Impact of vertical alveoloplasty on changes in keratinized mucosa width following full-arch immediate implant placement and rehabilitations: A prospective case series.

PURPOSE: This prospective case series aimed to investigate the effect of vertical alveoloplasty on the changes in keratinized mucosa width (KMW) following full-arch immediate implant placement and rehabilitation. MATERIALS AND METHODS: A total of 17 potential edentulous patients were enrolled and received implant placement and full-arch implant-supported immediate rehabilitations. The main outcome was to analyze the effect of vertical alveoloplasty on the changes in KMW. The amount of vertical alveoloplasty during implant surgery as well as the changes in KMW at buccal aspects from the day of surgery to 6 months post-surgery were recorded on the implant-level using a periodontal probe. The secondary outcome was to analyze the other possible factors that affected the changes in KMW. The included factors were the initial KMW, the distribution of implants in the maxilla and mandible, the distribution of implants in the anterior and posterior regions, the distribution of implants in extraction sockets and healed ridges, and gender. Mann-Whitney non-parametric tests and multiple linear regression adjusted by generalized estimating equations (GEE) were used to statistically analyze the data. RESULTS: A total of 121 implant positions were analyzed. The KMW was 4.1± 2.0 mm on the day of the surgery and 4.1± 1.7 mm 6 months post-surgery. The mean changes in KMW following 6 months were -0.1± 1.6 mm (p = 0.824). From the results of GEE, the vertical amount of alveoloplasty had no significant effect on changes in KMW. Both initial KMW and the distribution of implants in the anterior and posterior regions had significant impacts on the changes in KMW (p < 0.0001). CONCLUSION: The amount of vertical alveoloplasty during implant surgery has no significant impact on the KMW. The KMW remained stable from baseline to 6 months after alveoloplasty, implant placement, and immediate rehabilitations in potential edentulous arches. The initial KMW and the distribution of implants in the anterior and posterior regions were the possible factors affecting changes in KMW.

Adenosine receptors enhance the ATP-induced odontoblastic differentiation of human dental pulp cells.

Purinergic signaling regulates various biological processes through the activation of adenosine receptors (ARs) and P2 receptors. ATP induces the odontoblastic differentiation of human dental pulp cells (HDPCs) via P2 receptors. However, there is no information available about the roles of ARs in HDPC odontoblastic differentiation induced by ATP. Here, we found that HDPCs treated with ATP showed higher activity of ADORA1 (A1R), ADORA2B (A2BR), and ADORA3 (A3R). Inhibition of A1R and A2BR attenuated ATP-induced odontoblastic differentiation of HDPCs, whereas activation of the two receptors enhanced the odontoblastic differentiation induced by ATP. However, activation of ARs by adenosine did not induce the odontoblastic differentiation of HDPCs independently without induction of ATP. Our study indicates a positive role for ARs in ATP-induced odontoblastic differentiation of HDPCs, and demonstrates that ATP-induced odontoblastic differentiation of HDPCs may be due to the combined administration of ARs and P2 receptors. This study provides new insights into the molecular mechanisms of pulpal injury repair induced by ATP.

Effects of Adenosine Triphosphate on Proliferation and Odontoblastic Differentiation of Human Dental Pulp Cells.

INTRODUCTION: Adenosine 5'-triphosphate (ATP) is a potent signaling molecule that regulates diverse biological activities in cells. Its effects on human dental pulp cells (HDPCs) remain unknown. This study aimed to examine the effects of ATP on proliferation and differentiation of HDPCs. METHODS: Reverse transcription polymerase chain reaction was performed to explore the mRNA expression of P2 receptor subtypes. Cell Counting Kit-8 test and flow cytometry analysis were used to examine the effects of ATP on proliferation and cell cycle of HDPCs. The effects of ATP on differentiation of HDPCs were examined by using alizarin red S staining, energy-dispersive x-ray analysis, Western blot analysis, and real-time polymerase chain reaction. RESULTS: The purinoceptors P2X3, P2X4, P2X5, P2X7, and all P2Y receptor subtypes were confirmed to present in HDPCs. ATP enhanced HDPC proliferation at 10 µmol/L concentration. However, it inhibited cell proliferation by arresting the cell cycle in G0G1 phase (P < .05 versus control) and induced odontoblastic differentiation, ERK/MAPK activation, and dentin matrix protein 1 (DMP1) and dentin sialophosphoprotein (DSPP) mRNA transcriptions at 800 µmol/L concentration. Suramin, an ATP receptor antagonist, inhibited ERK/MAPK activation and HDPC odontoblastic differentiation (P < .05 versus control). CONCLUSIONS: Extracellular ATP activates P2 receptors and downstream signaling events that induce HDPC odontogenic differentiation. Thus, ATP may promote dental pulp tissue healing and repair through P2 signaling. Results provide new insights into the molecular regulation of pulpal wound healing.