Prostaglandins E2 and F2α Enhance Differentiation of Cementoblastic Cells

Background: The prostaglandins (PG) E2 and PGF2α are important cytokines in periodontal physiology and pathology. PGE2 and PGF2α alter cell function by binding and activating the plasmamembrane G‐protein‐coupled PG receptors. In this study, we examined the PGE2 and PGF2α effects on the immortalized cementoblastic OCCM cells. Methods: Confluent OCCM cells were treated with PGE2, PGF2α, specific activators/inhibitors of the EP prostanoid receptors, a specific activator of the FP prostanoid receptor, and direct activators/inhibitors of the protein kinase C (PKC) signaling pathway. Mineral nodule formation was assessed by the von Kossa stain. Results: PGE2 and PGF2α significantly increased mineralization of OCCM cells. The EP1 and EP3 PG receptor activators 16,16‐dimethyl‐prostaglandin E2 and sulprostone, also increased mineralization. In contrast, specific activators of the EP2 or the EP2/EP3/EP4 receptors did not have any effect. Fluprostenol, a specific activator of the FP receptor, significantly increased mineralization of OCCM cells. FP and EP (1 or 3) receptors signal through activation of the protein kinase C (PKC) pathway. Indeed, phorbol 12‐myristate 13‐acetate (PMA), a direct activator of the PKC pathway, significantly increase OCCM mineralization, while pre‐treatment of OCCM cells with the PKC inhibitor GF109203× (bisindolylmaleimide) significantly decreased mineralization. Conclusion: We conclude that PGE2 and PGF2α exert an anabolic effect on OCCM mineralization through activation of PKC signaling. J Periodontol 2005;76:303‐309.