An investigation of the fluid structure interaction in articular cartilage across disparate scales

Articular cartilage (AC) is found at opposing surfaces in mammalian joints. It provides a smooth bearing surface, promoting low friction articulation and facilitating continuous operation under relative motion. Its limited cellularity renders it incapable of intrinsic repair, leaving it susceptible to degeneration and disease, resulting in high clinical demand for effective cartilage repair strategies. To streamline treatment, an accurate computational model of the tissue is essential to inform rapid pre-screening of therapeutic interventions.

Current approaches often rely on single-scale models, which cannot capture the tissues intrinsic heterogeneity, zonal stratification and depth-dependent mechanical properties. In this thesis, the first accurately calibrated set of Biot poroelastic parameters for AC are established. Building on this foundation, a series of physiologically representative multi-scale modelling frameworks are developed, validated and refined to integrate micro-scale structural features, zonal composition, fibrous architecture, and pathological changes, enabling predictive investigation of cartilage mechanics and degeneration.

A generalised continuum-continuum framework is introduced to capture fluid-structure interactions, depth-dependent zonal behaviour, and progressive micro-scale damage. This is extended through a continuum-fiber coupling in which a fibrous network representation of the micro-scale enables modelling of collagen anisotropy, zonal organisation, and damage-driven structural degradation. A complementary mean-field homogenisation approach further incorporates stratified collagen fiber orientation data into a viscoelastic macro-scale model, allowing efficient representation of microstructural organisation. Across these frameworks, the models demonstrate how distinct micro-scale mechanisms can lead to comparable tissue level mechanical responses, while also revealing heterogeneous reductions in load-bearing capacity associated with degeneration.

Together, these frameworks provide a unified basis for linking micro-scale alterations to tissue-level mechanical responses, supporting predictive modelling of cartilage degeneration and informing the design and evolution of repair strategies. The implications can be extended to other fiber-reinforced biological tissues and porous engineered materials, advancing the theoretical and computational foundations of multi-scale tissue biomechanics.