Repeated Lipoteichoic Acid Injection at Low Concentration Induces Capsular Contracture by Activating Adaptive Immune Response through the IL-6/STAT3 Signaling Pathway.

BACKGROUND: Capsular contracture is the most common complication of breast implantation surgery. Bacterial contamination was considered to play an important role in the occurrence of capsular contracture, and Gram-positive bacteria such as Staphylococcus epidermidis were discovered in the clinical specimens. Lipoteichoic acid (LTA) was a component of the cell wall of Gram-positive bacteria and was sufficient in the pathogenicity of the bacteria. The authors assumed that LTA could trigger the immunologic response against the implant and cause capsular contracture. METHODS: The authors developed a rat model of capsular contracture by repeated injection of 10 µg/mL LTA. The histologic changes of the capsule tissue were measured by hematoxylin and eosin, sirius red, Masson, and immunohistochemical staining. The expression of related cytokines was measured by quantitative real-time polymerase chain reaction. The downstream pathway activation was shown by Western blot. The authors also applied tocilizumab, an interleukin (IL)-6 receptor antagonist, to verify the role of IL-6 in this pathologic process. RESULTS: The authors discovered that repeated LTA injection, at a low concentration, could induce the thickening of capsule tissue, the deposition of collagen fiber, and the activation of myofibroblasts. The IL-6/signal transducer and activator of transcription 3 signaling pathway was activated in this process, and the inhibition of IL-6 receptor could relieve the symptoms. B cells and T-helper cells, especially T-helper type 1, could be related to this phenomenon. CONCLUSIONS: The authors' research corroborated that subclinical infection could trigger capsular contracture, and the immune system played an important role in this process. The authors' results provided a possible research direction for the mechanism of bacterial infection-induced immune response against breast implants. CLINICAL RELEVANCE STATEMENT: The authors' research provides a possible research direction for the mechanism of bacterial infection-induced immune response against breast implants, and a potential target for predicting the prognosis of capsular contracture.

Exhaustive diagnosis of breast implants with capsular contracture: The microbiology laboratory as a major support.

The most frequent complications of post-mastectomy reconstructions are breast implant (BI) infection and capsular contracture (CC). The diagnosis of BI colonization is based on cultures from the sonicated BI and from the capsule tissue. Therefore, we first aimed to assess the yield of conventional culture and molecular techniques in periprosthetic fluid, in addition to BI and capsular tissue. Moreover, we compare colonization and biofilm production between patients with and without CC. During 19 months, we prospectively included patients whose BIs had been removed and divided them into two groups: A (CC, Baker III-IV) and B (no CC). Samples were obtained for conventional culture, 16 s rRNA PCR, and MALDI-TOF. Biofilm production was also evaluated. We included 81 BIs from 69 patients with CC (22) and without CC (53). Forty-three (53.1%) of the 81 BIs had ≥1 positive culture. The culture was positive in 57.1% and 50.9% in groups A and B, respectively (p = 0.645). The highest 16 s rRNA PCR positivity rate was detected in capsular tissue (40.5%). MALDI-TOF was unable to detect colonization in any of the samples. High biofilm production was the following: high biomass: A, 29.8%; B, 39.7% (p = 0.293); high metabolic activity: A, 36.2%; B, 34.5% (p = 0.857). We confirm that cultures from different sites are mandatory to ensure a proper diagnosis of BI colonization. Our study is the first to demonstrate that CC was not associated with BI colonization or high biofilm production. The application of molecular techniques in BI samples was not substantially useful for predicting colonization.

Microbial community compositions in breast implant biofilms associated with contracted capsules.

Subclinical bacterial infections (biofilms) are strongly implicated in breast augmentation failure due to capsular contracture, and while these infections are generally ascribed to common skin commensals, this remains largely unsubstantiated through robust cultivation independent analyses. To determine capsule biofilm microbial community compositions, we employed amplicon sequencing of the 16S rRNA gene using DNA extracted from breast implant capsule samples. These cultivation independent analyses revealed that capsule associated biofilms are more diverse than canonical single-species infections, but have relatively low diversity (~ <100 species) compared to many host-associated microbial communities. In addition to taxa commonly associated with capsular contracture, the biofilms analyzed comprised a number of taxa that escaped detection in cultivation-dependent work. We have also isolated several key taxa identified through the culture-independent analyses. Together our analyses reveal that capsule biofilms are more diverse than cultivation studies suggest and can be heterogeneous within an individual capsule, between breasts of the same patient, across similar implant types, and over a range in severity of contracture. The complex nature of these communities requires further study across a broader suite of patients in addition to higher resolution analyses including metagenomics to better assess the fundamental role of microorganisms in capsular contracture.

