No abstract

No abstract

We have developed a novel surgical/computational model for the investigation of unilat-eral vocal fold paralysis (UVFP) which will be used to inform future in silico approaches to improve surgical outcomes in type I thyroplasty. Healthy phonation (HP) was achieved using cricothyroid suture approximation on both sides of the larynx to generate symmetrical vocal fold closure. Following high-speed videoendoscopy (HSV) capture, sutures on the right side of the larynx were removed, partially releasing tension unilaterally and generating asymmetric vocal fold closure characteristic of UVFP (sUVFP condition). HSV revealed symmetric vibration in HP, while in sUVFP the sutured side demonstrated a higher frequency (10–11%). For the computational model, ex vivo magnetic resonance imaging (MRI) scans were captured at three configurations: non-approximated (NA), HP, and sUVFP. A finite-element method (FEM) model was built, in which cartilage displacements from the MRI images were used to prescribe the adduction, and the vocal fold deformation was simulated before the eigenmode calculation. The results showed that the frequency comparison between the two sides was consistent with observations from HSV. This alignment between the surgical and computational models supports the future application of these methods for the investigation of treatment for UVFP.

Objectives/HypothesisGlucocorticoids (GC)s are commonly employed to treat vocal fold (VF) pathologies. However, VF atrophy has been associated with intracordal GC injections. Dexamethasone‐induced skeletal muscle atrophy is well‐documented in other tissues and believed to be mediated by increased muscle proteolysis via upregulation of Muscle Ring Finger (MuRF)‐1 and Atrogin‐1. Mechanisms of dexamethasone‐mediated VF atrophy have not been described. This pilot study employed in vitro and in vivo models to investigate the effects of dexamethasone on VF epithelium, thyroarytenoid (TA) muscle, and TA‐derived myoblasts. We hypothesized that dexamethasone will increase atrophy‐associated gene expression in TA muscle and myoblasts and decrease TA muscle fiber size and epithelial thickness.Study DesignIn vitro, pre‐clinical.MethodsTA myoblasts were isolated from a female Sprague–Dawley rat and treated with 1 μM dexamethasone for 24‐h. In vivo, 15 New Zealand white rabbits were randomly assigned to three treatment groups: (1) bilateral intracordal injection of 40 μL dexamethasone (10 mg/ml; n = 5), (2) volume‐matched saline (n = 5), and (3) untreated controls (n = 5). Larynges were harvested 7‐days post‐injection. Across in vivo and in vitro experimentation, MuRF‐1 and Atrogin‐1 mRNA expression were measured via RT‐qPCR. TA muscle fiber cross‐sectional area (CSA) and epithelial thickness were also quantified in vivo.ResultsDexamethasone increased MuRF‐1 gene expression in TA myoblasts. Dexamethasone injection, however, did not alter atrophy‐associated gene expression, TA CSA, or epithelial thickness in vivo.ConclusionDexamethasone increased atrogene expression in TA myoblasts, providing foundational insight into GC induced atrophic gene transcription. Repeated dexamethasone injections may be required to elicit atrophy in vivo.Level of EvidenceNA Laryngoscope, 133:2264–2270, 2023