Abstract

We aimed to analyze the involvement of adipose-sourced mast cells in nerve repair. Sixteen Wistar rats underwent complete transection of the sciatic nerves followed by either direct neurorrhaphy or neurorrhaphy and processed abdominal fat. Four animals were used as controls. Specimens were obtained at 4 and 10 weeks and analyzed using luxol fast blue stain, mast cell tryptase and CD34 (for angiogenesis) per microscopic field ×200. When assessed by luxol fast blue, normal nerves showed an average of 2–3 mast cells/field. At 4 weeks, there were 9.25 for the simple nerve sutures and 16 for the augmented repairs. At 10 weeks, there were 23 and 27.6. When assessed by mast cell tryptase, there were no positives in the controls. At 4 weeks, we found an average of 4 in the simple sutures and 2.5 in the augmented repairs. At 10 weeks, there were 4.5 and 0.2. In controls, there were 1–2 CD34+ blood vessels per field. At 4 weeks, simple repairs showed an average of 4 and, in those with adipose addition, 5.5. At 10 weeks, there were 7 and 12. Mechanically processed adipose tissue augmented nerve repair does not seem to increase mast cell expression but may support angiogenesis in an experimental model.

Highlights

  • Peripheral nerve injuries are common and pose a therapeutic challenge

  • At 4 weeks, we found an average of 9.25 mast cells/microscopic field ×200 on the side with simple nerve suture, with one case showing 22 mast cells/microscopic field ×200

  • Repairs augmented with the adipose graft showed an average of 16 mast cells/microscopic field ×200 (Table 1, Figure 2)

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Summary

Introduction

Peripheral nerve injuries are common and pose a therapeutic challenge. Mast cells originate from hematopoietic progenitors and have terminal differentiation under local tissular environments [3]. They play key roles in inflammation modulation and tissue healing, but their role in nerve regeneration is not yet fully understood [1,2,3,4]. A recent study suggested that mast cells harvested from bone marrow could be involved in nerve injury repair, yet the authors could not specify which of the chemical mediators present in the cytoplasm have a more potent effect [5].

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