Such force is typically internal, related to the contact of one bone with a neighboring bone during the traumatic event (9). The compact subchondral bone and calcified cartilage are collectively termed the subchondral plate (4,5). These criteria were revised for juvenile OCD (62) with the addition of three secondary signs that all showed 100% specificity: (a) a T2-weighted high-signal-intensity rim surrounding a juvenile OCD lesion indicates instability only if it has the same signal intensity as that of joint fluid, (b) a second outer rim of T2-weighted low signal intensity, or (c) multiple breaks in the subchondral bone plate on T2-weighted MR images (Fig 18). 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). 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. Normal fatty signal intensity on T1-weighted images is lost and replaced with inhomogeneous low to intermediate signal intensity (30), most prominently in the weight-bearing area of the infarct (Fig 12). Once a characteristic pattern of osseous injury is recognized on MR images, the radiologist must seek specific additional soft-tissue and osseous injuries. Figure 8a. Similar findings were present on the tibial side. Figure 9a. This misnomer was entrenched in the medical lexicon for many years, persisting after recognition of this entity as a SIF (15,16). 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). Several typical patterns of osteochondral injuries have been described in association with certain types of internal derangement and instability (11–13). Note articular surface collapse of the medial femoral condyle (arrowhead in b and c), with depression of the subchondral bone plate (c) and loss of subchondral fatty signal intensity (b). (b) Subsequently, a frank articular collapse (arrowheads) has developed, followed by loss of fatty signal intensity in the necrotic area (arrows). As demonstrated in studies of osteonecrosis of the femoral head (35), bone marrow edema distal to the infarct constitutes an indirect sign of articular collapse. SIF involves a physiologic force applied to weakened trabeculae, often in association with osteopenia and diminished protective function of the articular cartilage and meniscus, which leads to a fracture along the subchondral area of the bone. (b–d) Sagittal T2-weighted fat-suppressed MR image (b), proton-density–weighted MR image (c), and CT image (d) show a curvilinear fracture (arrow in b and c) encircling a portion of subchondral bone and overlying cartilage. Typical patient demographics and clinical presentation, the etiologic role of trauma, and classic MRI features that help to guide appropriate treatment are described for each entity (Table). Note the peripheral extrusion of the medial meniscus (black arrow in b) from a posterior horn tear (not shown). 1, pp. The purpose of this study was to directly compare the MRI … SIFs are associated with meniscal tears in the same compartment in 76%–94% of patients (18,20,21). Although definitive evidence is lacking, when osteonecrosis is found in OCD, it actually may be secondary to fragment detachment and loss of blood supply rather than the primary cause of its formation (41,43,45,50). Additional secondary criteria are employed for a juvenile OCD lesion to increase specificity. Although there is evidence that both mechanisms may operate together, results of recent studies (71,72) support the bone contusion theory of osteoarthritis by showing that subchondral cysts arise in preexisting regions of subchondral bone marrow edema-like lesions, and their development is predicted much more strongly by bone marrow edema-like lesions than by full-thickness cartilage loss (71,72). Harding described the lateral X-ray as a method to identify the site of an OCD lesion. Figure 6b. Our results show that the integrity of the subchondral layer on MRI has a moderate role in predicting the need for an eventual autologous bone graft to augment ACI whereas in our cohort a depth of the lesion above 6.5 mm accurately predicts the need for a sandwich procedure. Note articular surface collapse of the medial femoral condyle (arrowhead in b and c), with depression of the subchondral bone plate (c) and loss of subchondral fatty signal intensity (b). This condition typically is seen in older patients after the 6th decade of life and more frequently in women. More important are the localized abnormalities in the subchondral region, best shown on T2-weighted and proton-density–weighted MR images. (b–d) Sagittal T2-weighted fat-suppressed MR image (b), proton-density–weighted MR image (c), and CT image (d) show a curvilinear fracture (arrow in b and c) encircling a portion of subchondral bone and overlying cartilage. Figure 4d. This segment, “a progeny,” may later develop laminar calcifications in the deep areas or may ossify partially or completely (45). Figure 12a. MR imaging of epiphyseal lesions of the knee: current concepts, challenges, and controversies, Presumptive subarticular stress reactions of the knee: MRI detection and association with meniscal tear patterns, Femoral condyle insufficiency fractures: associated clinical and morphological