Thomas Lange1, Benjamin R. Knowles1, Michael Herbst1,2, Kaywan Izadpanah3, and Maxim Zaitsev1
1Department of Radiology, University Medical Center Freiburg, Freiburg, Germany, 2John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, United States, 3Department of Orthopedic and Trauma Surgery, University Medical Center Freiburg, Freiburg, Germany
Synopsis
Robust T2 mapping of knee cartilage with in
situ mechanical loading using prospective motion correction is demonstrated for
the patellofemoral and tibiofemoral knee compartments. T2 maps are
reconstructed from multiple spin-echo data acquired with slice position updates
before every excitation. While T2 maps of the tibiofemoral joint do not show
significant changes in response to loading, maps of the patellofemoral joint
show a substantial load-induced T2 reduction in the superficial cartilage layers.
In particular, the T2 of tangential fibers at the cartilage surface appears to
undergo a strong reduction due to a load-induced increase of tissue anisotropy.Purpose
To date, only very few T2 mapping studies on
knee cartilage have been performed with in situ loading, mainly because such
experiments are strongly hampered by subject motion. The purpose of this work
is to investigate the response of knee cartilage T2 to in situ mechanical
loading in vivo for the patellofemoral and tibiofemoral joint compartments,
using prospective motion correction to mitigate artifacts from load-induced subject
motion.
Methods
All experiments were performed on a
Magnetom Trio 3T system (Siemens Healthcare, Germany), using an 8-channel
multipurpose coil (NORAS MRI products, Germany) for signal reception. Knee
loading was realized with an MR-compatible pneumatic loading device enabling
accurate load adjustment in the range 0-50 kg. Prospective motion correction
was performed with a moiré phase tracking (MPT) system (Metria Innovation Inc., Milwaukee, US), consisting
of a single in-bore camera and a tracking marker, which was taped to the
kneecap
1,2. For MRI of the patellofemoral joint under loading,
the subject was positioned on the scanner bed with a knee flexion angle of
40°-50° (Fig. 1). For MRI of the tibiofemoral cartilage, the leg was loaded in
nearly full extension. T2 mapping was conducted in healthy subjects with a 2D
multiple spin-echo sequence (TE = [13.8, 27.6, 41.4, 55.2, 69.0, 82.8] ms, 11
slices, slice thickness = 3 mm, in-plane resolution = 0.6 mm). Slice positions
were updated once per TR prior to the excitation pulse. Some T2 mapping
experiments were performed with fat suppression to reduce residual motion
artifacts from bright subcutaneous fat and bone signal. T2 maps were calculated from the acquired
data using the Matlab-based StimFit algorithm, accounting for stimulated echo
contributions arising from imperfect refocusing pulse profiles
3.
Results
Fig. 2 shows T2 maps of the patellofemoral
cartilage in a healthy subject under different loading conditions (0/20/40 kg),
acquired with and without motion correction and with and without fat
suppression. Images acquired without motion correction are not only strongly impaired
by load-induced subject motion during acquisition, but also by position offsets
increasing with the load. In contrast, the artifact level only mildly increases
with the load when prospective motion correction is used and can be further
reduced through fat suppression. Consistently higher T2 values were observed in
the maps acquired with fat suppression compared to those acquired without fat
suppression. The maps show a substantial load-induced T2 decrease in the superficial
cartilage layers (Fig. 3). In particular, there is a thin line of strongly
decreased T2 relaxation in the maps acquired with loading, marking the boundary
between patellar and femoral cartilage. On the other hand, there is a deep
cartilage layer with very short T2 values (T2 < 10 ms) close to the bone
which gets thinner with increasing loads. Such load-induced T2 changes could
not be observed in the T2 maps acquired from the tibiofemoral joint (Fig. 4).
Discussion
Motion was observed to be particularly severe
for load experiments on the patellofemoral joint, which required knee flexion.
However, the inter-scan position locking capability of our prospective motion
correction implementation
1 enables a direct comparison of T2 maps acquired with different loads. Interestingly,
substantial load-induced T2 changes could only be observed in the
patellofemoral joint, but not in the tibiofemoral joint as observed by others
4–6, suggesting that changes in the tibiofemoral joint are more subtle and
can only be unequivocally detected when results are averaged over larger
subject cohorts. The observed T2 decrease in superficial cartilage is in line
with results from the tibiofemoral joint by Souza et al.
6 and with in-situ NMR microscopy measurements on knee cartilage plugs
of pigs with concurrently acquired polarization light microscopic (PLM) reference
images
7. The PLM images in that work show that articular cartilage is composed
of a thin cartilage layer with tangential fiber orientation at the surface. By
applying mechanical loading to this cartilage structure, the anisotropy of this
superficial cartilage layer is increased. Larger fiber anisotropy gives rise to
increased residual dipolar coupling and thus enhances T2 relaxation. Therefore
mechanical loading leads to decreased T2 relaxation values at the cartilage
surface, which explains the thin boundary layer of very short T2 between
femoral and patellar cartilage observed in the presented work. Souza et al.
further reported a load-induced T2 increase in the deep cartilage layers,
explaining this phenomenon with a fluid transport from superficial to deep
cartilage layers
6. However, our results suggest that this apparent T2 increase might
rather be due to compression of the short T2 cartilage layers adjacent to the
bone, reducing their influence on the overall T2 of deep cartilage.
Acknowledgements
This work was funded in part by the NIH grant 2R01DA021146, in part by
the Helmholtz Alliance ICEMED - Imaging and Curing Environmental Metabolic
Diseases, and in part by the German Research Foundation (DFG), grant number LA 3353/2-1.References
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