タキタ　モリチカ   Morichika Takita   瀧田　守親    所属   医学部 医学科    職種   助教
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Prostaglandin E receptor EP4 antagonist suppresses lipopolysaccharide-induced osteoclast formation and inflammatory bone loss.
掲載誌名	正式名：Journal of Health Science 略　 称：J. Health Sci. ISSNコード：13449702/13475207
掲載区分	国内
出版社	Pharmaceutical Society of JAPAN
巻・号・頁	53(2),pp.234-239
著者・共著者	Matsumoto Chiho†, Takita Moirichika, Inada Masaki, Maruyama Takayuki, Miyaura Chisato*
担当区分	2nd著者
発行年月	2007/04
概要	PGE2 is mainly produced by osteoblasts in bone tissue, and acts as a potent stimulator of bone resorption. In osteoblasts, PGE2 production was greatly stimulated by lipopolysaccharide (LPS) following the expression of cyclooxygenase (COX)-2 and membrane-bound PGE synthase (mPGES)-1 mRNA. In the coculture of mouse bone marrow cells and osteoblasts, LPS induced PGE production and osteoclast formation, and EP4 antagonist completely suppressed osteoclast formation, indicating that PGE2-mediated EP4 signal is essential for LPS-induced osteoclast formation. Inflammatory bone diseases including periodontitis are known to be accompanied with the bone loss with increased osteoclastogenesis. To examine the role of EP4-medeiated PGE2 action in periodontitis, we examined the effects of EP4 antagonist on LPS-induced bone resorption using mouse alveolar bone. In organ culture of alveolar bone, LPS induced bone-resorbing activity and EP4 antagonist suppressed the LPS-induced bone resorption. In experimental model of periodontitis, LPS was injected into the lower gingiva and bone mineral density of alveolar bone was measured. LPS induced the loss of alveolar bone, which was recovered by the treatment of EP4 antagonist in vivo. Therefore, EP4 antagonist is a possible candidate for the therapy of inflammatory bone disease including periodontitis.
DOI	http://doi.org/10.1248/jhs.53.234