PubMed · 10554929
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A Atala. 1999. Tissue engineering applications for erectile dysfunction.. https://doi.org/10.1038/sj.ijir.3900483
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
A frequent long-term complication of total joint arthroplasty is aseptic loosening, the end result of wear debris accumulation, synovitis, and osteolysis about the implant-bone or cement-bone interface. Complement, an effector system in plasma, synovial fluid, and tissue, has powerful chemotactic, inflammatory, and osteoclast-activating potentials. This study explored the complement-activating ability of polyethylene, a material used in joint implants. In vitro hemolytic assays using sheep red blood cells (E(sh)), human serum, and particulate polyethylene suggested alternative pathway complement activation, as well as polyethylene adsorption of activated complement components. These results were confirmed by enzyme-linked immunosorbent assay (ELISA) quantification of activated complement factors Bb and C3b. In situ double antibody immunoperoxidase staining for factors Bb, C3a, iC3b, and SC5-9 in synovial tissue from revision hip specimens showed localized alternative pathway activation and component adsorption. These results introduce a likely role for complement activation in particle-mediated recruitment, proliferation, and activation of macrophages during early events in osteolysis and implant loosening.
The objective of this paper was to study the release of bovine serum albumin (BSA) from a series of biodegradable hydrogels having a wide range of hydrophilicity to hydrophobicity, swelling, and biodegradation properties. BSA was incorporated into a series of biodegradable hydrogels made from a dextran derivative of allyl isocyanate (dex-AI, as the hydrophilic constituent) and poly(DL-lactic acid) diacrylate macromer (PDLLAM, as the hydrophobic constituent). The release kinetics of BSA from these dex-AI/PDLLAM hydrogels was studied. Laser confocal scanning microscopy was used to investigate the morphological change of the hydrogels, as well as BSA distribution in the hydrogels, as a function of dex-AI to PDLLAM composition ratio and incubation time. We found that the incorporation of PDLLAM into dex-AI reduced the initial burst release of BSA due to its more homogeneous distribution in the hydrogels. As the PDLLAM component increased, the rate of formation of a loose three-dimensional (3D) network structure increased; consequently, the sustained rate and extent of BSA release increased. Both release index and diffusion coefficient (from release kinetics data) increased as the PDLLAM component increased in the hydrogels. The data suggest that the release of BSA was controlled by both diffusion of BSA through swelling of the hydrophilic phase during an early stage, and degradation of the hydrophobic phase during a late stage, and also that the magnitude of diffusion versus degradation controlled release is dependent on composition ratio and immersion time.
Isolated cell systems of human neutrophils (PMNs) and monocyte-derived macrophages (MDMs) were used to compare the destructive potential of these cells during the acute and chronic phases of inflammation, respectively. The contrast in the damage to poly(urethane)s (PUs) was monitored by measuring radiolabel release elicited from a (14)C-polyester-urea-urethane (PEUU) during incubation with both cell types. Human PMN were seeded onto polymer-coated glass slips and both radiolabel release as well as serine protease activity [assayed with N-benzyloxycarbonyl lysine thiobenzyl ester (BLT)] were measured 18 h later. Human monocytes were cultured on polystyrene tissue culture plates for 14 days, trypsinized, and seeded onto the polymer-coated glass slips; then, radiolabel release and esterase activity [assayed with p-nitrophenylbutyrate (PNB)] were measured after 18 h. Coverslips with MDM were also incubated for an additional 2 weeks. At 18 h postincubation with the PEUU, MDM elicited 25 times more radiolabel release per 10(6) cells than PMN at 18 h and continued to increase more than sevenfold over the 18-h value during the subsequent 14-day period. The BLT activity in PMN did not increase significantly during the 18-h incubation period, whereas the PNB activity in MDM increased more than fourfold. The MDM, but not the PMN elicited radiolabel release, was inhibited by the protein synthesis inhibitor cycloheximide, as was the increase in PNB activity. The data provide evidence for a hydrolytic role for MDM and, to a lesser extent PMN, in the biodegradation of implanted materials. The full implication of the release of polymer-derived chemical agents from this hydrolytic cleavage of the implanted biomaterials, on the propagation of the inflammatory response, remains to be elucidated.