ArticleJournal of the Royal Society, Interface2016
A homeostatic-driven turnover remodelling constitutive model for healing in soft tissues.
Article in Journal of the Royal Society, Interface, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 36 citations in OpenAlex.
- Prediction of tissue rupture from percolation of local strain heterogeneities for diagnostics.Communications medicine · 2025Article
- Residual Strain and Joint Pressurization Maintain Collagen Tension for On-Joint Lumbar Facet Capsular Ligaments.Journal of biomechanical engineering · 2024Article
- On modeling the multiscale mechanobiology of soft tissues: Challenges and progress.Biophysics reviews · 2022Review
- A Review on Damage and Rupture Modelling for Soft Tissues.Bioengineering (Basel, Switzerland) · 2022Review
- A Chemomechanobiological Model of the Long-Term Healing Response of Arterial Tissue to a Clamping Injury.Frontiers in bioengineering and biotechnology · 2020Article
- Three-dimensional numerical simulation of soft-tissue wound healing using constrained-mixture anisotropic hyperelasticity and gradient-enhanced damage mechanics.Journal of the Royal Society, Interface · 2020Article
- On the feasibility of the computational modelling of the endoluminal vacuum-assisted closure of an oesophageal anastomotic leakage.Royal Society open science · 2018Article
- A chemo-mechano-biological formulation for the effects of biochemical alterations on arterial mechanics: the role of molecular transport and multiscale tissue remodelling.Journal of the Royal Society, Interface · 2017Article
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Remodelling of soft biological tissue is characterized by interacting biochemical and biomechanical events, which change the tissue's microstructure, and, consequently, its macroscopic mechanical properties. Remodelling is a well-defined stage of the healing process, and aims at recovering or repairing the injured extracellular matrix. Like other physiological processes, remodelling is thought to be driven by homeostasis, i.e. it tends to re-establish the properties of the uninjured tissue. However, homeostasis may never be reached, such that remodelling may also appear as a continuous pathological transformation of diseased tissues during aneurysm expansion, for example. A simple constitutive model for soft biological tissues that regards remodelling as homeostatic-driven turnover is developed. Specifically, the recoverable effective tissue damage, whose rate is the sum of a mechanical damage rate and a healing rate, serves as a scalar internal thermodynamic variable. In order to integrate the biochemical and biomechanical aspects of remodelling, the healing rate is, on the one hand, driven by mechanical stimuli, but, on the other hand, subjected to simple metabolic constraints. The proposed model is formulated in accordance with continuum damage mechanics within an open-system thermodynamics framework. The numerical implementation in an in-house finite-element code is described, particularized for Ogden hyperelasticity. Numerical examples illustrate the basic constitutive characteristics of the model and demonstrate its potential in representing aspects of remodelling of soft tissues. Simulation results are verified for their plausibility, but also validated against reported experimental data.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.