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Purpose: To evaluate the influence of skeletal maturation on sodium (23Na) MRI relaxation parameters and the accuracy of tissue sodium concentration (TSC) quantification in human knee cartilage. Methods: Twelve pediatric knee specimens were imaged with whole‐body 10.5 T MRI using a density‐adapted 3D radial projection sequence to evaluate 23Na parameters: B1+, T1, biexponential T2*$$ {\mathrm{T}}_2^{\ast } $$, and TSC. Water, collagen, and sulfated glycosaminoglycan (sGAG) content were calculated from osteochondral biopsies. The TSC was corrected for B1+, relaxation, and water content. The literature‐based TSC (TSCLB) used previously published values for corrections, whereas the specimen‐specific TSC (TSCSP) used measurements from individual specimens. 23Na parameters were evaluated in eight cartilage compartments segmented on proton images. Associations between 23Na parameters, TSCLB − TSCSP difference, biochemical content, and age were determined. Results: From birth to 12 years, cartilage water content decreased by 18%; collagen increased by 59%; and sGAG decreased by 36% (all R2 ≥ 0.557). The short T2*$$ {\mathrm{T}}_2^{\ast } $$ (T2*S$$ {{\mathrm{T}}_2^{\ast}}_{\mathrm{S}} $$) decreased by 72%, and the signal fraction relaxing with T2*S$$ {{\mathrm{T}}_2^{\ast}}_{\mathrm{S}} $$ (fT2*S$$ {{\mathrm{fT}}_2^{\ast}}_{\mathrm{S}} $$) increased by 55% during the first 5 years but remained relatively stable after that. TSCSP was significantly correlated with sGAG content from biopsies (R2 = 0.739). Depending on age, TSCLB showed higher or lower values than TSCSP. The TSCLB − TSCSP difference was significantly correlated with T2*S$$ {{\mathrm{T}}_2^{\ast}}_{\mathrm{S}} $$ (R2 = 0.850), fT2*S$$ {{\mathrm{fT}}_2^{\ast}}_{\mathrm{S}} $$ (R2 = 0.651), and water content (R2 = 0.738). Conclusion: TSC and relaxation parameters measured with 23Na MRI provide noninvasive information about changes in sGAG content and collagen matrix during cartilage maturation. Cartilage TSC quantification assuming fixed relaxation may be feasible in children older than 5 years. [ABSTRACT FROM AUTHOR]

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]

Background: Female athletes have a higher incidence of anterior cruciate ligament injuries than do male athletes in similar sports. Hormones, particularly estrogen, have been indicated by some studies to be [...]

Background: Posterolateral knee instability is a difficult clinical problem to diagnose and treat. To best evaluate its natural history and the effects of interventional treatments, it is important to develop [...]

Extracellular modulators of cell-cell signaling control numerous aspects of organismal development. The Twisted gastrulation (Twsg1) gene product is a small, secreted cysteine-rich protein that has the unusual property of being able to either enhance or inhibit signaling by the bone morphogenetic protein (BMP) subfamily of TGF-[beta], type factors in a context-dependent manner. In this report, we characterize the early embryonic and skeletal phenotypes associated with loss of Twsg1 function in mice. All Twsg1 mutant mice, irrespective of genetic background, exhibit deletions of neural arches in the cervical vertebrae. In a C57BL/6 background, we also observe pronounced forebrain detects including rostral truncations, holoprosencephaly, cyclopia, as well as alterations in the first branchial arch (BA1) leading to lack of jaw (agnathia). Characterization of marker expression suggests that these defects are attributable to loss of signaling from forebrain-organizing centers including Fgf8 from the anterior neural ridge (ANR) and Shh from the prechordal plate (PrCP). In addition, we find defects in the foregut endoderm and a reduction in Hex expression, which may contribute to both the forebrain and BA1 defects. Keywords: Twisted gastrulation; Mouse; BMP; Holoprosencephaly; Forebrain; Neural arch; Agnathia; Foregut

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]