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University of Vienna A-1090 Vienna, Austria
In the article entitled "MR Imaging and T2 Mapping of Femoral Cartilage: In Vivo Determination of the Magic Angle Effect" [1], Mosher et al. reported that changes in T2 values of femoral cartilage with orientation were only 9-29% and that the least T2 variation was in the radial zone. On the basis of these results, they concluded that "it is unlikely that the magic angle effect accounts for regional differences in cartilage signal intensity observed in clinical imaging."
The authors wrote that "regional variation in cartilage T2 differs from that observed with signal intensity." However, assuming that their single-slice spin-echo images with the reported voxel size are almost unaffected by magnetization transfer or diffusion, signal intensity should depend only on T1, T2, and proton density. With the TR of 1500 msec used by the authors, there is very little T1 weighting in the images of cartilage. Proton density (i.e., the water concentration) is indeed decreased in the radial zone, but this decrease is not dramatic. The unimportance of proton density weighting is evident on common fat-suppressed short TE gradient-echo images, which show the full thickness of femoral cartilage with high signal intensity. Thus, T2 should be the only relevant parameter responsible for distinct regional differences of signal intensities in T2-weighted spin-echo images of weight-bearing cartilage.
The discrepancy between the signal intensities and the calculated T2 values
can be explained by multiexponential (or roughly biexponential) magnetization
decay with a short-T2 component (T2 
20 msec). We suggested this
hypothesis when we observed a similar regional difference between T2 and
signal intensities in a superficial cartilage layer in vitro
[2], and our experiments
excluded proton density as a potential cause of the difference. The concept of
the multiexponential magnetization decay is also supported by the
orientation-dependent T2 anisotropy in bulk cartilage and tendon observed by
Henkelman et al. [3].
In their experiments, Mosher et al. [1] used a multiecho imaging sequence consisting of 11 echoes in 10-msec steps, with the initial echo (TE, 10) excluded to minimize a systematic error. However, for the TEs from 20 to 110 msec, the short-T2 magnetization component is already extensively relaxed. As a result, in using a monoexponential fit, they calculated the T2 values corresponding mainly to the long-T2 component. This fact might also explain the unusually high T2 values reported for the radial cartilage region.
In summary, a finding of little orientation variability of the long-T2 component of the cartilage magnetization measured in vivo is not in contradiction with the expected role of the magic angle effect in regional differences of cartilage signal intensities.
References
Pennsylvania State University College of Medicine The Milton S.
Hershey Medical Center Hershey, PA 17033
The Children's Hospital Research Foundation Children's Hospital
Medical Center Cincinnati, OH 45229
We appreciate Dr. Mlynárik's comments regarding our recent article, "MR Imaging and T2 Mapping of Femoral Cartilage: In Vivo Determination of the Magic Angle Effect" [1]. His letter raises several points. First, it is necessary to clearly define the term "regional differences" as it applies to cartilage T2 measurements. As illustrated in figure 1 of our article, our conclusion applies to regions of cartilage within the femoral condyle. It does not refer to differences in T2 observed between histologic zones. Although he does not specifically state it in his letter, Mlynárik appears to be addressing differences in T2 and cartilage signal intensities of different histologic zones. Results of our study, as well as those of previous in vivo studies that showed a reproducible increase in cartilage T2 with distance from subchondral bone [2,3], are consistent with the hypothesis that a high density of collagen fibers contributes to the short T2 observed in the radial zone of cartilage. Our observation that the greatest difference in cartilage T2 as a function of orientation occurs in superficial cartilage suggests factors other than the magic angle effect—which should be greatest in the radial zone—are major contributors to regional variation in T2 and signal intensity.
Second, although we agree with Mlynárik that articular cartilage has a multiexponential T2 decay, this does not alter our stated conclusion that "it is unlikely that the magic angle effect accounts for regional differences in cartilage signal intensity observed in clinical imaging." In fact, the argument put forth by Mlynárik further supports this conclusion.
Prior studies with ex vivo cartilage samples suggest T2 relaxation of articular cartilage is multiexponential. Mlynárik et al. [4] hypothesized that cartilage T2 decay is biexponential, "with one component decaying rapidly in the first 10 msec or so." We previously showed multiexponential T2 decay in porcine cartilage plugs, which was indicative of three T2 populations [5]. The shortest component, consisting of approximately 20% of the total signal, had a T2 of 400 µsec. As Mlynárik proposes, this short T2 population is most likely to have a strong magic angle effect. However, because of rapid T2 relaxation, signal from this population of protons will be undetectable in the range of our T2 measurements (TE, 20-110). Likewise, this population will not contribute to the signal intensity of clinical fast spin-echo cartilage imaging, which uses TE values in the range of 30-50 msec. It is the population of protons with longer T2 values, in the range of 30-70 msec, that produces the MR imaging signal in clinical images. As Mlynárik suggests, this population is unlikely to show a magic angle effect.
In summary, we stand by our conclusions that regional differences in signal intensity of articular cartilage in clinical imaging are unlikely due to a magic angle effect.
References
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