Talc deposition in skin and tissues surrounding silicone gel-containing prosthetic devices

Periprosthetic capsule formation is the most common cause of morbidity associated with silicone gel-filled breast implants. All implant recipients develop capsules. However, the extent of capsule formation varies greatly among patients, ranging from a thin flexible membrane to a constrictive inelastic band of sclerotic collagen. Although silicone gel bleed has been proposed as the most likely cause of excessive capsular sclerosis, liquid silicone did not induce fibrosis in early clinical trials. Because many implant modifications have been introduced since the original studies were performed, a more plausible explanation for excess capsular sclerosis is the inadvertent introduction of a fibrogenic contaminant. The skin and periprosthetic tissues removed from 41 women during implant revision surgery were examined for the presence of foreign substances that might contribute to capsular sclerosis. Tissue was examined histologically with and without polarizing filters and with scanning electron microscopy equipped for energy-dispersive x-ray analysis.

A high incidence of talc was found within the skin and tissues adjacent to silicone-containing breast prostheses. Birefringent talc crystals, identified in 71% of the patients, were observed within nodular granulomas and perivascular histiocytes. Two specimens containing talc crystals were analyzed by energy-dispersive roentgenographic analysis, which confirmed the identity of the crystalline material as talc. Among 10 capsules examined by direct immunofluorescence, there was no evidence of immune complex deposition.

The high incidence of talc deposition in the skin and tissues surrounding silicone implants suggests that talc either is introduced at the time of implant surgery (possibly in association with the silicone elastomer bag, tissue sizers, or surgical gloves) or is released into the tissues as a silicone gel contaminant during gel bleed. Talc, a known sclerosing agent, may contribute to periprosthetic fibrosclerosis.