Most dental care products exert their antibacterial effects by eliminating oral bacteria. Instead, LPS from other types of bacterial cells, such as E. coli and Pseudomonas aeruginosa, have been used to induce the inflammation. Inflammatory events related to DPB-derived endotoxins have not been evaluated as intensively [29, 30], and the value of anti-microbial dental care products to treat periodontal disease has not been sufficiently verified. Thus, there was a need to simultaneously investigate inflammatory events due to DPB-derived endotoxin and elucidate an effective anti-microbial component for periodontal disease. Here we demonstrate that DPB and DPB- significantly increase inflammation-associated elements such as COX-2 and PGE2. Many inflammatory molecules and proteases are also upregulated by DPB-LPS and lead to matrix damage. In addition, DPB-LPS stimulation promotes osteoclast formation, causing bone resorption. The risk of bone loss tends to increase in patients with inflammatory conditions . Inflammatory cytokines modulate osteoblast and osteoclast activity . Interleukins (IL), tumor necrosis factor (TNF), and tumor necrosis factor receptor superfamily members (TNFRSF) perturb bone homeostasis, leading to increased cartilage degradation and bone resorption by osteoclasts and inhibiting bone formation by osteoblasts .