Physical signals and solute transport in human intervertebral disc during compressive stress relaxation: 3D finite element analysis.
A 3D finite element model for charged hydrated soft tissues containing charged/uncharged solutes was developed based on the multi-phasic mechano-electrochemical mixture theory (Lai et al., J. Biomech. Eng. 113 (1991), 245-258; Gu et al., J. Biomech. Eng. 120 (1998), 169-180). This model was applied to analyze the mechanical, chemical and electrical signals within the human intervertebral disc during an unconfined compressive stress relaxation test. The effects of tissue composition [e.g., water content and fixed charge density (FCD)] on the physical signals and the transport rate of fluid, ions and nutrients were investigated. The numerical simulation showed that, during disc compression, the fluid pressurization was more pronounced at the center (nucleus) region of the disc while the effective (von Mises) stress was higher at the outer (annulus) region. Parametric analyses revealed that the decrease in initial tissue water content (0.7-0.8) increased the peak stress and relaxation time due to the reduction of permeability, causing greater fluid pressurization effect. The electrical signals within the disc were more sensitive to FCD than tissue porosity, and mechanical loading affected the large solute (e.g., growth factor) transport significantly, but not for small solute (e.g., glucose). Moreover, this study confirmed that the interstitial fluid pressurization plays an important role in the load support mechanism of IVD by sharing more than 40% of the total load during disc compression. This study is important for understanding disc biomechanics, disc nutrition and disc mechanobiology.
Yao
Hai
H
Department of Bioengineering, Clemson University, Clemson, SC, USA.
Gu
Wei Yong
WY
D001692:Biological Transport / Q000502:physiology; D001834:Body Water / Q000378:metabolism; D004594:Electrophysiology; D020342:Finite Element Analysis; D006801:Humans; D007403:Intervertebral Disc / Q000378:metabolism / Q000502:physiology*; D040542:Mechanotransduction, Cellular / Q000502:physiology; D008954:Models, Biological; D016062:Porosity; D013314:Stress, Mechanical; D016474:Weight-Bearing / Q000502:physiology