In-situ measurements of chondrocyte deformation under transient loading.

Chondrocytes are responsible for the elaboration and maintenance of the extracellular (EC) matrix in articular cartilage, and previous studies have demonstrated that mechanical loading modulates the biosynthetic response of chondrocytes in cartilage explants. The goal of this study is to investigate the deformation behaviour of the chondrocyte and its microenvironment under transient loading, in order to address the relationship between the applied dynamic deformation and cellular strain. In-situ strain measurements were performed on cells in the middle (MZ) zone at early time points during ramp loading and at equilibrium. In this study, we characterized the behaviour of cartilage at the zonal and cellular levels under compressive loading using digital image analysis on miniature samples tested in a custom microscopy-based loading device. The experimental results indicate that significant strain amplification occurs in the microenvironment of the cell, with the minimum (compressive) principal strain found to be nearly 7X higher in the intracellular region (IC), and ~5X higher in the pericellular (PC) matrix than in the EC matrix at peak ramp. A similar strain amplification mechanism was observed in the maximum (tensile) principal strain, and this behaviour persisted even after equilibrium was reached. The experimental results of this study were interpreted in the context of a finite element model of chondrocyte deformation, which modelled the cell as a homogeneous gel, possessing either a spherical or ellipsoidal geometry, surrounded by a semi permeable membrane, and accounted for the presence of a PC matrix. The results of the FEA demonstrate significant strain amplification mechanism in the IC region, greater than had previously been suggested in earlier computational studies of cell-EC matrix interactions. Based on the FEA, this outcome is understood to result from the large disparity between EC matrix and intracellular properties. The results of this study suggest that mechanotransduction of chondrocytes may be significantly mediated by this strain amplification mechanism during loading.