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PGE₂ Activates Cementoclastogenesis by Cementoblasts via EP4

¹ Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan;
² Department of Bone and Joint Disease, Research Institute, National Center for Geriatrics and Gerontology, 36-3 Gengo, Obu, Aichi 474-8522, Japan;
³ Department of Periodontology, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan; and
⁴ Department of Periodontics, School of Dentistry, 1959 NE Pacific, D322-Health Science Center, University of Washington, Seattle, WA 98195-7444, USA

^* corresponding authors, mmiya{at}hiroshima-u.ac.jp and ttakata{at}hiroshima-u.ac.jp

Destruction of cementum and alveolar bone is the main causative event for the exfoliation of teeth as a consequence of periodontitis. Prostaglandin E₂ (PGE₂) and PGE receptor subtypes (EPs) play an important role in modulating osteoblast-mediated osteoclastogenesis; however, no information is available on the role of PGE₂ and EPs in regulating cementoblast-mediated cementoclastogenesis. We hypothesized that the PGE₂-EPs pathway also regulates cementoblasts’ ability to activate cementoclasts. For these studies, OCCM-30 cells (a mouse cementoblast cell line) were exposed to PGE₂ and specific EP agonists. PGE₂ (100 ng/mL) and EP4 agonist (1 µM) up-regulated RANKL and IL-6 mRNA levels, while they down-regulated OPG mRNA expression. The EP4 antagonist (1 µM) eliminated these effects of PGE₂. PGE₂ treatment of co-cultures of OCCM-30 cells with bone marrow cells induced TRAP-positive cells via the EP4 pathway. These findings suggest that PGE₂ promotes cementoblast-mediated cementoclastogenesis by regulating the expression of RANKL and OPG via the EP4 pathway.

KEY WORDS: prostaglandin E₂ • PGE receptor subtypes • cementoblasts • periodontal tissue