Journal
EUROPEAN RADIOLOGY
Volume 30, Issue 6, Pages 3401-3408Publisher
SPRINGER
DOI: 10.1007/s00330-020-06671-6
Keywords
Osteoarthritis; knee; Patellofemoral pain syndrome; Inflammation; Magnetic resonance imaging; Synovitis
Funding
- European Society of Musculoskeletal Radiology
- Radiological Society of North America (RSNA)
- EUR fellowship from the Erasmus University Rotterdam
- Dutch Arthritis Foundation
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Objective Infrapatellar fat pad (IPFP) fat-suppressed T2 (T2(FS)) hyperintense regions on MRI are an important imaging feature of knee osteoarthritis (OA) and are thought to represent inflammation. These regions are also common in non-OA subjects, and may not always be linked to inflammation. Our aim was to evaluate quantitative blood perfusion parameters, as surrogate measure of inflammation, within T2(FS)-hyperintense regions in patients with OA, with patellofemoral pain (PFP) (supposed OA precursor), and control subjects. Methods Twenty-two knee OA patients, 35 PFP patients and 43 healthy controls were included and underwent MRI, comprising T2 and DCE-MRI sequences. T2(FS)-hyperintense IPFP regions were delineated and a reference region was drawn in adjacent IPFP tissue with normal signal intensity. After fitting the extended Tofts pharmacokinetic model, quantitative DCE-MRI perfusion parameters were compared between the two regions within subjects in each subgroup, using a paired Wilcoxon signed-rank test. Results T2(FS)-hyperintense IPFP regions were present in 16 of 22 (73%) OA patients, 13 of 35 (37%) PFP patients, and 14 of 43 (33%) controls. DCE-MRI perfusion parameters were significantly different between regions with and without a T2(FS)-hyperintense signal in OA patients, demonstrating higher Ktrans compared to normal IFPF tissue (0.039 min(-1) versus 0.025 min(-1), p = 0.017) and higher Ve (0.157 versus 0.119, p = 0.010). For PFP patients and controls no significant differences were found. Conclusions IPFP T2(FS)-hyperintense regions are associated with higher perfusion in knee OA patients in contrast to identically appearing regions in PFP patients and controls, pointing towards an inflammatory pathogenesis in OA only.
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