Publications by authors named "Meghan E Kupratis"

Articular cartilage's remarkable low-friction properties are essential to joint function. In osteoarthritis (OA), cartilage degeneration (e.g.

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Healthy 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.

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Healthy articular cartilage supports load bearing and frictional properties unmatched among biological tissues and man-made bearing materials. Balancing fluid exudation and recovery under loaded and articulated conditions is essential to the tissue's biological and mechanical longevity. Our prior tribological investigations, which leveraged the convergent stationary contact area (cSCA) configuration, revealed that sliding alone can modulate cartilage interstitial fluid pressurization and the recovery and maintenance of lubrication under load through a mechanism termed 'tribological rehydration.

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Articular cartilage is a robust tissue that facilitates load distribution and wear-free articulation in diarthrodial joints. These biomechanical capabilities are fundamentally tied to tissue hydration, whereby high interstitial fluid pressures and fluid load support facilitate the maintenance of low tissue strains and frictions. Our recent studies of cartilage sliding biomechanics using the convergent stationary contact area (cSCA) configuration, first introduced by Dowson and colleagues, unexpectedly demonstrated that sliding alone can promote recovery of interstitial pressure and lubrication lost to static compression through a mechanism termed 'tribological rehydration.

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Injury to the growth plate is associated with growth disturbances, most notably premature cessation of growth. The goal of this study was to identify spatial changes in the structure and composition of the growth plate in response to injury to provide a foundation for developing therapies that minimize the consequences for skeletal development. We used contrast-enhanced microcomputed tomography (CECT) and histological analyses of a murine model of growth plate injury to quantify changes in the cartilaginous and osseous tissue of the growth plate.

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