Sleep-disordered breathing represents a broad spectrum of alterations, ranging from habitual snoring, through obstructive hypoventilation to obstructive sleep apnea-hypopnea syndrome, and produces breathing and architecture anomalies during sleep. There are some controversies on the physiopathological mechanisms of sleep-disordered breathing and its metabolic, neurocognitive and cardiovascular effects. The causes of comorbidity in obstructive sleep apnea-hypopnea syndrome in children are not yet well known and can include blood gasometric anomalies, fragmented sleep, and local and systemic inflammation, modulated by genetic, environmental and ethnic factors. The pathogenesis of pediatric sleep-disordered breathing undoubtedly involves complex interactions between anatomical or structural and functional factors, an airway prone to collapse and deficient neuromuscular compensation. Moreover, in children, sleep progresses in accordance with central nervous system development, which varies with age. This article reviews the role of the distinct anatomic, functional and inflammatory factors in the pathophysiology of pediatric sleep-disordered breathing.