Simulation of the disc degeneration with a poroelastic finite element model
To predict the degeneration process in the intervertebral disc, a finite element model of the spinal motion segment model was developed. The relationship between the biomechanical characteristics of fluid and solid matrix of the disc and cancellous core of the vertebral body, modeled as 20 node poroelastic elements, during the degeneration process was investigated. Excess von Mises stress in the disc element was assumed to be a possible source of degeneration under compressive loading condition. Recursive calculation was continued until the desired convergence was attained by changing the permeability and void ratio of those elements. The degenerated disc model showed that relatively small compressive stresses were generated in the nucleus elements compared to normal disc. Its distribution along the sagittal plane was consistent with a previously reported experimental result. Contrasts to this result, pore pressures in the nucleus were higher than those in the normal disc. Total stress, sum of compressive stress and pore pressure, indicated similar values for two different models. This study presented a new approach to study the likely mechanism responsible for the initiation and progression of the degenerative process within the intervertebral disc.
KeywordsDisc Degeneration FE model Poroelastic element Void ratio
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- Ghosh, P. and SC, B., 1988, “The Biology of the Intervertebral Disc,“CRC Press, USA, pp. 99–105.Google Scholar
- Kim, K. W., Lim, T. H., Kim, J. G., Jeong, S. T., Masuda, K. and An, H. S., 2003, “The Origin of Chondrocytes in the Nucleus Pulposus and Histologic Findings Associated with the Transition of a Notochordal Nucleus Pulposus to a Fibrocartilaginous Nucleus Pulposus in Intact Rabbit Intervertebral Discs,“Spine, Vol. 28, pp. 982–990.CrossRefGoogle Scholar
- Kuslich, S. D., Ulstrom, C. L. and Michael, C. J., 1991, “The Tissue Origin of Low Back Pain and Sciatica,“Orthop. Clin. N. Am., Vol. 22, pp. 181–187.Google Scholar