Szycher M, Siciliano A A
PolyMedica Industries, Inc., Woburn, MA 01801.
J Biomater Appl. 1991 Apr;5(4):282-322. doi: 10.1177/088532829100500403.
We have examined ten tissue capsules from patients ranging from five months to nine years of mammary implantation. Contrary to published reports of polyurethane foam "fragmentation" or "disappearance" in the capsules evaluated, the polyurethane foam was still present and embedded in the surrounding tissue capsule. The foam was nearly always invisible by gross observation, or manual palpation. Only after enzymatic digestion of the tissue capsule did the foam become clearly visible as continuous sheets. ESCA analyses show that explanted foams are devoid of nitrogen peaks. Only carbon, oxygen and silicone signals are observed. The same foams do show nitrogen peaks (due to urethane linkages) when probed by FTIR. Since ESCA only analyzes the first 40-50 Angstroms of a surface, we believe that a "protective coating" composed of soft segments has formed. Beneath this "coating" the original polyurethane composition is still present as evidenced by FTIR analysis. Three possible explanations are advanced: (1) The surface hydrolysis, which takes place within the soft segment of the polyurethane polymer, results in the formation of oligomer(s). These oligomers, devoid of urethane linkages, appear to protect the polymer from further bioresorption, by significantly retarding the rate of additional surface hydrolysis. (2) Chain cleavage occurs in the soft segment producing a hydrophilic polyester chain end which orients into the interfacial area. These chain ends then produce a skin effect which increases the distance from the surface to the hard segments, or urethane-containing linkages. (3) Macromolecular motion in the soft segment phases of the polymer could be reorienting under the influence of the in vivo environment, thus producing a surface layer or "coating" which is predominantly soft segment in composition. Regardless of which of the three hypotheses proves to be most plausible, we interpret the data as showing that the polyurethane foam cover undergoes very slow bioresorption, even after 9 years of human implantation. The data further suggests that the in vivo surface of the polyurethane foam cover is biocompatible and interfacial interactions with inflammatory cells are downregulated or reduced because of the apparent biocompatibility of the material.
我们检查了10个来自5个月至9年乳腺植入患者的组织包膜。与已发表的关于所评估包膜中聚氨酯泡沫“破碎”或“消失”的报告相反，聚氨酯泡沫仍然存在并嵌入周围的组织包膜中。通过肉眼观察或手动触诊，泡沫几乎总是不可见的。只有在对组织包膜进行酶消化后，泡沫才会作为连续的薄片清晰可见。电子能谱分析表明，取出的泡沫没有氮峰。只观察到碳、氧和硅的信号。当用傅里叶变换红外光谱探测时，同样的泡沫确实显示出氮峰（由于聚氨酯键）。由于电子能谱仅分析表面的前40-50埃，我们认为已经形成了由软段组成的“保护涂层”。傅里叶变换红外光谱分析证明，在这个“涂层”之下，原来的聚氨酯成分仍然存在。提出了三种可能的解释：（1）发生在聚氨酯聚合物软段内的表面水解导致低聚物的形成。这些没有聚氨酯键的低聚物似乎通过显著减缓额外表面水解的速度来保护聚合物免于进一步的生物吸收。（2）软段发生链断裂，产生亲水性聚酯链端，该链端定向到界面区域。然后这些链端产生一种趋肤效应，增加了从表面到硬段或含聚氨酯键的距离。（3）聚合物软段相中的大分子运动可能在体内环境的影响下重新定向，从而产生主要由软段组成的表面层或“涂层”。无论这三种假设中的哪一种被证明是最合理的，我们将这些数据解释为表明聚氨酯泡沫覆盖物即使在人体植入9年后也经历非常缓慢的生物吸收。数据进一步表明，聚氨酯泡沫覆盖物的体内表面具有生物相容性，并且由于材料明显的生物相容性，与炎症细胞的界面相互作用被下调或减少。
