Vasculogenesis is a pivotal procedure during dental implant osseointegration and bone repair process. Vascular endothelial growth factor (VEGF), regarded as one of the most important vasculogenesis factor, also plays a central role in bone repair, but its role around dental implants is still unknown. In the present study, rat primary osteoblasts seeded on titanium discs were tested using proliferation, enzyme-linked immunosorbent assay, Real-time PCR, and alkaline phosphatase (ALP) expression. Chicken embryo chorioallantoic membrane (CAM) was used to test the vasculogenesis property. In vivo VEGF-coated implants assay was used to test the osteocalcin (OCN)- and CD31-positive cells around an implant. VEGF could significantly promote osteoblasts seeded on titanium surfaces proliferation and secretion of VEGF protein (P < 0.05); increasing of VEGF, VEGFR1, VEGFR2, NRP-1, ALP and Runx2 mRNA expression (P < 0.05); up-regulating ALP expression on days 7 and 11 (P < 0.01). Supernatant of VEGF-induced osteoblasts could promote CAM vasculogenesis (P < 0.05). In vivo, VEGF-coated implants could promote OCN- and CD31-positive cells around bone lacunas. The present study shows that VEGF could induce primary rat osteoblasts proliferation, VEGF protein secretion, ALP expression, and VEGF-related mRNA expression in vitro. Osteoblasts co-cultured with VEGF could promote neovascularization in chicken embryos. In the in vivo experiments, coating the implant with VEGF could promote osteoblasts and endothelial cell expression.

Aging is associated with peripheral nerve degradation and bone destruction. The aim of the study is to elucidate the influence of sensory denervation on bone metabolism in different age groups by establishing a modified unilateral inferior alveolar nerve transection (IANT) model. The rats, divided into young, middle-aged and aged group, were sacrificed at 1, 2, 4 and 8 weeks after right IANT. The histological changes of mandibles were analyzed by fluorescent double labeling, micro-CT, HE, TRAP and anti-CGRP immunohistochemical staining. Molecular mechanisms underlying the changes were analyzed by qPCR and western blot. Differences between the test and control side were evaluated by paired-samples t test. The Friedman test and separate Wilcoxon signed-rank tests were applied to analyze age-dependent difference. The impact of IANT was the most intensive in developing bone, the most persistent in full grown bone and the faintest in the aged bone. The role of IAN in keeping homeostasis was closely related to the anabolic effect of CGRP, which suppressed the number of osteoclasts through OPG/RANKL ratio and controlled growth factors expression like BMP2. This study contributes to a better understanding of the molecular mechanisms of CGRP in vivo and the relationship among sensory nerve, bone metabolism and aging.

Objective. To investigate the genetic crosstalk mechanisms that link periodontitis and Alzheimer’s disease (AD). Background. Periodontitis, a common oral infectious disease, is associated with Alzheimer’s disease (AD) and considered a putative contributory factor to its progression. However, a comprehensive investigation of potential shared genetic mechanisms between these diseases has not yet been reported. Methods. Gene expression datasets related to periodontitis were downloaded from the Gene Expression Omnibus (GEO) database, and differential expression analysis was performed to identify differentially expressed genes (DEGs). Genes associated with AD were downloaded from the DisGeNET database. Overlapping genes among the DEGs in periodontitis and the AD-related genes were defined as crosstalk genes between periodontitis and AD. The Boruta algorithm was applied to perform feature selection from these crosstalk genes, and representative crosstalk genes were thus obtained. In addition, a support vector machine (SVM) model was constructed by using the scikit-learn algorithm in Python. Next, the crosstalk gene-TF network and crosstalk gene-DEP (differentially expressed pathway) network were each constructed. As a final step, shared genes among the crosstalk genes and periodontitis-related genes in DisGeNET were identified and denoted as the core crosstalk genes. Results. Four datasets (GSE23586, GSE16134, GSE10334, and GSE79705) pertaining to periodontitis were included in the analysis. A total of 48 representative crosstalk genes were identified by using the Boruta algorithm. Three TFs (FOS, MEF2C, and USF2) and several pathways (i.e., JAK-STAT, MAPK, NF-kappa B, and natural killer cell-mediated cytotoxicity) were identified as regulators of these crosstalk genes. Among these 48 crosstalk genes and the chronic periodontitis-related genes in DisGeNET, C4A, C4B, CXCL12, FCGR3A, IL1B, and MMP3 were shared and identified as the most pivotal candidate links between periodontitis and AD. Conclusions. Exploration of available transcriptomic datasets revealed C4A, C4B, CXCL12, FCGR3A, IL1B, and MMP3 as the top candidate molecular linkage genes between periodontitis and AD.

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