Abstract
The superior laryngeal nerve (SLN) is known to play an essential role in the laryngeal reflex and swallowing. Damage to the SLN causes difficulty swallowing, that is, dysphagia. We successfully developed a novel rat model of dysphagia by SLN injury, in which we could evaluate the neuroregenerative capacity of stem cell from human exfoliated deciduous teeth (SHED). The dysphagic rats exhibit weight loss and altered drinking patterns. Furthermore, SLN injury induces a delayed onset of the swallowing reflex and accumulation of laryngeal debris in the pharynx. This rat model was used to evaluate the systemic application of SHED-conditioned medium (SHED-CM) as a therapeutic candidate for dysphagia. We found that SHED-CM promoted functional recovery and significant axonal regeneration in SLNs through the polarization shift of macrophages from activated inflammatory macrophages (M1) to anti-inflammatory macrophages (M2) and angiogenesis. This chapter describes the establishment of SLN-injury induced dysphagia rat model and the preparation and application of SHED-CM.
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