findings and impact on outcome, Fat-suppressed T2-weighted MRI appearance of subchondral insufficiency fracture of the femoral head, MRI of subchondral fractures: a review, Subchondral insufficiency fractures of the knee: review of imaging findings, Dynamic contact mechanics of the medial meniscus as a function of radial tear, repair, and partial meniscectomy, Osteonecrosis of the knee after arthroscopic surgery: diagnosis with MR imaging, The importance of early diagnosis in spontaneous osteonecrosis of the knee: a case series with six year follow-up, Imaging of osteonecrosis: radiologic-pathologic correlation, Osteonecrosis and transient osteoporosis of the femoral head, MR imaging of avascular necrosis and transient marrow edema of the femoral head, Subchondral avascular necrosis: a common cause of arthritis, The role of sclerotic changes in the starting mechanisms of collapse: a histomorphometric and FEM study on the femoral head of osteonecrosis, Morphological analysis of collapsed regions in osteonecrosis of the femoral head, MRI evaluation of steroid- or alcohol-related osteonecrosis of the femoral condyle, Correlation between bone marrow edema and collapse of the femoral head in steroid-induced osteonecrosis, Subchondral fractures in osteonecrosis of the femoral head: comparison of radiography, CT, and MR imaging, Diagnostic performance of MR imaging in the assessment of subchondral fractures in avascular necrosis of the femoral head, Osteonecrosis of the femoral head: using CT, MRI and gross specimen to characterize the location, shape and size of the lesion, Osteochondritis dissecans: editorial comment, AAOS appropriate use criteria: management of osteochondritis dissecans of the femoral condyle, A review of knowledge in osteochondritis dissecans: 123 years of minimal evolution from König to the ROCK study group, American Academy of Orthopaedic Surgeons clinical practice guideline on: the diagnosis and treatment of osteochondritis dissecans, Osteochondritis dissecans 1887-1987: a centennial look at König’s memorable phrase, Studies on hereditary, multiple epiphyseal disorder, Hypertrophy and laminar calcification of cartilage in loose bodies as probable evidence of an ossification abnormality. The edema spares the devascularized infarcted segment. There are two theories of pathogenesis of subchondral cyst formation: the synovial fluid intrusion theory, which proposes that articular surface defects and increased intra-articular pressure allow intrusion of synovial fluid into the bone, leading to formation of cavities; and the bone contusion theory, according to which non-communicating cysts arise from subchondral foci of bone necrosis that are the result of opposing articular surfaces coming in contact with each other (67,69,70). This differs from the more localized bone marrow edema lesion subjacent to cartilage loss in osteoarthritis (10). Both a subchondral hypointense line (white arrow in b and c) and a subchondral area of low signal intensity (arrowhead in b and c) are observed along the weight-bearing aspect of the condyle and are associated with subtle flattening of the articular surface. Currently, to our knowledge, there are no data regarding which MRI features may predict improved outcomes in these patients. Healing juvenile OCD in a 13-year-old boy. This pattern of bone injury should prompt a search for additional findings of hyperextension with a varus or valgus component. AVN of the knee in a 59-year-old woman who was undergoing long-term corticosteroid treatment. Diagram of the fluid-sensitive MR image (a) and sagittal T2-weighted fat-suppressed (b), coronal T1-weighted (c), and proton-density–weighted fat-suppressed (d) MR images show a subchondral fracture (arrow in b and c) as a curvilinear hypointensity surrounded by bone marrow edema, without associated contour deformity. This article was corrected on August 23, 2018. Figure 8a. MRI is shown in Image A. The clinical scenario and histologic findings are typical of secondary osteonecrosis. Sagittal T2-weighted fat-suppressed MR images of the knee obtained through the medial compartment (a) and the posterior cruciate ligament (b) show a large crater at the medial femoral condyle (* in a) and an OCD fragment (arrow in b) displaced into the intercondylar notch. 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). Osteochondritis dissecans (OCD) is a term for a distinct clinical-pathologic entity: a pathologic condition that affects subchondral bone formation and may result in an unstable subchondral fragment, disruption of adjacent articular cartilage, and possible separation of the fragment. ■ Contrast and compare common entities that manifest as osteochondral lesions of the knee: acute traumatic osteochondral injuries, AVN, SIF of the knee, OCD, bone marrow edema-like lesions, and subchondral cystlike lesions in osteoarthritis. Note the lack of edema in the necrotic segment. Although it is adopted for osteochondral abnormalities of the talus (1), the term lacks specificity and should be only part of a description of a more specific diagnostic entity. 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