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Current clinical MRI of patients with juvenile osteochondritis dissecans (JOCD) is limited by the low reproducibility of lesion instability evaluation and inability to predict which lesions will heal after nonoperative treatment and which will later require surgery. The aim of this study is to verify the ability of apparent diffusion coefficient (ADC) to detect differences in lesion microstructure between different JOCD stages, treatment groups, and healthy, unaffected contralateral knees. Pediatric patients with JOCD received quantitative diffusion MRI between January 2016 and September 2020 in this prospective research study. A disease stage (I‐IV) and stability of each JOCD lesion was evaluated. ADCs were calculated in progeny lesion, interface, parent bone, cartilage overlying lesion, control bone, and control cartilage regions. ADC differences were evaluated using linear mixed models with Bonferroni correction. Evaluated were 30 patients (mean age, 13 years; 21 males), with 40 JOCD‐affected and 12 healthy knees. Nine patients received surgical treatment after MRI. Negative Spearman rank correlations were found between ADCs and JOCD stage in the progeny lesion (ρ = −0.572; p < 0.001), interface (ρ = −0.324; p = 0.041), and parent bone (ρ = −0.610; p < 0.001), demonstrating the sensitivity of ADC to microstructural differences in lesions at different JOCD stages. We observed a significant increase in the interface ADCs (p = 0.007) between operative (mean [95% CI] = 1.79 [1.56–2.01] × 10−3 mm2/s) and nonoperative group (1.27 [0.98–1.57] × 10−3 mm2/s). Quantitative diffusion MRI detects microstructural differences in lesions at different stages of JOCD progression towards healing and reveals differences between patients assigned for operative versus nonoperative treatment. [ABSTRACT FROM AUTHOR]

Juvenile osteochondritis dissecans (JOCD) is a pediatric orthopedic disorder that involves the articular–epiphyseal cartilage complex and underlying bone. Clinical disease is often characterized by the presence of radiographically apparent osteochondral flaps and fragments. The existence of early JOCD lesions (osteochondrosis latens [OCL] and osteochondrosis manifesta [OCM]) that precede the development of osteochondral flaps and fragments is also well recognized. However, identification of naturally occurring OCL lesions (confined to cartilage) using noninvasive imaging techniques has not yet been accomplished. We hypothesized that 10.5 T magnetic resonance imaging (MRI) can identify naturally occurring OCL lesions at predilection sites in intact joints of juvenile pigs. Unilateral elbows and knees (stifles) were harvested from three pigs aged 4, 8, and 12 weeks, and scanned in a 10.5 T MRI to obtain morphological 3D DESS images, and quantitative T2 and T1ρ relaxation time maps. Areas with increased T2 and T1ρ relaxation times in the articular–epiphyseal cartilage complex were identified in 1/3 distal femora and 3/3 distal humeri and were considered suspicious for OCL or OCM lesions. Histological assessment confirmed the presence of OCL or OCM lesions at each of these sites and failed to identify additional lesions. Histological findings included necrotic vascular profiles associated with areas of chondronecrosis either confined to the epiphyseal cartilage (OCL, 4‐ and 8‐week‐old specimens) or resulting in a delay in endochondral ossification (OCM, 12‐week‐old specimen). Future studies with clinical MR systems (≤7 T) are needed to determine whether these MRI methods are suitable for the in vivo diagnosis of early JOCD lesions in humans. Statement of Clinical Significance: Having identified quantitative and morphological markers useful for the early identification and characterization of juvenile osteochondritis dissecans lesions in ex vivo pig specimens on the highly sensitive 10.5 T magnetic resonance imaging platform, the methods are poised for future translation to human studies at clinical field strengths. [ABSTRACT FROM AUTHOR]

Juvenile osteochondritis dissecans (JOCD) is an orthopedic joint disorder of children and adolescents that can lead to premature osteoarthritis. Thirteen patients (mean age: 12.3 years, 4 females), 15 JOCD‐affected and five contralateral healthy knees, that had a baseline and a follow‐up magnetic resonance imaging (MRI) (mean interval of 8.9 months) and were treated nonoperatively during this interval were included. Retrospectively, patients were assigned to operative or nonoperative groups based on their electronic medical records. Volumetric mean T2* values were calculated within regions of interest (progeny lesion, interface, parent bone) and region matched control bone in healthy contralateral knees and condyles. The normalized percentage difference of T2* between baseline and follow up MRI in nonoperative patients significantly increased in progeny lesion (−47.8%, p < 0.001), parent bone (−13.9%, p < 0.001), and interface (−32.3%, p = 0.011), whereas the differences in operative patients were nonsignificant and below 11%. In nonoperative patients, the progeny lesion (p < 0.001) and interface T2* values (p = 0.012) were significantly higher than control bone T2* at baseline, but not at follow‐up (p = 0.219, p = 1.000, respectively). In operative patients, the progeny lesion and interface T2* values remained significantly elevated compared to the control bone both at baseline (p < 0.001, p < 0.001) and follow‐up (p < 0.001, p < 0.001), respectively. Clinical Significance: Longitudinal T2* mapping differentiated nonhealing from healing JOCD lesions following initial nonoperative treatment, which may assist in prognosis and improve the ability of surgeons to make recommendations regarding operative versus nonoperative treatment. [ABSTRACT FROM AUTHOR]

