Biomechanics and Modeling in Mechanobiology

, Volume 7, Issue 5, pp 405–416

A finite element model predicts the mechanotransduction response of tendon cells to cyclic tensile loading

Authors

    • Laboratory for Comparative Orthopaedic Research, College of Veterinary MedicineMichigan State University
  • Steven P. Arnoczky
    • Laboratory for Comparative Orthopaedic Research, College of Veterinary MedicineMichigan State University
  • Eugene Kepich
    • Orthopaedic Biomechanics Laboratories, College of Osteopathic MedicineMichigan State University
  • Oscar Caballero
    • Laboratory for Comparative Orthopaedic Research, College of Veterinary MedicineMichigan State University
  • Roger C. Haut
    • Orthopaedic Biomechanics Laboratories, College of Osteopathic MedicineMichigan State University
Original Paper

DOI: 10.1007/s10237-007-0104-z

Cite this article as:
Lavagnino, M., Arnoczky, S.P., Kepich, E. et al. Biomech Model Mechanobiol (2008) 7: 405. doi:10.1007/s10237-007-0104-z

Abstract

The importance of fluid-flow-induced shear stress and matrix-induced cell deformation in transmitting the global tendon load into a cellular mechanotransduction response is yet to be determined. A multiscale computational tendon model composed of both matrix and fluid phases was created to examine how global tendon loading may affect fluid-flow-induced shear stresses and membrane strains at the cellular level. The model was then used to develop a quantitative experiment to help understand the roles of membrane strains and fluid-induced shear stresses on the biological response of individual cells. The model was able to predict the global response of tendon to applied strain (stress, fluid exudation), as well as the associated cellular response of increased fluid-flow-induced shear stress with strain rate and matrix-induced cell deformation with strain amplitude. The model analysis, combined with the experimental results, demonstrated that both strain rate and strain amplitude are able to independently alter rat interstitial collagenase gene expression through increases in fluid-flow-induced shear stress and matrix-induced cell deformation, respectively.

Copyright information

© Springer-Verlag 2007