We propose a deterministic mathematical model to describe the biomechanics and cell biology of wound contraction, a ubiquitous feature in the normal healing of adult dermal excisional wounds. Our aim is to use the model to obtain a greater understanding of the mechanisms involved in wound contraction and in clinically important healing pathologies such as fibrocontractive diseases. The model consists of two cell types — fibroblasts aand myofibroblasts, a generic chemical growth factor and a viscoelastic extracellular matrix (which includes type I collagen). The essential processes of cell motility, proliferation, differentiation and mechanical interaction with the matrix are modelled from experimental data. A novel aspect of this approach is the inclusion of two cell types. The model is shown not only to simulate normal wound contraction (in good agreement with experimental data), but also to yield valuable insight into the fundamental mechanisms involved and the pathogenesis of fibrocontractive diseases, and makes experimentally testable predictions of the effects of varying biological parameters. Two important results are that collagen remodelling is more intrinsic to scar formation than to wound contraction and that dynamic gradients in the cell and matrix densities are the driving force for wound contraction
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