2007 Volume No 13 pages 100-111
Title: In-situ measurements of chondrocyte deformation
under transient loading |
Author: NO Chahine, CT Hung, GA Ateshian |
Address: Musculoskeletal Biomechanics Laboratory,
Department of Biomedical Engineering, Columbia University,
New York, NY 10027 |
E-mail: ateshian at columbia.edu |
Key Words: Cellular deformation, cartilage, cell-matrix
interaction |
Publication date: May 31st 2007 |
Abstract: 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. |
Article download: Pages
100-111 (PDF file) |