A cartilage growth mixture model for infinitesimal strains: solutions of boundary-value problems related to in vitro growth experiments.

A cartilage growth mixture (CGM) model is linearized for infinitesimal elastic and growth strains. Parametric studies for equilibrium and nonequilibrium boundary-value problems representing the in vitro growth of cylindrical cartilage constructs are solved. The results show that the CGM model is capable of describing the main biomechanical features of cartilage growth. The solutions to the equilibrium problems reveal that tissue composition, constituent pre-stresses, and geometry depend on collagen remodeling activity, growth symmetry, and differential growth. Also, nonhomogeneous growth leads to nonhomogeneous tissue composition and constituent pre-stresses. The solution to the nonequilibrium problem reveals that the tissue is nearly in equilibrium at all time points. The results suggest that the CGM model may be used in the design of tissue engineered cartilage constructs for the repair of cartilage defects; for example, to predict how dynamic mechanical loading affects the development of nonuniform properties during in vitro growth. Furthermore, the results lay the foundation for future analyses with nonlinear models that are needed to develop realistic models of cartilage growth.

A growth mixture theory for cartilage with application to growth-related experiments on cartilage explants.

In this paper, we present a growth mixture model for cartilage. The main features of this model are illustrated in a simple equilibrium boundary-value problem that is chosen to illustrate how a mechanical theory of cartilage growth may be applied to growth-related experiments on cartilage explants. The cartilage growth mixture model describes the independent growth of the proteoglycan and collagen constituents due to volumetric mass deposition, which leads to the remodeling of the composition and the mechanical properties of the solid matrix. The model developed here also describes how the material constants of the collagen constituent depend on a scalar parameter that may change over time (e.g., crosslink density); this leads to a remodeling of the structural and mechanical properties of the collagen constituent. The equilibrium boundary-value problem that describes the changes observed in cartilage explants harvested at different stages of a growth or a degenerative process is formulated. This boundary-value problem is solved using existing experimental data for developing bovine cartilage explants harvested at three developmental stages. The solution of the boundary-value problem in conjunction with existing experimental data suggest the types of experimental studies that need to be conducted in the future to determine model parameters and to further refine the model.

A new method for predicting the opening angle for soft tissues.

The purpose of this paper is to present a simple new method for calculating the opening angle produced by a given residual stress field in a soft biological tissue. The method uses minimization of potential energy, and is therefore named the MPE method. The accuracy of the MPE method is evaluated by comparing the opening angle it predicts to results from a finite element model of the opening angle experiment. We show that the MPE method provides good predictions of the opening angle, and that it is significantly more accurate than two other methods previously used in the literature.

Shear stress regulates the endothelial Kir2.1 ion channel.

Endothelial cells (ECs) line the mammalian vascular system and respond to the hemodynamic stimulus of fluid shear stress, the frictional force produced by blood flow. When ECs are exposed to shear stress, one of the fastest responses is an increase of K(+) conductance, which suggests that ion channels are involved in the early shear stress response. Here we show that an applied shear stress induces a K(+) ion current in cells expressing the endothelial Kir2.1 channel. This ion current shares the properties of the shear-induced current found in ECs. In addition, the shear current induction can be specifically prevented by tyrosine kinase inhibition. Our findings identify the Kir2.1 channel as an early component of the endothelial shear response mechanism.