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Objectives: Arthritis affects more than 21 million Americans, including millions of veterans. Focal arthritic defects are the target of a number of new techniques aimed at repair or regeneration. Techniques under development involve the use of growth factors, tissue engineering (autologous cell impregnated scaffolds) and periosteal/perichondral explants. Several of these techniques provide a source of pluripotential cells within the defect capable of differentiating into bone, cartilage, or fibrocartilage. The differentiation process and the resulting tissue phenotype are regulated by biochemical factors as well as local mechanical cues. The objective of this study is to examine the role of mechanobiology in the physical rehabilitation of articular cartilage.
Methods: In this study we created finite element models of an idealized joint both with and without an osteochondral defect. The surface of the joint was exposed to a sweeping pressure load representing an articulating joint during flexion and extension motion. The stress and strain distributions within the defect were examined in the context of a tissue differentiation theory used previously to study fracture healing1, distraction osteogenesis2, and implant fixation3.
Results: When the joint load passes over the defect region, the tissue throughout the defect experiences hydrostatic pressure that is similar in magnitude to that experienced by the adjacent undamaged cartilage. Although this stimulus is expected to be chondrogenic, the repair tissue may not have adequate initial strength to support the stresses associated with full weight bearing. In addition, due to the material property difference between regenerating tissue and the surrounding cartilage, high tensile (and distortional) strains are generated in the defect tissue that are not present in normal cartilage. According to our tissue differentiation theory these tensile strains are expected to promote fibrocartilage, rather than articular cartilage, development.
Conclusions: The predictions from this model are consistent with the results of numerous studies in animals and humans. Due to differences in tissue stiffness between the healthy cartilage and the regenerating tissue abnormal tensile and distortional strains are created at the interfaces of the two materials. This mechanical situation is problematic since not only will this encourage fibrous tissue formation in the defect, but elevated levels of octahedral shear stresses (and distortional strains) will be created in the adjacent cartilage. These octahedral shear stresses will tend to accelerate the degenerative process in the healthy adjacent cartilage. The study provides new insights into the role of mechanobiology in the repair of focal cartilage defects. These insights will influence the design of novel physical and biological techniques for the repair of articular cartilage defects leading to improved long- term clinical outcomes.
References: 1) Carter et al., J Orthop Res 6:736-748, 1988; 2) Carter et al., Clin Orthop & Rel Res 355S:S41-S55, 1998; Giori et al., J Arthro 10:514-522, 1995.
Acknowledgments: Supported by the VA Rehabilitation R&D project A501-4RA.