These osseous injuries are the result of impaction of the lateral femoral condyle against the posterolateral tibial plateau during internal rotation and anterior translation of the tibia accompanying an anterior cruciate ligament rupture (arrow in d). Figure 7b. Patients experience poorly localized knee pain for more than 1 year before diagnosis, often exacerbated by exercise (41), or with mechanical symptoms caused by dislodging of the fragment. Second, the subchondral bone marrow and subchondral bone plate must be examined and correlated with the radiographic appearance. (b, c) Coronal T1-weighted (b) and proton-density–weighted fat-suppressed (c) MR images show a progeny (P) fragment separated from the parent bone, with signal intensity equal to that of fluid (white arrow in c) and an additional outer rim of sclerosis (black arrow in c). The location of the abnormality is dictated by the mechanism of injury. Coronal proton-density–weighted fat-suppressed (a) and sagittal T2-weighted (b) MR images show articular surface collapse with a depression of the subchondral bone plate (arrowhead in a) and a fluid-filled fracture cleft underlying the subchondral bone plate (arrow). (b) Subsequently, a frank articular collapse (arrowheads) has developed, followed by loss of fatty signal intensity in the necrotic area (arrows). Histologic core biopsy specimens obtained in juvenile OCD lesions showed that osteonecrosis is either absent (47,50) or infrequent (48,51). In the quest to replace osteochondral defects with hyaline cartilage, Brittberg et al. (d) Sagittal T2-weighted fat-saturated MR image shows disruption of the subchondral bone plate (arrowhead). A peculiar clinical-radiologic entity originally designated as a so-called spontaneous osteonecrosis of the knee (SONK, a misnomer) was recognized early as a distinct form of epiphyseal osteonecrosis (14). The laminar configuration of the signal intensity in the fragment reflects the presence of calcifications in its deep zone (arrow in b). At MRI, SIF is associated with marked bone marrow edema emanating from the subchondral region and extending over large areas (10,17,18), often involving the entire femoral condyle. Anterior femoral condylar fracture and bone contusion at the anterior aspect of the tibia (* in b) are the results of an internal force that occurred during hyperextension as the femur and tibia collide. (d) Sagittal T2-weighted fat-saturated MR image shows disruption of the subchondral bone plate (arrowhead). (a) Coronal proton-density–weighted fat-suppressed image shows an extensive bone marrow edema pattern involving the medial femoral condyle (*), accompanied by a subchondral area of low signal intensity (arrowhead) located immediately subjacent to a subchondral bone plate, producing its apparent thickening. The compact subchondral bone and calcified cartilage are collectively termed the subchondral plate (4,5). Osteochondral lesions of the talus are common and difficult problems to treat. MRI features that aid in diagnosis include the location and extent of bone marrow edema, the presence of a fracture line, a hypointense area immediately subjacent to the subchondral bone plate, and deformity of the subchondral bone plate. The distal femoral growth plate is open (* in a and b). Figure 6a. Bone marrow edema surrounding the infarct is present on the femoral side (* in c) but not the tibial side. Several pathologic conditions may manifest as an osteochondral lesion of the knee at MRI and cause diagnostic difficulties, including acute and traumatic osteochondral injuries, subchondral insufficiency fracture of the knee, avascular necrosis, osteochondritis dissecans, and localized degenerative lesions; the typical patient demographics, clinical presentation, etiologic role of trauma, and pertinent MRI … MRI is a valuable diagnostic tool that provides critical information about the composition, stability, and integrity of the OCD fragment. Juvenile osteochondritis dissecans: is it a growth disturbance of the secondary physis of the epiphysis? Histologically, articular cartilage is organized into four layers, each characterized by a different cellular composition and orientation of collagen fibers that produce gradual variations in signal intensity: superficial, transitional, deep (radial), and calcified layers (2). 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