Surprisingly, it was found that ASP could not only reduce the production of TNF-α, IL-1β, IL-6 and RANKL in peri-implant tissues and attenuate alveolar bone loss in the peri-implantitis model, but also could inhibit osteoclast differentiation and bone resorption activity by suppressing the activation of NF-κB and ERK1/2 signaling pathways in vitro, which suggest ASP could inhibit osteoclast formation by indirect suppression of osteoclastogenesis caused by downregulating pro-inflammatory cytokines levels, as well as the direct effects on osteoclast differentiation. The gene discussed is IL6; the disease is Peri-Implantitis.