ABSTRACT
Articular cartilage is found at the distal end of long bones and is responsible for assisting in joint articulation. While articular cartilage has remarkable resistance to failure, once initially damaged, degeneration is nearly irreversible. Thus, understanding damage initiation is important. There are a few proposed mechanisms for articular cartilage failure initiation: (A) a single collagen fibril stress-based regime; (B) a rate-dependent regime captured by brittle failure at slow displacement rates (SDR) and ductile failure at fast displacement rates (FDR); and (C) a rate-dependent regime where failure is governed by pressurization fragmentation at SDR and governed by strain at FDR. The objective of this study was to use finite element (FE) models to provide evidence to support or refute these proposed failure mechanisms. Models were developed of microfracture experiments that investigated osmolarity (hypo-osmolar, normal osmolarity, and hyper-osmolar) and displacement rate (FDR and SDR) effects. Cartilage was modeled with a neo-Hookean ground matrix, strain-dependent permeability, nonlinear fibril reinforcement with viscoelastic fibril terms, and Donnan equilibrium swelling. Total stress, solid matrix stress, Lagrange strain, and fluid pressure were determined under the indenter tip at the moment of microfracture. Results indicated significant rate dependence across multiple outputs, which does not support (A) a single failure regime. Larger solid and fluid pressures at FDR than SDR did not support (C) a rate-dependent regime split by pressurization at SDR and strain at FDR. Consistent solid shear stresses at SDR and consistent third principal solid stresses at FDR support (B) the ductile-brittle failure regime. These findings help to shed light on the underlying mechanisms of articular cartilage failure, which have implications for the development of osteoarthritis.
