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Updated: Sep 19, 2025

Quantitative Magnetic Resonance Imaging of Skeletal Muscle Disease
Published on: December 18, 2016
Orientation-Independent T2 Mapping Enhances MRI-Based Cartilage Characterization
Henri P P Leskinen1,2, Juuso Tuppurainen1,3, Jiri Jäntti1,3
1Department of Technical Physics, University of Eastern Finland, Yliopistonranta 8, 70210, Kuopio, Finland.
Purpose:
Quantitative T2 mapping is an important MRI method for assessing degenerative changes in articular cartilage. Recently, in a measurement setup with automated sample re-orientation, it was demonstrated that T2 can be split into its orientation-independent components. This quantitative MRI study aims to assess the diagnostic significance of the automated approach with ex vivo human cartilage.
Methods:
T2 maps of 30 human osteochondral samples harvested from 5 cadaveric individuals were acquired at 9.4T in 13 orientations, allowing calculation of the T2 components. Additionally, T1, adiabatic T1ρ, and continuous wave T1ρ with two spin-lock frequencies were scanned in a single orientation. For reference, the collagen network anisotropy, proteoglycan content and biomechanical indentation properties were measured. The relationships between quantitative MRI and reference parameters were studied using Mann-Whitney U-test and Spearman's rank correlation. All parameters were compared between healthy and degenerated groups based on OARSI grading.
Results:
The anisotropic relaxation rate component of T2 (R2a), and all T1 and T1ρ parameters differed (p < 0.05) between the groups in superficial cartilage. R2a correlated moderately with PLM anisotropy (r = 0.44) and optical density (r = - 0.37) in the deep zone. Isotropic T2 component (R2i) correlated with instantaneous modulus (r = 0.48), and R2a with phase shift between stress and strain during indentation testing (r = - 0.44). T1 and T1ρ parameters correlated with both, instantaneous and dynamic modulus in several zones of cartilage.
Conclusion:
The elevation of T2 in degenerated cartilage is primarily driven by the R2a component, whereas the R2i component showed no significant difference between healthy and degenerated human articular cartilage.
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