Light at wavelength 405 nm is an effective bactericide. Previous studies showed that exposing mammalian cells to 405 nm light at 36 J/cm(2) (a bactericidal dose) had no significant effect on normal cell function, although at higher doses (54 J/cm(2)), mammalian cell death became evident. This research demonstrates that mammalian and bacterial cell toxicity induced by 405 nm light exposure is accompanied by reactive oxygen species production, as detected by generation of fluorescence from 6-carboxy-2',7'-dichlorodihydrofluorescein diacetate. As indicators of the resulting oxidative stress in mammalian cells, a decrease in intracellular reduced glutathione content and a corresponding increase in the efflux of oxidised glutathione were observed from 405 nm light treated cells. The mammalian cells were significantly protected from dying at 54 J/cm(2) in the presence of catalase, which detoxifies H2O2. Bacterial cells were significantly protected by sodium pyruvate (H2O2 scavenger) and by a combination of free radical scavengers (sodium pyruvate, dimethyl thiourea (OH scavenger) and catalase) at 162 and 324 J/cm(2). Results therefore suggested that the cytotoxic mechanism of 405 nm light in mammalian cells and bacteria could be oxidative stress involving predominantly H2O2 generation, with other ROS contributing to the damage.

Joint replacement has proven to be an extremely successful and cost-effective means of relieving arthritic pain and improving quality of life for recipients. Wear debris-induced osteolysis is, however, a major limitation and causes orthopaedic implant aseptic loosening, and various cell types including macrophages, monocytes, osteoblasts, and osteoclasts, are involved. During the last few years, there has been increasing concern about metal-on-metal (MoM) hip replacements regarding adverse reactions to metal debris associated with the MoM articulation. Even though MoM-bearing technology was initially aimed to extend the durability of hip replacements and to reduce the requirement for revision, they have been reported to release at least three times more cobalt and chromium ions than metal-on-polyethylene (MoP) hip replacements. As a result, the toxicity of metal particles and ions produced by bearing surfaces, both locally in the periprosthetic space and systemically, became a concern. Several investigations have been carried out to understand the mechanisms responsible for the adverse response to metal wear debris. This review aims at summarising in vitro analyses of the toxicity, immunological, and gene expression effects of cobalt ions and wear debris derived from MoM hip implants.