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LETTER TO THE EDITOR

The Breast Journal, Volume 6, Number 4, 2000 276–277 To the Editor: There have been many reports in the literature citing observations of macrophages, giant cells, vacuole formation, calcification, and necrotic adipocytes surrounding silicone gel-filled breast implants. In a previous study we observed that the morphology of vacuoles surrounding these implants was similar to that of fat necrosis of the breast (1). This led us to question the relationship between the presence of silicone gel-filled implants and fat tissue necrosis. In a recent study we compared the vacuoles observed in patients with silicone gel-filled implants to those observed in patients undergoing reduction mammoplasty. Our results suggest that the vacuoles seen in tissues from both sets of patients were similar in their morphologies and diameter distributions. In addition, the distribution of diameters for vacuoles was different than that of adipocytes based on mathematical analysis. These observations suggest that the pathogenesis of fat necrosis as a result of mammary reduction surgery may be similar to the pathogenesis of the inflammatory response seen in capsular tissue surrounding silicone gelfilled implants. Fat necrosis appears in part to be a consequence of mechanical (2) and enzymatic injury (3) to fat tissues at various sites in the body. In mechanical injury, excessive pressure may occur when breast implants are placed in a small tissue pocket (4). This could cut the blood supply to the surrounding adipose tissue. Smaller fill volumes and greater leakage rates seen in saline-filled implants may account for the decreased complications of these implants when compared to silicone gel-filled implants (5). Enzymatic injury to fat tissue has been reported to occur in pancreatitis as a result of the systemic release of lipases, resulting in fat cell necrosis at distal locations (3). Systemic release of lipases has been implicated in fat necrosis and arthritic changes to synovial structures (6). Similarities between morphologies of synovial tissues and capsules surrounding silicone-gel filled breast implants suggest that changes to these structures may occur by similar mechanisms (7). Fat necrosis appears to be a complication associated with the use of other polymers in addition to silicone gel-filled implants. Histologic reports of inflammatory responses seen with polyurethane, polyester, polypropylene, and other implant materials when implanted in the breast, show evidence of vacuoles surrounding these devices that are characteristic of fat necrosis (8). Therefore other polymeric materials besides silicone gel-filled implants appear to be able to induce fat necrosis. The purpose of this letter is to suggest that pressure induced by contact between an implant and fat tissue can lead to a subsequent inflammatory response due to fat tissue necrosis. The formation of vacuoles, release of macrophagic lipases, deposition of repair tissue, and subsequent calcification may all be attributable to fat cell necrosis. Although silicone gel-filled implants have received a great deal of attention, it is important to point out that any implant in contact with fat tissue may have the same adverse effects.