Prostaglandin E2 inhibits in‐vitro mineral deposition by human periodontal ligament cells via modulating the expression of TWIST1 and RUNX2

Abstract

The results of this study revealed that PGE2 modulates the osteogenic differentiation of HPDL cells via regulating the expression of RUNX2 and TWIST1. The results suggest a possible role for PGE2 in regulating the homeostasis of periodontal ligament tissue.

Tcf12, A Member of Basic Helix-Loop-Helix Transcription Factors, Mediates Bone Marrow Mesenchymal Stem Cell Osteogenic Differentiation In Vitro and In Vivo

“…At late time points during osteogenic differentiation, it was found that Tcf12 knockdown increased expression of OPN, OCN, and BSP, significantly increased ALP positive nodules and mineralization nodules when compared to scrambled and overexpression groups. This result is similar to that obtained with the homologous member Twist1, which has been shown to inhibit osteogenesis of C3H10T1/2 cells, bone osteosarcoma cells and human periodontal ligament cells . In these studies, Twist1 was proven to decrease the expression of osteogenic markers Bmp2, Alp, and Opn, whereas knockdown Twist1 increased their expression.…”

Anti‐Inflammatory and Osteoprotective Effects of Cannabinoid‐2 Receptor Agonist HU‐308 in a Rat Model of Lipopolysaccharide‐Induced Periodontitis

“…[6][7][8] It is known that PGE 2 is a prominent mediator of periodontal inflammation, making it a potent stimulator of bone resorption, and its production is associated with loss of periodontal attachment tissue. 7,8 Increase of these mediators of inflammation was reported to be involved in the imbalance between alveolar bone formation and resorption, by favoring resorption mediated by: 1) receptor activator of nuclear factor-kappa B ligand (RANKL), 2) its receptor RANK, and 3) a decoy receptor osteoprotegerin. 9,10 Nitric oxide (NO) is a free radical also involved in various pathophysiologic processes.…”

Regulation of inflammation by lipid mediators in oral diseases

“…PGE 2 is associated with periodontal disease and bone loss, and COX inhibitors have been proposed as a treatment (Lohinai et al, 2001;Yamaguchi and Kasai, 2005;Noguchi et al, 2007). Gingival biopsies from periodontal patients reveal that COX-2 expression leading to PGE 2 production correlates with connective tissue loss (Mesa et al, 2012(Mesa et al, , 2014, and it is hypothesized that PGE 2 inhibits in vitro mineral deposition by periodontal ligament cells via the modulation of TWIST1 & RUNX2 expression (Manokawinchoke et al, 2014). PGE 2 production can be inhibited by IL-4 and IFN-c in periodontal ligament fibroblasts (Noguchi et al, 1999b) and by lidocaine irrigation in periodontal treatment (Camargo et al, 2015b).…”