INFLAMMATORY INTERMEDIATES PRODUCED BY TISSUES ENCASING SILICONE BREAST PROSTHESES

Silicone prostheses, when implanted within the soft tissues of the bre ast, evoke an inflammatory reaction. In response to silicone exposure, inflammatory mediator production by individual cells has been observe d in various experimental studies. in this study, inflammatory mediato r production by periprosthetic tissues (whole organ) was measured. The mediator levels were correlated with both the tissue histopathology o f the periprosthetic capsules and the clinical symptorns noted by each patient. Tissue surrounding breast implants removed at surgery from t en 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 a nd (b) knee synovium from seven orthopedic surgery patients with arthr itis undergoing primary joint arthroplasty were similarly cultured. Th e mediators [interleukin-2 (IL2), tumor necrosis factor-alpha (TNF-alp ha), interleukin-6 (IL-6), and prostaglandin E2 (PGE(2))] liberated in to the culture media were measured by an enzyme linked immunosorbent a ssay. When compared to controls, the mediator levels of IL-6 and TNF-a lpha were substantially greater, although IL2 and PGE(2) were lower. L evels 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 PGE(2) from 100 to 10,000. The correlation between TNF-alpha and PGE(2) levels was .5 between IL-6 and PGE(2) wa s .6, and between IL6 and TNF-alpha was .77 The correlation between TN F-alpha and IL-6 was statistically significant at a p-value less than .01. Elevated levels of TNF-a production were associated with an incre ased number of macrophages and overall tissue cellularity (p < .05). N o significant relationship was observed between mediator production an d clinical symptoms. We conclude that overall cellularity specifically macrophages, in the periprosthetic capsule may lead to TNF-alpha prod uction but that cytokine production by periprosthetic tissues alone is not a predictor of clinical symptomatology in patients with silicone breast prostheses.