DFCs disturbs bone remodelling activity during tooth eruption through RANK/RANKL/OPG signalling pathway and may thus be responsible for impaired permanent tooth eruption in CCD patients.

Objectives The reconstruction of bone defects remains a major clinical issue. Our study aims to investigate the ability of RATEA16 (RA, [CH3CONH] RADARADARADARADA‐[CONH2]) for the sustained delivering VEGF and BMP‐2 to promote angiogenesis and osteogenesis in bone reconstruction. Materials and methods We prepared and investigated the characterization of RATEA16. The survival of human umbilical vein endothelial cells (HUVECs) and human stem cells of the apical papilla (SCAPs) encapsulated in RATEA16 hydrogel was detected. Then, we established RA‐VEGF/BMP‐2 drug delivery systems and measured their drug release pattern. The effects of RA‐VEGF scaffolds on HUVECs angiogenesis were investigated in vitro. Then, osteoblastic differentiation capacity of SCAPs with RA‐BMP‐2 scaffolds was analyzed by ALP activity and expression of osteoblast‐related genes. Results A porous nanofiber microstructure endowed this scaffold with the ability to maintain the survival of HUVECs and SCAPs. The RA‐VEGF/BMP‐2 drug delivery systems exhibited several advantagesin vitro: injectability, biodegradability, good biocompatibility, and noncytotoxicity. Released rhVEGF165/BMP‐2 were proved to promote angiogenesis of HUVECs as well as osteogenesis of SCAPs abilities. Conclusion RATEA16 loading with VEGF and BMP‐2 might be a potential clinical strategy for tissue engineering, especially in bone reconstruction, due to its ability of delivering growth factors effectively and efficiently.

ObjectiveThe aim of this study was to explore the regulatory effect of RUNX2 mutation on dental follicle cells (DFCs) senescence and clarify the underlying mechanism. This study aimed to explore the basis for a novel mechanism of delayed permanent tooth eruption in cleidocranial dysplasia (CCD) patients.Materials and MethodsDental follicles were collected from a CCD patient and healthy controls. Senescence‐associated β‐galactosidase (SA‐β‐gal) staining, Ki67 staining, cell cycle assays, and senescence‐related gene and protein expression assays were performed to assess DFCs senescence. Western blotting was performed to detect the activation of mitogen‐activated protein kinase (MAPK) signalling pathways, and the molecular mechanism underlying RUNX2 regulating in DFCs senescence was explored.ResultsRUNX2 mutation inhibited the cellular senescence of DFCs from the CCD patient compared with healthy controls. Ki67 staining showed that mutant RUNX2 promoted DFCs proliferation, and cell cycle assays revealed that the healthy control‐derived DFCs arrested at G1 phase. RUNX2 mutation significantly downregulated senescence‐associated gene and protein expression. RUNX2 mutation suppressed ERK signalling pathway activation, an ERK inhibitor decreased healthy control‐derived DFCs senescence, and an ERK activator promoted CCD patient‐derived DFCs senescence.ConclusionsRUNX2 mutation delayed DFCs senescence through the ERK signalling pathway, which may be responsible for delayed permanent tooth eruption in CCD patients.