Repair of large nerve defects with acellular nerve allografts (ANAs) is an appealing alternative to autografting and allotransplantation. ANAs have been shown to be similar to autografts in supporting axonal regeneration across short gaps, but fail in larger defects due to a poorly-understood mechanism. ANAs depend on proliferating Schwann cells (SCs) from host tissue to support axonal regeneration. Populating longer ANAs places a greater proliferative demand on host SCs that may stress host SCs, resulting in senescence. In this study, we investigated axonal regeneration across increasing isograft and ANA lengths. We also evaluated the presence of senescent SCs within both graft types. A sciatic nerve graft model in rats was used to evaluate regeneration across increasing isograft (~autograft) and ANA lengths (20, 40, and 60 mm). Axonal regeneration and functional recovery decreased with increased graft length and the performance of the isograft was superior to ANAs at all lengths. Transgenic Thy1-GFP rats and qRT-PCR demonstrated that failure of the regenerating axonal front in ANAs was associated with increased levels of senescence related markers in the graft (senescence associated β-galactosidase, p16INK4A, and IL6). Lastly, electron microscopy (EM) was used to qualitatively assess senescence-associated changes in chromatin of SCs in each graft type. EM demonstrated an increase in the presence of SCs with abnormal chromatin in isografts and ANAs of increasing graft length. These results are the first to suggest that SC senescence plays a role in limited axonal regeneration across nerve grafts of increasing gap lengths.

Frequently used LAs at traditional concentrations are toxic to and can injure the peripheral nerve. Any combination of motor and/or sensory sequelae may result due to the varying fascicular topography of a nerve.

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Background Previous studies have reported decreased rates of capsular contracture associated with the use of textured surface breast implants placed in the subglandular plane during breast augmentation. However, since the publication of these studies, our understanding of the pathophysiology of capsular contracture, as well as the surgical techniques utilized to minimize bacterial contamination of the implant, have advanced considerably. Objectives The purpose of this study was to re-evaluate the relation between implant surface texturization and capsular contracture rates for breast implants placed in the subglandular plane during primary breast augmentation. Methods Retrospective chart review was performed of all primary subglandular breast augmentation procedures involving the use of either smooth or textured round silicone gel implants, with or without simultaneous mastopexy. The primary outcome measures included clinically significant capsular contracture (Baker grade III/IV) and revision surgery for capsular contracture. Results Between 2010 and 2017, 526 patients underwent primary subglandular breast augmentation with either smooth (n = 212) or textured (n = 314) round silicone gel implants; 248 patients underwent breast augmentation, whereas 278 underwent breast augmentation-mastopexy. Average follow-up was 756 days in the textured group and 461 days in the smooth group. Five cases of capsular contracture were observed in the textured group, and 7 cases of capsular contracture were observed in the smooth group (P = 0.20). Conclusions Smooth surface implants placed in the subglandular plane were not at a significantly increased risk of capsular contracture compared with textured surface implants. We suggest that adherence to a surgical technique focused on minimizing bacterial contamination of the implant is of greater clinical significance than implant surface characteristics when discussing capsular contracture. Level of Evidence: 4

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