Background: Although dental pulp stem cells (DPSCs) isolated from periodontally compromised teeth (P-DPSCs) have been demonstrated to retain pluripotency and regenerative potential, their use as therapeutics remains largely unexplored. In this study, we investigated the proangiogenic effects of extracellular vesicles (EVs) secreted by P-DPSCs using in vitro and in vivo testing models. Methods: Patient-matched DPSCs derived from periodontally healthy teeth (H-DPSCs) were used as the control for P-DPSCs. Conditioned media (CMs) derived from H-DPSCs and P-DPSCs (H-CM and P-CM), CMs derived from both cell types pretreated with the EV secretion blocker GW4869 (H-GW and P-GW), and EVs secreted by H-DPSCs and P-DPSCs (H-EVs and P-EVs) were prepared to test their proangiogenic effects on endothelial cells (ECs). Cell proliferation, migration, and tube formation were assessed using the Cell Counting Kit-8 (CCK-8), transwell/scratch wound healing, and Matrigel assays, respectively. Specifically, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and western blot analysis were used to examine the expression levels of angiogenesis-related genes/proteins in ECs in response to EV-based incubation. Finally, a full-thickness skin defect model was applied to test the effects of EVs on wound healing and new vessel formation.

Long non-coding RNAs (lncRNAs) have been shown to play pivotal roles in various types of human cancer, including oral squamous cell carcinoma (OSCC). However, the potential mechanisms of action of lncRNAs in OSCC remain to be fully elucidated. The aim of the present study was to further explore the potential mechanisms of action of lncRNAs in OSCC. We first analyzed Gene Expression Omnibus (GEO) datasets to investigate aberrantly expressed lncRNAs which may be involved in the development of OSCC. Reverse transcription‑quantitative PCR (RT‑qPCR) was performed to analyze the expression levels of lncRNA H19. In addition, the correlation between H19 expression and the clinical characteristics and prognosis of patients with OSCC was statistically analyzed. The effects of H19 expression on OSCC cells were examined by using overexpression and RNA interference approaches in vitro and in vivo. To examine the competitive endogenous RNA (ceRNA) mechanisms, bioinformatics analysis and luciferase reporter assay were performed. In addition, the correlation between H19 and microRNA (miR)‑138 was detected. H19 was found to be upregulated in OSCC tissues and its high expression level was associated with the TNM stage and nodal invasion, and also correlated with a shorter overall survival of patients with OSCC. The knockdown of H19 significantly inhibited OSCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), and induced apoptosis in vitro; it also suppressed subcutaneous tumor growth in vivo. In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR‑138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. On the whole, our findings suggest that H19 functions as an oncogene by inhibiting miR‑138 and facilitating EZH2 expression in OSCC. Thus, lncRNA H1 may represent a potential therapeutic target for OSCC.

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Objectives: Previously, we found that by regulating T helper (Th) cell polarization, calcitriol intervention inhibited lipopolysaccharide (LPS)-induced alveolar bone loss in an animal periodontitis model, but the underlying cellular events remain unknown. Materials and methods:In this study, mouse Th cells were incubated in an inflammatory environment in the presence of dendritic cells (DCs) and LPS. Then, the potential of the Th cells to undergo Th2/Th17 polarization, the RANKL expression of the polarized Th cells and the subsequent influences of the polarized Th cells on RAW264.7 cell osteoclastogenesis in response to calcitriol administration were assessed. Finally, the effects of calcitriol on antigen presentation by DCs during these cellular events were evaluated. Results:In response to calcitriol administration, Th cells in an inflammatory environment exhibited an enhanced potential for Th2 polarization along with a decreased potential for Th17 polarization. In addition, RANKL expression in Th17-polarized cells was largely inhibited. Furthermore, inflammation-induced osteoclastogenesis in RAW264.7 cells was suppressed following coculture with calcitriol-treated Th cells.During these cellular events, increased expression of Th2 promoters (such as OX-40L and CCL17) and decreased expression of Th17 promoters (such as were found in DCs. Conclusions:Calcitriol can inhibit osteoclastogenesis in an inflammatory environment by changing the proportion and function of Th cell subsets. Our findings suggest that calcitriol may be an effective therapeutic agent for treating periodontitis.

Modification of the transmucosal site of an implant by plasmid-mediated pLAMA3-CM gene transfection is a potential method for future clinical applications.

