No abstract

SYNOPSISSurface degradation of implanted poly (ether urethane) s was studied quantitatively with a micro-ATR-FTIR technique. Substantial degradation was observed particularly in the soft segment a t the a-carbon adjacent to the ether linkage. The degradation caused changes in the concentration profiles of the soft-segment groups in the depth direction, and the affected depth was up to 10 microns after implantation for 10 weeks. Inhibition of degradation by antioxidants indicated the oxidative nature of degradation. An in uiuo poly (ether urethane) degradation mechanism was proposed.

Quantitative description of foreign body giant cell (FBGC) formation on poly(etherurethane urea) (PEUU) surfaces as a function of time can conceivably predict the effects of polymer characteristics on cellular responses in vivo. In the present study, the formation of FBGCs on strained and unstrained PEUUs was quantified with two parameters: the density of adherent macrophages present initially that participate in FBGC formation (d(o)) and the rate constant for cell fusion (k); both kinetic parameters were used to calculate the time-dependent FBGC density (dfc). Relationships were sought between results of the cellular analysis and the extent of environmental stress cracking (ESC), as characterized by scanning electron microscopy. Surface degradation was semiquantified with percent light transmittance. The materials used were: base PEUU, base PEUU with 1% Santowhite antioxidant powder, base PEUU with 5% Methacrol 2138F antifume agent, and base PEUU with both 1% Santowhite and 5% Methacrol 2138F. A comparison of unstrained base PEUU with base PEUU strained to 400% elongation indicated that the rate of cell fusion, but not d(o) and dfc, increased in the presence of strain. In all strained samples, additives that strongly affected the ESC also influenced FBGC kinetic parameters. Strained PEUU containing Santowhite had the lowest d(o), the slowest rate of cell fusion, and lowest dfc, and the least incidence of ESC. The results suggest that the incidence of ESC in PEUU was decreased in the presence of Santowhite, which also lowered the number of adherent macrophages participating in FBGC formation, the rate of FBGC formation and the subsequent FBGC density. These studies also indicate that strain in PEUUs does not directly modulate the adherent macrophage and FBGC density. Further studies are necessary to delineate the relationship between PEUU strain and adherent macrophage and FBGC activation, which leads to the exocytosis of degrading agents and the observed incidence of biodegradation.

Four materials based on a single poly-(etherurethane) (PEU) prepared from MDI and PTMEG but differing in additives were studied in the cage implant system. The two additives studied were Santowhite powder at the 1% level and Methacrol 2138F 5%. Methacrol 2138F appeared to be immiscible with the base PEU and was dispersed in discrete domains about 0.5-micron in size. The retrieved PEU specimens were also cleaned and examined in the optical and scanning electron microscopes, and the size and density of adherent foreign body giant cells (FBGCs) were measured at implantation times up to 10 weeks. Methacrol 2138F had no effect on the density, coverage or size distribution of adherent FBGCs, but leaching of Methacrol 2138F was considered to be responsible for extensive pitting of the PEU surface. On the other hand, Santowhite powder appeared to inhibit formation of FBGCs, and while surface cracking and flaking were observed as early as 3 weeks postimplantation on some PEUs, the Santowhite powder effectively inhibited surface cracking and flaking up to the longest implantation time studied.

The nature of in vivo leukocyte adhesion and foreign-body giant cell (FBGC) formation on polyurethanes was studied through theoretical and statistical analyses in terms of cell size distribution, density changes, and kinetics of FBGC formation. The results showed that the size distribution of FBGCs followed a "most probable" distribution. During FBGC formation, the densities of FBGCs changed with time. At an early stage, the number of FBGCs increased with time to a maximum at the expense of macrophages. As more FBGCs were formed and less macrophages were present, the fusion of FBGCs among themselves became significant. This, in turn, caused a gradual decrease of FBGC density with time. The rate of FBGC formation was characterized by a rate constant that represented certain characteristics of cell fusion and FBGC formation and the density of initial FBGC-forming macrophages that were a small fraction of leukocytes adhering to the surface. The direct correlations of surface cracking and pitting and adherent FBGCs demonstrated the influence of phagocytic actions of FBGCs on the biostability of implanted polyurethanes. While the cracking was thought to be caused by oxidative degradation facilitated by oxygen ion/radical release of FBGCs, the pitting appeared to result from the Methacrol 2138F aggregates diffusing out of the polymer in an acidic microenvironment under FBGCs, which in turn could be enhanced by the surface degradation and cell phagocytosis. The added Santowhite powder in polyurethane had a significant influence on FBGC formation: It reduced FBGC density and rate of FBGC formation by reducing leukocyte adhesion and the number of macrophages participating in FBGC formation.