Abstract:
Background: The hyoid is a mobile bone and central structure of the upper airway, serving as an anchor to several upper airway dilator muscles. As such, the hyoid is believed to play an important role in keeping the upper airway open (patent) during sleep and breathing. In cases where upper airway patency is compromised during sleep, repeated narrowing or complete collapse of the airway can occur. These events are characteristic of a disorder known as obstructive sleep apnea (OSA). OSA is a highly prevalent condition that is associated with serious health consequences, including cardiovascular disease and neurocognitive impairment. The most commonly observed anatomical difference between OSA and healthy individuals is a more caudally positioned hyoid bone in OSA. While surgical hyoid repositioning therapies have been performed as an attempt to treat OSA, outcomes are unpredictable and highly variable. In this thesis, in a bid to better understand the hyoid’s role in OSA and improve treatment outcomes with hyoid repositioning procedures, a previously validated two-dimensional finite element model of the rabbit upper airway was advanced to study the influence of hyoid bone position and surgical repositioning on upper airway patency and tissue mechanics.
Aims and Methods: Specifically, the aims of the current study were to investigate the influence of 1) baseline hyoid position (phenotype), 2) surgical hyoid re-positioning, and 3) combined changes in baseline hyoid position and surgical hyoid re-positioning on upper airway collapsibility (quantified as upper airway closing pressure, Pclose), airway lumen geometry (cross sectional area, CSA; anteroposterior diameter, APD) and tissue mechanics (displacement, stress and strain). Simulations involved displacement of the hyoid along cranial, caudal, anterior, anterior-caudal 45o and anterior-cranial 45o directions from 1-4mm (in 1mm increments) for both baseline hyoid position and surgical hyoid repositioning interventions.
Results: Changes in baseline hyoid position resulted in a linear increase in Pclose (i.e. increased collapsibility) for all directions, ranging between 29-43% at 4mm. Surgical hyoid repositioning outcomes were similarly dependent on both the direction and magnitude of hyoid displacement. Anterior, anterior-cranial and anterior-caudal directions caused the largest decrease in Pclose, dropping by ~115% at 4mm. Hyoid repositioning in the anterior-based directions also led to the greatest airway enlargement (increase in CSA and APD by 35% and 85 to 140%, repectively) and anterior-cranial repositioning generated the highest stress distributions across greater soft tissue areas. Combined baseline hyoid position changes and surgical hyoid repositioning simulations revealed that for a more caudal hyoid baseline position (4mm), like in the OSA condition, anterior-cranial and anterior caudal hyoid repositioning of 2mm (similar to clinical surgical hyoid procedures) were 25% and 8% less effective in decreasing Pclose, respectively.
Discussion: This unique computational modeling study has predicted that both baseline hyoid position and surgical hyoid re-positioning alter upper airway outcomes, and that these changes are dependent on both the direction and magnitude of hyoid displacement. The original baseline (“normal”) hyoid position was deemed the optimal airway anatomical configuration in terms of airway collapsibility. Position of the hyoid at baseline impacts the effectiveness of surgical hyoid repositioning procedures in reducing upper airway collapsibility. Furthermore, anterior-cranial surgical hyoid repositioning procedures lead to greater improvements in upper outcomes compared to anterior-caudal surgical hyoid repositioning procedures. Study findings have important implications to potentially guide hyoid surgeries to improve OSA treatment outcomes and provide further insight into OSA pathogenesis.