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The silicone surface and its associated biofilm matrix represent a critical therapeutic target in the prevention and treatment of medical device-related infections. Silicone is a widely used polymer in implants such as breast prostheses, catheters, and heart valves, but it is highly susceptible to microbial colonization. Once microbes adhere to the silicone surface, they secrete an extracellular polymeric substance (EPS) composed of polysaccharides, proteins, and extracellular DNA (eDNA) [Donlan, R. M. (2001). Biofilms and Device-Associated Infections. Emerging Infectious Diseases]. This matrix acts as a physical and chemical barrier, protecting the embedded microbes from the host immune system and increasing their resistance to systemic antibiotics by up to 1,000-fold [Stewart, P. S., & Costerton, J. W. (2001). Antibiotic resistance of bacteria in biofilms. The Lancet]. The presence of biofilms on silicone implants is linked to chronic inflammation and complications such as capsular contracture in breast implants [Ajdic, D., et al. (2016). Analysis of the Microbiome on Implants and in Explant Capsular Tissue. Aesthetic Surgery Journal]. Therapeutic strategies focus on modifying the silicone surface with hydrophilic or antimicrobial coatings to prevent initial attachment. Additionally, agents like Dispersin B or DNase I are being investigated to enzymatically degrade the matrix components, thereby exposing the microbes to conventional antibiotics. Targeting the biofilm matrix is essential for reducing the high failure rates and surgical revisions associated with infected medical devices.
Inhibition of microbial adhesion to the silicone surface, enzymatic degradation of the extracellular polymeric substance (EPS) matrix, and penetration of the protective barrier to deliver antimicrobial agents to sessile cells.
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