Formation of Scar Tissue Inside and Outside of a Conduit Used to Repair a Transected Sciatic Nerve in a Rabbit Model of Peripheral Nerve Injury
Michael Rivlin, MD1, Jolanta Fertala, PhD2, Andrzej Fertala, PhD3, Andrzej Steplewski, PhD2, Mark Wang, MD4 and Pedro K Beredjiklian, MD5, (1)Rothman Institute at Thomas Jefferson University, Philadelphia, PA, (2)Thomas Jefferson University, Philadelphia, PA, (3)Orthopaedic Surgery, Thomas Jefferson University, Philadelphia, PA, (4)Orthopaedics, Rothman Institute, Philadelphia, PA, (5)Rothman Institute, Philadelphia, PA
INTRODUCTION Peripheral nerve injury (PNI) occurs in about 2% of trauma patients. Many persistent functional deficits are due to neural fibrosis and scarring, which presents a mechanical barrier to peripheral nerve regeneration. Conduits are intended to bridge the neural defects guiding the regenerating axons. We studied the impact of conduits on the formation of neural scars.
METHODS Rabbits underwent surgery to transect the sciatic nerves. Conduits were employed to bridge the nerve gaps. The rabbits were sacrificed up to 10 weeks after surgery and then the sites of injury and contralateral uninjured nerves were dissected. The nerve samples were histologically analyzed for cellular markers of fibrosis, including α smooth muscle actin (αSMA), heat shock protein 47 (HSP47), and a neurofilaments marker. Corresponding histological sections were analyzed for overall cellularity and collagen-rich deposits indicating the formation of scar tissue.
RESULTS The αSMA-positive fibroblastic cells were primarily observed outside of the conduits and frequently co-localizingwith areas occupied by the fibrin glue.. The HSP47-positive cells were abundant on both sides of the conduit walls (Fig. 1). The sutures generated the formation of massive deposits of collagen-rich tissue elaborated by the HSP47-positive cells without αSMA-positive fibroblastic cells in these areas (Fig 2). The distribution of the neurofilament-specific marker within scar tissue indicated poor nerve regeneration ten weeks after surgery. H&E staining demonstrated inflammatory cells present through the entire 10-week experimental period.
DISCUSSION AND CONCLUSION The parallel organization of newly-formed collagen fibrils outside the conduits’ walls suggests that conduits may generate the torsional force due to some degree of rotation along the long axis. All fibroblastic cells around and within conduits actively produced collagen-rich matrices that facilitated the formation of adhesions and presented a formidable barrier for the axon regeneration through the 10-week experimental period. We cannot exclude a possibility that the conduit material, contributed to the prolonged inflammatory phase.
Back to 2020 Abstracts