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Rush-Presbyterian-St. Luke's Medical Center and Rush Medical College Chicago, IL 60612
Rubin et al. [1] reported in the April 2000 issue of AJR that treatable chondral injuries of the knee are frequently associated in MR images with focal edema in subchondral bone marrow. They concluded that subchondral bone marrow edema may be a useful marker for traumatic chondral injuries, serving to call the observer's attention to lesions that might otherwise be overlooked. They correctly pointed out that they cannot comment on the specificity of focal bone marrow edema for traumatic chondral injury because of the highly selective nature of their study population, and they cited a report [2] that illustrates "two knees in which subchondral edema was associated with degenerative chondrosis." The authors of that study, they note [1]:
did not indicate how frequently they saw subchondral bone changes [in degenerative chondrosis]. Nor did they comment on whether subchondral edema assisted in the search for surface defects, but we suspect that subchondral edema may be useful in identifying some degenerative cartilage lesions and traumatic cartilage injuries.
We have not formally studied the incidence of subchondral bone marrow edema in degenerative chondrosis, nor have we formally studied the usefulness of focal edema in identifying degenerative defects in articular cartilage. However, in viewing thousands of MR images of knees over a 16-year interval and using fat-suppression techniques in clinical imaging of the knee for the past 9 years, we have formed the distinct subjective impression that the educated intuition of Rubin et al. [1] is correct. Focal subchondral bone marrow edema is frequently seen in severe degenerative chondrosis, in which erosion of articular cartilage extends down to or nearly down to the subchondral bone plate. An example may be seen in figure 1C of the 1994 article by Broderick et al. [3], in which a fat-saturated fast spin-echo image (TR/TE, 2550/25) shows foci of high signal intensity in subchondral marrow adjacent to a deep focal erosion in the articular cartilage of the patella. The patient had severe osteoarthritis confirmed on arthroscopy. Moreover, we found in our clinical practice that the presence of focal bone marrow edema is useful in calling the observer's attention to these cartilage defects. The corollary, of course, is that focal subchondral bone marrow edema is not at all specific for traumatic chondral injury.
References
Washington University School of Medicine St. Louis, MO 63110
We thank Dr. Turner for his insightful comments regarding our article on the association between subchondral marrow edema and treatable cartilage injuries in the knee [1]. On the basis of our clinical experiences and reports in the literature [2], we fully agree with him on two points: subchondral edema is frequently seen underlying areas of severe degenerative chondrosis and idiopathic chondromalacia, and the finding is not specific to traumatic cartilage injuries. However, we believe that the finding has more practical use in drawing the radiologist's attention to traumatic cartilage lesions rather than to degenerative ones for two reasons. First, chondral fractures are radiographically occult, whereas knees with degenerative chondrosis often show osteoarthritis radiographically. Second, specific surgical therapy now exists for traumatic lesions, whereas degenerative ones are not amenable to specific surgical treatment.
No one should be surprised to learn that the subchondral bone reacts to degenerative changes in the overlying cartilage. We are all familiar with increased osseous activity on bone scintigrams and with subchondral bone sclerosis on radiographs as signs indicating osteoarthritis in the adjacent joint.
What we find more intriguing is the observation that not all knees with severe degenerative cartilage loss show subchondral edema on MR images. Our impression from interpreting clinical studies is that two populations exist. Some knees with severe chondrosis show edema in the subchondral bone, whereas others have nearly complete denudation of the cartilage with a smooth thickened subchondral plate and no subchondral edema. One wonders whether this phenomenon explains why some patients with radiographically severe osteoarthritis are relatively symptom-free, and other patients with less severe disease are in great pain. Our thought has been that in some knees the subchondral bone becomes polished by the bone-on-bone contact, sealing whatever tiny pores might exist in the bone end and preventing the ingress of edema fluid through the disrupted articular surface. At the same time, stress-related thickening of the subchondral trabeculae occurs, leaving less room for the accumulation of edema between the trabeculae. The histologic correlate would be bone eburnation and the radiographic correlate would be sclerosis [3]. We believe that these reactive mechanisms may prevent an increase in the interstitial pressure within the subchondral marrow due to edema and thus may mitigate the development of pain, but this hypothesis remains untested.
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