ArticleJournal of dental sciences2026
Antcin K suppresses osteoclastogenesis through modulation of the focal adhesion kinase and phosphoinositide 3-kinase pathways and attenuates ligature-induced periodontitis.
Article in Journal of dental sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
Background/purpose: Periodontitis is a chronic inflammatory condition characterized by host-mediated destruction of periodontal tissue and alveolar bone. Elevated proinflammatory cytokines and osteoclast activation are key factors contributing to this breakdown. Antcin K, a triterpenoid derived from Materials and methods: Receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis in murine macrophage cell line RAW 264.7 cells was evaluated following Antcin K treatment. RNA sequencing and pathway analysis revealed the involvement of the focal adhesion kinase (FAK)-phosphoinositide 3-kinase (PI3K) signaling axis, which was further validated by Western blotting. Results: Antcin K significantly suppressed RANKL-induced osteoclast formation Conclusion: Antcin K inhibits osteoclastogenesis by modulating the FAK-PI3K signaling pathway and attenuates alveolar bone loss. These findings suggest that Antcin K may serve as a potential host-modulatory therapeutic agent for the treatment of periodontitis.
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