The pathogenesis of fibrous capsular contracture after augmentation mammaplasty is still debated. One hypothesis implicates low-grade bacterial infections as a cause. The presence of a staphylococcal biofilm in a patient with recurrent capsular contracture was previously reported. A comparative, prospective, blinded, clinical study of implants and capsules removed from patients with or without significant capsular contracture was conducted to investigate the association of biofilm contamination, breast implants, and capsular contracture. Capsule and implant samples obtained during explantation were tested by routine microbiological culture, sensitive broth culture (after maceration and sonication), and scanning electron microscopy. Clinical parameters were correlated with microbiological findings. A total of 48 implant and/or capsule samples were obtained from 27 breasts during a 22-month period. Of the 27 breasts, 19 exhibited significant contracture (Baker grade III/IV). The mean duration of implantation was 9.2 years (range, 0.4 to 26.0 years). Routine swab cultures obtained at the time of explantation were negative for bacterial growth for all samples. The sensitive broth culture technique yielded 24 positive samples (50 percent, n = 48). An analysis of capsules demonstrated that 17 of 19 samples obtained from patients with significant contracture were positive, compared with only one of eight samples obtained from patients with minimal or no contracture (p = 0.0006). Fourteen of the 17 positive cultures from significantly contracted breasts yielded coagulase-negative staphylococci, mainly, species of the Staphylococcus epidermidis group. The presence of coagulase-negative staphylococci was also significantly associated with capsular contracture (p = 0.01). There was no significant difference in the frequency of culture positivity for saline versus silicone implants (p = 0.885). Scanning electron microscopy confirmed the presence of extensive biofilm on implants and within capsules.Biofilm, in particular, S. epidermidis biofilm, was detected for a significant proportion of patients with capsular contracture. This implicates biofilm disease in the pathogenesis of contracture, and strategies for its prevention should be explored.

Background: The association between breast implants and breast implant–associated anaplastic large cell lymphoma (ALCL) has been confirmed. Implant-related risk has been difficult to estimate to date due to incomplete datasets. Methods: All cases in Australia and New Zealand were identified and analyzed. Textured implants reported in this group were subjected to surface area analysis. Sales data from three leading breast implant manufacturers (i.e., Mentor, Allergan, and Silimed) dating back to 1999 were secured to estimate implant-specific risk. Results: Fifty-five cases of breast implant–associated ALCL were diagnosed in Australia and New Zealand between 2007 and 2016. The mean age of patients was 47.1 years and the mean time of implant exposure was 7.46 years. There were four deaths in the series related to mass and/or metastatic presentation. All patients were exposed to textured implants. Surface area analysis confirmed that higher surface area was associated with 64 of the 75 implants used (85.3 percent). Biocell salt loss textured (Allergan, Inamed, and McGhan) implants accounted for 58.7 percent of the implants used in this series. Comparative analysis showed the risk of developing breast implant–associated ALCL to be 14.11 times higher with Biocell textured implants and 10.84 higher with polyurethane (Silimed) textured implants compared with Siltex textured implants. Conclusions: This study has calculated implant-specific risk of breast implant–associated ALCL. Higher-surface-area textured implants have been shown to significantly increase the risk of breast implant–associated ALCL in Australia and New Zealand. The authors present a unifying hypothesis to explain these observations.

Background: A recent association between breast implants and the development of anaplastic large-cell lymphoma (ALCL) has been observed. The purpose of this study was to identify whether bacterial biofilm is present in breast implant–associated ALCL and, if so, to compare the bacterial microbiome to nontumor capsule samples from breast implants with contracture. Methods: Twenty-six breast implant–associated ALCL samples were analyzed for the presence of biofilm by real-time quantitative polymerase chain reaction, next-generation sequencing, fluorescent in situ hybridization, and scanning electron microscopy, and compared to 62 nontumor capsule specimens. Results: Both the breast implant–associated ALCL and nontumor capsule samples yielded high mean numbers of bacteria (breast implant–associated ALCL, 4.7 × 10⁶ cells/mg of tissue; capsule, 4.9 × 10⁶ cells/mg of tissue). Analysis of the microbiome in breast implant–associated ALCL specimens showed significant differences with species identified in nontumor capsule specimens. There was a significantly greater proportion of Ralstonia spp. present in ALCL specimens compared with nontumor capsule specimens (p < 0.05). In contrast, significantly more Staphylococcus spp. were found associated with nontumor capsule specimens compared with breast implant–associated ALCL specimens (p < 0.001). Bacterial biofilm was visualized both on scanning electron microscopy and fluorescent in situ hybridization. Conclusions: This novel finding of bacterial biofilm and a distinct microbiome in breast implant–associated ALCL samples points to a possible infectious contributing cause. Breast implants are widely used in both reconstructive and aesthetic surgery, and strategies to reduce their contamination should be more widely studied and practiced. CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, V.

There is increasing evidence that bacterial biofilm is responsible for the failure of medical devices, leading to device-associated infection. As plastic surgeons, we are among the leading users of prostheses in surgery, and it is important that we are kept informed of this growing problem. This article summarizes the pathogenesis of device-associated infection, outlines the evidence for such infection in a number of medical devices, and outlines operative strategies aimed at reducing the risk of bacterial contamination at the time of device deployment. It also outlines strategies under investigation to combat the development of device-associated infection.

Capsular contracture remains the most common complication following augmentation mammaplasty. The infective hypothesis implicates subclinical infection with biofilm in its pathogenesis. The authors developed an in vivo model of subclinical infection and biofilm formation to further investigate this. Adult female pigs underwent augmentation mammaplasty using miniature gel-filled implants. Staphylococcus epidermidis was inoculated into some of the periprosthetics as compared with control pockets, which were not inoculated. Implants were left in situ for 13 weeks, after which clinical assessment with the Baker technique was performed. Implants and capsules were then removed and subjected to laboratory analysis to detect biofilm. Fifty-one breast augmentations were performed in six pigs: 36 in submammary pockets inoculated with S. epidermidis and 15 in uninoculated pockets. Twenty-six of the 36 inoculated implants (72.2 percent) resulted in biofilm production. Pocket inoculation was strongly associated with biofilm formation (p = 0.0095). The presence of biofilm in the inoculated pockets was also significantly associated with the subsequent development of capsular contracture as compared with the uninoculated pockets (p < 0.05). Of the 15 uninoculated pockets, seven developed contracture. Five of these, however, demonstrated the presence of biofilm caused by native porcine S. epidermidis. Of the 31 biofilm-positive specimens, 25 (80.6 percent) developed capsular contracture. Using univariate analysis, biofilm formation was associated with a fourfold increased risk of developing contracture (odds ratio, 4.1667; 95 percent confidence interval, 1.1939 to 14.5413). Using this in vivo model, the authors have demonstrated a causal link between subclinical infection, biofilm formation, and capsular contracture.