PubMed · 7764242
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N Kossovsky, D Millett, A Gelman, E Sponsler, H Hnatyszyn. 1993. Self-assembling nanostructures.. https://doi.org/10.1038/nbt1293-1534
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Tissue ingrowth into porous-coated orthopedic and dental implants is commonly used as a means to achieve long-term fixation of these prostheses. However, the degree of tissue ingrowth is often inadequate and inconsistent. If the pores of these implants are impregnated with a controlled drug release system delivering relevant growth factors, then it might be possible to stimulate more tissue ingrowth. The present study introduces such a system based on biodegradable polymers and investigates its protein release profile and polymer degradation characteristics. Porous coated titanium implants were impregnated with a mixture of a 50%-50% polylactic acid-polyglycolic acid copolymer and a model protein, soybean trypsin inhibitor. Control implants contained only the polymer and no protein. The implants were subjected to hydrolytic degradation in phosphate buffered saline at 37 degrees C for periods of 3, 6, and 11 weeks. The protein release and the mass and molecular weight of the polymer were monitored. The results indicate that the protein is released in three distinct phases and the polymer loses almost all its mass and molecular weight by 11 weeks. There was a significant difference in the polymer degradation characteristics between the control and test implants, which might be the result of some complex polymer-protein interactions.
The authors examined the modifications of some markers of platelet activation after contact with biomaterials. Glycoprotein GMP-140 (CD62) was evaluated by flow cytometry; beta-thromboglobulin (beta-TG) and thromboxane B2 (TXB2) were determined by radioimmunoassay. Polyethylene terephthalate (PET) induced a remarkable platelet adhesion and a significant increase in beta-TG and TXB2, with no increase in CD62 on the nonadherent platelets. Pyrolytic carbon-coated PET (PC) did not induce platelet adhesion after 15 min of contact, but a significant increase in CD62 was detected. After 30 min a significant increase in platelet adhesion as well as the release of beta-TG and TXB2 were noted. The increase was lower than that observed for uncoated PET, and after 30 min of contact with PC the increase no longer was observed.
Inflammatory mediators such as cytokines produced by white blood cells (WBCs) at the site of implantation are important for the biocompatibility of vascular grafts. The aim of the present study was to demonstrate the tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) release from WBCs incubated with expanded polytetrafluoroethylene (ePTFE) or woven Dacron grafts. In a second series the effects of pentoxifylline (PTX) and iloprost (ILO), both known to inhibit white blood cell function, on this release were determined. Woven Dacron grafts induced significantly higher release of both TNF-alpha and IL-6 compared to ePTFE. TNF-alpha was detectable first after 2 h, whereas IL-6 was seen after 4 h. Maximum values were reached at 6 and 12 h, respectively. The addition of an endotoxin gave more pronounced patterns of cytokine release not influenced by time. Preincubation with both PTX and ILO at final concentrations of 100 and 10 micrograms/mL, respectively, reduced significantly the TNF-alpha release without differences between the two graft materials, whereas the effect on the IL-6 release varied and was graft material-dependent. In conclusion, graft material-dependent induction of TNF-alpha and IL-6 from WBCs was demonstrated. PTX and ILO influenced the cytokine release. It might be suggested that graft material-induced cytokine production could contribute to intimal hyperplasia in vivo. The present findings encourage further studies regarding graft material-induced WBC alterations and the role of pharmacologic agents influencing this function.