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Since PI3K\u03b3 is primarily responsible for PI3K activity during inflammation, we hypothesized that PI3K\u03b3 mediates particle\u2010induced osteolysis in vivo. Our results do not strongly support the hypothesis that PI3K\u03b3 regulates the overall amount of particle\u2010induced osteolysis in the murine calvarial model. However, our results strongly support the conclusion that variability in the amount of particle\u2010induced osteolysis between individual mice is reduced in the PI3K\u03b3<jats:sup>\u2212\/\u2212<\/jats:sup> mice. These results suggest that PI3K\u03b3 contributes to osteolysis to different degrees in individual mice and that the mice, and patients, that are most susceptible to osteolysis may be so, in part, due to an increased contribution from PI3K\u03b3.\u2003\u00a9 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. 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