Does bone-to-cartilage fluid transport exist and is it relevant to joint health?

Abstract

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.