A primary etiological factor underlying chronic middle ear disease is an inability to open the collapsible Eustachian tube (ET). However, the structure-function relationships responsible for ET dysfunction in patient populations at risk for developing otitis media (OM) are not known. In this study, three-dimensional (3D) finite element (FE) modeling techniques were used to investigate how changes in biomechanical and anatomical properties influence opening phenomena in three populations: normal adults, young children and infants with cleft palate. Histological data was used to create anatomically accurate models and FE techniques were used to simulate tissue deformation and ET opening. Lumen dilation was quantified using a computational fluid dynamic (CFD) technique and a sensitivity analysis was performed to ascertain the relative importance of the different anatomical and tissue mechanical properties. Results for adults suggest that ET function is highly sensitive to tensor veli palatini muscle (TVPM) forces and to periluminal mucosal tissue (PMT) elasticity. Young children and cleft palate subjects exhibited reduced sensitivity to TVPM forces while changes in PMT stiffness continued to have a significant impact on ET function. These results suggest that reducing PMT stiffness might be an effective way to restore ET function in these populations. Varying TVPM force vector relationships via changes in hamulus location had no effect on ET opening in young children and cleft palate subjects but did alter force transmission to the ET lumen during conditions of elevated adhesion. These models have therefore provided important new insights into the biomechanical mechanisms responsible for ET dysfunction.

Introduction-The prevalence of otitis media with effusion approaches 100% in infants with cleft palate (CP), and disease pathogenesis is believed to be caused by eustachian tube (ET) dysfunction.

The Eustachian Tube (ET) is a collapsible tube that connects the Middle Ear (ME) to the nasopharynx (NP). The ET is responsible for three primary functions: 1) regulation of ME pressure 2) protection of the ME from foreign pathogens and 3) drainage of fluid from the ME. [1] In healthy patients, the ET opens during swallowing because the surrounding tissue is deformed by muscle activity. If the ET fails to open, the ME develops painful sub-ambient pressure and fluid accumulates in the ME. ET dysfunction results in Otitis Media (OM), the most common ME disorder in children. The overall goal of our lab is to identify the mechanisms responsible for ET dysfunction and to develop novel treatments for OM that target the ET.

Otitis Media (OM) is the most commonly diagnosed childhood illness and has health care related cost of four billion dollars annually. [1] The onset of OM has been directly related to Eustachian Tube (ET) dysfunction. The ET has three main physiological functions, and when these functions are compromised, middle ear (ME) disorders arise. It is also known that specific populations of patients, such as those with cranio-facial abnormalities, such as a cleft palate, have a 100% onset rate of OM. Even though ET dysfunction has been related to OM, the underlying reasons for ET dysfunction in certain populations remains unknown. To gain an understanding of this system, we use fully coupled fluid-structure interaction (FSI) models of the ET based on geometries reconstructed from histological images. Using these models in systematic parameter variation studies allows us to identify which parameters of the ET can cause dysfunction. Using healthy adult subjects as a model for a well-functioning ET, we determined ET function to be sensitive to changes in TVP muscle force.

Otitis Media (OM) is an inflammation of the middle ear (ME) that is the most commonly diagnosed childhood illness and the cost of treating OM has been estimated at four billion dollars annually. [1] The onset of OM is typically due to bacterial/viral infections that cause tissue swelling, rapid ME gas exchange and painful sub-ambient ME pressures. Normally, periodic openings of the ET are used to relieve ME pressures. However, the up-regulation of various adhesion proteins within the ET lumen make it difficult for the surrounding muscles to open the ET. The goal of this study is to use computational models to investigate how changes in adhesion dynamics during inflammation influence ET function in three different patient populations: healthy adults, normal children, and CP infants. We have developed a multi-scale computational models of the ET based on histo-morphological data obtained in each population. Adhesive forces within the lumen are modeled as non-linear, reputable spring elements. These models indicate that tissue morphology and mechanics can significantly influence the ET’s response to inflammatory adhesion forces. Specifically, changes in mucosal tissue stiffness and TVP muscle forces are most effective in overcoming inflammatory adhesion forces.