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This study examined the effect of CB2 in the regulation of osteoclast differentiation in a murine macrophage cell line (RAW264.7), which has been shown to be stimulated by titanium (Ti) particles and receptor activator of the NF\u2010\u03baB ligand (RANKL). Results showed that CB2 expression in RAW cells cultured with Ti particles and RANKL. CB2 inactivation by AM630, a CB2 selective antagonist, effectively inhibited osteoclastogenesis in the differentiation medium system. AM630 treatment (\u2265100 n<jats:italic>M<\/jats:italic>) significantly reduced the number of tartrate\u2010resistant acid phosphatase\u2010positive cells when compared with the control. Real\u2010time reverse transcription polymerase chain reaction analysis revealed that AM630 (100 n<jats:italic>M<\/jats:italic>) inhibited mRNA expression of <jats:italic>RANK<\/jats:italic> and <jats:italic>cathepsin K<\/jats:italic> in RAW cells stimulated by Ti particles and RANKL. Moreover, enzyme\u2010linked immunosorbent assay showed that AM630 (100 n<jats:italic>M<\/jats:italic>) reduced protein expression of interleukin\u20101\u03b2 and tumor necrosis factor\u2010\u03b1 in RAW cells cultured with Ti particles. In addition, 3\u2010[4,5\u2010dimethylthiazol\u20102\u2010yl]\u20102,5\u2010diphenyltetrazoliumbromide revealed that AM630 had no toxic effect on RAW cells. These results suggested that CB2 inactivation by AM630 could provide a promising therapeutic target for treating or preventing aseptic loosening. \u00a9 2010 Wiley Periodicals, Inc. 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