Orthodontics and Sleep-Disordered Breathing

The pathophysiological mechanisms underpinning OSA are complex and it is no surprise the relationships between craniofacial growth, the airway, and sleep remain controversial in orthodontics. This chapter explores evidence from cases, imaging studies, observational and investigational cohort studies, randomized controlled trials, and systematic reviews that consider the myriad facets of pediatric and adult OSA. In pediatric OSA, certain features are suspected to be associated (e.g., lower facial height, posterior crossbite, small chin, increased ANB and SNB angles, retrognathism, a retrusive mandible, and reduced upper airway width); however, the influence of different types of structures and malocclusions remains unclear. In adult OSA, several correlations have been reported with differing measures of the cranial base, facial height, maxilla and mandible, pharyngeal airway space, the soft palate and tongue, and position of the hyoid bone, but direct causal evidence remains elusive. Evidence shows rapid maxillary expansion impacts the entire nasomaxillary complex, decreases nasal airway resistance, and decreases apnea–hypopnea index in adolescents. Still, long-term evidence is lacking, and no prior guideline has recommended optimal expansion widths or rates to improve symptoms. Research also suggests different orthodontic interventions (e.g., extractions, headgear, and other functional appliances) may impact airway dimensions, but opposing evidence is consid ered.