Subchondral fluid dynamics in a model of osteoarthritis: use of dynamic contrast-enhanced magnetic resonance imaging.
Publication Type | Academic Article |
Authors | Lee J, Dyke J, Ballon D, Ciombor D, Rosenwasser M, Aaron R |
Journal | Osteoarthritis Cartilage |
Volume | 17 |
Issue | 10 |
Pagination | 1350-5 |
Date Published | 04/17/2009 |
ISSN | 1522-9653 |
Keywords | Cartilage, Articular, Magnetic Resonance Imaging, Osteoarthritis, Knee, Tibia |
Abstract | OBJECTIVE: The hypothesis of this study is that changes in fluid dynamics in subchondral bone bear a functional relationship to bone remodeling and cartilage breakdown in osteoarthritis (OA). We have utilized dynamic contrast-enhanced (DCE) magnetic resonance imaging (MRI) to extract kinetic parameters of bone perfusion at various stages in the development of OA in the Dunkin-Hartley guinea pig. DESIGN: Animals of four different ages (6, 9, 12 and 15 months), representing various stages in the development of OA, were studied. All animals underwent DCE MRI and perfusion data were analyzed based on the Brix two-compartment pharmacokinetic model. Regions of interest were studied at the medial and lateral tibial plateaus and compared to histological-histochemical scores of articular cartilage and subchondral bone plate thickness. RESULTS: A decrease in perfusion as well as outflow obstruction was observed in animals between 6 and 9 months of age, only in the medial tibial plateau subchondral bone. The eventual cartilage and bone lesions of OA occurred also in the medial tibia. Changes in perfusion occurred in the lateral tibia but not until OA lesions were established. Kinetic parameters of inflow were unchanged in both the medial and lateral plateaus. CONCLUSIONS: DCE MRI can be used to extract kinetic information on bone perfusion in an animal model of OA. The signal enhancement in subchondral bone temporally precedes and spatially localizes at the same site of the eventual bone and cartilage lesions. Time-intensity curves suggest outflow obstruction as an underlying mechanism. |
DOI | 10.1016/j.joca.2009.03.019 |
PubMed ID | 19409292 |
PubMed Central ID | PMC2903730 |