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Micromolar sodium fluoride mediates anti-osteoclastogenesis in Porphyromonas gingivalis-induced alveolar bone loss

International Journal of Oral Science 2015年第4期7卷 242-249页

作者： Ujjal K Bhawal Hye-Jin Lee kazumune arikawa Michiharu Shimosaka Masatoshi Suzuki Toshizo Toyama Takenori Sato Ryota Kawamata Chieko Taguchi Nobushiro Hamada Ikuo Nasu Hirohisa Arakawa Koh Shibutani Department of Biochemistry and Molecular Biology Nihon University School of Dentistry at Matsudo Research Institute of Oral Health Nihon University School of Dentistry at Matsudo Department of Oral Health Graduate School of DentistryKanagawa Dental University Department of Dental Hygiene Howon University Department of Preventive and Public Oral Health Nihon University School of Dentistry at Matsudo Department of Anesthesiology Nihon University School of Dentistry at Matsudo Department of Infection Control Division of MicrobiologyKanagawa Dental University Department of Radiopraxis Science Kanagawa Dental University

Osteoclasts are bone-specific multinucleated cells generated by the differentiation of monocyte/macrophage lineage precursors. Regulation of osteoclast differentiation is considered an effective therapeutic approach to the treatment of bone-lytic diseases. Periodontitis is an inflammatory disease characterized by extensive bone resorption. In this study, we investigated the effects of sodium fluoride （NaF） on osteoclastogenesis induced by Porphyromonas gingivalis, an important colonizer of the oral cavity that has been implicated in periodontitis. NaF strongly inhibited the P. gingivalis-induced alveolar bone loss. That effect was accompanied by decreased levels of cathepsin K, interleukin （IL）-1β, matrix metalloproteinase 9 （MMP9）, and tartrate-resistant acid phosphatase, which were up-regulated during P. gingivalis-induced osteoclastogenesis. Consistent with the in vivo anti-osteoclastogenic effect, NaF inhibited osteoclast formation caused by the differentiation factor RANKL （receptor activator of nuclear factor KB ligand） and macrophage colony-stimulating factor （M-CSF）. The RANKL-stimulated induction of the transcription factor nuclear factor of activated T cells （NFAT） cl was also abrogated by NaF. Taken together, our data demonstrate that NaF inhibits RANKL-induced osteoclastogenesis by reducing the induction of NFATcl, ultimately leading to the suppressed expression of cathepsin K and MMP9. The in vivo effect of NaF on the inhibition of P. gingivalis-induced osteoclastogenesis strengthens the potential usefulness of NaF for treating periodontal diseases.

关键词： alveolar bone loss osteoclasts Porphyromonas gingivalis sodium fluoride

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