Subchondral bone circulation in osteoarthritis of the human knee.
| Publication Type | Academic Article |
| Authors | Aaron R, Racine J, Voisinet A, Evangelista P, Dyke J |
| Journal | Osteoarthritis Cartilage |
| Volume | 26 |
| Issue | 7 |
| Pagination | 940-944 |
| Date Published | 05/01/2018 |
| ISSN | 1522-9653 |
| Keywords | Contrast Media, Diffusion Magnetic Resonance Imaging, Knee Joint, Osteoarthritis, Knee |
| Abstract | OBJECTIVE: The hypothesis of this study is that human subchondral bone exhibits abnormal patterns of perfusion in osteoarthritis (OA) that can be characterized by kinetic parameters of blood flow using dynamic contrast enhanced (DCE) MRI. DESIGN: Fifteen subjects with advanced OA of the knee and seven control subjects without OA were studied at 1.5 T with DCE-MRI. Region of interest (ROIs) analysis of pharmacokinetic perfusion parameters were used to examine initial uptake and washout of the contrast agent in the lateral tibial plateau. RESULTS: Arterial and venous perfusion kinetics were abnormal in subchondral OA bone compared to those of normal controls. Time-intensity curves (TIC) exhibited delayed contrast clearance in OA knees compared to normal. Quantitatively, changes were observed in the kinetic parameters, kep, Akep, and kel. The mean kep and Akep were reduced in OA, compared to normal bone, indicating a reduction of arterial inflow and delayed signal enhancement. The kel in OA bone was lower than in normal bone, the negative kel indicating a reduction in venous outflow. The area under the TIC (AUC60) indicated greater residual contrast in OA bone. CONCLUSIONS: DCE-MRI can quantitatively assess subchondral bone perfusion kinetics in human OA and identify heterogeneous regions of perfusion deficits. The results are consistent with venous stasis in OA, reflecting venous outflow obstruction, and can affect intraosseous pressure, reduce arterial inflow, reduce oxygen content, and may contribute to altered cell signaling in, and the pathophysiology of, OA. |
| DOI | 10.1016/j.joca.2018.04.003 |
| PubMed ID | 29723635 |