Abstract

Despite advances in microsurgical technology and an improved understanding of nerve regeneration, obtaining satisfactory results after facial nerve injury remains a difficult clinical problem. Among existing peripheral nerve regeneration studies, relatively few have focused on the facial nerve, particularly how experimental studies of the facial nerve using animal models play an essential role in understanding functional outcomes and how such studies can lead to improved axon regeneration after nerve injury. The purpose of this article is to review current perspectives on strategies for applying potential therapeutic methods for facial nerve regeneration. To this end, we searched Embase, PubMed, and the Cochrane library using keywords, and after applying exclusion criteria, obtained a total of 31 qualifying experimental studies. We then summarize the fundamental experimental studies on facial nerve regeneration, highlighting recent bioengineering studies employing various strategies for supporting facial nerve regeneration, including nerve conduits with stem cells, neurotrophic factors, and/or other therapeutics. Our summary of the methods and results of these previous reports reveal a common feature among studies, showing that various neurotrophic factors arising from injured nerves contribute to a microenvironment that plays an important role in functional recovery. In most cases, histological examinations showed that this microenvironmental influence increased axonal diameter as well as myelination thickness. Such an analysis of available research on facial nerve injury and regeneration represents the first step toward future therapeutic strategies.

Highlights

  • Peripheral facial palsy is caused by a variety of disease pathologies, including congenital conditions, Bell’s palsy, Ramsay Hunt syndrome, Guillain-Barre syndrome, Lyme disease, HIV infection, Kawasaki disease, central nervous system disorders, temporal bone fracture, otitis media, Melkersson-Rosenthal syndrome, neoplasms, and malignant tumors of the parotid gland and temporal bone [1]

  • Scaffold-free nerve constructs generated from Gingiva-Derived Mesenchymal Stem Cells (GMSC) spheroids were found to eliminate the risk of existing scaffold-induced foreign body responses [50]. Transplantation of these constructs into a segmental defect of rat facial nerve during defective rat facial nerve regeneration showed a beneficial effect, similar to autografts. These findings suggested that GMSCs can represent promising and accessible stem cell sources for tissue engineering in neural tissues

  • Clinical and experimental studies conducted to date have investigated a number of potential factors that increase healing and improve functional outcome after traumatic facial nerve injury, as reviewed here

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Summary

Introduction

Peripheral facial palsy is caused by a variety of disease pathologies, including congenital conditions, Bell’s palsy, Ramsay Hunt syndrome, Guillain-Barre syndrome, Lyme disease, HIV infection, Kawasaki disease, central nervous system disorders, temporal bone fracture, otitis media, Melkersson-Rosenthal syndrome, neoplasms, and malignant tumors of the parotid gland and temporal bone [1]. As well as parotid and facial surgeries, are centered around the facial nerve, making it vulnerable to iatrogenic injuries [2]. Temporomandibular joint replacement is the most frequent cause of surgically associated iatrogenic facial nerve injury, with oral and maxillofacial surgical procedures accounting for 40% of injuries, resections of head and neck lesions for 25%, otologic procedures for 17%, cosmetic procedures for 11%, and other procedures for 7% [3]. If mechanical disruption of axons is excessive, the patient is more likely to have a longer recovery time and severe functional outcome with sequelae [4]. In cases of severe injury of the facial nerve, preventing extensive edema formation and inhibiting inflammatory responses are expected to shorten recovery time and improve outcome. Group 2: bFGF single shot (n = 8). HGF around the damaged nerve significantly accelerated the recovery of facial nerve function.

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