Equisetum arvense Inhibits Alveolar Bone Destruction in a Rat Model with Lipopolysaccharide (LPS)-Induced Periodontitis

Figure 6

Proposed mechanism of EA inhibition of osteoclast formation caused by LPS. (a) In LPS-induced periodontitis, TLR4-mediated phosphorylation of IκB kinase α and β (IKKα/β) and NF-κB induces the expression of inflammatory cytokines such as tumor necrosis factor (TNF)-α in periodontal tissue cells and the generation of the osteoclastogenic receptor activator of NF-κB ligand (RANKL), an osteoclastogenic factor. However, it inactivates the Wnt/β-catenin signaling pathway and promotes β-catenin degradation. Furthermore, production of the secreted protein semaphorin 3A (Sema3A) is decreased; Sema3A/neuropilin-1 (Nrp1)-mediated β-catenin degradation and nuclear translocation are suppressed, as is transcription and expression of osteoprotegerin (OPG), the decoy receptor for RANKL. Finally, the RANKL/OPG ratio is increased, leading to osteoclast formation and maturation and subsequent bone resorption. (b) Proposed mechanism of EA-induced suppression of osteoclastogenesis by LPS: EA strongly suppresses the activation of IKKα/β and NF-κB, indicating that the Wnt/β-catenin signaling pathway is activated and β-catenin degradation is suppressed. Furthermore, Sema3A production is elevated, Sema3A/Nrp1-mediated β-catenin degradation is suppressed, and nuclear migration is promoted. This suppresses osteoclast formation and excessive bone resorption.

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