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.
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.
The surgical field in breast augmentation is not rendered sterile by standard techniques and perioperative antibiotics.
Thus, a comprehensive strategy for maintaining implant sterility is critical in preventing bacterial contamination, and is supported by mounting clinical and laboratory evidence.
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 ).