Aside from the morphologic features of the fibrous capsule that surrounds silicone gel breast implants, knowledge about the nature of the inflammatory response is scant. In addition to a band of dense fibrous tissue, the implant capsule includes a variable number of inflammatory cells [9
]. Neutrophils are usually the first cells to arrive to the inflammatory process, digesting destroyed tissue. Monocytes, which are also identified, have phagocytic properties, becoming macrophages after engulfing any foreign substance. However, if the size of the particle to be eliminated is great, monocytes coalesce to form multinucleated giant cells. In addition to neutrophils and monocytes/macrophages, T and B lymphocytes are identified early. B cells are involved in the humoral response by producing circulating antibodies when they differentiate to plasma cells. T cells are involved in the cellular immunity. Nevertheless, the relationship between B and T lymphocytes, as well as the different proportions of T cell subtypes, has been infrequently reported in capsular implants.
Most of previously published studies, in which an immunophenotype for inflammatory cells in the capsular implants or fluid taken from the space between the implants and the surrounding fibrous capsule were determined, showed a predominance of T cells over B cells [2
]. Our findings are in agreement with those previous reports since the majority of inflammatory cells present in the implant capsule were T cells with a similar proportion for helper and cytotoxic subtypes. Thus, our findings support the hypothesis that silicone may induce a strong local T cell immune response. Even though the number of smooth-surfaced implants in our study was limited, they showed a lower tendency to elicit an inflammatory response. This finding would have to be confirmed by future studies. On the other hand, a variety of immunologic diseases (e.g., rheumatic diseases, including chronic rheumatoid arthritis, systemic lupus erythematosus, and Sjogren's syndrome, and the recently identified ALK-negative anaplastic large cell lymphoma) has been reported in association with breast implants [11
]. Of particular interest is the latter due to its clinical implications.
Primary lymphoma of the breast usually accounts for less than 1 % of all non-Hodgkin's lymphomas, and between 0.4 and 1 % of malignant breast neoplasms [13
]. Epidemiologic studies assessing the risk of non-Hodgkin's lymphoma in women with breast implants found no association between breast implants and an increased risk of non-Hodgkin's lymphoma [14
]. However, in 1997, Keech and Crech described a case of anaplastic large cell lymphoma negative for anaplastic lymphoma kinase-1 (ALCL-ALK1 negative) associated with a breast implant. Since this first report, 35 cases of ALCL in women with breast implants have been documented worldwide, turning it in a rare but emerging entity [16
Similar to other lymphomas reported in association with breast implants, ALCL shows, with rare exceptions, a T cell phenotype. In the present study, we documented a predominance of T cells when the inflammatory cells were present in the breast implant capsule. This predominance lead us to believe that there might exist conditions related to either the capsular component of implants or to the content of implants that could facilitate the proliferation of T cells over B cells. On the other hand, reported ALCL cases related to implants, for which a reference to the type of implants exists, have always been of textured surface. It is worth noting that even though the number of smooth surface implants in our study was limited, a T cell predominance tendency, as those seen in textured-type implants, was not observed. This fact backs up the hypothesis about smooth surfaced implants being less selective for T cells. Although the relationship between implants and these diseases is still unclear, a broader study is needed to confirm the present findings and determine its relationship with these diseases.
In summary, capsular contracture was associated with implant profile (low vs. high) but no with implant type (smooth vs. textured) or location (subglandular vs. submuscular). We also found evidence of inflammation in 92.5 % of all implant capsules, with a statistically significant higher proportion in textured breast implants. T cells predominated over B cells. Textured implants elicited a more marked response to T cells than smooth implants, with a similar proportion of helper and cytotoxic T cells. Textured implants showed statistically significant higher percentages of CD3 positive cells than smooth implants. Percentages of CD20 positive cells were similar in textured and smooth implants. These results suggest that the silicone present in breast implants might induce a strong local T cell immune response. Our findings could shed some light to understand the association of silicone breast implants and some cases of anaplastic large cell lymphomas.