Articular cartilage exhibits complex mechanical properties such as anisotropy, inhomogeneity and tension-compression nonlinearity. This study proposes and demonstrates that the application of compressive loading in the presence of osmotic swelling can be used to acquire a spectrum of incremental cartilage moduli (EYi) and Poisson's ratios (upsilon ij) from tension to compression. Furthermore, the anisotropy of the tissue can be characterized in both tension and compression by conducting these experiments along three mutually perpendicular loading directions: parallel to split-line (1-direction), perpendicular to split-line (2-direction) and along the depth direction (3-direction, perpendicular to articular surface), accounting for tissue inhomogeneity between the surface and deep layers in the latter direction. Tensile moduli were found to be strain-dependent while compressive moduli were nearly constant. The peak tensile (+) Young's moduli in 0.15M NaCl were E+Y1=3.1+/-2.3, E+Y2=1.3+/-0.3, E+Y3(Surface)=0.65+/-0.29 and E+Y3(Deep)=2.1+/-1.2 MPa. The corresponding compressive (-) Young's moduli were E-Y1=0.23+/-0.07, E-Y2=0.22+/-0.07, E-Y3(Surface)=0.18+/-0.07 and E-Y3(Deep)=0.35+/-0.11 MPa. Peak tensile Poisson's ratios were upsilon+12=0.22+/-0.06, upsilon+21=0.13+/-0.07, upsilon+31(Surface)=0.10+/-0.03 and upsilon+31(Deep)=0.20+/-0.05 while compressive Poisson's ratios were upsilon-12=0.027+/-0.012, upsilon-21=0.017+/-0.07, upsilon-31(Surface)=0.034+/-0.009 and upsilon-31(Deep)=0.065+/-0.024. Similar measurements were also performed at 0.015 M and 2 M NaCl, showing strong variations with ionic strength. Results indicate that (a) a smooth transition occurs in the stress-strain and modulus-strain responses between the tensile and compressive regimes, and (b) cartilage exhibits orthotropic symmetry within the framework of tension-compression nonlinearity. The strain-softening behavior of cartilage (the initial decrease in EYi with increasing compressive strain) can be interpreted in the context of osmotic swelling and tension-compression nonlinearity.

Traumatic brain injury (TBI) is caused by brain deformations resulting in the pathophysiological activation of cellular cascades which produce delayed cell damage and death. Understanding the consequences of mechanical injuries on living brain tissue continues to be a significant challenge. We have developed a reproducible tissue culture model of TBI which employs organotypic brain slice cultures to study the relationship between mechanical stimuli and the resultant biological response of living brain tissue. The device allows for the independent control of tissue strain (up to 100%) and strain rate (up to 150 s-1) so that tolerance criteria at the tissue level can be developed for the interpretation of computational simulations. The application of texture correlation image analysis algorithms to high speed video of the dynamic deformation allows for the direct calculation of substrate strain and strain rate which was found to be equi-biaxial and independent of radial position. Precisely controlled, mechanical injuries were applied to organotypic hippocampal slice cultures, and resultant cell death was quantified. Cell death was found to be dependent on both strain magnitude and rate and required several days to develop. An immunohistological examination of injured cultures with antibodies to amyloid precursor protein revealed the presence of traumatic axonal injury, suggesting that the model closely replicates in vivo TBI but with advantages gained in vitro. We anticipate that a combined in vitro approach with optical strain mapping will provide a more detailed understanding of the dependence of brain cell injury and death on strain and strain rate.

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