Induced Secretion of IL-1β from THP-1 Cells after Titanium Exposure

Within the orthopedic field, a post-installation complication such as aseptic inflammation occurs around orthopedic prosthetic implants. Immunological studies within the field have so far been correlating the aseptic osteolytic process to activated macrophages due to phagocytosis of implant wear debris. The activated macrophages respond with an inflammasome mediated secretion of pro-inflammatory mediators Macrophage-polarization is another theory behind the mechanism of aseptic inflammation induced by orthopedic prosthetic implants, leading to a higher ratio of the pro-inflammatory subtype M1-macrophage in the local peri-implant tissue. Together with the lack of a true definition of peri-implantitis of dental implants, the mechanisms involved in the pathogenesis remain unravelled. Hence, the aim of our study was to investigate if mechanisms previously mentioned could be correlated to factors involved in pathogenesis of peri-implantitis. We hypothesized that samples of solid titanium and titanium-ions in combination with microbial stimuli could induce an enhanced pro-inflammatory interleukin-1β (IL-1β) secretion from macrophages. This hypothesis was tested in our in vitro experiments, where THP-1 cells (human monocyte cancer cell line) and freshly isolated human macrophages were exposed to solid titanium samples and titanium-ions in the presence of microbial stimuli (Escherichia coli LPS). Results showed that a pro-inflammatory response could be induced from THP-1 cells, due to exposure of titanium-metal and titanium-ions, dependent on the dose/purity of titanium. This indicates that a bacteria-induced inflammatory response could be further enhanced in vicinity to titanium implants