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dc.contributor.authorKupratis, Meghan E.
dc.contributor.authorGonzalez, Uriel
dc.contributor.authorRahman, Atia
dc.contributor.authorBurris, David L.
dc.contributor.authorCorbin, Elise A.
dc.contributor.authorPrice, Christopher
dc.date.accessioned2024-04-24T22:40:57Z
dc.date.available2024-04-24T22:40:57Z
dc.date.copyright3/19/2024 12:00:00 AM
dc.date.issued2024
dc.identifier.issn0148-0731
dc.identifier.otherbio_146_07_071001.pdf
dc.identifier.urihttp://yetl.yabesh.ir/yetl1/handle/yetl/4295675
dc.description.abstractHealthy articular cartilage is a remarkable bearing material optimized for near-frictionless joint articulation. Because its limited self-repair capacity renders it susceptible to osteoarthritis (OA), approaches to reinforce or rebuild degenerative cartilage are of significant interest. While exogenous collagen crosslinking (CXL) treatments improve cartilage's mechanical properties and increase its resistance to enzymatic degradation, their effects on cartilage lubrication remain less clear. Here, we examined how the collagen crosslinking agents genipin (GP) and glutaraldehyde (GTA) impact cartilage lubrication using the convergent stationary contact area (cSCA) configuration. Unlike classical configurations, the cSCA sustains biofidelic kinetic friction coefficients (μk) via superposition of interstitial and hydrodynamic pressurization (i.e., tribological rehydration). As expected, glutaraldehyde- and genipin-mediated CXL increased cartilage's tensile and compressive moduli. Although net tribological rehydration was retained after CXL, GP or GTA treatment drastically elevated μk. Both healthy and “OA-like” cartilage (generated via enzymatic digestion) sustained remarkably low μk in saline- (≤0.02) and synovial fluid-lubricated contacts (≤0.006). After CXL, μk increased up to 30-fold, reaching values associated with marked chondrocyte death in vitro. These results demonstrate that mechanical properties (i.e., stiffness) are necessary, but not sufficient, metrics of cartilage function. Furthermore, the marked impairment in lubrication suggests that CXL-mediated stiffening is ill-suited to cartilage preservation or joint resurfacing.
dc.publisherThe American Society of Mechanical Engineers (ASME)
dc.titleExogenous Collagen Crosslinking is Highly Detrimental to Articular Cartilage Lubrication
dc.typeJournal Paper
dc.journal.volume146
dc.journal.issue7
dc.journal.titleJournal of Biomechanical Engineering
dc.identifier.doi10.1115/1.4064663
dc.journal.fristpage71001-1
dc.journal.lastpage71001-11
dc.page11
dc.treeJournal of Biomechanical Engineering:;2024:;volume( 146 ):;issue: 007
dc.contenttypeFulltext


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