Reply: Capsular Biofilm Formation at the Interface of Textured Implants and Acellular Dermal Matrix: A Comparative Scanning Electron Microscopy Study.

Abstract

Sir: We are thankful for the opportunity to respond to Dr. Minqiang Xin’s letter regarding our study entitled “Capsular Biofilm Formation at the Interface of Textured Implants and Acellular Dermal Matrix: A Comparative Scanning Electron Microscopy Study.”1 This is the first study investigating biofilm formation at the interface of textured expanders and acellular dermal matrix in the literature, and Dr. Xin and colleagues raise important questions to fuel this discussion. We have advocated the use of negative-pressure drainage with the insertion of Biocell (Allergan, Inc., Dublin, Ireland) macrotextured implants since our initial description of the “Velcro effect.”2 Our hypothesis is that biofilm formation within dead spaces of macrotextured implants originates from skin flora and on-table contamination during initial insertion of the device.3 Ingrowth of capsular tissue into these pores might decrease the propensity for bacterial proliferation, a process that is facilitated by negative-pressure drainage. Furthermore, it has been demonstrated that blood can accelerate the formation of biofilm, thereby emphasizing the necessity of reducing the amount of fluid accumulation around the implant with a drainage system. In addition, as Dr. Xin and colleagues point out, the force of gravity is also responsible for pooling of liquid in the lower pole of the breast, where acellular dermal matrices are located. This can contribute to the formation of biofilm if no negative-pressure drains are inserted, but in our opinion, it is not the sole mechanism. Indeed, in the case of acellular dermal matrices, no tissue ingrowth is expected to occur within the pores of macrotextured implants such as Biocell because neovascularization of the matrix has yet to occur. We believe that our findings demonstrating higher rates of biofilm formation at the acellular dermal matrix interface rather than the muscular aspect is more likely to be explained by this delay in capsular ingrowth into these dead spaces. Bacterial proliferation within these pores will occur regardless of the presence of a negative-pressure drainage system in this case. Furthermore, the formation of biofilm around closed-suction devices has been previously described by Dower and Turner in Plastic and Reconstructive Surgery in 2012.4 The authors studied under scanning electron microscopy a group of 12 patients with drains removed between 2 and 42 hours after insertion. Their findings revealed that biofilm formation was evident as soon as 2 hours after insertion at the three sites that were investigated (i.e., skin junction, middle of drain, and tip of drain). Contamination of the drain before insertion seemed to be origin of this biofilm formation, which corresponds to our hypothesis that bacterial proliferation around macrotextured implants originates at the time of insertion. Dr. Xin and colleagues also raise an important point when inquiring about the timing of filling and volume of expanders, and what impact it can have on biofilm formation. In a previous study published in Plastic and Reconstructive Surgery in 2015, we reported on the timing of postoperative expansion and the formation of biofilm around macrotextured implants as seen under scanning electron microscopy.5 Our findings demonstrated that a delayed approach to postoperative filling of expanders resulted in lower rates of biofilm formation and double capsules. In our institution, the initial volume expansion varies from 100 to 200 cc (representing roughly one-third of total expander implant volume) and the timing of postoperative initiation varies with surgeon experience, wherein some chose the conventional rapid expansion and others opted for a delayed approach. In the current study, regardless of the timing of postoperative expansion, all patients demonstrated thick biofilms at the acellular dermal matrix interface. This could indicate that the impact of expander filling is more negligible than the impact of lack of acellular dermal matrix ingrowth into the pores with regard to biofilm formation. DISCLOSURE Dr. Danino is a consultant and speaker for Allergan, Inc. None of the other authors has any commercial associations or financial interests to declare with respect to any of the information or products presented in this communication. Operational study costs were partially supported by an Allergan, Inc., industry research grant. Michel A. Danino, M.D., Ph.D.Johnny I. Efanov, M.D.Laurence Paek, M.D., M.Sc.Monica Iliescu Nelea, Ph.D.Plastic and Reconstructive Surgery DepartmentUniversity of Montreal Hospital CenterMontreal, Quebec, Canada