Articular cartilage is a dense connective tissue that lines the bony surfaces of diarthrodial joints, providing low friction and wear during joint motion. Mechanical loading of cartilage has been shown to be efficacious and necessary for the maintenance of normal metabolic activities of chondrocytes. The primary objective of this thesis is to examine the roles of physical stimulation and/or nutrient transport as possible mechanisms leading to such cartilaginous growth. The effect of dynamic loading on nutrient transport in tissue engineering of replacement constructs is investigated. Moreover, the effect of loading on the in-situ deformation behavior of the chondrocyte microenvironment is also examined.

Interpreting the effects of physical loading on cells hinges on our understanding of its surrounding extracellular matrix, and the structure-function relationships that the tissue possesses. Therefore the mechanical properties of cartilage were investigated, examining the anisotropy, inhomogeneity, and tension-compression nonlinearity of bovine shoulder and human patellar tissues. These findings are interpreted in the context of contributions from proteoglycan molecules and organization of type II collagen.

Based on the findings described in this thesis, mechanical loading appears to dramatically modulate the physical signals in and around chondrocytes, resulting in strain amplification in the cellular microenvironment relative to the applied deformation. Additionally, dynamic loading was found to enhance the rate of transport of growth factor like solutes into tissue constructs. Consequently, dynamic loading of cartilage or engineered constructs results in an environment that is simultaneously physically and metabolically stimulating.