Juvenile osteochondritis dissecans (JOCD) lesions contain cartilaginous, fibrous and osseous tissues which are difficult to distinguish with clinical, morphological magnetic resonance imaging (MRI). Quantitative T2* mapping has earlier been used to evaluate microstructure and composition of all aforementioned tissues as well as bone mineral density. However, the ability of T2* mapping to detect changes in tissue composition between different JOCD lesion regions, different disease stages, and between stable and unstable lesions has not been demonstrated. This study analyzed morphological and T2* MRI data from 25 patients (median age, 12.1 years) with 34 JOCD‐affected and 13 healthy knees. Each lesion was assigned a stage reflecting the natural history of JOCD, with stages I and IV representing early and healed lesion, respectively. T2* values were evaluated within the progeny lesion, interface and parent bone of each lesion and in the control bone region. T2* was negatively correlated with JOCD stage in progeny lesion (ρ = −0.871; p < 0.001) and interface regions (ρ = −0.649; p < 0.001). Stage IV progeny showed significantly lower T2* than control bone (p = 0.028). T2* was significantly lower in parent bone than in control bone of patients with stable lesions (p = 0.009), but not in patients with unstable lesions (p = 0.14). Clinical significance: T2* mapping enables differentiation between different stages of JOCD and quantitative measurement of the ossification degree in progeny lesion and interface. The observed T2* decrease in healed and stable lesions may indicate increased bone density as a result of the active repair process. T2* mapping provides quantitative information about JOCD lesion composition. [ABSTRACT FROM AUTHOR]

This study investigated the sensitivity of T1ρ and T2 relaxation time mapping to detect acute ischemic injury to the secondary ossification center (SOC) and epiphyseal cartilage of the femoral head in a piglet model of Legg–Calvé–Perthes disease. Six piglets underwent surgery to induce global right femoral head ischemia and were euthanized 48 h later. Fresh operated and contralateral‐control femoral heads were imaged ex vivo with T1, T2, and T1ρ mapping using a 9.4T magnetic resonance imaging scanner. The specimens were imaged a second time after a freeze/thaw cycle and then processed for histology. T1, T2, and T1ρ measurements in the SOC, epiphyseal cartilage, articular cartilage, and metaphysis were compared between operated and control femoral heads using paired t tests. The effects of freeze/thaw, T1ρ spin‐lock frequency, and fat saturation were also investigated. Five piglets with histologically confirmed ischemic injury were quantitatively analyzed. T1ρ was increased in the SOC (101 ± 15 vs. 73 ± 16 ms; p = 0.0026) and epiphyseal cartilage (84.9 ± 9.2 vs. 74.3 ± 3.6 ms; p = 0.031) of the operated versus control femoral heads. T2 was also increased in the SOC (28.7 ± 2.0 vs. 22.7 ± 1.7; p = 0.0037) and epiphyseal cartilage (57.4 ± 4.7 vs. 49.0 ± 2.7; p = 0.0041). No changes in T1 were detected. The sensitivities of T1ρ and T2 mapping in detecting ischemic injury were maintained after a freeze/thaw cycle, and T1ρ sensitivity was maintained after varying spin‐lock frequency and applying fat saturation. In conclusion, T1ρ and T2 mapping are sensitive in detecting ischemic injury to the SOC and epiphyseal cartilage of the femoral head as early as 48 h after ischemia induction. [ABSTRACT FROM AUTHOR]

ABSTRACT In vivo visualization of subclinical osteochondrosis (OC) lesions, characterized by necrosis of epiphyseal growth cartilage, is necessary to clarify the pathogenesis of this disease. Hence, our objectives were to demonstrate induced necrosis of the epiphyseal cartilage in vivo using MRI and to monitor progression or resolution of resulting lesions. We also aimed to improve the goat model of OC by introducing controlled exercise. Vascular supply to the epiphyseal cartilage was surgically interrupted in four 5-day-old goats to induce ischemic cartilage necrosis in a medial femoral condyle. Starting 3 weeks postoperatively, goats underwent daily controlled exercise until euthanasia at 6, 10, 11 ( n = 2) weeks postoperatively. T2 maps of operated and control femora were obtained in vivo at 3 ( n = 4), 6 ( n = 4), 9 ( n = 3), and 11 ( n = 2) weeks postoperatively using a 3 T MR scanner. In vivo MRI findings were validated against MRI results obtained ex vivo at 9.4 T in three goats and compared to histological results in all goats. Surgical interruption of the vascular supply caused ischemic cartilage necrosis in three out of four goats. T2 maps obtained in vivo at 3 T identified regions of increased relaxation time consistent with discrete areas of cartilage necrosis 3-11 weeks postoperatively and demonstrated delayed progression of the ossification front at 9 ( n = 1) and 11 ( n = 2) weeks postoperatively. In vivo MRI findings were confirmed by ex vivo MRI at 9.4 T and by histology. Identification of cartilage necrosis in clinical patients in the early stages of OC using T2 maps may provide valuable insight into the pathogenesis of this condition. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:868-875, 2017. [ABSTRACT FROM AUTHOR]