Exploring the Intricate Links between Adenotonsillar Hypertrophy, Mouth Breathing, and Craniofacial Development in Children with Sleep-Disordered Breathing: Unraveling the Vicious Cycle

Abstract

Adenotonsillar hypertrophy has been well-acknowledged as the primary instigator of sleep-disordered breathing in the pediatric population. This condition spans a spectrum, from typical age-related growth that the immune system influences to persistent pathological hypertrophy. Reduction in air spaces, metabolic changes, neurobehavioral alterations, and chronic inflammation characterizes the latter form. As the go-to treatment, adenotonsillectomy has proven effective. However, it is not a guarantee for all patients, leaving us without reliable predictors of treatment success. Evidence suggests a connection between adenotonsillar hypertrophy and specific oral breathing patterns resulting from craniofacial development. This finding implies an intricate interdependence between the two, hinting at a self-sustaining vicious cycle that persists without proper intervention. The theories regarding the relationship between craniofacial conformation and sleep-disordered breathing have given rise to intriguing perspectives. In particular, the “gracilization theory” and the “gravitational hypothesis” have provided fascinating insights into the complex interaction between craniofacial conformation and SDB. Further investigation is crucial to unraveling the underlying pathophysiological mechanisms behind this relationship. It is also vital to explore the risk factors linked to adenotonsillectomy failure, study the long-term effects of adenotonsillar hypertrophy on craniofacial growth, and devise innovative diagnostic techniques to detect upper airway compromise early. Moreover, to assess their efficacy, we must delve into novel therapeutic approaches for cases that do not respond to traditional treatment, including positional therapy and orofacial myofunctional therapy. Though complex and unpredictable, these challenges promise to enhance our understanding and treatment of adenotonsillar hypertrophy and its related complications in children. By taking on this task, we can pave the way for more effective and targeted interventions, ultimately improving affected individuals’ well-being and quality of life.

Sleep Disordered Breathing in Children with Autism Spectrum Disorder: An In-Depth Review of Correlations and Complexities

“…Hypotonia was the most common motor symptom in a cohort of 154 children with ASD (51%), and it appears to improve over time. In the 2-6-year-old group, the prevalence of hypotonia was approximately 63% [36] at the age in which there is a high prevalence of SDB, mainly due to adenotonsillar hypertrophy [38,39]. In general, the atonia of skeletal muscles present during REM sleep might be exacerbated by the underlying hypotonia in children [40], and in ASD might increase the risk of OSA.…”

Insights into Pediatric Sleep Disordered Breathing: Exploring Risk Factors, Surgical Interventions, and Physical and Scholastic Performance at Follow-Up

“…Drug-induced sleep endoscopy (DISE) is essential for diagnosing upper airway obstructions in OSA patients, guiding treatment decisions, and improving surgical outcomes [39]. Evidence suggests a connection between upper airway obstruction and specific patterns of oral breathing stemming from craniofacial development, implying an intertwined interdependence between the two factors [40]. Improper alignment of teeth and jaw, known as malocclusion, can also contribute to SDB by restricting air passage through the nose and throat [41].…”

Exploring the Complex Interplay of Obesity, Allergic Diseases, and Sleep-Disordered Breathing In Children

“…This increased nasal resistance forces individuals to switch from nasal to mouth breathing, potentially contributing to upper airway collapse and apnoea generation. Studies have shown that nasal obstruction, whether due to anatomical issues or chronic allergies, can destabilize the upper airways and worsen sleep apnoea by disrupting normal breathing patterns [48,49]. Lofaso et al demonstrated that persistent vasomotor and non-vasomotor rhinitis are risk factors for SDB and OSA [50].…”