Oka H, Miyauchi M, Sakamoto K, Moriwaki S, Niida S, Noguchi K, Somerman M J, Takata T
Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
J Dent Res. 2007 Oct;86(10):974-9. doi: 10.1177/154405910708601011.
Destruction of cementum and alveolar bone is the main causative event for the exfoliation of teeth as a consequence of periodontitis. Prostaglandin E(2) (PGE(2)) and PGE receptor subtypes (EPs) play an important role in modulating osteoblast-mediated osteoclastogenesis; however, no information is available on the role of PGE(2) and EPs in regulating cementoblast-mediated cementoclastogenesis. We hypothesized that the PGE(2)-EPs pathway also regulates cementoblasts' ability to activate cementoclasts. For these studies, OCCM-30 cells (a mouse cementoblast cell line) were exposed to PGE(2) and specific EP agonists. PGE(2) (100 ng/mL) and EP4 agonist (1 microM) up-regulated RANKL and IL-6 mRNA levels, while they down-regulated OPG mRNA expression. The EP4 antagonist (1 microM) eliminated these effects of PGE(2). PGE(2) treatment of co-cultures of OCCM-30 cells with bone marrow cells induced TRAP-positive cells via the EP4 pathway. These findings suggest that PGE(2) promotes cementoblast-mediated cementoclastogenesis by regulating the expression of RANKL and OPG via the EP4 pathway.
