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Commentary |
1 Department of Radiology, Hospital of the University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104.
Received February 23, 2001;
accepted after revision March 9, 2001.
This article is a commentary on the preceding article by Mosher et al.
Introduction
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The magic angle effect has been noted in those structures of the musculoskeletal system in which there are highly ordered collagen fibers such as tendons [2]. The water molecules present in collagen are rigidly bound to the collagen macromolecules and, as a result, exhibit very short T2 relaxation times. This very short T2 time results in the almost complete absence of signal at TEs typically used in clinical MR imaging. By lengthening T2 time of these bound water molecules, the magic angle effect results in signal that is visible on short-to-moderate length TE sequences used clinically. Because we "visualize" tendons as regions of absent signal surrounded by structures with higher signal, such as fat, the presence of magic angle effect has the paradoxical result of rendering the tendon less visible. In addition, because increased signal within a tendon is often associated with the presence of injury, degeneration, or inflammation, the magic angle effect is a potential cause of a false-positive diagnosis of tendon abnormality.
What the author of this commentary has found most surprising about magic angle effect is the variability with which it is observed in actual clinical practice. Thus, for example, although it is clearly seen in some patients when the ankle tendons are at the magic angle with respect to the static field, it is not well seen in others. The reason for this variability is unknown, but it may be caused by differences in the orientation of the collagen fibers. Whatever the cause, the effect of this variability is to render more difficult the interpretation of the significance of increased signal in the tendons in regions in which the magic angle effect could be present. Thus, as a diagnostic radiologist, one is often faced with the question of whether increased signal in the posterior tibial tendon as it courses around the medial malleolus is the result of magic angle effect or if it represents tendon degeneration. Although it is certainly true that the magic angle effect does not result in bright (fluidlike) signal on T2-weighted images, the presence of increased signal on short TE sequences is compatible with either degeneration or magic angle effect.
Organized collagen fibers are also present in articular cartilage, as illustrated in figure 4 of the accompanying article by Mosher et al. The apparent similarity of the MR-visible layers to the orientation of the collagen fibers established by light microscopy (and in particular the sheets of collagen revealed by scanning electronic microscopy [3] and represented in figure 4) has led many investigators to conclude that the collagen is predominantly responsible for the layers seen in cartilage with MR imaging [4]. In addition, the increase in signal intensity of the basilar layer of cartilage with rotation of in vitro specimens to 55° noted by several investigators [4, 5] has been assumed to result from the presence of ordered collagen fibers and the magic angle effect. Furthermore, the focus of increased signal seen with the trochlear cartilage on T2-weighted MR images, and shown in Figure 1A,1B of this commentary, has been assumed to be a result of this same phenomenon. The importance of this explanation is that it can account for the presence of increased signal within the cartilage in the absence of degeneration or injury.
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As reasonable as these explanations may seem, direct correlation of collagen fibril orientation with the MR images of cartilage has proven problematic. A carefully controlled investigation by Goodwin et al. [6] failed to establish a precise correlation between the two, leading them to speculate that the collagen network acts indirectly on water molecules, perhaps through its influence on the orientation of proteoglycan macromolecules.
The accompanying article by Mosher et al. casts further doubt on the magic angle effect as the primary cause of increased signal seen in the trochlear cartilage in vivo. The authors were able to show the same increase in signal intensity of the deep layer of the trochlear cartilage as just discussed and illustrated in the accompanying images. The T2 measurements that they made, however, implied that the magic angle effect, which operates by increasing the T2 relaxation times, is not responsible for this increased signal. They marshaled two pieces of evidence from their data to support this contention: the measured increase on T2 ranged from 9% to 29%, a value the authors believed insufficient to account for the observed ex vivo changes in signal intensity; and the greatest measured increase in T2 was present in the superficial 20% of the cartilage, likewise not in keeping with the large increase seen in the basilar layers ex vivo.
The authors went on to speculate that regional differences in compression of the cartilage associated with walking might be the major cause of the observed signal differences.
Figure 1A,1B of this commentary illustrates an increase in signal intensity of the articular cartilage in the trochlear groove of the femur as seen with both short (Fig. 1A) and long TE (Fig. 1B) sequences obtained on a 1.5-T system. As with all high-field superconducting magnets used in clinical MR imaging, B0 is oriented along the long axis of the body, which corresponds to the vertical direction of these figures. A few observations regarding these images are in order:
First, the increased signal in the cartilage seen in this patient is more pronounced than we generally see. In some cases there is little if any change. Given the nature of the sequences used to acquire the images, an actual measurement of T2 times in the cartilage is not feasible. Thus, it is difficult to determine whether an increase in T2 actually could be responsible for the signal increase that is typically seen or even what is seen here.
Second, although the bright signal in the trochlear cartilage is seen at the expected region of the magic angle, bright signal is also seen at angles that are more vertically oriented than the 55° that represents the magic angle (arrow). This is also true for the patellar cartilage (black arrowhead). These findings do not support the magic angle effect as the cause of the increased signal.
Third, the increase in signal is also seen to extend through the entire thickness of the cartilage, a finding that does not correspond to greater increase in T2 of the superficial cartilage noted by Mosher et al.
Finally, although the cartilage located on the most inferior region of the trochlear groove has the lowest signal (white arrow-head), there is very little compression of the cartilage in this region because it is located close to the midline and is subject to only limited pressure from weight bearing.
The relation between cartilage structure and its MR appearance is clearly in need of more investigative work. Mosher et al. were willing to question previous assumptions. Their study is a good reminder that we should not just accept as fact what seems reasonable; we should critically assess the quality of the scientific evidence available before reaching a conclusion.
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