MRI findings of growth plate fractures of the knee: are there age- and fracture-dependent differences?

OBJECTIVE: To investigate MRI findings in children with physeal fractures of the knee with respect to age, location, and articular involvement. METHODS: Children with physeal fractures who underwent knee MRI between 2008 and 2021 were included. Two radiologists retrospectively reviewed all examinations to determine articular involvement, findings of physeal instability (perichondral disruption, periosteal entrapment), and internal derangement (cruciate ligament injury, meniscal tear, chondromalacia). Independent samples t, Mann-Whitney U, Pearson's chi-square, and Fisher's exact tests were used to compare findings. RESULTS: Fifty-six patients (37 boys, 19 girls; mean age: 12.2 ± 2.5 years; 32 distal femur, 24 proximal tibial fractures) included 24(43%) intraarticular fractures. Fractures were more common in the tibia than the femur (67% versus 25%, p = 0.004) and intraarticular fractures were more common in older than younger children (13.1 ± 2.0 versus 11.5 ± 2.7 years, p = 0.01), to associate with chondromalacia (46% versus 12%, p = 0.02) and undergo surgery (33% versus 10%, p = 0.04) when compared to extraarticular fractures. Perichondral disruption (n = 44, 79%) and periosteal entrapment (n = 13, 23%) did not significantly differ based on location or articular involvement (p > 0.05). At a median follow-up of 17.5 months (interquartile range: 1.25-34), 3 patients (2 intraarticular, 1 extraarticular fractures) developed osteoarthritis, osteochondral lesion, and leg-length discrepancy from growth arrest, which required additional surgery. CONCLUSION: Intraarticular physeal fractures were more common with older children, associate with chondromalacia, and underdo surgical intervention when compared to extraarticular fractures of the knee. While MRI findings of physeal instability were common, no significant differences were found between fractures based on anatomic location or fracture pattern.

Dicumarol inhibition of NADPH:quinone oxidoreductase induces growth inhibition of pancreatic cancer via a superoxide-mediated mechanism.

NADPH:quinone oxidoreductase (NQO(1)), a homodimeric, ubiquitous, flavoprotein, catalyzes the two-electron reduction of quinones to hydroquinones. This reaction prevents the one-electron reduction of quinones by cytochrome P450 reductase and other flavoproteins that would result in oxidative cycling with generation of superoxide (O(2)(.-)). NQO(1) gene regulation may be up-regulated in some tumors to accommodate the needs of rapidly metabolizing cells to regenerate NAD(+). We hypothesized that pancreatic cancer cells would exhibit high levels of this enzyme, and inhibiting it would suppress the malignant phenotype. Reverse transcription-PCR, Western blots, and activity assays demonstrated that NQO(1) was up-regulated in the pancreatic cancer cell lines tested but present in very low amounts in the normal human pancreas. To determine whether inhibition of NQO(1) would alter the malignant phenotype, MIA PaCa-2 pancreatic cancer cells were treated with a selective inhibitor of NQO(1), dicumarol. Dicumarol increased intracellular production of O(2)(.-), as measured by hydroethidine staining, and inhibited cell growth. Both of these effects were blunted with infection of an adenoviral vector containing the cDNA for manganese superoxide dismutase. Dicumarol also inhibited cell growth, plating efficiency, and growth in soft agar. We conclude that inhibition of NQO(1) increases intracellular O(2)(.-) production and inhibits the in vitro malignant phenotype of pancreatic cancer. These mechanisms suggest that altering the intracellular redox environment of pancreatic cancer cells may inhibit growth and delineate a potential strategy directed against pancreatic cancer.