Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL.
Aesthet Surg J. 2019 Jan 31;39(Suppl_1):S36-S48. doi: 10.1093/asj/sjy335.
Currently, there is a dearth of information regarding the degree of particle shedding from breast implants (BIs) and what are the general biological consequences of BI debris. Thus, it is unclear to what degree BI debris compromises the long-term biological performance of BIs. For orthopedic implants, it is well established that the severity of biological reactivity to implant debris governs long-term clinical performance. Orthopedic implant particulate debris is generally in the range of 0.01 to 100 μm in diameter. Implant debris-induced bioreactivity/inflammation is mostly a peri-implant phenomenon caused by local innate immune cells (eg, macrophages) that produce proinflammatory cytokines such as tumor necrosis factor-α, interleukin-1β, interleukin-6, and prostaglandin 2 (PGE2). In orthopedics, there have been few systemic concerns associated with polymeric implant debris (like silicone) other than documented dissemination to remote organs (eg, liver, spleen, etc.) with no known associated pathogenicity. This is not true of metal implant debris where normal (well-functioning) implants can induce systemic reactions such as delayed type hypersensitivity. Diagnostic analysis of orthopedic tissues has focused on innate (macrophage mediated) and adaptive (lymphocyte-mediated hypersensitivity) immune responses. Orthopedic implant debris-associated lymphocyte cancers have not been reported in over 40 years of orthopedic literature. Adaptive immune responses such as hypersensitivity reactions to orthopedic implant debris have been dominated by certain implant types that produce specific kinds of debris (eg, metal-on-metal total joint prostheses). Orthopedic hypersensitivity responses and atypical BI bioreactivity such as BI-associated anaplastic large cell lymphoma share crossover markers for diagnosis. Differentiating normal innate immune reactivity to particles from anaplastic large cell lymphoma reactions from delayed type hypersensitivity reactions to BI-associated implant debris remains unclear but vital to patients and surgeons.
目前,关于乳房植入物(BI)的颗粒脱落程度以及 BI 碎片的一般生物学后果的信息很少。因此,尚不清楚 BI 碎片在多大程度上影响 BI 的长期生物学性能。对于骨科植入物,已经明确的是,对植入物碎片的生物学反应的严重程度决定了长期的临床性能。骨科植入物颗粒性碎片的直径通常在 0.01 至 100μm 之间。植入物碎片诱导的生物反应/炎症主要是由局部固有免疫细胞(如巨噬细胞)引起的植入物周围现象,这些细胞会产生促炎细胞因子,如肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6 和前列腺素 2(PGE2)。在骨科领域,除了已记录的聚合物植入物碎片(如硅酮)向远处器官(如肝、脾等)的传播外,很少有与聚合植入物碎片(如硅酮)相关的全身问题,而且这些传播没有已知的致病性。金属植入物碎片则不然,正常(功能正常)的植入物会引起全身性反应,如迟发型超敏反应。对骨科组织的诊断分析主要集中在固有(巨噬细胞介导)和适应性(淋巴细胞介导)免疫反应上。在超过 40 年的骨科文献中,没有报道与骨科植入物碎片相关的淋巴细胞癌。对骨科植入物碎片的适应性免疫反应,如对骨科植入物碎片的超敏反应,主要由某些产生特定类型碎片(如金属对金属全关节假体)的植入物类型主导。骨科超敏反应和非典型 BI 生物反应(如 BI 相关间变大细胞淋巴瘤)具有相同的诊断交叉标记物。区分正常的固有免疫反应与间变大细胞淋巴瘤反应以及对 BI 相关植入物碎片的迟发型超敏反应仍然不清楚,但对患者和外科医生至关重要。