silicon and Fibrosis

Dear Editor, Silicone is a hydrophobic polymer containing silicon. Silicon is an essential compound of soft tissue proteoglycans. Reports about morphea and other autoimmune connective tissue disorders in association with silicone implants have stimulated the discussion of a possible link between the two, such as immunological cross-reactivity of silicone and connective tissue components (1). A number of case reports suggested a possible link to adjuvant autoimmune syndrome (2), morphea of the breast (3-5), and systemic scleroderma (6-8), among others. One study measured tissue silicon levels in women with silicone breast implants with and without symptoms or signs and compared these data with women who had either a saline breast implant or no augmentation at all. The authors detected higher levels of silicon in capsular tissue of patients with silicone implants, independent of the presence of any symptoms or signs (9,10). The conclusion was that there is no evidence of an association between silicone implants and autoimmune connective tissue disorders. Three other clinical trials investigating the role of silicone implants and induction of autoimmune connective tissue disorders also failed to find an association between the two (11-13). We report the case of a 32-year-old female patient who developed morphea of the breasts after silicone implants for augmentation after risk-reducing mastectomy for Cowden syndrome. She presented with pronounced capsule fibrosis of the implants. With a delay of several years, an ill-defined slightly hyperpigmented area developed on the breasts and ventral chest (Figure 1). The lesion was analyzed by dermoscopy (Figure 2), which found mild erythema, reduced vessels, and white areas (ill-defined dull white globules, fibrotic beams). A skin biopsy was taken. Histopathological analysis showed a normal epidermal layer, minor papillary edema, and some vascular ectasias in the papillary dermis and upper corium (Figure 3). There was mild perivascular inflammatory infiltrate of the deep dermal vascular plexus, composed of lymphocytes and monocytes with some plasma cells (Figure 4). Elastic fibers seemed unaffected (Figure 5). The diagnosis of an early morphea of the edematous-inflammatory stage was established. Treatment with topical corticosteroids and UVB-311 nm irradiation was recommended. Morphea of the breasts is an uncommon disorder. It may occur after radiotherapy of breast cancer, after silicone augmentation, or without any

Topics: Adult; Autoimmune Diseases; Breast Neoplasms; Female; Fibrosis; Humans; Mastectomy; Scleroderma, Localized; Silicon; Silicones

Topics: Aging; Animals; Anti-Inflammatory Agents; Arthritis; Autoimmune Diseases; Blood Coagulation; Bone and Bones; Cartilage; Chemical Phenomena; Chemistry, Physical; Connective Tissue; Embryonic and Fetal Development; Exudates and Transudates; Fibronectins; Fibrosis; Gene Expression Regulation; Glycosaminoglycans; Humans; Inflammation; Macrophages; Molecular Structure; Organ Specificity; Proteoglycans; Silicon; Wound Healing

Over the past decade, various implantable devices have been developed to treat diseases that were previously difficult to manage such diabetes, chronic pain, and neurodegenerative disorders. However, translation of these novel technologies into clinical practice is often difficult because fibrotic encapsulation and/or rejection impairs device function after body implantation. Ideally, cells of the host tissue should perceive the surface of the implant being similar to the normal extracellular matrix. Here, we developed an innovative approach to provide implant surfaces with adhesive protein micropatterns. The patterns were designed to promote adhesion of fibroblasts and macrophages by simultaneously suppressing fibrogenic activation of both cell types. In a rat model, subcutaneously implanted silicone pads provided with the novel micropatterns caused 6-fold lower formation of inflammatory giant cells compared with clinical grade, uncoated, or collagen-coated silicone implants. We further show that micropatterning of implants resulted in 2-3-fold reduced numbers of pro-fibrotic myofibroblast by inhibiting their mechanical activation. Our novel approach allows controlled cell attachment to implant surfaces, representing a critical advance for enhanced biointegration of implantable medical devices.

