In vivo biostability of shore 55D polyether polyurethanes with and without fluoropolymer surface modifying endgroups.

Abstract

Polyether polyurethanes are subject to autooxidation and environmental stress cracking (ESC) because of interactions with lysosomal oxygen-free radicals. Oxidation can also be catalyzed by and caused by direct (redox) reaction with transition metal ions (metal ion oxidation, MIO). The source of the ions is corrosion of metallic parts within an implanted device. A previous study on a Shore 80A polyether polyurethane modified with fluoropolymer surface modifying end groups demonstrated improved biostability over unmodified controls. We predicted that this could be extrapolated to the inherently more biostable Shore 55D version (E55DF). While it is difficult to demonstrate significant biodegradation in the harder polymers within a reasonable time frame, we did see excellent biologic autooxidation and ESC resistance for both E55DF and its unmodified Shore 55D (P55D) control. E55DF was slightly, but significantly more resistant to MIO than P55D. This was particularly evident in molecular weight distributions with P55D exhibiting a large decrease in number average molecular weight compared to no change for E55DF. Both were markedly superior to the softer Shore 80A control. It does appear that one can extrapolate accelerated in vivo biostability results with the softer polymers to their harder analogues.