From the Division of Plastic and Reconstructive Surgery, Department of Surgery, National Cheng Kung University Hospital.
Institute of Clinical Medicine.
Plast Reconstr Surg. 2024 Jan 1;153(1):109-120. doi: 10.1097/PRS.0000000000010464. Epub 2023 Mar 28.
Capsular contracture is the most common reason for having a secondary breast implant operation. The failure of the implanted device and discomfort are related to foreign body response, which involves a pathologic encapsulation. An up-regulated expression of CD248 was previously demonstrated to modulate inflammation and fibrosis. The authors hypothesized that CD248 contributes to foreign body reaction and contracture during silicone-stimulated capsule formation.
A murine capsular contracture model was established to correlate CD248 with capsular contracture. The timing and site of CD248 expression were characterized by protein analysis and histologic examination. The capsules between wild-type mice and CD248 knockout mice were compared in this model to verify the possible role of CD248 in silicone-related capsule formation.
CD248 was expressed in the peri-silicone implant capsule by stromal fibroblast and perivascular fibroblast. CD248 was overexpressed on day 4 and down to a constant level, but it was still up-regulated through day 21 to day 56 after silicone implantation. The CD248 knockout mice showed a prolonged inflammation period, whereas the wild-type mice developed a thinner but more collagenous capsule.
In conclusion, an effective murine capsular contracture model was established to study the relationship between CD248 and capsular contracture. CD248 may play a role in inflammation and encapsulation during silicone implantation. CD248 deletion in mice contributed to a loose and irregular collagen bundle in a capsule area, implying a decrease in contracture. Therefore, CD248 could be a potential therapeutic target in capsular contracture.
CD248 may play a role in inflammation and encapsulation during silicone implantation. It could be a potential therapeutic target in clinical capsular contracture.
包膜挛缩是进行二次乳房植入手术的最常见原因。植入装置失效和不适与异物反应有关，异物反应涉及病理性包膜形成。先前的研究表明，CD248 的表达上调可调节炎症和纤维化。作者假设 CD248 有助于硅胶刺激囊形成过程中的异物反应和挛缩。
建立了一种鼠类包膜挛缩模型，以将 CD248 与包膜挛缩相关联。通过蛋白质分析和组织学检查来描述 CD248 的表达时间和部位。在该模型中比较了野生型小鼠和 CD248 敲除小鼠之间的包膜，以验证 CD248 在硅胶相关包膜形成中的可能作用。
CD248 在间质成纤维细胞和血管周成纤维细胞的硅胶植入包膜中表达。CD248 在硅胶植入后第 4 天表达上调，并在第 21 天至第 56 天持续上调，但仍处于上调状态。CD248 敲除小鼠表现出较长的炎症期，而野生型小鼠形成的包膜较薄但胶原含量更高。
总之，建立了一种有效的鼠类包膜挛缩模型，用于研究 CD248 与包膜挛缩之间的关系。CD248 可能在硅胶植入过程中的炎症和包膜形成中起作用。CD248 在小鼠中的缺失导致包膜区域胶原束疏松且不规则，提示挛缩减少。因此，CD248 可能是包膜挛缩的潜在治疗靶点。
CD248 可能在硅胶植入过程中的炎症和包膜形成中起作用。它可能是临床包膜挛缩的潜在治疗靶点。
