Browsing by Author "Hislop, Brady David"

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Does bone-to-cartilage fluid transport exist and is it relevant to joint health?
(Montana State University - Bozeman, College of Engineering, 2024) Hislop, Brady David; Chairperson, Graduate Committee: Ronald K. June II; This is a manuscript style paper that includes co-authored chapters.
Osteoarthritis (OA) afflicts millions of people each year. The onset of OA has been associated with many factors including increased bone-cartilage fluid transport, yet a cure remains elusive. To implicate bone-cartilage fluid transport in the progression of OA, further studies are needed on fluid transport in health. Recent studies have challenged the assumption that no fluid transport occurs between bone and cartilage in healthy joints. However, many gaps remain in our understanding of bone-to-cartilage fluid transport, including 1) do fluid pressure gradients develop at the bone-cartilage interface, 2) do traumatic injuries impact subchondral bone stiffness, and synovial fluid metabolism 3) do larger molecules move from bone-to-cartilage and does cyclic loading enhance such movement, 4) what material properties influence bone-to-cartilage fluid transport 5) do distinct metabolism changes occur with osteoarthritis, evaluated using a novel clustering method. Our results showed the development of fluid pressure gradients at the osteochondral interface, and that cyclic compression enhances bone-cartilage fluid transport. Furthermore, our results showed that proteoglycan loss, and decreased subchondral bone stiffness increased bone-cartilage fluid transport. Finally, we showed that in the first week after traumatic joint injuries (e.g., ACL tears) subchondral bone volume decreases, and subchondral bone stiffness increases, while the synovial fluid metabolism shifts. In conclusion, we showed that osteochondral fluid transport is enhanced by cyclic compression for larger molecules than previously studied (3kDa dextran), and that material parameters changes associated with the progression of OA alter bone-cartilage fluid transport. These studies provide novel understanding of bone-to-cartilage fluid transport, leading us one step closer to understanding OA as a whole joint disease.
Osteochondral fluid transport in an ex vivo system
(Elsevier BV, 2024-04) Hislop, Brady David; Mercer, Ara K.; Whitley, Alexandria G.; Myers, Erik P.; Mackin, Marie; Heveran, Chelsea M.; June, Ronald K.
Objective: Alterations to bone-to-cartilage fluid transport may contribute to the development of osteoarthritis (OA). Larger biological molecules in bone may transport from bone-to-cartilage (e.g., insulin, 5 kDa). However, many questions remain about fluid transport between these tissues. The objectives of this study were to (1) test for diffusion of 3 kDa molecular tracers from bone-to-cartilage and (2) assess potential differences in bone-to-cartilage fluid transport between different loading conditions. Design: Osteochondral cores extracted from bovine femurs (N = 10 femurs, 10 cores/femur) were subjected to either no-load (i.e., pure diffusion), pre-load only, or cyclic compression (5 ± 2% or 10 ± 2% strain) in a two-chamber bioreactor. The bone was placed into the bone compartment followed by a 3 kDa dextran tracer, and tracer concentrations in the cartilage compartment were measured every 5 min for 120 min. Tracer concentrations were analyzed for differences in beginning, peak, and equilibrium concentrations, loading effects, and time-to-peak tracer concentration. Results: Peak tracer concentration in the cartilage compartment was significantly higher compared to the beginning and equilibrium tracer concentrations. Cartilage-compartment tracer concentration and maximum fluorescent intensity were influenced by strain magnitude. No time-to-peak relationship was found between strain magnitudes and cartilage-compartment tracer concentration. Conclusion: This study shows that bone-to-cartilage fluid transport occurs with 3 kDa dextran molecules. These are larger molecules to move between bone and cartilage than previously reported. Further, these results demonstrate the potential impact of cyclic compression on osteochondral fluid transport. Determining the baseline osteochondral fluid transport in healthy tissues is crucial to elucidating the mechanisms OA pathology.