A fibril-reinforced poroviscoelastic swelling model for articular cartilage

Wilson, W.; Donkelaar, Corrinus C. van; Rietbergen, Bert van; Huiskes, R.

doi:10.1016/j.jbiomech.2004.07.003

Cited by 259 publications

(315 citation statements)

References 30 publications

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“…A fibril-reinforced poroviscoelastic swelling model of Wilson et al [24], based on the theory of Biot [29], Mow et al [30] and Lanir [15,16], is used to describe the intervertebral disc; it consists of a swelling nonfibrillar part and a fibrillar part [24,25]. The model distinguishes between an elastic non-fibrillar solid matrix, a 3D viscoelastic collagen fiber structure and an osmotically prestressed extrafibrillar fluid.…”

Section: Methodsmentioning

confidence: 99%

“…The key equations of the main components are given here, for further details refer to [24] and Appendix.…”

Section: Methodsmentioning

confidence: 99%

“…Wilson et al [24] combined the bicomponent model [21] with their fibril-reinforced poroviscoelastic model [25]. This allows the inclusion of the fibril structure of articular cartilage.…”

Section: Introductionmentioning

confidence: 99%

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Osmoviscoelastic finite element model of the intervertebral disc

et al. 2006

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Intervertebral discs have a primarily mechanical role in transmitting loads through the spine. The disc is subjected to a combination of elastic, viscous and osmotic forces; previous 3D models of the disc have typically neglected osmotic forces. The fibrilreinforced poroviscoelastic swelling model, which our group has recently developed, is used to compute the interplay of osmotic, viscous and elastic forces in an intervertebral disc under axial compressive load. The unloaded 3D finite element mesh equilibrates in a physiological solution, and exhibits an intradiscal pressure of about 0.2 MPa. Before and after axial loading the numerically simulated hydrostatic pressure compares well with the experimental ranges measured. Loading the disc decreased the height of the disc and results in an outward bulging of the outer annulus. Fiber stresses were highest on the most outward bulging on the posterior-lateral side. The osmotic forces resulted in tensile hoop stresses, which were higher than typical values in a non-osmotic disc. The computed axial stress profiles reproduced the main features of the stress profiles, in particular the characteristic posterior and anterior stress which were observed experimentally.

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Section: Methodsmentioning

confidence: 99%

“…The key equations of the main components are given here, for further details refer to [24] and Appendix.…”

Section: Methodsmentioning

confidence: 99%

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Osmoviscoelastic finite element model of the intervertebral disc

et al. 2006

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“…The computational tool uses the finite element method and includes mechanical effects of swelling pressure by charged proteoglycans, as well as constraints against swelling by a Noonan et al (1998) reinforcing network of collagen fibrils. The total tissue stress (σ tot ) is given by (Wilson et al 2006b(Wilson et al , 2007(Wilson et al , 2005(Wilson et al , 2004)…”

Section: Model Descriptionmentioning

confidence: 99%

“…Therefore, we adapt our model for cartilage mechanics (Wilson et al 2006b(Wilson et al , 2007(Wilson et al , 2005(Wilson et al , 2004, such that proteoglycan and collagen concentrations can change with time, and we implement a description for collagen turnover. Input parameters are obtained from epiphyseal plate studies, and unknown parameters are fitted to experimental data.…”

Section: Introductionmentioning

confidence: 99%

Mechanics of chondrocyte hypertrophy

Donkelaar

Wilson

2011

Biomech Model Mechanobiol

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Chondrocyte hypertrophy is a characteristic of osteoarthritis and dominates bone growth. Intra-and extracellular changes that are known to be induced by metabolically active hypertrophic chondrocytes are known to contribute to hypertrophy. However, it is unknown to which extent these mechanical conditions together can be held responsible for the total magnitude of hypertrophy. The present paper aims to provide a quantitative, mechanically sound answer to that question. To address this aim requires a quantitative tool that captures the mechanical effects of collagen and proteoglycans, allows temporal changes in tissue composition, and can compute cell and tissue deformations. These requirements are met in our numerical model that is validated for articular cartilage mechanics, which we apply to quantitatively explain a range of experimental observations related to hypertrophy. After validating the numerical approach for studying hypertrophy, the model is applied to evaluate the direct mechanical effects of axial tension and compression on hypertrophy (Hueter-Volkmann principle) and to explore why hypertrophy is reduced in case of partially or fully compromised proteoglycan expression. Finally, a mechanical explanation is provided for the observation that chondrocytes do not hypertrophy when enzymatical collagen degradation is prohibited (S1Pcko knock-out mouse model). This paper shows that matrix turnover by metabolically active chondrocytes, together with externally applied mechanical conditions, can explain quantitatively the volumetric change of chondrocytes during hypertrophy. It provides a mechanistic explanation for the observation that collagen degradation results in chondrocyte hypertrophy, both under physiological and pathological conditions.

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