Objective:?To investigate the effect of LncRNA small nucleolar RNA host genes (SNHG) 8 on osteogenic differentiation of jaw bone marrow mesenchymal stem cells (JBMMSCs). Methods:?LncRNA SNHG8 was eliminated or overexpressed in JBMMSCs by lentivirus transfection; gene expression was detected by qRT-PCR; alkaline phosphatase (ALP) activity detection, alizarinred staining, calcium ion quantification and Western blot were used to determine the osteogenic differentiation ability of JBMMSCs in vitro. JBMMSCs were mixed with HA/TCP materials and subcutaneous transplanted in nude mice, and the osteogenic differentiation ability of JBMMSCs in vivo was detected by hematoxylin-eosin (HE) staining, Masson staining and immunofluorescence staining; reactive oxygen species (ROS) staining was used to detect ROS levels; and the protein expression of the mitogen-activated protein kinase (MAPK) signaling pathway was detected by Western blot. Results: After lncRNA SNHG8 was knocked down, ALP activity and in vitro mineralization ability of JBMMSCs were increased (P＜0.01, and bone sialprotein (BSP) protein expression bands were increased. After lncRNA SNHG8 was overexpressed, ALP activity and in vitro mineralization ability were decreased (P＜0.01), and BSP protein expression bands were decreased. The expression of phosphorylated c-Jun N-terminal kinase (p-JNK) in MAPK pathway was up-regulated by knocking down of lncRNA SNHG8, and overexpression of lncRNA SNHG8 inhibited p-JNK expression. LncRNA SNHG8 deletion can enhance intracellular ROS staining, and overexpression of lncRNA SNHG8 can inhibit intracellular ROS staining. After lncRNA SNHG8 knockout, new bone formation increased in vivo (P＜0.01), and the expression bands of BSP and osteocalcin (OCN) were enhanced. Conclusions:?LncRNA SNHG8 may inhibit the osteogenic differentiation function of JBMMSCs in vitro and in vivo via JNK signaling pathway.

Objective：To investigate the effect of dynein WDR63 on the differentiation ability of human stem cells from the apical papilla (SCAPs) and the expression of neural differentiation-related markers in vitro. Methods: Using lentiviral transfection, stable over-expression and knockdown of WDR63 in SCAPs were obtained. The neural differentiation of the cells was induced through a neurosphere formation experiment, and the diameter of the neurospheres was quantitatively analyzed. qRT-PCR was used to detect the expression changes of WDR63 gene in untransfected lentivirus SCAPs at 3, 6 and 9 days after induction of neurogenic differentiation. The expression of Nestin and βIII-tubulin in SCAPs was detected by immunofluorescence staining and quantitatively analyzed. qRT-PCR was used to detect the expression of neural differentiation-related indicators such as βIII-tubulin, NeuroD, NCAM, and Nestin genes. Results: The expression level of WDR63 in untransfected lentivirus SCAPs gradually increased at 3, 6, and 9 days after neuronal differentiation (P<0.05). Overexpression of WDR63 led to the increase of WDR63 gene and protein expression (P＜0.001), significant increase in neuronal ball diameter (P＜0.01), and obvious increased in Nestin and βIII-tubulin-positive neural ball-like cells with significantly enhanced fluorescence intensity (P＜0.01). βⅢ-tubulin, NeuroD, NCAM, and Nestin gene expression also increased (P＜0.05). Conversely, knockdown of WDR63 led to decreased WDR63 gene and protein expression (P＜0.01), significant reduction in neuronal ball diameter (P＜0.05), and significant decrease in Nestin and βⅢ-tubulin-positive neural ball-like cells (P＜0.05) with decreased βⅢ-tubulin, NeuroD, NCAM, and Nestin gene expression (P＜0.05). Conclusions: WDR63 promotes the neural differentiation potential of SCAPs.

