This paper was presented at the symposium by Alan J. Grodzinsky to whom correspondence should be addressed.
Tissue-Engineered Versus Native Cartilage: Linkage between Cellular Mechano-Transduction and Biomechanical Properties
- Gregory Bock Organizer and
- Jamie Goode
Published Online: 7 OCT 2008
Copyright © Novartis Foundation 2003
Tissue Engineering of Cartilage and Bone: Novartis Foundation Symposium 249
How to Cite
Lee, J. H., Kisiday, J. and Grodzinsky, A. J. (2003) Tissue-Engineered Versus Native Cartilage: Linkage between Cellular Mechano-Transduction and Biomechanical Properties, in Tissue Engineering of Cartilage and Bone: Novartis Foundation Symposium 249 (eds G. Bock and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470867973.ch5
- Published Online: 7 OCT 2008
- Published Print: 11 MAR 2003
Book Series Editors:
- Novartis Foundation
Print ISBN: 9780470844816
Online ISBN: 9780470867976
Recent studies demonstrate that chondrocytes in native articular cartilage and in tissue-engineered constructs respond to mechanical stimuli through multiple regulatory pathways. Responses of the cells are manifested by intra- and intercellular signalling, alterations in transcription level, protein translation, post-translational modifications, and synthesis of intracellular and extracellular macromolecules. In addition, mechanical stimuli can alter the balance between anabolic and catabolic processes that are critically important to cell-mediated extracellular assembly and degradation of the tissue matrix and, therefore, to the survival of tissue engineered constructs. Chondrocyte mechanotransduction is therefore a critically important link to the biomechanical properties of native cartilage and to developing constructs. Since implanted cartilage repair tissue will be subjected to mechanical loads throughout its lifetime, it is essential that the resident cells respond appropriately to the range of static and dynamic compressive and shear deformations in vivo in a manner that enables adaptive remodelling and minimizes catabolic degradation. The in vivo environment should thereby signal tissue-specific maturation and integration processes in order to achieve the most appropriate tissue morphology and biomechanical function.