Capsular contracture around silicone miniimplants following bacterial contamination: an in vivo comparative experimental study between textured and polyurethane implants.

BACKGROUND: Capsular contracture remains a problem following breast implant surgery. Although impact of biofilm and implant surface on capsule formation has been demonstrated, interaction of microorganisms with different surface types has not been clarified yet. We aimed to compare the ability of biofilm formation of implants with different surfaces, under standard conditions and to demonstrate its impact on capsular contracture. METHODS: Twenty-four rats were divided into four groups. Mini-implants with three different surfaces (fine-textured, rough-textured and polyurethane) were placed on the dorsum of each rat. In Group-1, sterile implants were placed in submuscular pockets. In Group-2, implants were incubated in Staphylococcus epidermidis medium before implantation. In Group-3, before implantation, implants were immersed in Rifamycin solution following bacterial contamination. In Group-4, sterile implants were immersed in Rifamycin solution before implantation, and served as the control group. Rats were sacrificed at three months. Clinical, microbiological, histological and immunohistochemical evaluations were performed. RESULTS: Capsule contracture developed only on infected rough-textured implants. Rough-textured and polyurethane implants showed more biofilm formation than fine-textured implants. Capsule thickness and inflammatory cell density were higher on rough-textured implants compared to fine-textured implants (p = 0.004). Actin sequence was parallel and concentric on fine-textured and rough-textured implants; but was in irregular array on polyurethane implants. CONCLUSION: In presence of bacterial contamination, rough-textured implants have the most propensity of developing capsular contracture comparing to fine-textured and polyurethane implants at three months after implantation. Despite high bacterial load and biofilm formation, polyurethane implants are resistant to capsule contracture due to surface characteristics.

PCR Characterization of Microbiota on Contracted and Non-Contracted Breast Capsules.

BACKGROUND: The aetiology of capsular contracture around breast implants remains unclear. The leading theory is that a subclinical infection around the implant plays a role in the development of capsular contractions. Several studies found associations between the presence of bacteria and the occurrence of capsular contraction. However, it is unclear whether detected bacteria originate from the breast capsule, breast glandular tissue or skin contamination. Moreover, this has never been investigated with molecular techniques. The aim of this study was to assess the bacterial microbiota on breast capsules, glandular tissue and skin using a highly sensitive PCR assay. MATERIALS AND METHODS: Fifty breast capsules were collected during implant removal or replacement. Ten specimens of glandular breast tissue and breast skin were collected in females who were undergoing reduction mammoplasty. A sample specimen (4 mm) was sterilely obtained from all tissues. All specimens were analysed by IS-pro, a 16S-23S interspace region-based PCR assay. RESULTS: Low numbers of Staphylococcus spp. (four species in four capsules) were found on breast capsules. There was no difference in bacterial presence between normal and contracted capsules. The skin of the breast-harboured Streptococcus spp. and Staphylococcus spp. while the glandular tissue was sterile. CONCLUSION: The low numbers of bacteria found on the capsules are most likely caused by contamination during capsule removal. More and larger studies are needed to investigate the bacterial presence on breast capsules using a PCR assay. This is the first study in which breast capsules have been studied using a highly sensitive PCR assay. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Back to Basics: Could the Preoperative Skin Antiseptic Agent Help Prevent Biofilm-Related Capsular Contracture?