Aim This study aimed to determine whether periodontitis in early pregnancy and periodontal therapy during gestation affect the incidence of gestational diabetes mellitus (GDM) through a population‐based clinical study. Materials and methods Subjects without periodontitis at 1–4 weeks of gestation who met our inclusion criteria were enrolled in the non‐periodontitis group. Periodontitis patients who agreed or refused to receive periodontal therapy during pregnancy were separately enrolled in the periodontitis treated or untreated group. At 12–16 weeks of gestation, gingival crevicular fluid (GCF) and venous blood were collected for analyses of bacterial species and serum inflammatory mediators, respectively. At 24–28 weeks of gestation, GDM patients were identified by oral glucose tolerance tests. The association tests were performed using Chi‐squared statistics and regression analyses. Results The complete data of 3523 pregnant women were recorded during the study period. GDM incidence among the untreated periodontitis participants (84/749, 11.21%) was significantly higher than that among the non‐periodontitis participants (108/2255, 4.79%) (p < .05), and periodontal treatment during gestation reduced the incidence from 11.21% (untreated group) to 7.32% (38/519, treated group) (p < .05). Based on multiple logistic regression analyses, it was found that periodontitis in early pregnancy was associated with GDM, and three‐step regression analyses showed that Porphyromonas gingivalis (P. gingivalis) and the serum TNF‐α and IL‐8 levels played a role in the association between untreated periodontitis and GDM. Furthermore, Pearson's correlation test indicated that the existence of P. gingivalis in GCF was positively correlated with high serum levels of these two inflammatory mediators. Conclusions This study establishes a connection between periodontitis in early pregnancy and GDM and demonstrates that the presence of P. gingivalis is associated with high levels of inflammatory mediators in serum, and thereby may contribute to the development of GDM. In‐depth mechanistic studies are needed to further support these findings.

Following the publication of this article, we realize that the title appeared incorrectly: This appeared in print as "Long non-coding RNA H1 promotes cell proliferation and invasion by acting as a ceRNA of miR-138 and releasing EZH2 in oral squamous cell carcinoma", and the corrected title is now featured above ("H1" should have read as "H19").Note that this error did not have any bearing on the results reported in the paper, or on the conclusions therein. We regret any inconvenience that this mistake has caused.

Background: Salivary adenoid cystic carcinoma (SACC) is one of the most common malignant cancers of the salivary gland, and 32.4-72.0% of SACC cases exhibit neural invasion (NI), however, the molecular mechanism underlying the high invasion potential of SACC remains unclear. Methods: The present study investigated the role of epidermal growth factor receptor (EGFR) in the AKT inhibition- or mitogen-activated protein kinase kinase (MEK)-induced NI and epithelial-mesenchymal transition (EMT) in SACC cells using EGFR, PI3K and MEK inhibitors. SACC 83 cell viability was assessed using an MTT assay, and a wound healing assay was performed to evaluate cell migration. Immunohistochemical staining with streptavidin peroxidase was used to detect the positive expression rate of EMT, AKT, phosphorylated (p)-AKT, ERK and p-ERK proteins. The impact of EGFR, PI3K and MEK inhibitors on tumor growth and NI was examined in a xenograft model in nude mice. Results: EGF and EGFR are effective in increasing cell viability, migration and invasion. SACC metastasis is affected by the PI3K/AKT and MEK/ERK pathways, both of which are initiated by EGF/EGFR. The EMT and NI are regulated by the EGF/EGFR, PI3K/AKT and MEK/ERK pathways. The present findings demonstrate the importance of suppressed EGFR/AKT/MEK signaling in NI in SACC by neural-tumor co-culture in vitro. Furthermore, our preclinical experiment provides solid evidence that injection of EGFR, PI3K and MEK inhibitors obviously suppressed the tumor growth and NI of SACC cells in nude mice. Conclusion: It was identified that inhibitors of EGFR, PI3K/AKT or MEK/ERK suppressed the proliferation, migration and NI of SACC-83 cells via downregulation of the PI3K/AKT or MEK/ERK pathways. It was also demonstrated that inhibition of EGFR abolishes EMT in SACC by inhibiting the signaling of PI3K/AKT and MEK/ERK. The present results suggest the potential effectiveness of targeting multiple oncogenes associated with downstream pathways of EGF/EGFR, as well as potential therapeutic targets to limit NI in SACC by PI3K/AKT or MEK/ERK inhibition.