Finite element analysis of eustachian tube function in cleft palate infants based on histological reconstructions

Abstract

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.

Objectives: Quantify the functional consequences of ET anatomy in infant CP specimens, and identify the relative importance of various tissue biomechanical properties on ET function in infants with CP.

Methods: Finite element models of ET anatomy and physiology were developed by using image analysis and three-dimensional (3D) reconstruction techniques. Models were developed using histological images of ET structures obtained from five infant CP specimens. The models were parameterized, and the effects of varying model parameters, which included tensor veli palatini and levator veli palatini force, ET cartilage, periluminal mucosal compliance, and hamular position on resistance to airflow through the tubal lumen, were determined.

Results: Of the evaluated parameters, only applied tensor veli palatini muscle force and compliance of the periluminal mucosa and cartilage tissues were significant predictors of resistance to airflow through the ET during muscle-assisted opening.

Conclusions: Finite element models of ET function in the CP infant identified tensor veli palatini muscle force as a direct predictor and mucosal/cartilage compliance as an indirect predictor of ET opening during muscle-assisted lumen dilations. Hamular position and levator veli palatini force were not found to have an effect on ET function in CP infants.

FIGURE 1

a, b, c: Distal, middle, and proximal histological sections of a CP specimen showing regional tracing/outlines of the cartilage, mucosal tissue, and ET lumen. Sections 1 through 5 represent the locations of loads/ boundary conditions as follows: 1, cranial base attachment; 2, mTVP attachment to the cartilage; 3, mTVP attachment to the mucosal tissue; 4, mLVP attachment to the mucosal tissue; and 5, mLVP attachment to the cartilage.

FIGURE 2

Locations of loading and boundary conditions on finite element ET models. a: Location of mTVP and mLVP force vectors. b: Location of fixed boundary condition on medial cartilage surface (black surface) and of zero z-displacment on the proximal and distal ends of the ET (gray surfaces).

FIGURE 3

a: Deformed finite element mesh of the ET with opened lumen caused by the action of muscle forces (gray = deformed cartilage, black = deformed mucosal tissue). b: Calculation of airflow velocity magnitude in the deformed lumen for an applied pressure drop of 200 mm H₂O. Integration of velocity field in the midsection was used to calculate flow rate.

FIGURE 4

Solid models of the ET cartilage (dark gray) and mucosal tissue (light gray) in the five CP specimens demonstrating wide variation in ET size and morphology.

FIGURE 5

Effects of varying (a) mTVP force, (b) mLVP force, (c) mucosal tissue elastic modulus, and (d) cartilage elastic modulus on resistance to airflow through the dilated ET. Data represent independent parameter variations with all other model parameters held at baseline values.

FIGURE 6

Effects of varying the pterygoid hamulus position in the (a) lateral or x direction, (b) superior or y direction, and (c) distal or z direction on resistance to airflow through the dilated ET. Data represent independent parameter variations with all other model parameters held at baseline values.