Knee subchondral bone perfusion and its relationship to marrow fat and trabeculation on multi-parametric MRI and micro-CT in experimental CKD

Abstract

The pathogenesis of chronic kidney disease (CKD) is multifactorial. In the progression of CKD arthropathy, arteriosclerosis may alter the knee subchondral bone marrow by altering blood flow through the bone vasculature. Herein, multi-parametric MRI assessment, including dynamic contrast enhanced magnetic resonance imaging (DCE-MRI), magnetic resonance spectroscopy (MRS), MRI T2*, contrast enhanced MR angiography (CE-MRA), and micro-CT were applied in a rodent nephrectomy model to: 1) investigate the blood perfusion of subchondral bone marrow and its relationship to fat water content and trabeculation pattern in CKD and 2) demonstrate the feasibility of using multi-parametric MRI parameters as imaging biomarkers to evaluate the disease’s progression. Two groups of rats in our study underwent either 1) no intervention or 2) 5/6 nephrectomy. We found that in the CKD group, perfusion amplitude A and elimination constant k el values were significantly decreased, and vascular permeability k ep was significantly increased. MRS showed that fat fraction (FF) was significantly lower, water fraction (WF) was significantly higher in the CKD group. Micro-CT showed a significant loss of trabecular bone. Knee subchondral bone marrow perfusion deficiency in experimental CKD may be associated with decreased fat content, increased water content, and sparse trabeculation.

How We Manage Bone Marrow Edema—An Interdisciplinary Approach

“…The second major cause is renal insufficiency, which ultimately causes a complex bone disorder called chronic kidney disease-mineral and bone disorder (CKD-MBD). Although data regarding the incidence of BME in the several CKD stages are scarce, CKD-MBD may accompany BME, as suggested by animal models [79]. In addition, CKD-MBD causes an osteoporosis-like syndrome with impaired bone quality and increased risk of fragility (micro-) fractures.…”

Disease-modifying interactions between chronic kidney disease and osteoarthritis: a new comorbid mouse model

“…Increased differentiation of circulating inflammatory monocytes into osteoclasts is part of the CKD-MBD syndrome associated with secondary hyperparthathyroidism and vascular pathology. [37][38][39] While partially offset by later-stage OA-induced focal bone formation, the persistence of 5/6Nx-induced subchondral bone turnover and reduced BMD may ameliorate excessive mechanical loading on the overlying cartilage associated with OA-induced subchondral sclerosis as well as abnormal biological cross-talk from diseased subchondral osteocytes. 15 In addition to subchondral bone remodelling, osteoclasts are critical in regulating calcified cartilage turnover in endochondral ossification.…”

Hypoperfusion of the infrapatellar fat pad and its relationship to MRI T2* relaxation time changes in a 5/6 nephrectomy model

“…Three perfusion parameters can be extracted such as the amplitude, A , the elimination constant of the contrast medium from the plasma, k el , and the exchange rate constant from the extravascular extracellular space (EES) to plasma, k ep . In previous reports, DCE-MRI has been used to study synovial vascularity and inflammation in diseases such as rheumatoid arthritis (RA) 18 and osteoarthritis (OA) 19 , but few reports have examined its use to study the pathogenesis of CKD-related OA 20 . To clarify the hemodynamic response to CKD in the highly vascularized infrapatellar fat pad, longitudinal DCE-MRI was used to explore the role of perfusion at different stages of CKD.…”