Background: Avascular necrosis (AVN) is a major complication after closed reduction for developmental dysplasia of the hip. The factors that predispose to AVN remain controversial. The purpose of this study was to analyze the risk factors, especially patient factors, such as age at reduction, grade of dislocation, and ossific nucleus development, related to AVN. Materials and Methods: We retrospectively reviewed children with dysplasia of the hip treated by closed reduction between 1997 and 2006. AVN was evaluated using Salter criteria and Kalamchi and MacEwen classification. Related factors were analyzed. Results: One hundred and eight children (140 hips) with an average age of 16.6 months at closed reduction (range: 6-24 mo) were included in the study. For an average duration of 10.1 years (range 7–16 y) of follow-up, 44 hips (31.4%) developed AVN. Grade II or higher AVN occurred in 14 hips (10%). The incidence of AVN increased with the grade of dislocation (P=0.022) and underdevelopment of the ossific nucleus (P<0.001). Underdevelopment of the ossific nucleus was also found to be positively correlated with the dislocation grade (P=0.047). The age at the time of reduction, sex, and side were not significant factors. Children who underwent secondary operation were all older than 1 year at reduction. Conclusions: High-grade dislocation correlates with the underdevelopment of the ossific nucleus. Patients with these 2 characteristics are predisposed to AVN. As underdevelopment of the ossific nucleus occurred regardless of age, it is not advisable to delay reduction because it does not alter the AVN rate, and instead, it increases the secondary operation rate. Level of Evidence: Level IV case series.

Background: Mutations in the ZMIZ1 gene have been implicated in neurodevelopmental disorder with dysmorphic facies and distal skeletal anomalies (NEDDFSA). However, the underlying cellular and physiological mechanisms remain poorly understood. Methods: Exome sequencing was performed to identify candidate variants. qPCR, Western blot, immunofluorescence, CCK-8, and wound-healing assays were employed to assess gene function in human skeletal muscle cells (HSkMCs). RNA-seq and co-immunoprecipitation coupled with mass spectrometry (Co-IP/MS) were used for transcriptomic and interactome profiling. Results: Here, we identified a novel de novo missense variant c.910G>C (p.A304P) in ZMIZ1 in a patient with NEDDFSA. The p.A304P variant significantly increased ZMIZ1 mRNA and protein expression levels and altered its subcellular localization. Functional assays demonstrated enhanced proliferation and migration in HSkMCs expressing the mutant ZMIZ1 . qPCR validation revealed significant dysregulation of key genes in the TGF-β1 signaling pathway. Transcriptome analysis identified the cytokine-cytokine receptor interaction pathway as the most significantly enriched pathway. Additionally, we identified a novel interaction between ZMIZ1 and the transcription factor GTF2I. Conclusion: Our study identifies a novel likely pathogenic variant in ZMIZ1 associated with NEDDFSA. These findings provide new insights into the cellular and physiological mechanisms underlying NEDDFSA, highlighting ZMIZ1’s role as a regulatory hub in multiple signaling pathways. Impact: Our study identifies a novel likely pathogenic variant in the ZMIZ1 gene associated with NEDDFSA, the second in China, and demonstrates its functional impact on cellular processes and signaling pathways, particularly in muscle cells. This finding expands the known ZMIZ1 mutation spectrum and provides the first functional evidence of its role in muscle cells, highlighting its potential as a regulatory hub in multiple pathways beyond the nervous system. These results offer new insights into the cellular mechanisms underlying NEDDFSA, especially in non-neurological tissues, and may facilitate the development of targeted therapies for related disorders.

In the field of orthopedic surgery, particularly distraction osteogenesis (DO), the mechanical environment plays a decisive role in the quality of bone regeneration and the safety of the soft tissue envelope. The continuous monitoring and accurate prediction of distraction resisting forces (DRF) are critical for preventing soft tissue complications such as nerve ischemia, joint contractures, and mechanical failure of the lengthening device. However, current clinical practice relies heavily on subjective assessment or passive monitoring tools that lack predictive capabilities. To address this gap, this study proposes a comprehensive solution combining a custom mechanical acquisition system with a high-fidelity finite element (FE) prediction method. The system design features a novel “double-ring” sensor interface specifically engineered to decouple axial distraction forces from parasitic bending moments generated by asymmetric muscle tension. Furthermore, a patient-specific FE model utilizing the Ogden hyperelastic constitutive law was derived, explicitly based on the patient’s muscle volume from preoperative CT imaging, to predict the non-linear force evolution. The feasibility and accuracy of the system were validated in a pilot in vivo study using a single ovine model ($N=1$). To isolate the soft tissue resistance from callus formation, distraction was performed immediately postoperatively up to a total length of 4 cm. Experimental results demonstrated the system’s high linearity ($R^2>0.999$) and its ability to capture the characteristic viscoelastic relaxation of living tissues. The FE model successfully predicted the peak distraction forces, showing improved agreement with experimental data at larger distraction magnitudes. By integrating mechanical sensing with predictive modeling, this framework lays the foundation for future closed-loop, patient-specific control in distraction osteogenesis.

To analyze the 10-year epidemiological trends of pediatric fracture and injuries in Beijing from 2010 to 2019.Methods: This retrospective study included children presenting with fracture or injuries at the emergency department of Beijing Jishuitan Hospital (National Orthopedic Medical Center) during the study period. Demographic and clinical data (age, sex, seasonal distribution) were analyzed using linear regression. The number of fracture and injury in children increased (R = 0.856 and 0.828, P = 0.002 and 0.003); The mean age of children with fracture and injury increased (R = 0.946 and 0.744, p = 0.000 and 0.009). The number of fracture increased in the 6 ~ 8 years old, 9 ~ 11 years old and 12 ~ 14 years old age group (R = 0.748, 0.986 and 0.874, p = 0.013, 0.000 and 0.001). The number of injury in the 9 ~ 11 years old and 12 ~ 14 years old age group increased (R = 0.914 and 0.762, p = 0.000 and 0.010). The number of fracture in boys and girls increased (R = 0.806 and 0.912, p = 0.005 and 0.000). The number of injury in boys and girls increased (R = 0.646 and 0.935, p = 0.044 and 0.000). The number of fracture in spring and winter increased (R = 0.844 and 0.932, p = 0.002 and 0.000). The number of injury in spring, autumn and winter increased (R = 0.851, 0.701 and 0.918, p = 0.002, 0.024 and 0.000). Beijing children experienced progressively rising fracture and injury rates during the study decade, with notable increases in older age groups. The proportional rise of fracture among injured children suggests changing injury patterns. While seasonal and gender differences persist, their relative impact appears to be diminishing over time.