SMI-Capsular Fibrosis and Biofilm Dynamics: Molecular Mechanisms, Clinical Implications, and Antimicrobial Approaches
Abstract
:1. Introduction
1.1. Foundations of Wound Healing: Implications for Health and Recovery
1.2. Wound Healing Dynamics, Microbial Biofilms, and Fibrotic Responses in Silicone Mammary Implants
2. From Wound to Peri-SMI Capsular Fibrosis
2.1. Immediate Inflammatory Response and Early Fibrosis
2.1.1. Acute Inflammatory Response
2.1.2. Early Fibrotic Changes
2.1.3. Molecular Signaling Pathways
2.2. Chronic Inflammation and Capsular Contracture
2.2.1. Chronic Inflammatory Response
2.2.2. Capsular Contracture Formation
2.2.3. Chronic Inflammatory Pathways in Sustained Fibroblast Activation and Fibrosis
2.2.4. Immune Cell Interactions
2.2.5. S100 Proteins on Inflammation and Fibrosis
2.3. Immediate and Chronic Inflammatory Triggers Following SMI Insertion
2.3.1. Immediate Post-Implantation Response
2.3.2. Early-Stage Fibrosis (Months Post-Implantation)
2.4. Influence of Surface Characteristics on Inflammation and Fibrotic Pathways
2.4.1. Surface Texture and Inflammation
2.4.2. Surface Characteristics and Cellular Responses
3. Microbial Adhesion, Colonization, and Biofilm Formation on SMI
3.1. Microbial Transmission and Surface Adhesion
3.2. Colonization and Biofilm Formation
4. Reducing Capsular Contracture: Antimicrobial Strategies in Breast Implant Surgery
4.1. Antimicrobial Approaches to Mitigate Postoperative Infections and Biofilm Formation
4.2. Surgical Techniques for Minimizing Bacterial Contamination
4.3. Translating Preclinical Findings to Clinical Applications
5. Advances in Implant-Shell-Material and Non-Pharmacological Strategies to Prevent Biofilm-Associated Fibrosis
5.1. Surface Characteristics and Their Influence on Biofilm Dynamics
5.1.1. Surface Modification
5.1.2. Polyurethan Coatings
5.2. Advances in Coating Technologies to Prevent Bacterial Adhesion
5.2.1. Antiadhesive Coatings
5.2.2. Nanoparticles
5.2.3. Biomimetic Coatings
6. Pharmacological Strategies to Prevent Biofilm-Associated Fibrosis in Implants
6.1. Antibacterial Drugs
6.1.1. Systemic Antibacterials
6.1.2. Topical Antibacterials
6.1.3. Drug Incorporation into Implants
6.2. Antifibrotic and Anti-Inflammatory Drugs
6.2.1. Pirfenidone
6.2.2. Halofuginone
6.2.3. Dexamethasone
6.3. Integration of Antimicrobial Strategies
6.4. Long-Term Effects of Antimicrobial Strategies in Implant Surgery
7. Clinical Implications and Future Directions
8. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Biological Mechanisms | Wound Healing Dynamics | Fibrotic Responses in SMI |
---|---|---|
Pathophysiological Process | Restoration of tissue integrity and function through hemostasis, inflammation, proliferation, and remodeling. | Formation of a fibrous capsule around implants due to inflammatory response and biofilm formation. |
Initial Response | Hemostasis: Constriction of blood vessels, platelet activation, clot formation to prevent blood loss and provide a scaffold for healing. | Immediate Immune Response: Activation of innate immune system, recruitment of immune cells (neutrophils, macrophages) due to microbial contamination and protein adsorption. |
Molecular Components | Platelets, Fibrinogen, Fibrin: Form a clot that acts as a barrier and temporary scaffold. | Microorganisms, Proteins: Microbial biofilm formation on the implant surface, leading to persistent immune stimulation. |
Inflammatory Phase | Neutrophils and Macrophages: Clear debris, combat infection, release cytokines and MMPs to modulate the inflammatory response. | Chronic Inflammation: Persistent inflammation due to biofilm, leading to prolonged immune response and ongoing ECM remodeling. |
Proliferation Phase | Fibroblast Proliferation, ECM Deposition, Angiogenesis, Epithelialization: Formation of new tissue, collagen production, and blood vessel formation. | Fibrous Capsule Formation: Collagen and ECM deposition around the implant, leading to capsule formation. |
Remodeling Phase | Collagen Realignment, Cross-Linking, Continual ECM Remodeling: Strengthening of new tissue and refinement of the wound architecture. | Capsular Contracture: Excessive collagen deposition and ECM remodeling leading to a contracted and thickened fibrous capsule. |
Impact on Healing | Prevention of Infection, Scar Formation: Effective healing reduces infection risk, minimizes scar formation, and restores tissue function. | Infection Risk: Biofilms create a persistent infection risk that complicates healing and exacerbates fibrosis. |
Category | Strategy | Mechanism | Key Points |
---|---|---|---|
Physical Modifications with Antimicrobial Properties | Polyurethane Foam Coatings | Surface modification to disrupt fibrotic tissue formation | Initial reduction in fibrotic capsule formation, concerns over toxicity from degradation products [168,169,170,171,172]. |
Surface Topography | Rough surfaces increase biofilm formation | Rougher surfaces (Ra 60 µm) enhance bacterial adhesion and biofilm maturity, leading to infections and capsular contracture [45,47,105,174]. | |
Biological Matrices with Antimicrobial Properties | Antibiotic- Impregnated Meshes | Localized antibiotic delivery to reduce biofilm formation | Promising in reducing bacterial colonization and biofilm formation with sustained antimicrobial activity [175,176,177,178]. |
Spider Silk- Based Meshes | Inhibits bacterial adhesion and fibrotic tissue formation | Biocompatible, reduces fibroblast proliferation and collagen deposition [179,180,181,182,183,184,185]. | |
