Clinical trials using dental stem cells: 2022 update.

For nearly 20 years, dental stem cells (DSCs) have been successfully isolated from mature/immature teeth and surrounding tissue, including dental pulp of permanent teeth and exfoliated deciduous teeth, periodontal ligaments, dental follicles, and gingival and apical papilla. They have several properties (such as self-renewal, multidirectional differentiation, and immunomodulation) and exhibit enormous potential for clinical applications. To date, many clinical articles and clinical trials using DSCs have reported the treatment of pulpitis, periapical lesions, periodontitis, cleft lip and palate, acute ischemic stroke, and so on, and DSC-based therapies obtained satisfactory effects in most clinical trials. In these studies, no adverse events were reported, which suggested the safety of DSC-based therapy. In this review, we outline the characteristics of DSCs and summarize clinical trials and their safety as DSC-based therapies. Meanwhile, we also present the current limitations and perspectives of DSC-based therapy (such as harvesting DSCs from inflamed tissue, applying DSC-conditioned medium/DSC-derived extracellular vesicles, and expanding-free strategies) to provide a theoretical basis for their clinical applications.

Analysis of Coding RNA and LncRNA Expression Profile of Stem Cells from the Apical Papilla After Depletion of Sirtuin 7.

OBJECTIVE: To explore the effects of Sirtuin 7 (SIRT7) on the gene expression profile of stem cells from the apical papilla (SCAPs). METHODS: SCAPs were isolated and cultured. SIRT7 short hairpin ribonucleic acid (shRNA) was used to knock down the expression of SIRT7 in SCAPs. After library construction and RNA sequencing (RNA-seq), differentially expressed genes were identified using Cuffdiff with a false discovery rate (FDR) ≤ 0.05 and fold change ≥ 2. Pathway and Gene Ontology (GO) analyses were conducted to elucidate the changes in important functions and pathways after SIRT7 gene knockdown. Gene set enrichment analysis (GSEA) was performed and enrichment of a gene set with an FDR lower than 0.25 was considered significant. RESULTS: The most striking GO terms related to SIRT7sh SCAPs and Consh SCAPs were response to nucleus, nucleolus, cytoplasm, protein binding and intrinsic apoptotic signalling pathway. Signalling pathway analysis revealed the top five pathways to be metabolic, pyrimidine metabolism, protein processing in endoplasmic reticulum, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signalling and p53 signalling. The results of GSEA showed that genes were mainly enriched in cell cycle, cell proliferation, transforming growth factor beta (TGF-ß) signalling and cytokine-cytokine receptor interaction pathways. CONCLUSION: SIRT7 may affect the functions of SCAPs through cell cycle, cell proliferation and apoptosis pathways.

[Protective effect of allicin on human periodontal ligament cells with nicotine-induced oxidative damage].

OBJECTIVE: To explore the protective effect of allicin on nicotine-induced oxidative damage to human periodontal ligament cells (HPDLCs). METHODS: (1) Establish nicotine-induced oxidative damage model on HPDLCs. Use water-soluble tetrazolium (WST) colorimetric method to find out the nicotine concentration (X) that could inhibit HPDLCs' growth for the following experiments. (2) HPDLCs of the fifth passage were divided into 5 groups: The control group, the nicotine group and the nicotine+allicin groups(the concentration of allicin was 15, 30, and 60 microg x mL(-1) respectively). Different kinds of culture media were added. Similarly, use WST colorimetric method to choose the allicin concentration (Y) that could significantly improve the survival rate of HPDLCs. (3) HPDLCs were divided into 3 groups: The control group, the nicotine group, the nicotine+allicin group and different media were added. The glutathion (GSH) concentrations in HPDLCs were determined in 1, 4, 8, 12 and 24h respectively. RESULTS: 0.8 mg x mL(-1) nicotine could inhibit the HPDLCs survival rate significantly (77% of the control, P < 0.05). But 60 microg x mL(-1) allicin could prevent the inhibition effects evidently, improving the survival rate to 112% of that of the nicotine group (P < 0.05) and reaching the survival rate level of control group (P > 0.05). The GSH concentrations of nicotine+allicin group were higher than that of the nicotine group always (P < 0.05) and by 82% at 8 h after culture, but had no difference with that of the control group (P > 0.05). CONCLUSION: 60 microg x mL(-1) allicin can protect the HPDLCs against oxidative damage induced by nicotine.

[Maxillofacial deformity caused by cancrum oris: a case report].

Cancrum oris is a kind of gangrenous disease happening on the maxillofacial region. It is characterized by developing rapidly, high lethality and deforming rate. This article reported a case of maxillofacial deformity caused by cancrum oris, and discussed based on relevant literatures.