BACKGROUND: Capsular contracture (CC) has remained an unresolved issue throughout history. Strong evidence focuses on bacterial biofilm as its main source. A literature review revealed that more than 90% of bacteria found in capsules and implants removed from patients with Baker grade III-IV CC belong to the resident skin microbiome (Staphylococcus epidermidis, predominant microorganism). The use of an adequate preoperative skin antiseptic may be a critical step to minimize implant contamination and help prevent biofilm-related CC. OBJECTIVES: The authors sought to compare the effect of 2 different antiseptic skin preparations: povidone-iodine (PVP-I) vs chlorhexidine gluconate (CHG) on CC proportions after primary breast augmentation through a periareolar approach. METHODS: In June of 2014, The Society for Healthcare Epidemiology of America proposed to use CHG for preoperative skin preparation in the absence of alcohol-containing antiseptic agents as strategy to prevent surgical site infection. The clinical safety committee of a surgical center in Colombia decided to change PVP-I to CHG for surgical site preparation thereafter. The medical records of 63 patients who underwent to primary breast augmentation through a periareolar approach during 2014 were reviewed. In the first 6 months PVP-I was used in 32 patients, and later CHG was employed in 31 patients. RESULTS: Pearson's chi-squared test to compare CC proportions between subgroups showed a statistically significant difference. The CC proportion was higher for patients who had antisepsis with PVP-I. CC was absent when CHG was employed. CONCLUSIONS: CHG as preoperative skin antiseptic for primary breast augmentation surgery was more effective than PVP-I to help prevent biofilm-related CC.

The aetiopathogenesis of capsular contracture: A systematic review of the literature.

BACKGROUND: Capsular contracture is the most frequent complication after breast augmentation or reconstruction with breast implants. The immune system plays a prominent role in capsular contracture formation, albeit to an unknown extent. Bacterial contamination in situ has been hypothesized to be causative for capsular contracture. How this relates to the immunological processes involved is unknown. This article aims to provide an overview of immunological and bacterial factors involved in development of capsular contracture. MATERIALS AND METHODS: We undertook a systematic literature review focused on immunological factors and microbiota in relation to capsular contraction around implants. This systematic review was performed in accordance with the PRISMA guidelines. PubMed, EMBASE, and the Cochrane databases were searched from inception up to October 2016. Included studies were assessed for the following variables: subject characteristics, number of capsules, primary indication for surgery, surgical procedure, follow-up or implant duration, study methods, type of antibiotics or medical therapies and outcomes related to microbiota and immunological factors. RESULTS: Data on immunological factors and bacterial contamination were retrieved from 64 included studies. Notably the presence of macrophages and Staphylococcus epidermidis within capsules was often associated with capsular contracture. CONCLUSION: This review provides a clear overview of the immunological factors associated with capsular contracture and provides a hypothetical immunological model for development of the disease. Furthermore, an overview of bacterial contamination and associations with capsular contracture has been provided. Follow-up research may result in clinical recommendations to prevent capsular contracture.

Plasma Activation of a Breast Implant Shell in Conjunction With Antibacterial Irrigants Enhances Antibacterial Activity.

BACKGROUND: Infection and capsular contracture are two of the most significant complications of breast-implant surgery. Both complications are associated with bacterial contamination of the implant surface. Plasma activation of the surface of a silicone breast implant changes its surface properties from water repelling (hydrophobic) to water absorbing (hydrophilic), thus making it possible for antibacterial irrigants to temporarily adsorb onto the implant surface. OBJECTIVES: To support our hypothesis that by changing the surface properties we could render antibacterial irrigation more effective in inhibiting bacterial growth on a breast implant shell. METHODS: An in vitro study using silicone discs cut from a textured silicone breast implant shell was performed by treating some of the discs with plasma activation and then exposing the discs to contamination with either Staphylococcus aureus or Pseudomonas aeruginosa and then variously treating the discs with 10% povidone iodine, Cefazolin, or Gentamicin. Bacterial contamination was verified and counted using contact plates as well as culture media. RESULTS: Plasma activation changed the wetting properties of the disc's surface from hydrophobic to hydrophilic. Nonplasma activated contaminated discs demonstrated clear bacterial growth both in the untreated group and in the antibacterial-treated group. Combining antibacterial treatment with plasma activation resulted in complete inhibition of bacterial growth in each of the groups treated with antibacterial irrigants. CONCLUSIONS: Combining plasma activation with topical antibacterial irrigants can inhibit the growth of bacteria on implant shell discs. By changing the properties of the surface from hydrophobic to hydrophilic, the adsorption of the antibacterial irrigants is enhanced.

