Silicone-reactive disorder...breast implant toxicity

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Silicon and matrix macromolecules: new research opportunities for old diseases from analysis of potential mechanisms of breast implant toxicity

Medical Hypotheses, Volume 51, Issue 1, July 1998, Pages 27-35

A. E. Brawer

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Abstract

An understanding of the normal and essential integration of the element silicon in biosystems, as well as knowledge of its fundamental chemistry, are crucial to understanding its role in health and disease. Modern organosilicon chemistry, based in part on the artificial silicon-carbon bond, coincided with the emergence of the biomaterials and bioengineering fields fifty years ago, and was thought to be a fortunate coincidence according to conventional wisdom that high-molecular-weight polymeric siloxanes were chemically and biologically inert. These concepts have been challenged by reports of silicone migration and degradation following insertion of gel-filled breast implants, claims of a novel systemic illness appearing in many breast implant recipients, and investigations implicating varied and permeating immunotoxic mechanisms of disease causation by breast devices. The present study develops additional potential pathogenetic ideas based on alterations of cell biochemistry by silicon-containing compounds, and offers correlation of the patients' diverse clinical features with plausable disruption of basic biological processes. This in turn raises new questions concerning everyday environmental exposure, has broad implications for multiple other diseases, can provide alternative directions for future investigative research, and may contribute to the ongoing redefinition of immune dysfunction and inflammation.

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Silicone-reactive disorder: A new autoimmune disease caused by immunostimulation and superantigens

Medical Hypotheses, Volume 41, Issue 4, October 1993, Pages 348-352

M. A. Lappe

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Abstract

Over 100 cases of disorders closely resembling classic autoimmune diseases have been reported among patients who were injected or implanted with a diverse group of chemicals including paraffins, vegetable oils or silicone (1–30). Most cases have occurred in silicone breast implant recipients, especially those who received their prostheses 2–10 years prior to onset of symptoms (5, 30). A high proportion of patients exhibit classic signs and symptoms of Sjogren's syndrome or scleroderma (15, 18, 21, 24, 26, 30). Affected patients typically experience some combination of fatigue, myalgia, joint pain, sicca syndrome (dry eyes and mouth), synovitis, rash, alopecia, muscular weakness or lymphadenopathy, and autoantibody formation. Less commonly, patients may have the CREST syndrome (calcinosis, Raynaud's phenomena, eosophageal hypomotility, sclerodactyl and talangiectasias), hypertension, pulmonary fibrosis, or central nervous system pathology.

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Immunotoxicity of silicone: Implications of oxidant balance towards adjuvant activity

Food and Chemical Toxicology, Volume 32, Issue 11, November 1994, Pages 1089-1100

S. H. Yoshida, S. S. Teuber, J. B. German, M. E. Gershwin

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Abstract

A variety of mechanisms can be proposed to explain the potential effects of silicone and silicone by-products on the immune response. In this paper, we discuss information on the chemistry of silicon and silicon gels/elastomers, and the manufacture of silicone breast implants as they pertain to the bioreactivity of silicone. Moreover, with reference to silicone-mediated human adjuvant disease, an overview of experimental adjuvant-induced arthritis is presented; comparisons with graft-versus-host disease and chemically induced autoimmunity then follow. Particular attention is paid to similarities in the characteristics of silicone and classic lipid adjuvants. For example, macrophage activation is presumed to be a central event in silicone-induced autoimmunity. Since those genes uniquely expressed in macrophages activated by plastic adherence are similar to those induced by lipopolysaccharide, adherence to silicone rubber may initiate an inflammatory response by the same mechanism. Macrophage effects would also include the erosion of implants through the generation of oxidants and localized pH changes. The degradation products of silicone are also implicated in the adjuvant effects of silicone implants. There is evidence to suggest that oxidants produced by inflammatory cells preferentially inactivate CD8+ suppressor T cells. This could then lead to an inflammatory state, perhaps through oxidant-induced transcription factors such as NF-kB, resulting in a long-term pro-oxidant imbalance that manifests itself as a breakdown in immunological self-tolerance. The authors hypothesize that autoreactivity following oxidant stress evolved to enhance inflammatory repair mechanisms after tissue, cell or molecular damage by oxidants.

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