Kai D. Ludwig1, Casey P. Johnson1,2, Stefan Zbyn1,2, Shelly Marette2, Takashi Takahasi2, Jeffrey A. Macalena3, Bradley J. Nelson3, Marc A. Thompkins3, Cathy S. Carlson4, and Jutta M. Ellermann1,2
1Center for Magnetic Resonance Research (CMRR), University of Minnesota, Minneapolis, MN, United States, 2Radiology, University of Minnesota, Minneapolis, MN, United States, 3Orthopaedic Surgery, University of Minnesota, Minneapolis, MN, United States, 4Veterinary Clinical Sciences, University of Minnesota, St. Paul, MN, United States
Synopsis
Juvenile osteochondritis dissecans (JOCD) is a disease
affecting the knee joint of young active patients that can lead to early
osteoarthritic changes. JOCD lesions are formed deep to the articular cartilage
with late changes in the overlying articular cartilage. Our study was motivated
by clinical observations that the opposing articular cartilage might be
affected early. In this study, we observed a significant increase in T2*
relaxation times in the articular cartilage of the medial tibia directly
opposing the lesions when compared to the control region on the lateral site. These
findings might indicate compositional changes in the tibial cartilage matrix
due to increased biomechanical loading. Further study of T2* mapping as a
potentially clinically realizable method to stage and prognosticate JOCD are
warranted.
Purpose
Juvenile
osteochondritis dissecans (JOCD) is a disease characterized by the formation of
lesions initiating in the sub-articular epiphyseal cartilage and, later, ossifying
as the joint develops. The articular cartilage overlying the lesion remains clinically-normal
for a long period, and changes are noted clinically only in very late stages of
the disease. Current clinical protocols based on qualitative assessments cannot
detect whether the intact overlying articular cartilage is injured. Thus, it is
of potential clinical interest to non-invasively evaluate the health of the
femoral and tibial articular cartilage in the vicinity of the JOCD lesion. Our
interest in these location was motivated by arthroscopic observations noted by
orthopaedic surgeons in subtle changes of the opposing tibial articular
surface. It has been previously shown that T2 and T2* relaxation times can quantitative
measure cartilage integrity in JOCD [1,2]. The
purpose of this study was to investigate whether T2* relaxation times are
altered in the articular cartilage of the distal femur (adjacent to JOCD
lesions) and proximal tibial (opposing the JOCD lesions) compared to cartilage
on the opposite side of the joint.Methods
Subjects. The institutional review board approved all
procedures. Eight patients with suspected JOCD (6M/2F; average age = 14.0 years;
range: 11-19 years) were enrolled.
Imaging. MRI data was acquired on a 3T Magnetom
Prisma MRI system (Siemens Medical Systems) with a 15-channel transmit/receive
knee RF coil. Clinical T1-weighted, T2-weighted, and PD-weighted images were
collected in three orthogonal planes. A gradient-recalled-echo T2* mapping
sequence (TR/TE/ΔTE = 1150/2.63/2.96 ms, 6 echoes, matrix = 352×352, resolution = 0.43×0.43, slice thickness/gap
= 2.0/0.0 mm, 39 slices, flip angle = 60°, voxel bandwidth = 395-405 Hz, and
acquisition time = 6min:57sec) was acquired. All lesions were radiologically classified
as stable lesions without obvious articular cartilage fissures or defects.
Analysis.
T2* maps: Articular cartilage T2* relaxation time maps
were fit from the six measured TEs on a voxel-wise basis. For segmentation, the
final three echo images of the T2* mapping sequence were averaged to enhance
the cartilage-to-bone contrast. The cartilage tissue was segmented
semi-automatically using ITK-SNAP [3]. Region-of-interests (ROIs) for
T2* measurements were defined from the segmented cartilage masks as shown in Figure 1.
Statistics: We hypothesized that T2* relaxation times
are altered in: (i) the central aspect of the medial femoral condyle (MFCC) vs. the lateral femoral
condyle (LFCC); and (ii) the medial tibia (MTC) vs. the lateral
tibia (LTC). These hypotheses were tested using a Wilcoxon-rank-sum
test with p<0.05 considered
statistically significant.
Results
All lesions occurred on the central aspect of the medial femoral
condyle (MFCC). No macroscopic abnormalities of the femoral or
tibial articular cartilage were observed in any of the knees. Cartilage depth
and parent bone edges were clearly visible on clinical PD- or T2-weighted
images and T2*-first-echo images, respectively, as shown in Figure 2. Cartilage T2* values for all
subjects are shown in Table 1. The MFCC had increased T2* values
compared to the same location on the lateral femoral condyle (LFCC)
(26.4 ± 4.4 ms vs. 23.1 ± 3.0 ms; p=0.090),
though not statistically significant. The opposing articular cartilage on the
medial tibia (MTC) had significantly increased T2* values compared
to the lateral tibia (LTC) (18.8 ± 2.8 ms vs. 15.8 ± 2.5 ms; p=0.029).Discussion
We observed a significant increase in T2* relaxation
times in the articular cartilage of the medial tibia directly opposing the
lesions compared to the lateral tibia. In contrast, there was no significant
difference in T2* relaxation times noted in the articular cartilage of the
medial femur immediately superficial to the lesion compared to the lateral
femur. Our results in the femur are consistent with a prior study of JOCD
patients that found no T2 differences in the cartilage overlying the JOCD
lesion versus cartilage adjacent to the lesion nor in the cartilage adjacent to
the lesion versus cartilage in controls [2].
No prior reports have assessed the tibial articular cartilage opposing the
lesions. Our tibial findings may relate to compositional changes in the tibial cartilage
matrix due to abnormal contact with the femoral cartilage lesion site. These
findings are considered to be preliminary due to the low number of patients
included in the study and motivate further study of T2* mapping as a
potentially clinically-realizable method to stage and prognosticate JOCD.Acknowledgements
This study was supported by the NIH (R01AR070020, K01AR070894,
and P41EB015894) and the W. M. Keck Foundation.References
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