Acellular Dermal Matrix, Smooth Tissue Expanders, and Betadine: Histologic Assessment in a Primate Model

Abstract

INTRODUCTION: It is known that an overabundance of pathogens in the setting of prosthetic breast devices can lead to infection, prolonged inflammation, and capsular contracture. As such, there has been increasing emphasis on the use of aseptic techniques that include antimicrobial irrigation solutions such as Betadine. The increasing use of human acellular dermal matrices (HADM) and prosthetic devices have raised questions as to whether exposure of the implant or tissue expander (TE) to Betadine may lead to deleterious effects related to HADM incorporation. The aim of this study was to determine if exposure of HADM to a Betadine-saturated TE would affect the corresponding biological response. METHODS: Samples (1.5 × 1.5 cm) cut from custom-made smooth silicone TEs (Allergan plc) were soaked in 100% Betadine for 2 minutes, without a subsequent saline rinse, or soaked in control saline alone, and then sutured to equivalently sized HADM samples (AlloDerm, Allergan plc) to form an HADM:TE construct. Eighteen African Green monkeys were each implanted subcutaneously with a pair of Betadine and saline-treated HADM:TE constructs and evaluated for overall biologic response to Betadine treatment following implantation at 2 or 4 weeks as demonstrated by hematoxylin and eosin histologic staining and using a subjective scoring scale (0–9) inclusive of recellularization, neovascularization, and inflammatory responses. The presence of individual cell types involved in inflammation (eosinophils, lymphocytes, neutrophils, histiocytes, foreign body giant cells) and HADM remodeling (fibroblasts) was also evaluated based on hematoxylin and eosin histologic staining (0–3 scoring scale) and in some cases corroborated by immunohistochemical staining (CD-3, CD-20, CD-68). Betadine-treated constructs were compared at 2-week (n = 9) and 4-week (n = 9) implantation to saline control-treated constructs with no exposure to Betadine also at 2-week (n = 9) and 4-week (n = 9) implantation. RESULTS: Overall biologic response to the HADM in the presence of Betadine or saline control was similar at 2-week implantation, scoring 5.6 ± 0.5 and 5.3 ± 0.9, respectively (P = 0.41) and remained similar at 4 weeks, scoring 4.6 ± 1.0 and 4.2 ± 0.8, respectively (P = 0.46). Although the presence of individual inflammatory cell types appeared to trend higher in the saline control group than in the Betadine-treated group at 2 weeks, the difference was not statistically significant, and the trend did not persist at 4 weeks. Likewise, differences in HADM fibroblast infiltration were not significant between Betadine-treated and control groups. However, the presence of fibroblasts within the implanted HADM did increase over time between 2 and 4 weeks, for both the Betadine-treated (increase from 1.0 ± 0.9 to 1.8 ± 1.0) and saline control groups (increase from 1.4 ± 0.9 to 1.8 ± 0.8), indicative of ongoing HADM incorporation. CONCLUSIONS: The data suggest that exposure of the HADM to a Betadine-treated TE did not negatively impact the host response to the implanted HADM in terms of inflammation, vascularization, recellularization, or overall HADM incorporation.