Microbial Evaluation in Capsular Contracture of Breast Implants.

BACKGROUND: Capsular contracture around breast implants is a severe and unpredictable complication experienced by up to 50 percent of patients after breast augmentation and reconstruction, and represents a major cause leading to reoperation. Several lines of evidence point to the involvement of subclinical infections and of bacterial biofilm formation. METHODS: To reduce the incidence of capsular contracture following mammaplasty, the authors studied the correlation between contamination by exogenous and endogenous bacterial flora and the capacity to develop bacterial biofilm in mammary implants. The authors performed a microbiological study assessing microbial growth of swabs from breast skin, nipple-areola complex, and mammary gland biopsy specimens. Furthermore, the authors compared the results with the data resulting from cultural experiments from biopsy specimens of periprosthetic capsule, contracted or not, and from the surfaces of the relative prosthesis. RESULTS: Between July of 2012 and July of 2013, a series of 65 female patients from the area of Naples, Italy, and its province, who underwent breast plastic surgery with the use of implants for aesthetic or reconstructive reasons, were included in the study. The authors noticed that there is a greater tendency for capsular contracture to form in oncologic patients who received radiotherapy, patients with precedent capsular contracture, and patients with cutaneous contamination by biofilm-producing microbes. CONCLUSIONS: Although all of the new technical procedures tend to reduce the amount of bacterial charge that comes into contact with the prosthesis at the time of its introduction, a minimal amount must always be taken for granted. This is the rationale for a preventative personalized antibiotic therapy. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.

The Relationship of Bacterial Biofilms and Capsular Contracture in Breast Implants.

Capsular contracture is a common sequelae of implant-based breast augmentation. Despite its prevalence, the etiology of capsular contracture remains controversial. Numerous studies have identified microbial biofilms on various implantable materials, including breast implants. Furthermore, biofilms have been implicated in subclinical infections associated with other surgical implants. In this review, we discuss microbial biofilms as a potential etiology of capsular contracture. The review also outlines the key diagnostic modalities available to identify the possible infectious agents found in biofilm, as well as available preventative and treatment measures.

Histologic, Molecular, and Clinical Evaluation of Explanted Breast Prostheses, Capsules, and Acellular Dermal Matrices for Bacteria.

BACKGROUND: Subclinical infections, manifest as biofilms, are considered an important cause of capsular contracture. Acellular dermal matrices (ADMs) are frequently used in revision surgery to prevent recurrent capsular contractures. OBJECTIVE: We sought to identify an association between capsular contracture and biofilm formation on breast prostheses, capsules, and ADMs in a tissue expander/implant (TE/I) exchange clinical paradigm. METHODS: Biopsies of the prosthesis, capsule, and ADM from patients (N = 26) undergoing TE/I exchange for permanent breast implant were evaluated for subclinical infection. Capsular contracture was quantified with Baker Grade and intramammary pressure. Biofilm formation was evaluated with specialized cultures, rtPCR, bacterial taxonomy, live:dead staining, and scanning electron microscopy (SEM). Collagen distribution, capsular histology, and ADM remodeling were quantified following fluorescent and light microscopy. RESULTS: Prosthetic devices were implanted from 91 to 1115 days. Intramammary pressure increased with Baker Grade. Of 26 patients evaluated, one patient had a positive culture and one patient demonstrated convincing evidence of biofilm morphology on SEM. Following PCR amplification 5 samples randomly selected for 16S rRNA gene sequencing demonstrated an abundance of suborder Micrococcineae, consistent with contamination. CONCLUSIONS: Our data suggest that bacterial biofilms likely contribute to a proportion, but not all diagnosed capsular contractures. Biofilm formation does not appear to differ significantly between ADMs or capsules. While capsular contracture remains an incompletely understood but common problem in breast implant surgery, advances in imaging, diagnostic, and molecular techniques can now provide more sophisticated insights into the pathophysiology of capsular contracture. LEVEL OF EVIDENCE: 4 Therapeutic.

Chronic biofilm infection in breast implants is associated with an increased T-cell lymphocytic infiltrate: implications for breast implant-associated lymphoma.

