Abstract
Traumatic injuries of articular cartilage result in the formation of a cartilage lesion and contribute to cartilage degeneration and the risk of osteoarthritis (OA). A better understanding of the framework for the formation of a cartilage lesion formation would be helpful in therapy development. Toward this end, we present an age and space-structured model of articular cartilage lesion formation after a single blunt impact. This model modifies the reaction-diffusion-delay models in Graham et al. (2012) (single impact) and Wang et al. (2014) (cyclic loading), focusing on the “balancing act” between pro- and anti-inflammatory cytokines. Age structure is introduced to replace the delay terms for cell transitions used in these earlier models; we find age structured models to be more flexible in representing the underlying biological system and more tractable computationally. Numerical results show a successful capture of chondrocyte behavior and chemical activities associated with the cartilage lesion after the initial injury; experimental validation of our computational results is presented. We anticipate that our in silico model of cartilage damage from a single blunt impact can be used to provide information that may not be easily obtained through in in vivo or in vitro studies.
Highlights
The degenerative joint disease known as osteoarthritis (OA) is among the most common causes of disability worldwide
Age structure is introduced to replace the delay terms for cell transitions used in these earlier models; we find age structured models to be more flexible in representing the underlying biological system and more tractable computationally
These functions are attributable to the unique composition and structure of cartilage extracellular matrix (ECM), which consists of water (>70%), proteoglycan (15%), and collagen (15%) (Martin et al, 2011)
Summary
The degenerative joint disease known as osteoarthritis (OA) is among the most common causes of disability worldwide. While OA involves multiple joint tissues including bone, tendons, ligaments and synovium, articular cartilage degeneration, and erosion is the proximal cause of loss of joint function. Articular cartilage is a thin layer of connective tissue that covers the ends of long bones in synovial joints such as the shoulder, hip, knee, and ankle, where it distribute mechanical loads and allows for smooth joint motion. These functions are attributable to the unique composition and structure of cartilage extracellular matrix (ECM), which consists of water (>70%), proteoglycan (15%), and collagen (15%) (Martin et al, 2011). The resistance of cartilage to compression and its ability to distribute loads is largely due to this macromolecular arrangement, and aggrecan depletion or collagen degradation radically reduces mechanical strength (Farndale et al, 1982; Lu et al, 2011)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