Objective: To investigate the formation and potential regulatory mechanisms of diacylglycerol (DG)-induced neutrophil extracellular traps (NETs), and to assess the effect of NETs on the gingival epithelial keratinization and barrier. Methods: Lipidomics data from periodontitis and healthy subjects were obtained from the MTBLS4684 database, normalized and analyzed for differences of DG content between the two groups. Human peripheral blood-derived polymorphonuclear neutrophils (PMNs) were treated with DG, followed by detection of citrullinated histone H3 (CitH3) expression by Western blot, extracellular nucleic acid changes by Sytox green staining, and changes of CitH3 expression and distribution by immunofluorescence. After pretreatment of PMNs with protein kinase C (PKC) inhibitor and then stimulated with DG, NETs formation was detected by Western blot, Sytox green staining and immunofluorescence. Human gingival keratinocytes (HGKs) were stimulated by extracted NETs, and changes in the expression of loricrin (LOR) and claudin-2 (CLDN2) were examined by qRT-PCR and Western blot. The levels of LOR and CLDN2 expression in the gingival epithelium of the healthy and periodontitis groups were detected by immunohistochemistry, and the markers of NETs, CitH3 and myeloperoxidase (MPO), in epithelium were assayed by Western blot. Results: Multiple DG was raised in the gingival epithelium of patients with periodontitis. After stimulation of PMNs by DG, CitH3 protein expression was enhanced (P<0.01), nucleic acids were released into the extracellular zone, and CitH3 fluorescence expression was elevated with its distribution to the extracellular region; the above processes were effectively blocked by the application of PKC inhibitor. After stimulation of HGKs by NETs, the expressions of keratinization marker LOR and barrier marker CLDN2 were decreased at the transcriptional and protein levels (P<0.05). In the periodontitis group, the levels of LOR and CLDN2 were reduced, and the expressions of CitH3 and MPO were increased in the gingival epithelium (P<0.05). Conclusions: DG promotes the formation and accumulation of NETs by activating PKC in PMNs, which in turn exerts a destructive effect on keratinization and barrier of epithelium.

Objective:?To clarify the phenotype-genotype correlations of non-syndromic tooth agenesis (NSTA) caused by WNT10A gene mutation. Methods:?We retrieved literature on WNT10A related NSTA from PubMed database between January 2007 to December 2023. This process was conducted by two researchers independently and followed the exclusion and inclusion criteria. The clinical features (such as gender, age, position and number of missing teeth) and related WNT10A variants were analyzed. Results: The 35 articles reporting WNT10A related NSTA included 225 patients with 45 different mutations. The patients age ranged from 6 to 54, with female being more affected than male. Oligodontia was found in most patients and the average number of missing teeth was 9.5. The most prevalent missing teeth were the mandibular second premolar, maxillary second premolar and maxillary lateral incisor, with the same teeth in opposite side frequently affected at the same time. And the c. 682T＞A (p. Phe228Ile) mutation was the most common ones. Conclusions:?The mutations in WNT10A cause selective tooth agenesis. And the mandibular second premolars，maxillary second premolars and maxillary lateral incisors are the most prevalent missing teeth. There is a significant genotype-phenotype association in WNT10A related NSTA.

Objective:?To Explore the function and mutual regulatory mechanism of miR-615-3p and its target gene fibronectin 1 (FBLN1) in osteogenic differentiation of adipose derived stem cells (ADSCs). Methods：Using lentivirus transfection to obtain miR-615-3p knockdown ADSCs and FBLN1 overexpressing ADSCs, qRT-PCR and Western blot were used to detect the knockdown efficiency of miR-615-3p and FBLN1 overexpression efficiency, as well as the expression of FBLN1 after knocking down miR-615-3p. The effects of knocking down miR-615-3p and overexpressing FBLN1 on the osteogenic differentiation ability of ADSCs were evaluated by alkaline phosphatase (ALP) activity assay and alizarin Red staining. Detection of gene expression of osteogenic cell specific transcription factors Osterix (OSX), dentin sialoprotein (DSPP), and dentin matrix protein-1 (DMP1) in knocking down miR-615-3p and overexpressing FBLN1 ADSCs by qRT-PCR. The expression changes of DMP1 and DSPP were detected by Western blot in knocking down miR-615-3p and overexpression of FBLN1. Results：After knocking down miR-615-3p in ADSCs, miR-615-3p gene expression decreased, ALP activity increased (P>0.05), mineralized nodules increased, OSX, DMP1, DSPP gene expression levels increased (P>0.05), and DMP1 and DSPP protein expression increased. The expression of FBLN1 was increased in ADSCs with low expression of miR-615-3p. After overexpression of FBLN1, the expression of FBLN1 gene increased, ALP activity increased (P>0.05), mineralized nodules increased, and the expression levels of osteogenic related indicators such as OSX, DMP1, DSPP increased (P>0.05). Conclusions：miR-615-3p inhibits osteogenic differentiation of ADSCs by downregulating FBLN1.

