Biodegradation of metallic magnesium elicits an inflammatory response in primary nasal epithelial cells.

摘要

Resorbable magnesium-based implants hold great promise for various biomedical applications, such as osteosynthesis and coronary stenting. They also offer a new therapeutic option for the treatment of chronic rhinosinusitis, but little data is yet available regarding the use of magnesium in the nasal cavity. To model this field of application, primary porcine nasal epithelial cells were used to test the biocompatibility of degrading pure magnesium and investigate whether the degradation products may also affect cellular metabolism. Magnesium specimens did not induce apoptosis and we found no major influence on enzyme activities or protein synthesis, but cell viability was reduced and elevated interleukin 8 secretion indicated proinflammatory reactions. Necrotic damage was most likely due to osmotic stress, and our results suggest that magnesium ion build-up is also involved in the interleukin 8 release. Furthermore, the latter seems to be mediated, at least in part, by the p38 signaling pathway. These effects probably depended on the accumulation of very high concentrations of magnesium ions in the in vitro set-up, which might not be achieved in vivo, although we cannot exclude that further, as yet unknown, factors played a role in the inflammatory response during the degradation process. In conclusion, the biocompatibility of pure magnesium with cells in the immediate vicinity appears less ideal than is often supposed, and this needs to be considered in the evaluation of magnesium materials containing additional alloying elements.