Abstract
The design of medical devices could be very much improved if robust tools were available for computational simulation of tissue response to the presence of the implant. Such tools require algorithms to simulate the response of tissues to mechanical and chemical stimuli. Available methodologies include those based on the principle of mechanical homeostasis, those which use continuum models to simulate biological constituents, and the cell-centred approach, which models cells as autonomous agents. In the latter approach, cell behaviour is governed by rules based on the state of the local environment around the cell; and informed by experiment. Tissue growth and differentiation requires simulating many of these cells together. In this paper, the methodology and applications of cell-centred techniques—with particular application to mechanobiology—are reviewed, and a cell-centred model of tissue formation in the lumen of an artery in response to the deployment of a stent is presented. The method is capable of capturing some of the most important aspects of restenosis, including nonlinear lesion growth with time. The approach taken in this paper provides a framework for simulating restenosis; the next step will be to couple it with more patient-specific geometries and quantitative parameter data.
Highlights
The potential of computational models for understanding biological systems is increasingly recognized, and their use in biomedical device design is increasing
The system is slow to react to the mechanical environment; it reacts over months, whereas at the other extreme, mechanics affect the system very rapidly, by opening ion channels, or altering the morphology of the cells
We explore the use of the cell-centred approach to develop a predictive model for restenosis
Summary
The potential of computational models for understanding biological systems is increasingly recognized, and their use in biomedical device design is increasing. Tissue adaptation can be represented as a system striving to achieve a homeostatic mechanical state by altering its geometry (growth/resorption) or material properties (stiffness, porosity, etc.) This concept has been successfully applied to bone remodelling (Cowin & Hegedus 1976; Huiskes et al 1987; Prendergast & Taylor 1994) and arterial remodelling (Rachev et al 2000; Kuhl et al 2003; Alastrue et al 2008). There may be no adequate equations available to model this relationship At this level, the system is slow to react to the mechanical environment; it reacts over months, whereas at the other extreme, mechanics affect the system very rapidly, by opening ion channels, or altering the morphology of the cells. The key to effective modelling of tissue adaptation is a multi-scale approach (Evans et al 2008)—where processes at the continuum/tissue level (for example stress/strain), and at the intercellular level (perhaps gene transcription) can inform processes at the cell level (differentiation, proliferation, etc.)
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