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Simulating the multiphysics of the intervertebral disc and the likely implications of disc cell nutrition in disc degeneration
Intervertebral disc (IVD) cells can easily develop catabolic activities and die under limited nutrition. Lumbar IVD are the largest avascular organs in human bodies, and cell nutrition relies on diffusion processes, in interaction with the mechanical response of the tissues. But the role of nutrition in disc degeneration or ageing is unclear. This research exploits the strength of numerical modelling and explores cause-and-effect relationships among IVD mechanics and morphology, cell nutrition, and tissue condition and regulation.3D porohyperelastic IVD finite element models incorporated the annulus fibrosus (AF) composite structure and the nucleus pulposus (NP) osmotic pressure, in function of tissue composition and/or condition. Poromechanical calculations were coupled to metabolic transport models that predicted the diffusion of oxygen, glucose and lactate, in function of coupled solute reactions and of glucose- and pH-dependent cell viability. This framework was used to simulate the effect of: 1) mechanical cues on the nutrition-dependent cell viability, 2) tissue alterations and disc geometries on cell nutrition and viability, and 3) effective cell nutrition on the proteoglycan turnover.
Under compressive loads representative of human daily activity, deformation-induced reductions of diffusion distances competed with tissue consolidation, in terms of effect on solute distributions. For standard disc heights (c.a. 10 mm), consolidation largely hindered glucose diffusion, but mechanical overloads or endplate sclerosis were necessary to induce cell death. Nutrition seemed to control the proteoglycan loss characteristic of ageing. However, simulated NP dehydration with healthy proteoglycan contents already caused drops of glucose in the inner AF, suggesting that nutrition-induced catabolic activities may locally precede the commonly reported NP degeneration. In (e.g. 14 mm) thick IVDs, increased diffusion distances affected directly the NP cell viability independently on tissue condition. All in all, the different mechanical and biophysical interplays identified might help to explain the diversity of disc degeneration phenotypes.
Acknowledgments: EC (MySpine-GA-269909)
Author(s):
Jerome Noailly
Biomechanics and Mechanobiology, Institute for Bioengineering of Catalonia (IBEC)
Spain
Carlos Ruiz Wills
Biomechanics and Mechanobiology, Institute for Bioengineering of Catalonia (IBEC)
Spain
Andrea Malandrino
Biomechanics and Mechanobiology, Institute for Bioengineering of Catalonia (IBEC)
Spain