A Surgical Mouse Model for Advancing Laryngeal Nerve Regeneration Strategies.

Iatrogenic recurrent laryngeal nerve (RLN) injury is a morbid complication of anterior neck surgical procedures. Existing treatments are predominantly symptomatic, ranging from behavioral therapy to a variety of surgical approaches. Though laryngeal reinnervation strategies often provide muscle tone to the paralyzed vocal fold (VF), which may improve outcomes, there is no clinical intervention that reliably restores true physiologic VF movement. Moreover, existing interventions neglect the full cascade of molecular events that affect the entire neuromuscular pathway after RLN injury, including the intrinsic laryngeal muscles, synaptic connections within the central nervous system, and laryngeal nerve anastomoses. Systematic investigations of this pathway are essential to develop better RLN regenerative strategies. Our aim was to develop a translational mouse model for this purpose, which will permit longitudinal investigations of the pathophysiology of iatrogenic RLN injury and potential therapeutic interventions. C57BL/6J mice were divided into four surgical transection groups (unilateral RLN, n = 10; bilateral RLN, n = 2; unilateral SLN, n = 10; bilateral SLN, n = 10) and a sham surgical group (n = 10). Miniaturized transoral laryngoscopy was used to assess VF mobility over time, and swallowing was assessed using serial videofluoroscopy. Histological assays were conducted 3 months post-surgery for anatomical investigation of the larynx and laryngeal nerves. Eight additional mice underwent unilateral RLN crush injury, half of which received intraoperative vagal nerve stimulation (iVNS). These 8 mice underwent weekly transoral laryngoscopy to investigate VF recovery patterns. Unilateral RLN injury resulted in chronic VF immobility but only acute dysphagia. Bilateral RLN injury caused intraoperative asphyxiation and death. VF mobility was unaffected by SLN transection (unilateral or bilateral), and dysphagia (transient) was evident only after bilateral SLN transection. The sham surgery group retained normal VF mobility and swallow function. Mice that underwent RLN crush injury and iVNS treatment demonstrated accelerated and improved VF recovery. We successfully developed a mouse model of iatrogenic RLN injury with impaired VF mobility and swallowing function that can serve as a clinically relevant platform to develop translational neuroregenerative strategies for RLN injury.

Nonsurgical options to treat giant-cell tumors of the head and neck: A case report and brief review of the literature.

Central giant-cell granulomas (CGCGs) are relatively uncommon. When they do occur, they typically arise in the mandible and maxilla. Some lesions are more destructive than others, and the destructive subtype has a tendency to recur. Unfortunately, there is no reproducible way to differentiate aggressive from nonaggressive subtypes. Treatment of CGCG has historically been based on surgical curettage or wide local excision. However, surgery has been associated with significant morbidity, disfigurement, and expense, as well as a high recurrence rate. Pharmacologic treatments-either as an alternative or an adjunct to surgery-have been shown to yield acceptable results. These agents include intralesional and/or systemic corticosteroids, bisphosphonates, calcitonin, and interferon alfa. These options are typically less expensive than surgery, and they are associated with few side effects, which makes them potentially more desirable. We report the case of a 36-year-old woman with a CGCG who was successfully treated with a combination of an intralesional steroid and an oral steroid over a period of 5 months. As evidenced by this case, medical management can be effective for tumor regression in treating CGCG of the head and neck, and it is ultimately associated with less morbidity and is less costly. To the best of our knowledge, no randomized controlled studies have been published on this topic. Such a study would be welcome, particularly considering the presence of both aggressive and nonaggressive subtypes of CGCG. We also briefly review the literature.