59. Characterization of the Differences in Cellular Response yo Silicone Particles in Smooth and Textured Breast Implant Capsules

PURPOSE: Fibrous encapsulation of breast implants following placement is typically a benign process. However, deposition of silicone particles within the capsule induces chronic inflammation that leads to capsular contracture and is hypothesized to stimulate other breast implant capsule pathologies such as breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) and primary squamous cell carcinoma. Textured breast implants have a lower incidence of capsular contracture compared to smooth devices, but are linked to ALCL. While both smooth and textured breast implants can bleed small silicone particles into the capsule, textured implants may also shed larger surface silicone fragments into the capsule. This key difference could have important implications for breast implant capsule pathophysiology. To date, the localized cellular response surrounding silicone particles has not been investigated. We aim to determine the differences in silicone infiltration in smooth and textured breast implant capsules and characterize the specific cellular responses to silicone particles in the capsule. METHODS: Capsule tissue from macrotextured silicone (N=15) and smooth silicone (N=15) breast implants was collected from consenting patients undergoing revisions. Silicone infiltration and capsular thickness were assessed histologically. Capsular cell populations were measured by immunohistochemistry (macrophages, CD3+ total T-cells, CD4+ helper T-cells, fibroblasts, and myofibroblasts). RESULTS: Silicone infiltration was greater in textured implant capsules (radius=4.87 µm) than smooth implant capsules (radius= 4.28 µm) (p=0.47). Smooth implant capsules had an increased thickness (smooth implant capsule thickness=1058 µm, textured implant capsule thickness=848 µm) (p=0.27). In addition, smooth implant capsules displayed increased total macrophages (p=0.01), M2 macrophages (p=0.03), myofibroblasts (p=0.04) and fibrotic cells (p=0.08). Textured implant capsules had increased CD4+ T-cells (p=0.88). The presence of all immune cells was enriched in silicone-dense areas, irrespective of implant surface (p<0.001). CONCLUSION: Our results suggest that the immune response to silicone particles in capsular tissue varies according to both implant surface and amount of silicone infiltration. Smooth implant capsules exhibit a macrophage-dominant response with thicker capsules. Textured implant capsules display enhanced CD4+ T-cell infiltration, which may alter baseline capsular physiology and susceptibility to distinct capsular pathologies. The global increased immune response to silicone particles could underscore the link between the presence of silicone and capsular contracture. Expanding our knowledge of these differences could yield meaningful advancements in our understanding of the mechanisms underlying breast implant capsule-related pathology.