BACKGROUND: Biofilm infection of breast implants significantly potentiates capsular contracture. This study investigated whether chronic biofilm infection could promote T-cell hyperplasia. METHODS: In the pig study, 12 textured and 12 smooth implants were inserted into three adult pigs. Implants were left in situ for a mean period of 8.75 months. In the human study, 57 capsules from patients with Baker grade IV contracture were collected prospectively over a 4-year period. Biofilm and surrounding lymphocytes were analyzed using culture, nucleic acid, and visualization techniques. RESULTS: In the pig study, all samples were positive for bacterial biofilm. There was a significant correlation between the bacterial numbers and grade of capsular contracture (p = 0.04). Quantitative real-time polymerase chain reaction showed that all lymphocytes were significantly more numerous on textured compared with smooth implants (p < 0.001). T cells accounted for the majority of the lymphocytic infiltrate. Imaging confirmed the presence of activated lymphocytes. In the human study, all capsules were positive for biofilm. Analysis of lymphocyte numbers showed a T-cell predominance (p < 0.001). There was a significant linear correlation between the number of T and B cells and the number of detected bacteria (p < 0.001). Subset analysis showed a significantly higher number of bacteria for polyurethane implants (p < 0.005). CONCLUSIONS: Chronic biofilm infection around breast prostheses produces an increased T-cell response both in the pig and in humans. A possible link between bacterial biofilm and T-cell hyperplasia is significant in light of breast implant-associated anaplastic large-cell lymphoma. CLINICAL QUESTION/LEVEL OF EVIDENCE: Risk, V.

The effect of a bacterial contamination on the formation of capsular contracture with polyurethane breast implants in comparison with textured silicone implants: an animal study.

INTRODUCTION: One of the most common complications following breast augmentation is capsular contracture. The subclinical infection of the implant is often considered to be one of the main risk factors. It is believed that polyurethane (PU) implants, because of their larger foam-like surface, have lower capsular contracture rates due to better tissue integration. It remains unclear if bacterial contamination and biofilm formation result in higher capsular contracture rates under the condition of the increased surface of PU implants compared to textured silicone-gel implants. The effect of this bacterial contamination was examined in an animal-based study. METHODS: A total of 80 mini implants (40 textured silicone-gel implants and 40 PU implants) were implanted in the dorsum of female Wistar rats. In each group, 20 implants were inoculated before implantation with a standard amount of Staphylococcus epidermidis. Capsules and implants were explanted after 60 days, followed by double-blind histological, immunohistochemical, and microbiological examinations. RESULTS: Macroscopic separation of the total capsule in the textured implant group was possible whereas the growth of surrounding tissue into the foam structure of PU implants made separation in that group difficult. After contamination, a thicker capsule could be observed in both groups without significant differences. Histologically, capsules around PU implants showed significantly lower expression of parallel myofibrils. We were able to describe a significant higher infiltration with inflammatory cells in capsules around PU implants both with and without contamination. Microbiological investigations revealed positive growth of S. epidermidis around one PU implant without related signs of capsular contracture. DISCUSSION: This study demonstrates that aside from the surface of silicone implants, bacterial contamination has major impact on the architecture of capsule formation. In our study, we were able to demonstrate that bacterial contamination leads to a thicker capsule and an increased tissue reaction with a higher amount of inflammatory cells. However, a resulting bacterial infection was only demonstrated in one case and had an insignificant influence on capsule architecture. The observed inflammatory reaction around PU implants was observed as a nonbacterial, granulomatose foreign body reaction. EBM RATING: Level I: Evidence obtained from at least one properly designed randomized controlled trial.

The ever-changing role of biofilms in plastic surgery.

The goal of this article is to present a brief background of biofilms and how they pertain to plastic surgery. Of particular interest are how biofilms affect breast prosthesis and their subsequent complications. The authors also present information on how biofilms are involved in soft-tissue filler complications. After a brief review of the pathophysiology of biofilms and their effect on plastic surgery, the authors propose a revised algorithm to assist in guiding the plastic surgeon when faced with complications that involve biofilms that involves more rapid diagnosis and treatment using polymerase chain reaction technology. This article is a review of recent literature.

Prevention of biofilm-induced capsular contracture with antibiotic-impregnated mesh in a porcine model.

