LOCAL INCREASE IN HYALURONIC ACID AND INTERLEUKIN-2 IN THE CAPSULES SURROUNDING SILICONE BREAST IMPLANTS
Wells AF; Daniels S; Gunasekaran S; Wells KE
Address: Dept. Internal Medicine, U. of South Florida, College Medicine,
Tampa, FL. Source: Ann Plast Surg,
1994 Jul, 33:1, 1-5
Abstract: Connective tissue disease-like illness has been
associated with silicone breast implants. However, no data are currently available on the immunopathology of the capsule surrounding
the breast implants. Sera from women with breast implants were collected and assayed for interleukin-6 (IL-6), IL-2, and hyaluronic
acid. Capsular biopsies were stained with a probe for HYA or with monoclonal antibodies specific for human macrophages (CD68),
T cells (CD4), IL-6, and IL-2. Control specimens consisted of breast biopsies from women undergoing reduction mammoplasty.
Our results revealed an increased local amount of hyaluronic acid in the capsule of patients with breast implants
compared with control breast tissue. The HYA was localized extracellularly in areas containing fibrosis and cellular infiltrates.
The infiltrating cells were determined to be primarily macrophages and T cells. No IL-6 was localized in any of the tissue
sections. In contrast, large amounts of IL-2 were found in regions of infiltrating lymphocytes. No significant increase in
IL-6, IL-2, or hyaluronic acid was found in the sera. The role of hyaluronic acid and cytokines in the inflammatory response
in the capsules of silicone breast implants is discussed.
PHYSIOLOGIC AND PATHOLOGIC PATTERNS OF REACTION TO SILICONE
Author: Friemann J; Bauer M; Golz B; Rombeck N; Hhr D; Erbs G; Steinau HU; Olbrisch RR
fur Umweltpathologie des Medizinischen Instituts fur Umwelthygiene,
Heinrich-Heine-Universitat Dusseldorf. Source: Zentralbl
Chir, 1997, 122:7, 551-64
Abstract: Local morphological reaction patterns on breast implants can be of high significance
as possible starting point for controversely discussed systemic immune response triggered by silicon or silicone. Therefore,
the collagenous capsules of 149 explanted mammoplasty prostheses were examined macroscopically, under a scanning electron
microscope and light- microscopically using antibodies to the macrophage antigen CD68, vimentin, muscle actin, and the proliferation
antigen MIB1, and were then correlated with anamnestic data (implanted type of prosthesis, indication for im- or explantation).
According to our examinations, the in-vivo durability of the prostheses' shells is considerably decreasing with the expansion
of their surfaces.
Regardless of the type of the prostheses' surface regularly a chronic- proliferating inflammation
pattern could be identified in the periprosthetic capsulectomy specimens starting with a synovial metaplasia of proliferating
CD-68-negative and vimentin- positive mesenchymal cells in the area surrounding the implants and ending by its transformation
into a stage of dense hyaline collagenous fibrous tissue after an advanced implantation period ( 2 years).
the texturing of the prosthesis surface modifies only the course, but not the quality of the chronically fibrosing inflammation.
Bleeding of prosthesis as well as the incorporation of the polyurethane- foam coating of different prosthesis types into the
periprosthetic breast capsule lead to a significant lymphoplasmacytic infiltration, partly with participation of local vessels
as defined in a "silicone vasculitis".
Morphological signs of an at least local immune response are detectable
in 8.3% of the examined fibrotic capsules even without a morphologically identifiable foreign-body embedding. They can be
possibly referred to-as well as the complete absence of hyaline collagenous fibrous tissue in 30% of the cases-a yet not causally
clarified, inter-individually different susceptibility of the implant bearers. Only the systematic registration of the above-mentioned
morphological reaction patterns in a "prosthesis-passport" together with the additional clinical observation of
the patients can ensure in future the realistic estimation of potential health risks caused by silicone breast implants.
INFLAMMATORY INTERMEDIATES PRODUCED BY TISSUES ENCASING SILICONE BREAST PROTHESES
Author: Mena EA; Kossovsky
N; Chu C; Hu C
Address: Department of Pathology and Laboratory Medicine, School of Medicine,
University of California,
Los Angeles 90024-1732, USA.
Source: J Invest Surg, 1995 Jan, 8:1, 31-42
Abstract: Silicone prostheses, when
implanted within the soft tissues of the breast, evoke an inflammatory reaction.
In response to silicone exposure,
inflammatory mediator production by individual cells has been observed in various experimental studies. In this study, inflammatory
mediator production by periprosthetic tissues (whole organ) was measured.
The mediator levels were correlated with
both the tissue histopathology of the periprosthetic capsules and the clinical symptoms noted by each patient. Tissue surrounding
breast implants removed at surgery from ten women (average age and implant duration 40 and 7 years respectively) was cultured
in vitro for 24 hours. Control tissues consisting of (a) augmentation mammaplasty skin scars from eight additional patients
and (b) knee synovium from seven orthopedic surgery patients with arthritis undergoing primary joint arthroplasty were similarly
cultured. The mediators [interleukin-2 (IL-2), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and prostaglandin
E2 (PGE2)] liberated into the culture media were measured by an enzyme linked immunosorbent assay.
to controls, the mediator levels of IL-6 and TNF-alpha were substantially greater, although IL-2 and PGE2 were lower. Levels
varied greatly from patient to patient: in pg/ml per 10 g tissue, IL-2 ranged from 10 to over 1,000; TNF-alpha from 100 to
1,000; IL-6 from 100 to 1,000,000; and PGE2 from 100 to 10,000. The correlation between TNF-alpha and PGE2 levels was .5 between
IL-6 and PGE2 was .6, and between IL-6 and TNF-alpha was .77.
The correlation between TNF-alpha and IL-6 was statistically
significant at a p-value less than .01.
Elevated levels of TNF-alpha production were associated with an increased
number of macrophages and overall tissue cellularity (p .05). No significant relationship was observed between mediator production
and clinical symptoms.
We conclude that overall cellularity, specifically macrophages, in the periprosthetic capsule
may lead to TNF-alpha production but that cytokine production by periprosthetic tissues alone is not a predictor of clinical
symptomatology in patients with silicone breast prostheses