avascular organ in humans and the metabolism of the relatively few disk cells has to ensure the maintenance of a large amount of extracellular matrix (ECM), while it mainly relies on proper diffusion of metabolites from and to the periphery of the disk. Such a situation can have deleterious effects in the innermost regions of the disk (Huang et al, 2014), which might be worsen by the fact that disk cells seem prone to catabolic responses in presence of limited nutrition (Rinkler et al, 2010; Neidlinger-Wilke et al, 2012). Disk cell biology should be considered along with the mechanical competence of the disk tissues
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