Prostaglandin E2 inhibits mineralization and enhances matrix metalloproteinase-13 in mature cementoblasts mainly via the EP4 pathway

Objectives glandin E2 (PGE2) is an important factor in the pathogenesis of periodontal disease because of bone resorbing 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 in mature cementoblasts, and to examine the effect of PGE2 and EPs on their cellular function. sion of EPs in immortalized mouse cementoblasts (OCCM-30 cells), which were characterized as mature cementoblasts, was determined using reverse transcriptase polymerase chain reaction (RT-PCR). The effects of PGE2 and EP agonists on mineralization were examined by studying nodule formation with alizarin red S staining. Alkaline phosphatase (ALP) activity with PGE2 and EP4 agonist was examined using the Bessey–Lowry enzymologic method. Effects of the PGE2-EP4 pathway on expression levels of osteocalcin (OCN) and matrix metalloproteinase-13 (MMP-13) mRNA were examined using real-time RT-PCR. s 0 cells expressed EP1, EP2, EP3 and EP4 mRNA. PGE2 and EP4 agonist led to downregulation of mineralized nodule formation and ALP activity in OCCM-30 cells. OCN mRNA expression was suppressed and MMP-13 mRNA expression was stimulated via the PGE2-EP4 pathway in OCCM-30 cells. sions oblasts may downregulate their mineralization ability and upregulate MMP-13 production through the PGE2-EP4 pathway, and may contribute to destruction of connective tissue attachment under inflammatory conditions.