Abstract / Summary
Pediatric obstructive sleep apnea syndrome (OSAS) is a common sleep-related breathing disorder increasingly recognized as a multisystem disease rather than an isolated disorder of the upper airway. Recurrent episodes of upper airway obstruction generate intermittent hypoxia, reoxygenation, and sleep fragmentation, promoting excessive production of reactive oxygen and nitrogen species and disruption of antioxidant defenses. This narrative review summarizes current evidence regarding the mechanisms, biomarkers, and clinical consequences of oxidative stress in pediatric OSAS. Intermittent hypoxia activates several redox-sensitive pathways, including NADPH oxidases, hypoxia-inducible factor-1α, nuclear factor-κB, mitochondrial dysfunction, and endoplasmic reticulum stress, thereby creating a bidirectional relationship between oxidative stress and systemic inflammation. Pediatric studies have demonstrated alterations in lipid peroxidation products, glutathione redox balance, urinary 8-hydroxy-2′-deoxyguanosine, isoprostanes, NOX2-related markers, and inflammatory mediators. These abnormalities are associated with endothelial dysfunction and cardiovascular, neurocognitive, metabolic, hepatic, renal, and immune consequences, and several may improve following effective treatment. Importantly, the magnitude of oxidative and end-organ injury does not consistently parallel the apnea-hypopnea index, suggesting that hypoxic burden, obesity, genetic susceptibility, antioxidant capacity, and disease duration influence individual biological vulnerability. Although several oxidative biomarkers show potential for disease characterization and treatment monitoring, methodological heterogeneity and the absence of standardized pediatric reference values currently limit their clinical application. Future integration of polysomnographic hypoxic-burden metrics with oxidative, inflammatory, metabolomic, and genomic biomarkers may improve risk stratification and facilitate more personalized management of pediatric OSAS.