Objective: PGE2 is an important factor in pathogenesis of periodontal disease because of bone resorting activity and association with attachment loss. PGE2 and PGE receptor subtypes (EPs) play an important role in modulating bone metabolism via osteoblasts. However, little is known about the effects of PGE2 on cementoblasts. The aims of this study were to determine the expression of EPs on matured cementoblasts and to examine the effect of PGE2 and EPs on their cellar function. Design: Expression of EPs in immortalized mouse cementoblasts (OCCM-30), which were characterized as matured cementoblasts, was determined using RT-PCR. Then effects of PGE2 and EP agonists on mineralization were examined by studying nodule formation with alizarin red S (ALZ) staining. Alkaline phosphatase (ALP) activity with PGE2, EP4 agonist was examined by Bessey-Lowry enzymologic method. Effects of PGE2-EP4 pathway on expression levels of osteocalcin (OCN) and matrix metalloproteinase (MMP)-13 mRNA were examined by real-time RT-PCR. Results: OCCM-30 expressed EP1, 2, 3 and 4 mRNA. PGE2 and EP4 agonist caused downregulation of mineralized nodule formation and ALP activity in OCCM-30. OCN mRNA expression was suppressed and MMP-13 mRNA expression was stimulated via PGE2-EP4 pathway in OCCM-30. Conclusions: Cementoblasts may downregulate their mineralization ability and upregulate MMP-13 production through PGE2-EP4 pathway and may contribute to destruction of connective tissue attachment under inflammatory condition.