
Effects of O ‐methylated (−)‐epigallocatechin gallate ( EGCG ) on LPS ‐induced osteoclastogenesis, bone resorption, and alveolar bone loss in mice
Author(s) -
Tominari Tsukasa,
Ichimaru Ryota,
Yoshinouchi Shosei,
Matsumoto Chiho,
Watanabe Kenta,
Hirata Michiko,
Grundler Florian M.W.,
Inada Masaki,
Miyaura Chisato
Publication year - 2017
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12340
Subject(s) - bone resorption , resorption , osteoclast , chemistry , dental alveolus , epigallocatechin gallate , prostaglandin e2 , periodontitis , lipopolysaccharide , rankl , in vivo , endocrinology , pharmacology , biochemistry , medicine , in vitro , antioxidant , biology , receptor , polyphenol , dentistry , microbiology and biotechnology , activator (genetics)
(−)‐Epigallocatechin‐3‐ O ‐gallate ( EGCG ), present in green tea, exhibits antioxidant and antiallergy effects. EGCG 3″Me, a 3‐ O ‐methylated derivative of EGCG , has been reported to show similar biological functions; the inhibitory activity of EGCG 3″Me in a mouse allergy model was more potent than that of EGCG , probably due to the efficiency of absorption from the intestine. However, the functional potency of these EGCG s is controversial in each disease model. We previously observed that EGCG suppressed inflammatory bone resorption and prevented alveolar bone loss in a mouse model of periodontosis. In this study, we examined the role of EGCG 3″Me in bone resorption using a mouse model of periodontitis. Lipopolysaccharide ( LPS )‐induced osteoclast formation was suppressed by adding EGCG 3″Me to cocultures of osteoblasts and bone marrow cells, and LPS ‐induced bone resorption was also inhibited by EGCG 3″Me in calvarial organ cultures. EGCG 3″Me acted on osteoblasts and suppressed prostaglandin E ( PGE ) production, which is critical for inflammatory bone resorption, by inhibiting the expression of COX ‐2 and mPGES ‐1, key enzymes for PGE synthesis. In osteoclast precursor macrophages, EGCG 3″Me suppressed RANKL ‐dependent differentiation into mature osteoclasts. In a mouse model of periodontitis, LPS ‐induced bone resorption was suppressed by EGCG 3″Me in organ culture of mouse alveolar bone, and the alveolar bone loss was further attenuated by the treatment of EGCG 3″Me in the lower gingiva in vivo . EGCG 3″Me may be a potential natural compound for the protection of inflammatory bone loss in periodontitis.