Collagen damage is one of the earliest signs of cartilage degeneration and the onset of osteoarthritis (OA), but the connection between the microscale damage and macroscale tissue function is unclear. We argue that a multiscale model can help elucidate the biochemical and mechanical underpinnings of OA by connecting the microscale defects in collagen fibrils to the macroscopic cartilage mechanics. We investigated this connection using a multiscale fibril reinforced hyperelastoplastic (MFRHEP) model that accounts for the structural architecture of the soft tissue, starting from tropocollagen molecules that form fibrils, and moving to the complete soft tissue. This model was driven by reported experimental data from unconfined compression testing of cartilage. The model successfully described the observed transient response of the articular cartilage in unconfined and indentation tests with low and high loading rates. We used this model to understand damage initiation and propagation as a function of the cross-link density between tropocollagen molecules. This approach appeared to provide a realistic simulation of damage when compared with certain published studies. The current construct presents the first attempt to express the aggregate cartilage damage in terms of the cross-link density at the microfibril level.
- Cartialge damage
- Multiscale model
ASJC Scopus subject areas
- Biomedical Engineering
- Orthopedics and Sports Medicine