BACKGROUND: A growing body of evidence implicates subclinical (biofilm) infection around breast implants as an important cause of capsular contracture (CC). OBJECTIVES: The authors use an in vivo porcine model to investigate the potential of antibiotic-impregnated mesh as a prophylactic measure against biofilm formation and CC. METHODS: A total of 28 implants (14 untreated controls, 14 treated with antibiotic mesh) were inserted into 5 adult female pigs. All implants and pockets were inoculated with a human clinical strain of Staphylococcus epidermidis. The implants were left in situ for 16 weeks and then analyzed for contracture using both Baker grading and applanation tonometry. The presence of biofilm infection was assessed by subsequent microbiological analysis of implants and capsules. RESULTS: One untreated implant had extruded and was excluded from analysis. The tissue surrounding the 13 untreated control implants had Baker Grade III/IV CC, whereas no CC was identified around the 14 antibiotic mesh-treated implants. This difference was highly significant (P < .001). Tonometry findings were consistent with the Baker assessments. Although bacterial biofilm was detected on all implants and capsules, the biofilms on the antibiotic-treated implants and surrounding capsules were generally single-layered or isolated in contrast to the multilayer biofilms found on untreated implants and capsules. CONCLUSIONS: Based on the findings from this study of a porcine model, the use of antibiotic-impregnated mesh reduces bacterial access to breast implants at the time of surgical insertion and may subsequently protect against subclinical infection and CC.

Risk of breast implant bacterial contamination from endogenous breast flora, prevention with nipple shields, and implications for biofilm formation.

BACKGROUND: Capsular contracture (CC) is a common complication of breast augmentation that is thought to arise from bacterial contamination and subsequent biofilm formation on the implant. Endogenous breast flora expressed through the nipple may contaminate the sterile field during breast augmentation, acting as a possible source for initiation of biofilm formation. OBJECTIVES: The authors investigate the incidence of nipple bacterial contamination with endogenous breast flora after standard chest wall sterilization during breast augmentation. METHODS: Bacterial contamination of nipples and nipple shields was assessed in a series of 32 consecutive patients presenting for breast augmentation (63 breasts: 31 bilateral procedures and 1 unilateral procedure). After standard sterilization of the chest wall, occlusive nipple shields were applied and breast augmentation was performed. At the conclusion of breast augmentation, the nipple shields were removed and, using the same swab, both the nipple/areolar area and occlusive dressings were cultured. RESULTS: Data from 63 cultured nipples and nipple shields revealed that 22 nipples/nipple shields (34.9%) were positive for bacterial contamination. Three patients, all of whom had negative cultures, developed CC after augmentation. CONCLUSIONS: The exposed nipple is a potential source of implant contamination during breast augmentation. An improved understanding of biofilms and related risk factors for CC can provide surgeons with insights for addressing this common complication. Meticulous hemostasis, use of nipple shields, and submuscular device placement may contribute to a lower incidence of CC.

Animal model of implant capsular contracture: effects of chitosan.

BACKGROUND: The mechanism(s) responsible for breast capsular contracture (CC) remain unknown, but inflammatory pathways play a role. Various molecules have been attached to implant shells in the hope of modifying or preventing CC. The intrinsic antibacterial and antifungal activities of chitosan and related oligochitosan molecules lend themselves well to the study of the infectious hypothesis; chitosan's ability to bind to growth factors, its hemostatic action, and its ability to activate macrophages, cause cytokine stimulation, and increase the production of transforming growth factor (TGF)-ß1 allow study of the hypertrophic scar hypothesis. OBJECTIVE: The authors perform a comprehensive evaluation, in a rabbit model, of the relationship between CC and histological, microbiological, and immunological characteristics in the presence of a chitooligosaccharide (COS) mixture and a low molecular weight chitosan (LMWC). METHODS: Eleven adult New Zealand rabbits were each implanted with three silicone implants: a control implant, one impregnated with COS, and one impregnated with LMWC. At four-week sacrifice, microdialysates were obtained in the capsule-implant interfaces for tumor necrosis factor alpha (TNF-α) and interleukin-8 (IL-8) level assessment. Histological and microbiological analyses were performed. RESULTS: Baker grade III/IV contractures were observed in the LMWC group, with thick capsules, dense connective tissue, and decreased IL-8 levels (p < .05) compared to control and COS groups. Capsule tissue bacterial types and microdialysate TNF-α levels were similar among all groups. CONCLUSIONS: Chitosan-associated silicone implantation in a rabbit model resulted in Baker grade III/IV CC. This preclinical study may provide a model to test various mechanistic hypotheses of breast capsule formation and subsequent CC.

