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.