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

Tsukasa Tominari; Chiho Matsumoto; Kenta Watanabe; Michiko Hirata; Florian M W Grundler; Chisato Miyaura; Masaki Inada

doi:10.1016/j.fob.2015.06.003

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. eCollection 2015.

Authors

Tsukasa Tominari¹, Chiho Matsumoto², Kenta Watanabe², Michiko Hirata², Florian M W Grundler³, Chisato Miyaura¹, Masaki Inada¹

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.

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.