The effect of fibrillar degradation on the mechanics of articular cartilage

a computational model

Tanvir R. Faisal*, Malek Adouni, Yasin Y Dhaher

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

The pathogenesis and pathophysiological underpinnings of cartilage degradation are not well understood. Either mechanically or enzymatically mediated degeneration at the fibril level can lead to acute focal injuries that will, overtime, cause significant cartilage degradation. Understanding the relationship between external loading and the basic molecular structure of cartilage requires establishing a connection between the fibril-level defects and its aggregate effect on cartilage. In this work, we provide a multiscale constitutive model of cartilage to elucidate the effect of two plausible fibril degradation mechanisms on the aggregate tissue: tropocollagen crosslink failure (β) and a generalized surface degradation (δ). Using our model, the mechanics of aggregate tissue shows differed yield stress and post-yield behavior after crosslink failure and surface degradation compared to intact cartilage, and the tissue-level aggregate behaviors are different from the fibrillar behaviors observed in the molecular dynamics simulations. We also compared the effect of fibrillar defects in terms of crosslink failure and surface degradation in different layers of cartilage within the macroscale tissue construct during a simulated nanoindentation test. Although the mechanical properties of cartilage tissue were largely contingent upon the mechanical properties of the fibril, the macroscale mechanics of cartilage tissue showed ~ 10% variation in yield strain (tissue yield strain: ~ 27 to ~ 37%) compared to fibrillar yield strain (fibrillar yield strain: ~ 16 to ~ 26%) for crosslink failure and ~ 7% difference for the surface degradation (yield strain variations at the tissue: ~ 30 to ~ 37% and fibril: ~ 24 to ~ 26%) at the superficial layer. The yield strain was further delayed in middle layers at least up to 30% irrespective of the failure mechanisms. The cartilage tissue appeared to withstand more strain than the fibrils. The degeneration mechanisms of fibril differentially influenced the aggregate mechanics of cartilage, and the deviation may be attributed to fiber–matrix interplay, depth-dependent fiber orientation and fibrillar defects with different degradation mechanisms. The understanding of the aggregate stress–strain behavior of cartilage tissue, cartilage degradation and its underlying biomechanical factors is important for developing engineering approaches and therapeutic interventions for cartilage pathologies.

Original languageEnglish (US)
Pages (from-to)733-751
Number of pages19
JournalBiomechanics and Modeling in Mechanobiology
Volume18
Issue number3
DOIs
StatePublished - Jun 15 2019

Fingerprint

Cartilage
Articular Cartilage
Mechanics
Computational Model
Degradation
Tissue
Defects
Degeneration
Mechanical Properties
Tropocollagen
Nanoindentation
Fiber Orientation
Mechanical properties
Multiscale Model
Failure Mechanism
Yield Stress
Pathology
Molecular Dynamics Simulation
Fiber reinforced materials
Constitutive Model

Keywords

  • Cartilage degradation
  • Crosslink failure
  • Multiscale modeling
  • Surface degradation

