Mechanical response of the spine to various dynamic loading conditions can be analyzed by way of in vitro and in vivo studies. Ethical concerns, interpretation of conclusions reached in animal studies, and lack of detailed stress distributions in the disc components are the major disadvantages of relying solely on in vivo studies. Intraspecimen variability, difficulty in including muscle activity, and inability to mimic fluid exchange into the disc during unloading are some of the disadvantages of in vitro models. The poroelastic finite element models can provide a method of understanding the relationship between biomechanical performance of the disc due to cyclic loading and disc degeneration. A poroelastic finite element model, including regional variation of strain-dependent permeability and osmotic pressure, was used to study the effect of disc degeneration on biomechanical properties as well as propagation of failure in the disc components when cyclic loading was applied to the lumbar disc. The results predicted that healthy discs were much more flexible than degenerated discs, and the disc stiffness decreased with increasing the number of load cycles independent of degenerative condition. Failure was found to progress as the drained elastic properties of the disc components decreased due to the presence of failure.
Poroelastic finite element modeling, including strain-dependent permeability and osmotic pressure, is the most advanced analytical tool currently available that can be used to understand how cyclic loading affects the biomechanical characteristics of a degenerated lumbar disc. However, a complete understanding of behavior of the intervertebral disc will ultimately be achieved only with use of a combination of computational models together with in vitro and in vivo experimental methods.
Finite element models of discs with varying degrees of disc degeneration will help clinicians understand the initiation and progression of disc failure and degeneration and will assist in the development of approaches to stimulate the regeneration of disc tissues.
In support of their research for or preparation of this manuscript, one or more of the authors received grants or outside funding from the National Institutes of Health (NIH:AR 48152-02). None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.
- Copyright © 2006 by The Journal of Bone and Joint Surgery, Incorporated
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