4.6 Article

Repairing whole facial nerve defects with xenogeneic acellular nerve grafts in rhesus monkeys

Journal

NEURAL REGENERATION RESEARCH
Volume 17, Issue 5, Pages 1131-1137

Publisher

WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4103/1673-5374.324853

Keywords

acellular nerve; compound muscle action potentials; facial nerve defect; facial symmetry; monkey; nerve graft; nerve regeneration; retrograde labeling test; synaptophysin; xenogeneic

Funding

  1. National Natural Science Foundation of China [81770990]
  2. Jiangsu Provincial Key Research and Development Program of China [BE2018628]
  3. Six Talent Peaks Project in Jiangsu Province of China [2019-WSW-141]
  4. Major Medicine Projects of Wuxi Health Commission of Jiangsu, China [Z201802]
  5. Precision Medicine Projects of Wuxi Health Commission of Jiangsu, China [J202002]

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Acellular nerve allografts achieved satisfactory results in bridging facial nerve defects, but limited allogeneic donors are available. This experiment constructed a monkey model of whole nerve defect and studied xenogeneic acellular nerve grafts. The results showed that xenogeneic acellular nerve grafts were safe and effective for repairing facial nerve defects, similar to autografts.
Acellular nerve allografts conducted via chemical extraction have achieved satisfactory results in bridging whole facial nerve defects clinically, both in terms of branching a single trunk and in connecting multiple branches of an extratemporal segment. However, in the clinical treatment of facial nerve defects, allogeneic donors are limited. In this experiment, we exposed the left trunk and multiple branches of the extratemporal segment in six rhesus monkeys and dissected a gap of 25 mm to construct a monkey model of a whole left nerve defect. Six monkeys were randomly assigned to an autograft group or a xenogeneic acellular nerve graft group. In the autograft group, the 25-mm whole facial nerve defect was immediately bridged using an autogenous ipsilateral great auricular nerve, and in the xenogeneic acellular nerve graft group, this was done using a xenogeneic acellular nerve graft with trunk-branches. Examinations of facial symmetry, nerve-muscle electrophysiology, retrograde transport of labeled neuronal tracers, and morphology of the regenerated nerve and target muscle at 8 months postoperatively showed that the faces of the monkey appeared to be symmetrical in the static state and slightly asymmetrical during facial movement, and that they could actively close their eyelids completely. The degree of recovery from facial paralysis reached House-Brackmann grade II in both groups. Compound muscle action potentials were recorded and orbicularis oris muscles responded to electro-stimuli on the surgical side in each monkey. FluoroGold-labeled neurons could be detected in the facial nuclei on the injured side. Immunohistochemical staining showed abundant neurofilament-200-positive axons and soluble protein-100-positive Schwann cells in the regenerated nerves. A large number of mid-graft myelinated axons were observed via methylene blue staining and a transmission electron microscope. Taken together, our data indicate that xenogeneic acellular nerve grafts from minipigs are safe and effective for repairing whole facial nerve defects in rhesus monkeys, with an effect similar to that of autologous nerve transplantation. Thus, a xenogeneic acellular nerve graft may be a suitable choice for bridging a whole facial nerve defect if no other method is available.

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