Capsular contracture remains a common and preventable complication of implanted breast prostheses. As our understanding of the pathophysiology continues to develop, it is prudent to reexamine existing beliefs in a contemporary context. This article presents a current summary of clinical and laboratory evidence, expressed as an interaction between potentiating and suppressing factors, and how this understanding can be applied to practice.
Key points
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Chronic inflammation attributable to the presence of bacterial biofilm is currently the predominant theorem of capsular contracture formation. Conversely, maintenance of implant sterility will prevent capsular contracture.
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The surgical field in breast augmentation is not rendered sterile by standard techniques and perioperative antibiotics.
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Thus, a comprehensive strategy for maintaining implant sterility is critical in preventing bacterial contamination, and is supported by mounting clinical and laboratory evidence.
Introduction
In an ideal world a medical device, once inserted into the human body, will undergo biological integration with complete tolerance and without any remote-to-implant effects, leading to long-term successful functional and aesthetic outcomes. In the real world, however, medical devices continue to be plagued with a wide spectrum of adverse outcomes, ranging from acute infection to long-term device failure necessitating removal. For breast implants, capsular contracture (CC) represents the most common and most problematic adverse outcome. Following primary augmentation, CC occurs in up to 59% of patients, and is the commonest indication for reoperation. Patients undergoing revision surgery for contracture can expect to have recurrence in 18.1% to 39.7% of cases. Furthermore, revision surgery is technically more difficult, and satisfaction rates are lower ( Fig. 1 ).
