In this study, we demonstrated that inhibition of S1PR2 by its specific antagonist (JTE013) reduced IL-1β, IL-6, TNF-α, and S1P production induced by the oral bacterial pathogen Aa; inhibited BMMs chemotaxis induced by bacterial infection; as well as suppressed osteoclastogenesis and bone resorption induced by RANKL. The gene discussed is S1PR2; the disease is bacterial infectious disease.