ASJC Scopus subject areas

  • Biotechnology
  • Modeling and Simulation
  • Mechanical Engineering

Cite this

@article{b63f24166b644e04baa5998d02b519d0,
title = "The effect of fibrillar degradation on the mechanics of articular cartilage: a computational model",
abstract = "The pathogenesis and pathophysiological underpinnings of cartilage degradation are not well understood. Either mechanically or enzymatically mediated degeneration at the fibril level can lead to acute focal injuries that will, overtime, cause significant cartilage degradation. Understanding the relationship between external loading and the basic molecular structure of cartilage requires establishing a connection between the fibril-level defects and its aggregate effect on cartilage. In this work, we provide a multiscale constitutive model of cartilage to elucidate the effect of two plausible fibril degradation mechanisms on the aggregate tissue: tropocollagen crosslink failure (β) and a generalized surface degradation (δ). Using our model, the mechanics of aggregate tissue shows differed yield stress and post-yield behavior after crosslink failure and surface degradation compared to intact cartilage, and the tissue-level aggregate behaviors are different from the fibrillar behaviors observed in the molecular dynamics simulations. We also compared the effect of fibrillar defects in terms of crosslink failure and surface degradation in different layers of cartilage within the macroscale tissue construct during a simulated nanoindentation test. Although the mechanical properties of cartilage tissue were largely contingent upon the mechanical properties of the fibril, the macroscale mechanics of cartilage tissue showed ~ 10{\%} variation in yield strain (tissue yield strain: ~ 27 to ~ 37{\%}) compared to fibrillar yield strain (fibrillar yield strain: ~ 16 to ~ 26{\%}) for crosslink failure and ~ 7{\%} difference for the surface degradation (yield strain variations at the tissue: ~ 30 to ~ 37{\%} and fibril: ~ 24 to ~ 26{\%}) at the superficial layer. The yield strain was further delayed in middle layers at least up to 30{\%} irrespective of the failure mechanisms. The cartilage tissue appeared to withstand more strain than the fibrils. The degeneration mechanisms of fibril differentially influenced the aggregate mechanics of cartilage, and the deviation may be attributed to fiber–matrix interplay, depth-dependent fiber orientation and fibrillar defects with different degradation mechanisms. The understanding of the aggregate stress–strain behavior of cartilage tissue, cartilage degradation and its underlying biomechanical factors is important for developing engineering approaches and therapeutic interventions for cartilage pathologies.",
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The effect of fibrillar degradation on the mechanics of articular cartilage : a computational model. / Faisal, Tanvir R.; Adouni, Malek; Dhaher, Yasin Y.

In: Biomechanics and Modeling in Mechanobiology, Vol. 18, No. 3, 15.06.2019, p. 733-751.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The effect of fibrillar degradation on the mechanics of articular cartilage

T2 - a computational model

AU - Faisal, Tanvir R.

AU - Adouni, Malek

AU - Dhaher, Yasin Y

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AB - The pathogenesis and pathophysiological underpinnings of cartilage degradation are not well understood. Either mechanically or enzymatically mediated degeneration at the fibril level can lead to acute focal injuries that will, overtime, cause significant cartilage degradation. Understanding the relationship between external loading and the basic molecular structure of cartilage requires establishing a connection between the fibril-level defects and its aggregate effect on cartilage. In this work, we provide a multiscale constitutive model of cartilage to elucidate the effect of two plausible fibril degradation mechanisms on the aggregate tissue: tropocollagen crosslink failure (β) and a generalized surface degradation (δ). Using our model, the mechanics of aggregate tissue shows differed yield stress and post-yield behavior after crosslink failure and surface degradation compared to intact cartilage, and the tissue-level aggregate behaviors are different from the fibrillar behaviors observed in the molecular dynamics simulations. We also compared the effect of fibrillar defects in terms of crosslink failure and surface degradation in different layers of cartilage within the macroscale tissue construct during a simulated nanoindentation test. Although the mechanical properties of cartilage tissue were largely contingent upon the mechanical properties of the fibril, the macroscale mechanics of cartilage tissue showed ~ 10% variation in yield strain (tissue yield strain: ~ 27 to ~ 37%) compared to fibrillar yield strain (fibrillar yield strain: ~ 16 to ~ 26%) for crosslink failure and ~ 7% difference for the surface degradation (yield strain variations at the tissue: ~ 30 to ~ 37% and fibril: ~ 24 to ~ 26%) at the superficial layer. The yield strain was further delayed in middle layers at least up to 30% irrespective of the failure mechanisms. The cartilage tissue appeared to withstand more strain than the fibrils. The degeneration mechanisms of fibril differentially influenced the aggregate mechanics of cartilage, and the deviation may be attributed to fiber–matrix interplay, depth-dependent fiber orientation and fibrillar defects with different degradation mechanisms. The understanding of the aggregate stress–strain behavior of cartilage tissue, cartilage degradation and its underlying biomechanical factors is important for developing engineering approaches and therapeutic interventions for cartilage pathologies.

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