Osteochondral fluid transport in an ex vivo system

Brady David Hislop; Ara K Mercer; Alexandria G Whitley; Erik P Myers; Marie Mackin; Chelsea M Heveran; Ronald K June

doi:10.1016/j.joca.2024.02.946

Osteochondral fluid transport in an ex vivo system

Osteoarthritis Cartilage. 2024 Apr 15:S1063-4584(24)01155-5. doi: 10.1016/j.joca.2024.02.946. Online ahead of print.

Authors

Brady David Hislop¹, Ara K Mercer², Alexandria G Whitley³, Erik P Myers¹, Marie Mackin², Chelsea M Heveran¹, Ronald K June⁴

Affiliations

¹ Department of Mechanical and Industrial Engineering, Montana State University, Bozeman, MT, USA.
² Department of Chemistry and Biochemistry, Montana State University, Bozeman, MT, USA.
³ Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA.
⁴ Department of Mechanical and Industrial Engineering, Montana State University, Bozeman, MT, USA; Department of Cell Biology and Neurosciences, Montana State University, Bozeman, MT, USA; Department of Orthopaedics and Sports Medicine, University of Washington, Seattle, WA, USA. Electronic address: rjune@montana.edu.

PMID: 38631555
DOI: 10.1016/j.joca.2024.02.946

Abstract

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.

Keywords: Bone-to-cartilage fluid transport; Cyclic compression; Mechanotransduction; Osteoarthritis.