Zwitterionic Polymers | Superior hydrophilicity, preventing protein adsorption and microbial adhesion | Resistant to microbial colonization, preventing foreign body response and fibrotic capsules [186,187,188,189,190]. | |
Pharmacological Strategies | Systemic Antibacterials (Cefazolin, Gentamicin) | Prophylactic antibiotics to prevent infections before and during surgery | Effective against Gram-positive and Gram-negative bacteria in breast implant surgeries [191,192]. |
Topical Antibacterials (Bacitracin, Chlorhexidine) | Direct application to reduce bacterial load and biofilm formation | Applied during surgery to prevent contamination and infection [191,193,194,195]. | |
Drug Incorporation into Implants (Rifampin) | Localized, sustained antimicrobial effect from drug-coated implant surfaces | Reduces bacterial colonization and biofilm formation directly at the implant site [196]. | |
Antifibrotic and Anti-inflammatory Drugs | Pirfenidone | Reduces inflammation and fibroblast activity | Shown to reduce capsule thickness in preclinical models, potential use in biofilm-associated fibrosis [197,198,199,200]. |
Halofuginone | Inhibits collagen synthesis and T helper 17 cell differentiation | Reduces fibrosis and capsule formation around implants, promising antifibrotic properties [201,202,203,204]. | |
Dexamethasone | Reduces inflammation and collagen production by modulating cytokine activity | Decreases fibrous tissue formation and inflammation, improving implant surgery outcomes [193,206,207]. | |
Integration of Antimicrobial and Antifibrotic Strategies | Combined Approaches | Use of both antimicrobial and antifibrotic strategies to prevent biofilm formation and fibrosis | Combining antibiotics with local antiseptic irrigation and antifibrotic agents enhances efficacy in preventing biofilm-associated fibrosis. |
Clinical Aspect | Challenges | Current Strategies | Future Directions |
---|---|---|---|
Biofilm Formation on SMIs | Persistent biofilms protect bacteria from immune responses and antimicrobials, leading to chronic inflammation and fibrosis. | Antimicrobial prophylaxis, antimicrobial coatings, and advanced material surfaces designed to reduce biofilm formation. | Develop targeted antimicrobial strategies that penetrate biofilms. Biomimetic materials that release antimicrobials in response to biofilm formation. |
Chronic Inflammation and Fibrosis | Biofilm matrix limits immune cell infiltration and antimicrobial effectiveness, leading to thick fibrous capsules. | Anti-inflammatory and antifibrotic agents (pirfenidone, halofuginone, dexamethasone) to reduce fibrosis. | Incorporate anti-inflammatory and antifibrotic agents into implant materials. Personalized treatment approaches based on patient immune responses. |
Antimicrobial Resistance | Resistance to traditional antimicrobial treatments is rising, making it difficult to manage biofilm infections. | Preoperative prophylaxis with systemic antibiotics; antimicrobial materials such as antibiotic-impregnated meshes. | Novel drug delivery systems (e.g., nanoparticles or localized reservoirs) that enhance antimicrobial efficacy and overcome resistance. |
Advanced Materials | Existing materials may not fully prevent microbial adhesion or fibrosis. | Antibiotic-impregnated and spider silk-based meshes, zwitterionic polymers. | Development of smart materials that dynamically respond to microbial threats, change surface properties, or release antimicrobials. |
Clinical Guidelines and Practice | Variability in practices and lack of standardized guidelines lead to inconsistent management of biofilm complications. | General antimicrobial prophylaxis and surface modifications for reducing biofilm risk. | Standardized clinical guidelines for antimicrobial prophylaxis, coatings, and antifibrotic treatments across clinical settings. |
Personalized Medicine | Generalized treatments may not consider individual patient factors, leading to suboptimal outcomes. | Uniform antibiotic and antifibrotic regimens based on general risk profiles. | Personalized treatments tailored to patient-specific factors (microbial flora, immune responses, genetic predisposition). |
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Schoberleitner, I.; Lackner, M.; Coraça-Huber, D.C.; Augustin, A.; Imsirovic, A.; Sigl, S.; Wolfram, D. SMI-Capsular Fibrosis and Biofilm Dynamics: Molecular Mechanisms, Clinical Implications, and Antimicrobial Approaches. Int. J. Mol. Sci. 2024, 25, 11675. https://doi.org/10.3390/ijms252111675
Schoberleitner I, Lackner M, Coraça-Huber DC, Augustin A, Imsirovic A, Sigl S, Wolfram D. SMI-Capsular Fibrosis and Biofilm Dynamics: Molecular Mechanisms, Clinical Implications, and Antimicrobial Approaches. International Journal of Molecular Sciences. 2024; 25(21):11675. https://doi.org/10.3390/ijms252111675
Chicago/Turabian StyleSchoberleitner, Ines, Michaela Lackner, Débora C. Coraça-Huber, Angela Augustin, Anja Imsirovic, Stephan Sigl, and Dolores Wolfram. 2024. "SMI-Capsular Fibrosis and Biofilm Dynamics: Molecular Mechanisms, Clinical Implications, and Antimicrobial Approaches" International Journal of Molecular Sciences 25, no. 21: 11675. https://doi.org/10.3390/ijms252111675
APA StyleSchoberleitner, I., Lackner, M., Coraça-Huber, D. C., Augustin, A., Imsirovic, A., Sigl, S., & Wolfram, D. (2024). SMI-Capsular Fibrosis and Biofilm Dynamics: Molecular Mechanisms, Clinical Implications, and Antimicrobial Approaches. International Journal of Molecular Sciences, 25(21), 11675. https://doi.org/10.3390/ijms252111675