Sleep-Disordered Breathing in Children: Long-Term Health Impacts

Introduction

Sleep-disordered breathing (SDB) in children has been recognized and treated since the 1800s with adenotonsillectomy (AT surgery) [1]. What once might have been dismissed as simple snoring is now understood as a serious health concern with potential lifelong consequences. Proper sleep is critically important for children’s development, with disturbances linked to increased risk of cardiac, metabolic, and neurocognitive issues that can persist into adulthood [2, 3]. Children with obstructive sleep apnea (OSA) utilize healthcare resources 2.3 times more frequently than their peers [2, 3], highlighting both the health and economic implications of this condition.

The rising prevalence of childhood obesity shows a bidirectional relationship with sleep apnea, each condition potentially exacerbating the other [4, 2, 1]. The disturbed sleep and nocturnal hypoxia associated with SDB can initiate pathophysiological cascades resulting in left ventricular hypertrophy and childhood hypertension, potentially leading to significant cardiovascular morbidity decades later [5, 6]. As dental professionals, we occupy a privileged position to identify early warning signs during routine examinations of orofacial structures [7, 8].

Epidemiology of Pediatric SDB

According to the European Respiratory Society [9], obstructive SDB represents a spectrum of airway dysfunctions that may progress from primary snoring to full OSA (Figure 1).

Figure 1. The Progression Spectrum of Sleep-Disordered Breathing: From primary snoring to upper airway resistance syndrome to obstructive sleep apnea, illustrating the potential linear progression of respiratory disturbance during sleep in pediatric patients.

SDB in childhood typically peaks between ages 2-8 due to disproportionate lymphoid tissue growth compared to airway development. Among overweight children aged 10-16, prevalence ranges from 13-39%, reflecting the concerning rise in childhood obesity rates [10, 11, 4]. Cases in children under 2 years are typically associated with syndromic, neuromuscular, or congenital factors [4].

The overall prevalence of primary snoring is approximately 7.45% (range 3-35%), while pediatric OSA affects 1-4% of children (range 0.1-13%). Of clinical significance, 2-3% of children diagnosed with primary snoring will develop clinical OSA, underscoring the importance of careful evaluation [4]. Known risk factors include craniofacial abnormalities, asthma, obesity, premature birth, Down syndrome, African American ethnicity, tobacco exposure, low socioeconomic status, facial trauma history, and untreated allergic rhinitis [9, 4].

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Clinical Symptoms and Diagnosis

Dental practitioners and healthcare practitioners should be alert to signs of adenotonsillar hypertrophy [4] and associated malocclusions, including posterior crossbite [12, 13], increased vertical dimension, retrognathia, steep mandibular plane, and macroglossia. Sleep bruxism merits particular attention, as it may present in up to 50% of children with SDB [15]. These are important risk factors and clinical symptoms (Figure 2).

Parental reports often include snoring, mouth breathing, bedwetting, frequent night-time arousals, daytime sleepiness, and witnessed apneas [16]. Associated symptoms include nasal congestion and allergic rhinitis, the latter increasing OSA risk threefold [17, 4]. Behavioral manifestations range from exhaustion to hyperexcitability, aggression, ADHD-like symptoms, and cognitive difficulties [9].

Definitive diagnosis requires polysomnography (PSG) with pediatric-specific scoring criteria: mild (1-4.9 events/hr), moderate (5-9.9 events/hr), and severe (>10 events/hr) [16]. Treatment is generally indicated when the apnea-hypopnea index (AHI) exceeds 5 events/hour, as spontaneous resolution becomes unlikely at this threshold [9].

Figure 2. Comprehensive Clinical Assessment Framework: Key risk factors and diagnostic indicators for pediatric sleep-disordered breathing, including craniofacial features, sleep behaviors, and comorbid conditions that should trigger further evaluation.

Treatment Options

Management approaches vary based on severity and associated factors (Figure 3). Mild-moderate pediatric OSA may respond to pharmacological interventions such as montelukast or intranasal steroids [16]. Improved sleep hygiene and watchful waiting can lead to normalized results in up to 46% of cases, particularly given that adenoid tissue naturally decreases in size beginning around age 10 [16].

For cases with significant adenotonsillar hypertrophy, the American Academy of Otolaryngology recommends tonsillectomy [18]. AT surgery results in significant improvement in more than 70% of otherwise healthy children, though up to 70% of children with additional risk factors may experience residual OSA following surgery [19].

Additional interventions include CPAP, BiPAP, and myofunctional therapy [20]. Orthodontic approaches, particularly rapid maxillary expansion (RME), can effectively increase nasal airway size while reducing adenoid and tonsil volume by up to 51.6% and 75.4% respectively [21, 8, 20]. Post-treatment polysomnography is essential due to the high risk of residual OSA and adenoid regrowth, which occurs in more than 12% of cases within 1.5 years [9].

Figure 3. Evidence-Based Treatment Algorithm for Pediatric SDB: A systematic approach to intervention based on severity, age, and associated factors, highlighting the range of options from watchful waiting to surgical and orthodontic interventions.

Long-term Consequences

The implications of untreated pediatric SDB extend far beyond childhood sleep disturbances. Affected children may develop ADHD, learning disabilities, impaired growth, memory deficits, and executive function disorders [2] (Figure 4).

Cardiovascular consequences include ventricular hypertrophy [5], increased oxidative stress [22], and elevated inflammatory markers [24]. The bidirectional relationship with obesity manifests as higher cholesterol levels, insulin resistance, and increased leptin levels that encourage overeating [2, 23].

Even primary snoring which is often considered benign is associated with poorer endothelial function, elevated blood pressure [25], and cognitive issues regardless of AHI severity [26, 27]. This suggests that any degree of SDB warrants clinical attention and appropriate intervention.

Figure 4. Multisystem Consequences of Untreated Sleep-Disordered Breathing: The cascade of long-term health impacts across cardiovascular, metabolic, neurocognitive, and behavioral domains, illustrating the importance of early identification and intervention.

Conclusion

Untreated childhood sleep-disordered breathing establishes lifelong health risks through mechanisms of chronic intermittent hypoxia and systemic inflammation that increase the likelihood of cardiovascular and metabolic disease. As dental practitioners, we are uniquely positioned to recognize SDB’s clinical manifestations in orofacial structures during routine examinations.

By incorporating targeted screening, recognizing early warning signs, and facilitating appropriate referrals, dentists and healthcare practitioners serve as guardians of systemic well-being beyond oral health. The thorough orofacial examination and intervention may prevent premature cardiovascular mortality and significantly improve the quality of life across our patients’ lifespans.

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