Topics: Animals; Equipment Failure Analysis; Fibrosis; Male; Prostheses and Implants; Prosthesis Design; Rats; Rats, Wistar; Silicon; Surface Properties

Myocardial infarction (MI), commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia, which is an increasing problem in terms of morbidity, mortality and healthcare costs worldwide. Along with the idea to develop nanocarriers that efficiently deliver therapeutic agents to target the heart, in this study, we aimed to test the in vivo biocompatibility of different sizes of thermally hydrocarbonized porous silicon (THCPSi) microparticles and thermally oxidized porous silicon (TOPSi) micro and nanoparticles in the heart tissue. Despite the absence or low cytotoxicity, both particle types showed good in vivo biocompatibility, with no influence on hematological parameters and no considerable changes in cardiac function before and after MI. The local injection of THCPSi microparticles into the myocardium led to significant higher activation of inflammatory cytokine and fibrosis promoting genes compared to TOPSi micro and nanoparticles; however, both particles showed no significant effect on myocardial fibrosis at one week post-injection. Our results suggest that THCPSi and TOPSi micro and nanoparticles could be applied for cardiac delivery of therapeutic agents in the future, and the PSi biomaterials might serve as a promising platform for the specific treatment of heart diseases.

Topics: Animals; Biocompatible Materials; Cells, Cultured; Drug Carriers; Drug Delivery Systems; Fibrosis; Gene Expression Regulation; Inflammation; Male; Myocardial Infarction; Myocardium; Myocytes, Cardiac; Porosity; Rats; Rats, Sprague-Dawley; Silicon

Capsular fibrosis is one of the most severe complications that can occur in connection with silicone breast implants. Should this case arise, a periprosthetic deposition of fibroid tissue may evolve. Transforming growth factor (TGF)-beta is one of the most important mediators in relation to such processes.. The chinazolinone derivative halofuginone is a type I collagen synthesis inhibitor that interferes with the TGF-beta signaling pathway. The work at hand examines the local antifibrotic effectiveness of halofuginone lactate, which has been biotechnologically bound to the silicone implant's surface. The experiments in relation to this were conducted in vivo on two groups of seven Sprague-Dawley rats. Group I received untreated silicone implants, and group II received halofuginone-coated silicone implants.. Submusculary embedded halofuginone-coated silicone implants have shown no systemic side effects. The histologic and immunohistologic examinations of the periprostatic capsules revealed a significant decrease of CD68 histiocytes, TGF-beta, fibroblasts, collagen type I and type III, and capsular thickness after a 3-month period.. The results confirmed a decrease in foreign body responses to halofuginone surface-modified silicone implants and mark their potential for obtaining a lessened capsular fibrosis by way of a local antifibrotic effect.

Topics: Animals; Breast Implants; Coated Materials, Biocompatible; Collagen Type I; Disease Models, Animal; Female; Fibrosis; Foreign-Body Reaction; Mammary Glands, Animal; Piperidines; Protein Synthesis Inhibitors; Quinazolinones; Rats; Rats, Sprague-Dawley; Silicon; Treatment Outcome

A novel immunoassays for screening of disease markers in human serum are presented by miniaturizing interdigitated array (IDA) of microelectrodes via micro electro-mechanical system (MEMS) on a silicon chip for multi-channel electrochemical measurement. Different selected antibodies (Abs) are incorporated site-specifically into the electrochemically deposited polypyrrole (PPy) formed on the IDA of the silicon chip, which was characterized by fluorescence microscope photo and the electrochemical quartz crystal microbalance (EQCM) measurements. The selective recognition of Ab to the corresponding antigen (Ag) is monitored through the measurable conductivity change, which is directly visualized by cyclic voltammograms (CVs) in presence of the redox probe, Fe (CN)6(3-/4-). By using the strategy presented here, three liver fibrosis markers, hyaluronic acid (HA), lamin (LN) and collagen type IV (IV-C), are detected simultaneously and specifically at the surface of the chip with calibration curves, y = 21.75 + 0.84x (R = 0.995), y = 57.54 + 0.47x (R = 0.999) and y = 37.92 + 0.28x (R = 0.999), separately. Either the standard or the serum samples can be detected at ng/mL concentration level in a tiny amount of volume, approximately 50 microL. The chip-based immunoassay shows the advantages of high sensitivity, good specificity, high throughput, low sample consumption, and the stability offered via batch production by MEMS as well, which is expected to benefit the multi-target screening of desired clinical analytes.

Topics: Biomarkers; Blood Chemical Analysis; Blood Proteins; Electrochemistry; Equipment Design; Equipment Failure Analysis; Fibrosis; Humans; Immunoassay; Microelectrodes; Miniaturization; Protein Array Analysis; Silicon