Abstract

The mechanism and management of periprosthetic capsular contracture (CC) following breast augmentation have been the subject of debate for more than half a century, and Costagliola et al,1 authors of “An Innovative Procedure for the Treatment of Primary and Recurrent Capsular Contracture (CC) Following Breast Augmentation,” have continued the discussion. The surgical implantation of a prosthesis in every patient incites an inflammatory response that results in a well-ordered process of cellular events culminating in the deposition of collagen around the prosthesis. This can be viewed as the body's attempt to exclude the prosthesis from the immune system. It consists of the laminar deposition of a collagen envelope around the prosthesis. The cellular makeup of this envelope influences the degree of “constriction” around the prosthesis and, in the case of a breast implant, the softness or firmness of the overlying tissue. Inflammation is the initial stimulus for this process. Ongoing inflammation has been posited as the primary mechanism for continued cellular activity within the periprosthetic capsule. The 2 main hypotheses for the factors involved in the production of CC are a “hypertrophic scar induction” and continued inflammation based on a “subclinical infection.” There has been much focus during the past decade on addressing the latter for its potential as an inciting stimulus. Specific attention has been given to identifying bacterial organisms cultured from periprosthetic capsular fluid and formulating antibiotic irrigation solutions2 effective in suppressing or eliminating these bacteria in the periprosthetic capsular space. Data on the efficacy of this approach remain forthcoming. Most recently, the science of biofilms and their role in the process of bacteria-induced inflammation has been highlighted as an area for study.3 The hypertrophic scar hypothesis has many proponents, and authors have tried approaches for modulating the inflammatory stimulus thought to be an important inducing …

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