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Cannabinoids possess anti-inflammatory, analgesic, and osteogenic effects in different cell types and tissues. The null hypothesis is delta-9-tetrahydrocannabinol (THC) might induce dental tissue repair and regeneration. The aim of this study was to investigate the effect of THC on human dental pulp cell (HDPC) viability and biomineralization as well as the molecular mechanism of THC-induced odonto/osteogenic differentiation of HDPCs. The toxicity of THC on HDPCs was determined by 3-(4,5-dimethylthiazolyl-2-yl)-2,5-diphenyltetrazolium bromide assay. The odonto/osteogenic differentiation marker genes of HDPCs were assessed by real-time polymerase chain reaction with or without THC treatment. HDPC biomineralization was examined by collagen synthesis and calcium nodule deposition. The molecular mechanism of THC on HDPCs was investigated by examining the mitogen-activated protein kinase (MAPK) signaling pathway via blocking cannabinoid receptor type 1 or 2 receptors. We found that THC had no inhibition of HDPC vitality in the testing concentration (0–100 μmol/L). THC showed biphasic effects on HDPC proliferation. At a low dose (<5 μmol/L), THC considerably increased HDPC cell division. HDPC proliferation reduced with higher THC concentrations (>5 μmol/L). The expression of odonto/osteogenic marker genes were up-regulated in the presence of cannabinoids. These were confirmed by increased collagen synthesis and mineralized calcium nodule formation in the cannabinoid group. The effect of THC-induced odonto/osteogenesis occurred via MAPK signaling. THC was biocompatible to HDPCs by promoting their mitogenic division in a biphasic pattern depending on the concentration. THC induced HDPC odonto/osteogenic differentiation through the activation of MAPK mediated by CB1 and CB2 receptors. Cannabinoids may play an important role in the HDPC regeneration process and potentially be used as a pulp-capping agent. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effects of mandible advanced device (MAD) therapy for obstructive sleep apnea-hypopnea syndrome (OSAHS) on nitric oxide (NO) release and changes in pulmonary artery pressure and structure.Methods: Thirty male New Zealand white rabbits were randomly divided into OSAHS, MAD, and control groups (n = 10 per group). The soft palate of rabbits in the OSAHS and MAD groups was injected with hydrophilic polyacrylamide gel to induce OSAHS. The MAD group wore a MAD, and the control group was not treated. Cone-beam computed tomography scans and polysomnography recordings were performed to confirm successful model establishment. All rabbits slept in a supine position for 4 to 6 hours daily and were observed for 8 consecutive weeks. The pulmonary artery pressure was measured by right heart catheterization. Pulmonary artery morphometry was analyzed by hematoxylin and eosin staining. NO levels in plasma and lung homogenate supernatants were detected by Griess reaction assay kits.Results: The OSAHS group exhibited higher pulmonary artery pressure (57.74 ± 1.79 mm Hg) than the MAD (19.99 ± 2.04 mm Hg) and control (14.49 ± 0.54 mm Hg) groups. The media thickness percentage of the pulmonary artery was higher in the OSAHS group (46.89 ± 2.72%) than the control group (15.87 ± 1.18%) and was markedly reduced by MAD (21.64 ± 1.45%). Blood oxygen saturation was positively correlated with the NO concentration in both the lung and plasma, and the NO concentration was negatively correlated with the media thickness percentage and media section percentage.Conclusions: OSAHS induced a decrease in NO and pulmonary hypertension, which was relieved by MAD therapy. [ABSTRACT FROM AUTHOR]