SMI-Capsular Fibrosis and Biofilm Dynamics: Molecular Mechanisms, Clinical Implications, and Antimicrobial Approaches

Abstract

Silicone mammary implants (SMIs) frequently result in capsular fibrosis, which is marked by the overproduction of fibrous tissue surrounding the implant. This review provides a detailed examination of the molecular and immunological mechanisms driving capsular fibrosis, focusing on the role of foreign body responses (FBRs) and microbial biofilm formation. We investigate how microbial adhesion to implant surfaces and biofilm development contribute to persistent inflammation and fibrotic responses. The review critically evaluates antimicrobial strategies, including preoperative antiseptic protocols and antimicrobial-impregnated materials, designed to mitigate infection and biofilm-related complications. Additionally, advancements in material science, such as surface modifications and antibiotic-impregnated meshes, are discussed for their potential to reduce capsular fibrosis and prevent contracture of the capsule. By integrating molecular insights with clinical applications, this review aims to elucidate the current understanding of SMI-related fibrotic responses and highlight knowledge gaps. The synthesis of these findings aims to guide future research directions of improved antimicrobial interventions and implant materials, ultimately advancing the management of capsular fibrosis and enhancing patient outcomes.

Keywords: antimicrobial-impregnated materials; biofilm formation; capsular fibrosis; fibrotic response; foreign body response (FBR); implant surface modification; silicone mammary implants (SMIs).

Figure 1

Stages of the inflammatory and fibrotic response SMI insertion, illustrating the transition from immediate post-implantation inflammation to long-term fibrosis and implant encapsulation, with a detailed schematic of the cellular and molecular events driving these processes. Schematic representation of the cellular and molecular events involved in the inflammatory and fibrotic processes: (1) Lymphocyte Activation: CD4+ T cells are activated by dendritic cells (DCs) presenting antigens through major histocompatibility complex (MHC) molecules. Heat shock proteins (HSP60) and other danger-associated molecular patterns (DAMPs) interact with pattern recognition receptors (PRR) and toll-like receptors (TLR), initiating the immune response. (2) Th1/Th17 Immune Response: Activated T cells differentiate into Th1 and Th17 subsets, secreting pro-inflammatory cytokines (IL-1β, IFN-γ, TNF-α, IL-17), which drive the inflammatory response while suppressing regulatory T cells (Treg). (3) Macrophage Activation: M1 macrophages, stimulated by the inflammatory environment, contribute to chronic inflammation. Over time, there may be a transition to M2 macrophages associated with tissue repair and fibrosis. (4) Fibrogenesis: Myofibroblasts arise from fibroblasts under the influence of cytokines like TGF-β, leading to the production of ECM components and the development of fibrotic tissue. (5) ECM Remodeling: The ECM undergoes significant changes, with increased production of proteins such as COL1 < 3, vimentin, and decorin. Matrix metalloproteinases (MMP2, MMP8) are involved in the remodeling process, regulated by factors like HSP60. (6) Implant Encapsulation: The final outcome is the encapsulation of the implant by fibrotic tissue, forming a dense fibrous capsule around the implant due to the accumulation and remodeling of ECM components.

Figure 2

Mechanisms triggering immediate and chronic inflammation in response to silicone mammary implants. (a) Immediate Inflammatory Triggers Post-Implantation: The acute inflammatory response is initiated immediately after silicone mammary implant (SMI) insertion due to tissue damage, skin microbiome contamination, and the introduction of DAMPs and PAMPs. Silicone microparticle shedding, microbial attachment, and protein adsorption on the implant surface further intensify the inflammatory response, with mediators like MCP-1, collagen (COL1/3), and CD44 accumulating in the wound environment. (b) Chronic Inflammatory Triggers and Early-Stage Fibrosis: Months after implantation, persistent inflammation is driven by biofilm formation on the implant surface and the adhesion of proinflammatory and profibrotic factors. Microbial infiltration into fibrotic tissue and extensive ECM remodeling, involving vimentin, decorin, and fibronectin, result in the development of a dense fibrotic capsule.

Figure 3

Bacterial contamination and biofilm development contribute to capsular contracture. Microbial colonization during implant placement begins with the transfer of the skin microbiome to the implant surface through surgical tools and incision, embedding the implant into the lower tissue layers. Microbial Proliferation in the Acute Wound: The patient’s skin microbiome is transferred to the implant surface during surgery, via the scalpel, incision, and implant placement. Reversible Phase: In this early stage, planktonic bacteria adhere to the implant surface and the adhesive proteome through electrostatic and hydrophobic forces. At this point, the bacterial adhesion is reversible, and appropriate interventions can still prevent colonization. Irreversible Phase: As time progresses, bacteria establish a firm attachment to the surface, proliferating and forming a biofilm. The biofilm matrix shields the bacteria from the host’s immune system and antimicrobial treatments, promoting a persistent infection. Capsule Formation and Contracture: The persistent presence of biofilms triggers an ongoing antimicrobial inflammatory reaction, contributing to the development of a fibrous capsule around the implant. This process can result in capsular contracture, where the capsule thickens and tightens, causing complications.

Figure 4

Strategies for Reducing Capsular Contracture in Breast Implant Surgery. Infection Control and Sterilization: Proper sterilization and disinfection of medical instruments are emphasized to prevent pathogen transmission in healthcare settings. Guidelines tailored to the specific use of medical devices and associated infection risks are critical for avoiding severe infections. Antimicrobial Approaches: The effectiveness of preoperative antiseptics, including chlorhexidine gluconate and povidone-iodine, is compared, with a focus on their role in reducing biofilm-related capsular contracture. The use of irrigation solutions such as Triple Antibiotic Solution (TAS), polyhexanide, and hypochlorous acid is also explored for biofilm eradication. Surgical Techniques: Preoperative preparation, including antisepsis methods and hair removal techniques, is combined with intraoperative strategies like the no-touch technique and antimicrobial pocket irrigation to reduce bacterial exposure. The use of sterile devices like Keller funnels and the selection of specific incision types, such as inframammary incisions, are recommended to minimize contamination risks. Postoperative Care: Proper wound management, including keeping the surgical site clean and monitoring for infections, is crucial for preventing complications and ensuring optimal surgical outcomes.