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Abstract Posttraumatic osteoarthritis (PTOA) is typically initiated by momentary supraphysiologic shear and compressive forces delivered to articular cartilage during acute joint injury and develops through subsequent degradation of cartilage matrix components and tissue remodeling. PTOA affects 12% of the population who experience osteoarthritis and is attributed to over $3 billion dollars annually in healthcare costs. It is currently unknown whether articulation of the joint post‐injury helps tissue healing or exacerbates cellular dysfunction and eventual death. We hypothesize that post‐injury cartilage articulation will lead to increased cartilage damage. Our objective was to test this hypothesis by mimicking the mechanical environment of the joint during and post‐injury and determining if subsequent joint articulation exacerbates damage produced by initial injury. We use a model of PTOA that combines impact injury and repetitive sliding with confocal microscopy to quantify and track chondrocyte viability, apoptosis, and mitochondrial depolarization in a depth‐dependent manner. Cartilage explants were harvested from neonatal bovine knee joints and subjected to either rapid impact injury (17.34 ± 0.99 MPa, 21.6 ± 2.45 GPa/s), sliding (60 min at 1 mm/s, under 15% axial compression), or rapid impact injury followed by sliding. Explants were then bisected and fluorescently stained for cell viability, caspase activity (apoptosis), and mitochondria polarization. Results show that compared to either impact or sliding alone, explants that were both impacted and slid experienced higher magnitudes of damage spanning greater tissue depths. 

We present a new framework to understand how changes to the microstructure of cartilage lead to a mechanical phase transition. 

Tunable mechanics and fracture resistance are hallmarks of biological tissues whose properties arise from extracellular matrices comprised of double networks. To elucidate the origin of these desired properties, we study the shear modulus and fracture properties of a rigidly percolating double network model comprised of a primary network of stiff fibers and a secondary network of flexible fibers. We find that when the primary network density is just above its rigidity percolation threshold, the secondary network density can be tuned to facilitate stress relaxation via non-affine deformations and provide mechanical reinforcement. In contrast, when the primary network is far above its rigidity threshold, the double network is always stiff and brittle. These results highlight an important mechanism behind the tunability and resilience of biopolymer double networks: the secondary network can dramatically alter mechanical properties from compliant and ductile to stiff and brittle only when the primary network is marginally rigid.