Subchondral bone circulation in osteoarthritis of the human knee.

TitleSubchondral bone circulation in osteoarthritis of the human knee.
Publication TypeJournal Article
Year of Publication2018
AuthorsAaron RK, Racine JR, Voisinet A, Evangelista P, Dyke JP
JournalOsteoarthritis Cartilage
Volume26
Issue7
Pagination940-944
Date Published2018 07
ISSN1522-9653
KeywordsAged, Biomechanical Phenomena, Blood Flow Velocity, Bone and Bones, Case-Control Studies, Contrast Media, Diffusion Magnetic Resonance Imaging, Female, Humans, Knee Joint, Male, Middle Aged, Osteoarthritis, Knee, Reference Values, Severity of Illness Index
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, k, Ak, and k. The mean k and Ak were reduced in OA, compared to normal bone, indicating a reduction of arterial inflow and delayed signal enhancement. The k in OA bone was lower than in normal bone, the negative k indicating a reduction in venous outflow. The area under the TIC (AUC) 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.

DOI10.1016/j.joca.2018.04.003
Alternate JournalOsteoarthritis Cartilage
PubMed ID29723635
Related Institute: 
MRI Research Institute (MRIRI)

Weill Cornell Medicine
Department of Radiology
525 East 68th Street New York, NY 10065