Effects of coagulase-negative staphylococci and fibrin on breast capsule formation in a rabbit model.

BACKGROUND: The etiology and ideal clinical treatment of capsular contracture (CC) remain unresolved. Bacteria, especially coagulase-negative staphylococci, have been previously shown to accelerate the onset of CC. The role of fibrin in capsule formation has also been controversial. OBJECTIVE: The authors investigate whether fibrin and coagulase-negative staphylococci (CoNS) modulate the histological, microbiological, and clinical outcomes of breast implant capsule formation in a rabbit model and evaluate contamination during the surgical procedure. METHODS: Thirty-one New Zealand white female rabbits were each implanted with one tissue expander and two breast implants. The rabbits received (1) untreated implants and expanders (control; n = 10), (2) two implants sprayed with 2 mL of fibrin and one expander sprayed with 0.5 mL of fibrin (fibrin; n = 11), or (3) two implants inoculated with 100 µL of a CoNS suspension (10(8)CFU/mL-0.5 density on the McFarland scale) and one expander inoculated with a CoNS suspension of 2.5 × 10(7) CFU/mL (CoNS; n = 10). Pressure/volume curves and histological and microbiological evaluations were performed. Operating room air samples and contact skin samples were collected for microbiological evaluation. The rabbits were euthanized at four weeks. RESULTS: In the fibrin group, significantly decreased intracapsular pressures, thinner capsules, loose/dense (<25%) connective tissue, and negative/mild angiogenesis were observed. In the CoNS group, increased capsular thicknesses and polymorph-type inflammatory cells were the most common findings. Similar bacteria in capsules, implants, and skin were cultured from all the study groups. One Baker grade IV contracture was observed in an implant infected with Micrococcus spp. CONCLUSIONS: Fibrin was associated with reduced capsule formation in this preclinical animal model, which makes fibrin an attractive potential therapeutic agent in women undergoing breast augmentation procedures. Clinical strategies for preventing bacterial contamination during surgery are crucial, as low pathogenic agents may promote CC.

Effects of fibrin, thrombin, and blood on breast capsule formation in a preclinical model.

BACKGROUND: The root cause of capsular contracture (CC) associated with breast implants is unknown. Recent evidence points to the possible role of fibrin and bacteria in CC formation. OBJECTIVES: The authors sought to determine whether fibrin, thrombin, and blood modulated the histological and microbiological outcomes of breast implant capsule formation in a rabbit model. METHODS: The authors carried out a case-control study to assess the influence of fibrin, thrombin, and blood on capsule wound healing in a rabbit model. Eighteen New Zealand white rabbits received four tissue expanders. One expander acted as a control, whereas the other expander pockets received one of the following: fibrin glue, rabbit blood, or thrombin sealant. Intracapsular pressure/volume curves were compared among the groups, and histological and microbiological evaluations were performed (capsules, tissue expanders, rabbit skin, and air). The rabbits were euthanized at two or four weeks. RESULTS: At four weeks, the fibrin and thrombin expanders demonstrated significantly decreased intracapsular pressure compared to the control group. In the control and fibrin groups, mixed inflammation correlated with decreased intracapsular pressure, whereas mononuclear inflammation correlated with increased intracapsular pressure. The predominant isolate in the capsules, tissue expanders, and rabbit skin was coagulase-negative staphylococci. For fibrin and thrombin, both cultures that showed an organism other than staphylococci and cultures that were negative were associated with decreased intracapsular pressure, whereas cultures positive for staphylococci were associated with increased intracapsular pressure. CONCLUSIONS: Fibrin application during breast implantation may reduce rates of CC, but the presence of staphylococci is associated with increased capsule pressure even in the presence of fibrin, so care should be taken to avoid bacterial contamination.