Grade I Lesions

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In the surgical form of the Outerbridge classification, Grade I lesions are identified by a subjective assessment of cartilage softening or cartilage discoloration with an intact articular surface. Because there is no direct MRI finding that corresponds to cartilage softening, this has been modified to reflect MRI signal changes without morphologic changes of the cartilage surface. Early studies found poor correlation between Grade I MRI lesions and arthroscopy [70,71], as well a low sensitivity in MRI detection of patellar cartilage softening found at arthroscopy [72]. It has been postulated that elevation in cartilage signal intensity on T2-weighted sequences is a result of alterations in the organization of the collagen matrix that lead to lower anisotropy and increased cartilage water content [73]. As seen in Fig. 3A, remote areas of T2 hyperinten-sity are frequently found in patients with more advanced areas of focal cartilage injury. Although the clinical significance of this finding is unknown, small longitudinal studies suggest that Grade I lesions are common and progress to sites of morphologic damage [74].

A more diffuse heterogeneous pattern of high T2-weighted signal can be observed following acute trauma, frequently in association with hypertensity in the adjacent subchondral bone marrow. Isolated areas of T2 hyperintensity may be observed in cartilage of patients who have no reported history of trauma. As demonstrated in Fig. 4, this can be associated with a focal blister or smooth contour abnormality of the overlying articular surface. Similar findings of focal swelling and alterations in the fibril density in the superficial zone of patellar cartilage have been reported in the electron microscopy literature [75,76], supporting the hypothesis that these lesions represent structural reorganization/degeneration of the collagen matrix. In addition to T2 hyperintensity, which is frequently present in the acute setting, focal areas of decreased T2-weighted cartilage signal are frequently observed adjacent to sites of cartilage injury (see Fig. 3). Decreased T2-weighted signal is generally not observed immediately after trauma, but as demonstrated by the case illustrated in Fig. 5, can develop several weeks following cartilage injury. The etiology of the decreased T2 signal intensity has not been determined, but may reflect a hypertro-phic healing response, or fragmentation of the collagen fibrils leading to a greater concentration of water binding sites on collagen. Areas of low T2-weighted signal intensity are also observed with sites of chondrocalcinosis, particularly with gradient echo techniques [77], or with high magnetic field strengths [78].

Grade Meniscus TearGrade Cartilage Damage

Fig. 3. Heterogeneous T2 elevation: 29-year-old male with chronic knee pain and history of skiing injury 1 6 years earlier. (A) Diffuse T2 elevation is present in cartilage of the lateral patella facet on this fat-suppressed, PD-weighted FSE image. (B) More superiorly, there is a flap tear extending to bone (Grade III lesion) associated with abnormal marrow hyperintensity in subchondral bone. Note the decreased signal intensity of cartilage adjacent to the flap tear. This is frequently seen in subacute or chronic cartilage injuries.

Grade Meniscus Tear

Fig. 4. Cartilage blister: 3.0 T fat-suppressed, PD-weighted FSE MRI image in 18-year-old male with anterior knee pain. Focally elevated, T2-weighted signal consistent with altered organization of the collagen matrix is observed in the deep radial zone of cartilage (arrow), with a smooth contour elevation of the overlying chondral surface.

Fig. 4. Cartilage blister: 3.0 T fat-suppressed, PD-weighted FSE MRI image in 18-year-old male with anterior knee pain. Focally elevated, T2-weighted signal consistent with altered organization of the collagen matrix is observed in the deep radial zone of cartilage (arrow), with a smooth contour elevation of the overlying chondral surface.

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