Abstract

Bone resorption is regulated by cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and by the balance of a receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG). The aim of this study was to investigate the mechanism of particle-induced osteolysis in murine calvariae by assessing the extent of osteolysis and the expression of inflammatory cytokines, RANKL and OPG after implantation of metal and polyethylene particles. The murine calvariae implanted with Ti6Al4V, CoCr or high-density polyethylene (HDP) particles showed significantly more extensive osteolysis and elevated levels of inflammatory cytokines. The ratio between RANKL and OPG was high in the mice implanted with Ti6Al4V and HDP particles, but not in the mice implanted with CoCr particles. These observations suggested that CoCr particle-induced osteoclastogenesis may be caused directly by inflammatory cytokines rather than by the RANKL-RANK pathway. There might be different mechanisms at work in particle-induced osteolysis between Ti6Al4V, HDP and CoCr.

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