To explore the impact of different concentrations of lanthanum chloride (LaCl3) on critical components of wear particle-mediated signaling pathways in inflammation and osteoclastogenesis, RAW264.7 cells were naturally divided into eight groups and analyzed by CCK-8 assay, flow cytometry, ELISA, RT-PCR and western blot after treatments. The results showed that three concentrations of LaCl3 had no influence on viability of RAW264.7 cells and down-regulated receptor activator of nuclear factor κB (RANK) instead of macrophage colony-stimulating factor receptor (M-CSFR). Additionally, 2.5 and 10 μmol/L LaCl3 could signifi- cantly inhibit gene and protein levels of pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β, i.e., TNF-α and IL-1β) and NF-κB/p65, but 100 μmol/L LaCl3 did not exert an obvious inflammation-inhibiting effect, and even induced inflammation. In conclusion, these findings demonstrated that LaCl3 was able to suppress wear particle-induced inflammation and activation of NF-κB in a certain range of concentrations in vitro and mainly decrease the expression of RANK, but not M-CSFR, all of which were generally recognized to play a pivotal role in osteoclastogenesis. To explore the impact of different concentrations of lanthanum chloride (LaCl3) on critical components of wear particle-mediated signaling pathways in inflammation and osteoclastogenesis, RAW264.7 cells were naturally divided into eight groups and analyzed by CCK-8 assay, flow cytometry, ELISA , RT-PCR and western blot after treatments. The results showed that three concentrations of LaCl3 had no influence on viability of RAW264.7 cells and down-regulated receptor activator of nuclear factor κB (RANK) instead of macrophage colony-stimulating factor receptor ( M-CSFR). Additionally, 2.5 and 10 μmol / L LaCl3 could signifi- cantly inhibit gene and protein levels of pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β, ie, TNF- α and IL- 1β) and NF-κB / p65, but 100 μmol / L LaCl3 did not exert an obvious inflammation-inhibiting effect, and even induced inflammation. In conclusion, these findings demonstrated that LaCl3 was able to suppress wear particle-induced inflammacy tion and activation of NF-κB in a certain range of concentrations in vitro and mainly decrease the expression of RANK, but not M-CSFR, all of which were generally recognized to play a pivotal role in osteoclastogenesis.