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Register a new userLattice and Continuum Modelling of a Bioactive Porous Tissue Scaffold
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A contemporary procedure to grow artificial tissue is to seed cells onto a porous biomaterial scaffold and culture it within a perfusion bioreactor to facilitate the transport of nutrients to growing cells. Typical models of cell growth for tissue engineering applications make use of spatially homogeneous or spatially continuous equations to model cell growth, flow of culture medium, nutrient transport, and their interactions. The network structure of the physical porous scaffold is often incorporated through parameters in these models, either phenomenologically or through techniques like mathematical homogenization. We derive a model on a square grid lattice to demonstrate the importance of explicitly modelling the network structure of the porous scaffold, and compare results from this model with those from a modified continuum model from the literature. We capture two-way coupling between cell growth and fluid flow by allowing cells to block pores, and by allowing the shear stress of the fluid to affect cell growth and death. We explore a range of parameters for both models, and demonstrate quantitative and qualitative differences between predictions from each of these approaches, including spatial pattern formation and local oscillations in cell density present only in the lattice model. These differences suggest that for some parameter regimes, corresponding to specific cell types and scaffold geometries, the lattice model gives qualitatively different model predictions than typical continuum models. Our results inform model selection for bioactive porous tissue scaffolds, aiding in the development of successful tissue engineering experiments and eventually clinically successful technologies.
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We study dynamics emergent from a two-dimensional reaction--diffusion process modelled via a finite lattice dynamical system, as well as an analogous PDE system, involving spatially nonlocal interactions. These models govern the evolution of cells in a bioactive porous medium, with evolution of the local cell density depending on a coupled quasi--static fluid flow problem. We demonstrate differences emergent from the choice of a discrete lattice or a continuum for the spatial domain of such a process. We find long--time oscillations and steady states in cell density in both lattice and continuum models, but that the continuum model only exhibits solutions with vertical symmetry, independent of initial data, whereas the finite lattice admits asymmetric oscillations and steady states arising from symmetry-breaking bifurcations. We conjecture that it is the structure of the finite lattice which allows for more complicated asymmetric dynamics. Our analysis suggests that the origin of both types of oscillations is a nonlocal reaction-diffusion mechanism mediated by quasi-static fluid flow.
A continuum model of epithelial tissue mechanics was formulated using cellular-level mechanical ingredients and cell morphogenetic processes, including cellular shape changes and cellular rearrangements. This model can include finite deformation, and incorporates stress and deformation tensors, which can be compared with experimental data. Using this model, we elucidated dynamical behavior underlying passive relaxation, active contraction-elongation, and tissue shear flow. This study provides an integrated scheme for the understanding of the mechanisms that are involved in orchestrating the morphogenetic processes in individual cells, in order to achieve epithelial tissue morphogenesis.
Several biological tissues undergo changes in their geometry and in their bulk material properties by modelling and remodelling processes. Modelling synthesises tissue in some regions and removes tissue in others. Remodelling overwrites old tissue material properties with newly formed, immature tissue properties. As a result, tissues are made up of different patches, i.e., adjacent tissue regions of different ages and different material properties, within evolving boundaries. In this paper, generalised equations governing the spatio-temporal evolution of such tissues are developed within the continuum model. These equations take into account nonconservative, discontinuous surface mass balance due to creation and destruction of material at moving interfaces, and bulk balance due to tissue maturation. These equations make it possible to model patchy tissue states and their evolution without explicitly maintaining a record of when/where resorption and formation processes occurred. The time evolution of spatially averaged tissue properties is derived systematically by integration. These spatially-averaged equations cannot be written in closed form as they retain traces that tissue destruction is localised at tissue boundaries. The formalism developed in this paper is applied to bone tissues, which exhibit strong material heterogeneities due to their slow mineralisation and remodelling processes. Evolution equations are proposed in particular for osteocyte density and bone mineral density. Effective average equations for bone mineral density (BMD) and tissue mineral density (TMD) are derived using a mean-field approximation. The error made by this approximation when remodelling patchy tissue is investigated. The specific time signatures of BMD or TMD during remodelling events may provide a way to detect these events occurring at lower, unseen spatial resolutions from microCT scans.
In this paper we introduce a new mathematical model for the active contraction of cardiac muscle, featuring different thermo-electric and nonlinear conductivity properties. The passive hyperelastic response of the tissue is described by an orthotropic exponential model, whereas the ionic activity dictates active contraction incorporated through the concept of orthotropic active strain. We use a fully incompressible formulation, and the generated strain modifies directly the conductivity mechanisms in the medium through the pull-back transformation. We also investigate the influence of thermo-electric effects in the onset of multiphysics emergent spatiotemporal dynamics, using nonlinear diffusion. It turns out that these ingredients have a key role in reproducing pathological chaotic dynamics such as ventricular fibrillation during inflammatory events, for instance. The specific structure of the governing equations suggests to cast the problem in mixed-primal form and we write it in terms of Kirchhoff stress, displacements, solid pressure, electric potential, activation generation, and ionic variables. We also propose a new mixed-primal finite element method for its numerical approximation, and we use it to explore the properties of the model and to assess the importance of coupling terms, by means of a few computational experiments in 3D.
The growth of several biological tissues is known to be controlled in part by local geometrical features, such as the curvature of the tissue interface. This control leads to changes in tissue shape that in turn can affect the tissues evolution. Understanding the cellular basis of this control is highly significant for bioscaffold tissue engineering, the evolution of bone microarchitecture, wound healing, and tumour growth. While previous models have proposed geometrical relationships between tissue growth and curvature, the role of cell density and cell vigor remains poorly understood. We propose a cell-based mathematical model of tissue growth to investigate the systematic influence of curvature on the collective crowding or spreading of tissue-synthesising cells induced by changes in local tissue surface area during the motion of the interface. Depending on the strength of diffusive damping, the model exhibits complex growth patterns such as undulating motion, efficient smoothing of irregularities, and the generation of cusps. We compare this model with in-vitro experiments of tissue deposition in bioscaffolds of different geometries. By accounting for the depletion of active cells, the model is able to capture both smoothing of initial substrate geometry and tissue deposition slowdown as observed experimentally.
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