Finite Element Modeling of Hyoid Bone Position, Mobility, and Surgical Repositioning in Mandibular Advancement: Effects on Upper Airway Patency and Mechanics

Abstract

Background: Obstructive sleep apnea (OSA) is characterized by recurrent collapse of the upper airway during sleep, resulting in intermittent oxygen desaturation and sleep fragmentation. Mandibular advancement (MA) is a commonly used treatment for OSA; however, treatment response is highly variable and the underlying reasons for this variability remain poorly understood. The hyoid bone, a mobile structure with muscular attachments to both the mandible and upper airway, has the potential to influence airway patency during MA. Despite this, the role of the hyoid bone in modulating the effectiveness of MA has been underexplored. Aim: To investigate the role of the hyoid bone in modifying upper airway patency, collapsibility, and tissue mechanics during mandibular advancement using computational modeling. Methods A validated two-dimensional midsagittal finite element model of the rabbit upper airway was employed to simulate MA from 0-3 mm in 1 mm increments, across a range of hyoid conditions, alone and combined. Various simulations were incorporated: 1) baseline, natural hyoid positions at increasingly caudal levels (0, 2, and 4 mm) representative of the OSA phenotype; 2) a free versus fixed hyoid bone; and 3) surgical hyoid repositioning (HR) in the anterior, anterior-cranial, anterior-caudal, cranial, and caudal directions from 0-2 mm (1 mm increments). For each simulation, upper airway collapsibility was quantified using closing pressure (Pclose), defined as the negative pressure at which the upper airway collapsed. Airway cross-sectional area (CSA) and anterior-posterior diameter (APD) were measured, and tissue mechanics (displacement, stress, and strain) were analyzed. Results: Progressive MA (0-3 mm) consistently improved upper airway patency and mechanics: Pclose decreased incrementally, while CSA and APD increased. The magnitude of these effects depended on the natural hyoid position, mobility, and direction and magnitude of surgical HR. At MA of 3 mm with the hyoid free to move, the initial (healthy) baseline hyoid position demonstrated the lowest Pclose (-62.86%). Under the same conditions, a more caudal baseline hyoid position (4 mm) exhibited markedly greater collapsibility (-5.71). Airway enlargement with MA was greater when the hyoid was free to move and slightly augmented at more caudal baseline positions (up to 16.4% vs 12.8% at MA 3 mm for free vs. fixed hyoid). Anterior-directed HR (anterior, anterior-cranial, and anterior-caudal) most effectively amplified MA-induced improvements. Anterior HR yielded the greatest airway expansion (30%), while anterior-cranial HR resulted in the highest reduction of Pclose (-111.43%). Cranial or caudal HR provided only modest, non-dose dependent changes. Conclusion: The response of the upper airway to mandibular advancement depended on the intrinsic hyoid phenotype, including its natural position and mobility, as well as the direction and magnitude of surgical hyoid bone repositioning. A caudally positioned and/or mechanically constrained hyoid bone limited the effectiveness of mandibular advancement in improving airway patency. Combining anterior-cranial hyoid repositioning with mandibular advancement enhances airway patency and compensates for unfavorable baseline anatomy. The results suggest that accounting for hyoid biomechanics in clinical evaluation and treatment planning may enhance patient selection, optimize therapeutic strategies, and possibly reduce treatment failure for OSA management with mandibular advancement.