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Background/Objectives: Limb lengthening and deformity correction techniques, particularly distraction osteogenesis, have significantly evolved in pediatric orthopedics. This study examines the temporal changes of key biochemical markers—vascular endothelial growth factor (VEGF), fibroblast growth factor 1 (FGF-1), and the propeptide of type I collagen (P1NP)—during the limb lengthening process. Methods: Twenty pediatric patients (aged 13–16) underwent distraction osteogenesis using the Circular Hexapod External Fixator. Peripheral blood samples were collected pre-treatment, three weeks after initiating distraction, and one month post-lengthening. Marker levels were measured using ELISA. Results: Serum VEGF concentrations significantly increased during treatment, peaking at T2 (T1 35.91 ± SD 5.54 vs. T2 293.47 ± SD 69.57, p < 0.0001), then declined at T3 (293.47 ± SD 69.57 vs. 40.86 ± SD 6.26, p < 0.0001). FGF-1 showed minor fluctuations initially but significantly increased by T3 (18.14 ± SD 4.57 vs. 41.56 ± SD 17.15, p < 0.01), about 2.3 times higher than baseline. P1NP concentrations exhibited a linear increase, with a significant rise from T2 to T3 (234.06 ± SD 36.57 vs. 280.68 ± SD 35.63, p < 0.05), while the T1 to T2 increase was not statistically significant, indicating ongoing osteoblastic activity and bone formation. Conclusions: This study highlights the dynamic changes in VEGF, FGF-1, and P1NP during distraction osteogenesis, emphasizing their roles as biomarkers of bone regeneration. These findings enhance the understanding of bone healing mechanisms and could inform future therapeutic strategies for pediatric limb lengthening. Further research is warranted to explore their clinical utility. [ABSTRACT FROM AUTHOR]

Background. Legg–Calvé–Perthes (LCPD) disease is a complex condition affecting the femoral head's epiphysis in children. It occurs with a prevalence ranging from 0.4 to 29.0 cases per 100,000 children under the age of 15. It involves various factors, including genes associated with coagulation and fibrinolysis, pro-inflammatory factors, and vasoactive substances. Methods. We investigated the relationship between genetic mutations associated with coagulation and vascular disorders and the occurrence of LCPD in Polish patients. We performed a study involving 25 patients with LCPD and 100 healthy controls. All subjects were genotyped for eNOS4, Factor V Leiden, prothrombin, tPA25, and MTHFR polymorphism. Results. The analysis revealed that the frequencies of eNOS4 genotypes were significantly different in LCPD patients than in the control group (p = 0.018). The frequencies of 4a allele were significantly higher in patients with LCPD than in the healthy population (26% vs. 9%, p = 0.0012). There were no significant differences in genotype and allele frequencies for Factor V Leiden, prothrombin tPA 25, and MTHFR gene polymorphisms between patients with LCPD and the controls. Conclusions. Genotype and allele frequencies of eNOS4 were significantly higher in patients with LCPD. These findings suggest a potential association between the eNOS gene polymorphism and an increased risk of developing LCPD. [ABSTRACT FROM AUTHOR]