Details
| Original language | English |
|---|---|
| Pages (from-to) | 254-271 |
| Number of pages | 18 |
| Journal | Journal of the Mechanical Behavior of Biomedical Materials |
| Volume | 97 |
| Early online date | 4 May 2019 |
| Publication status | Published - Sept 2019 |
Abstract
The present experimental-modelling study provides a quantitative interpretation of mechanical data and damage measurements obtained from collagen hybridizing peptide (CHP) techniques on overstretched sheep cerebral arterial tissues. To this aim, a structurally-motivated constitutive model is developed in the framework of continuum damage mechanics. The model includes two internal variables for describing the effects of collagen triple-helical unfolding via interstrand delamination: one governs plastic mechanisms in collagen fibers, leading to a stress softening response of the tissue at the macroscale; the other one describes the loss of fiber structural integrity, leading to tissue final failure. The proposed model is calibrated using the obtained mechanical experimental data, showing excellent fitting capabilities. The predicted evolution of internal variables agree well with independent measurements of molecular-level CHP-based damage data, obtaining an independent a posteriori validation of damage predictions. Moreover, available data on inelastic tissue elongation following supraphysiological loads are successfully reproduced. These outcomes further the hypothesis that the accumulation of interstrand delamination is a primary cause for the evolution of inelastic mechanisms in tissues, and in particular of stress softening up to failure.
Keywords
- Arterial mechanics, Elasto-damage constitutive model, Fiber yielding, Molecular damage mechanisms, Tissue softening and failure
ASJC Scopus subject areas
- Materials Science(all)
- Biomaterials
- Engineering(all)
- Biomedical Engineering
- Engineering(all)
- Mechanics of Materials
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In: Journal of the Mechanical Behavior of Biomedical Materials, Vol. 97, 09.2019, p. 254-271.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Molecular-level collagen damage explains softening and failure of arterial tissues
T2 - A quantitative interpretation of CHP data with a novel elasto-damage model
AU - Marino, Michele
AU - Converse, Matthew I.
AU - Monson, Kenneth L.
AU - Wriggers, Peter
N1 - Funding Information: M. Marino acknowledges that this work has been carried out within the framework of the SMART BIOTECS alliance between the Technical University of Braunschweig and the Leibniz University of Hannover. This initiative is financially supported by the Ministry of Science and Culture (MWK) of Lower Saxony, Germany .
PY - 2019/9
Y1 - 2019/9
N2 - The present experimental-modelling study provides a quantitative interpretation of mechanical data and damage measurements obtained from collagen hybridizing peptide (CHP) techniques on overstretched sheep cerebral arterial tissues. To this aim, a structurally-motivated constitutive model is developed in the framework of continuum damage mechanics. The model includes two internal variables for describing the effects of collagen triple-helical unfolding via interstrand delamination: one governs plastic mechanisms in collagen fibers, leading to a stress softening response of the tissue at the macroscale; the other one describes the loss of fiber structural integrity, leading to tissue final failure. The proposed model is calibrated using the obtained mechanical experimental data, showing excellent fitting capabilities. The predicted evolution of internal variables agree well with independent measurements of molecular-level CHP-based damage data, obtaining an independent a posteriori validation of damage predictions. Moreover, available data on inelastic tissue elongation following supraphysiological loads are successfully reproduced. These outcomes further the hypothesis that the accumulation of interstrand delamination is a primary cause for the evolution of inelastic mechanisms in tissues, and in particular of stress softening up to failure.
AB - The present experimental-modelling study provides a quantitative interpretation of mechanical data and damage measurements obtained from collagen hybridizing peptide (CHP) techniques on overstretched sheep cerebral arterial tissues. To this aim, a structurally-motivated constitutive model is developed in the framework of continuum damage mechanics. The model includes two internal variables for describing the effects of collagen triple-helical unfolding via interstrand delamination: one governs plastic mechanisms in collagen fibers, leading to a stress softening response of the tissue at the macroscale; the other one describes the loss of fiber structural integrity, leading to tissue final failure. The proposed model is calibrated using the obtained mechanical experimental data, showing excellent fitting capabilities. The predicted evolution of internal variables agree well with independent measurements of molecular-level CHP-based damage data, obtaining an independent a posteriori validation of damage predictions. Moreover, available data on inelastic tissue elongation following supraphysiological loads are successfully reproduced. These outcomes further the hypothesis that the accumulation of interstrand delamination is a primary cause for the evolution of inelastic mechanisms in tissues, and in particular of stress softening up to failure.
KW - Arterial mechanics
KW - Elasto-damage constitutive model
KW - Fiber yielding
KW - Molecular damage mechanisms
KW - Tissue softening and failure
UR - http://www.scopus.com/inward/record.url?scp=85066047541&partnerID=8YFLogxK
U2 - 10.1016/j.jmbbm.2019.04.022
DO - 10.1016/j.jmbbm.2019.04.022
M3 - Article
C2 - 31132662
AN - SCOPUS:85066047541
VL - 97
SP - 254
EP - 271
JO - Journal of the Mechanical Behavior of Biomedical Materials
JF - Journal of the Mechanical Behavior of Biomedical Materials
SN - 1751-6161
ER -