Epigallocatechin gallate (EGCG) suppresses lipopolysaccharide-induced inflammatory bone resorption, and protects against alveolar bone loss in mice

  • FEBS Open Bio. 2015 Jun 12;5:522-7. doi: 10.1016/j.fob.2015.06.003.
Tsukasa Tominari  1 ,  Chiho Matsumoto  2 ,  Kenta Watanabe  2 ,  Michiko Hirata  2 ,  Florian M W Grundler  3 ,  Chisato Miyaura  1 ,  Masaki Inada  1
Affiliations
  • 1. Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakamachi, Koganei, Tokyo 184-8588, Japan ; Global Innovation Research Organization, Tokyo University of Agriculture and Technology, 2-24-16 Nakamachi, Koganei, Tokyo 184-8588, Japan.
  • 2. Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakamachi, Koganei, Tokyo 184-8588, Japan.
  • 3. Institute of Crop Science and Resource Conservation, University of Bonn, Karlrobert-Kreiten-Strasse 13, 53115 Bonn, Germany.
PMID: 26155460 DOI: 10.1016/j.fob.2015.06.003
Abstract

Epigallocatechin gallate (EGCG), a major polyphenol in green tea, possesses antioxidant properties and regulates various cell functions. Here, we examined the function of EGCG in inflammatory bone resorption. In calvarial organ cultures, lipopolysaccharide (LPS)-induced bone resorption was clearly suppressed by EGCG. In osteoblasts, EGCG suppressed the LPS-induced expression of COX-2 and mPGES-1 mRNAs, as well as prostaglandin E2 production, and also suppressed RANKL expression, which is essential for osteoclast differentiation. LPS-induced bone resorption of mandibular alveolar bones was attenuated by EGCG in vitro, and the loss of mouse alveolar bone mass was inhibited by the catechin in vivo.

Keywords
BMN, bone mineral density; Bone resorption; COX, cyclo-oxygenase; EGCG, (−)-epigallocatechin-3-gallate; Epigallocatechin gallate; LPS, lipopolysaccharide; Lipopolysaccharide; OCPC, o-cresolphthalein complexon; OPG, osteoprotegerin; Osteoblasts; PGE2, prostaglandin E2; PSD, polymicrobial synergy and dysbiosis; Periodontitis; Prostaglandin E; RANKL, receptor activator of NF-kB ligand; mPGES, membrane-bound PGE synthase.
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