Inflammatory intermediates produced by tissues encasing silicone breast prostheses.
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. When compared 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.
Mena
E A
EA
Department of Pathology and Laboratory Medicine, School of Medicine, University of California, Los Angeles 90024-1732, USA.
Kossovsky
N
N
Chu
C
C
Hu
C
C
D000328:Adult; D018427:Breast Implants / Q000009:adverse effects*; D015232:Dinoprostone / Q000096:biosynthesis; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D007376:Interleukin-2 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008875:Middle Aged; D012828:Silicones / Q000009:adverse effects*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D018836:Inflammation Mediators; D007376:Interleukin-2; D015850:Interleukin-6; D012828:Silicones; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone