Abstract
Orthopaedic metal implants are routinely used in bone fracture repair and for joint replacement therapies. However, approximately 15% of recipients suffer from inflammatory reactions and aseptic loosening. One possible cause is an immune reactivity towards the metal implants. Metal implants in patients undergo biocorrosion releasing metal ions and wear particles. Metal ions are able to circulate in the body and bind to extracellular and/or intracellular proteins. Any immune reactivity by patients would be initiated by professional antigen presenting cells, dendritic cells (DCs) and effected by CD4+ T‐cell.For this in vitro study, Titanium (IV) and Vanadium (IV) ions were chosen as they are major components in current metal implants. Using energy filtered transmission electron microscopy, uptake of Titanium (IV) by human DCs showed intracellular accumulation as phosphorus containing titanium complexes at the surface and intracellular membranes, as well as in ribosomal and nuclear chromatin structures. Changes in the DC surface markers after exposure to metal ions measured using flow cytometry. Increase in expression of co‐stimulatory molecules (CD80, CD86 and CD40) was seen in vanadium exposed DCs. Upregulation of cytokines IL4, IL10, IFN‐g and TNF‐a was detected in the supernatants of DCs exposed to titanium (IV). Finally, the ability of metal exposed DCs to interact with lymphocytes was also investigated through flow cytometry. Decrease in T‐lymphocytic CD25 was seen after 5 day culture with Titanium (IV) treated DCs whilst vanadium treated DCs were able to maintain CD25 expression.The reactivity towards various metal ions varies with individuals. It is suggested that responders towards metals would have a reduced regulatory capability through CD4+CD25+ cells, allowing the proliferation of inflammatory osteo‐immune Th17cells.
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