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J.Health Sci., 53(2), 234-239, 2007
Prostaglandin E Receptor EP4 Antagonist Suppresses Lipopolysaccharide-Induced Osteoclast Formation and Inflammatory Bone Loss
Chiho Matsumoto,a Morichika Takita,a
Masaki Inada,a Takayuki Maruyama,b
and Chisato Miyaura*, a
aDepartment of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakamachi, Koganei, Tokyo 184-8588, Japan and
bDiscovery Research Laboratories I, Minase Research Institute, Ono Pharmaceutical Co., Ltd., 3-1-1 Sakurai, Shimamoto-cho, Mishima-gun, Osaka, Japan
Prostaglandin E2 (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 the PGE2-mediated EP4 signal is essential for LPS-induced osteoclast formation. Inflammatory bone diseases including periodontitis are known to be accompanied by bone loss with increased osteoclastogenesis. To examine the role of EP4-mediated PGE2 action in periodontitis, we examined the effects of EP4 antagonist on LPS-induced bone resorption using mouse alveolar bone. In an organ culture of alveolar bone, LPS-induced bone resorbing activity and EP4 antagonist suppressed this LPS-induced bone resorption. In an experimental model of periodontitis, LPS was injected into the lower gingiva, and the bone mineral density of alveolar bone was measured. LPS-induced the loss of alveolar bone, which was recovered by the treatment with EP4 antagonist in vivo. Therefore, EP4 antagonist is a possible candidate for the therapy of inflammatory bone disease including periodontitis.
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