Fatigue of soft fibrous tissues: Multi-scale mechanics and constitutive modeling
[Display omitted] In recent experimental studies a possible damage mechanism of collagenous tissues mainly caused by fatigue was disclosed. In this contribution, a multi-scale constitutive model ranging from the tropocollagen (TC) molecule level up to bundles of collagen fibers is proposed and utili...
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Published in | Acta biomaterialia Vol. 71; pp. 398 - 410 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Ltd
15.04.2018
Elsevier BV |
Subjects | |
Online Access | Get full text |
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Summary: | [Display omitted]
In recent experimental studies a possible damage mechanism of collagenous tissues mainly caused by fatigue was disclosed. In this contribution, a multi-scale constitutive model ranging from the tropocollagen (TC) molecule level up to bundles of collagen fibers is proposed and utilized to predict the elastic and inelastic long-term tissue response. Material failure of collagen fibrils is elucidated by a permanent opening of the triple helical collagen molecule conformation, triggered either by overstretching or reaction kinetics of non-covalent bonds. This kinetics is described within a probabilistic framework of adhesive detachments of molecular linkages providing collagen fiber integrity. Both intramolecular and interfibrillar linkages are considered. The final constitutive equations are validated against recent experimental data available in literature for both uniaxial tension to failure and the evolution of fatigue in subsequent loading cycles. All material parameters of the proposed model have a clear physical interpretation.
Irreversible changes take place at different length scales of soft fibrous tissues under supra-physiological loading and alter their macroscopic mechanical properties. Understanding the evolution of those histologic pathologies under loading and incorporating them into a continuum mechanical framework appears to be crucial in order to predict long-term evolution of various diseases and to support the development of tissue engineering. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1742-7061 1878-7568 |
DOI: | 10.1016/j.actbio.2018.03.010 |