Objective:?To study the deposition and its distribution of light energy in dental tissue under different laser input modes and establish the qualitative relationship between laser input parameters and the temperature rise distribution in dental tissue. Methods:?Based on the Pennes equation of bio-heat transfer, a heat transport model of the dental tissue irradiated by Er: YAG laser was constructed, in which the layered structure and the heat exchange between the outer surface and surrounding environment was considered. By means of the finite difference method, the time-space distribution properties of temperature rise in dental tissue under different laser input modes were numerically simulated and compared. Results:?The change of the input modes of laser energy (pulse power, pulse width, pulse number and pulse interval) has a significant effect on the temperature rise of dental tissue, and this effect decreases gradually with the increase of depth. Under the premise that the total input energy is fixed, the effect of the change of input modes is only concentrated near the irradiation surface, but has almost no effect on the temperature rise of the pulp cavity wall. In addition, the heat exchange between the outer surface and surrounding environment will inhibit the temperature rise of the dental tissue to a certain extent and accelerate its cooling process. Conclusions:?The laser input method has an important effect on the temperature rise of the dental tissue, and the heat exchange between the external surface and the environment should be considered before and after the process with the dental tissue.

Caries and trauma may cause pulpo-dentinal complex injury, and the existing clinical treatment can not effectively promote the regeneration of pulpo-dentinal complex. In recent years, dental tissue regeneration based on mesenchymal stem cells has been the forefront of current research. Multiple factors may significantly affect the efficacy of pulpo-dentinal complex regeneration, including stem cells, extracellular signaling molecules and biomaterial scaffolds. Based on this, this paper will briefly discuss the effects of dental pulp stem cells (DPSCs) and other odontogenic stem cells on the regeneration of pulpo-dentinal complex, as well as the possible regulatory roles of extracellular matrix (ECM) proteins, extracellular signaling molecules and biomaterial scaffolds, in order to promote the repair and regeneration of pulpo-dentinal complex mediated by stem cells or stem cell derivatives.

Enhanced metabolism of periodontal tissues, microcirculatory disturbances, and proliferation of periodontal bacteria within periodontal pockets resulting in a hypoxic microenvironment are significant pathophysiological features of periodontitis. Important risk factors for the occurrence and progression of periodontitis include high-altitude residence, obstructive sleep apnea syndrome, smoking, which induce low oxygen levels in periodontal tissues and periodontal pockets. The interaction between hypoxia and periodontitis promotes the occurrence and development of periodontitis. This review explores the interaction between hypoxia and periodontitis, as well as the latest research progress on treatment strategies based on the hypoxic microenvironment within periodontal pockets, providing insights for the prevention and treatment of periodontitis.

As a kind of mesenchymal stem cells, dental stem cells can promote angiogenesis by interacting with endothelial cells or secreting a variety of angiogenesis-related cytokines. Several major types of dental stem cells have been isolated and characterized, including dental pulp stem cells, exfoliated deciduous teeth stem cells, periodontal ligament stem cells, apical papilla stem cells, gingival mesenchymal stem cells and dental follicle stem cells. Based on the analysis of the literature in recent years, this paper summarizes and reviews the related research progress of the above-mentioned dental stem cells in promoting angiogenesis and tissue regeneration.

Enterococcus faecalis, a Gram-positive bacterium, is the leading cause of refractory periapical periodontitis. Iron is an essential micronutrient for E. faecalis to survive. To obtain iron from its host, E. faecalis has evolved a variety of mechanisms, and it can tolerate high iron concentrations that are toxic to any other bacteria. E. faecalis is able to sense changes in iron levels in the environment and adjust accordingly, enabling it to grow in different host niches and initiate infection, in this review, the mechanism of maintaining iron homeostasis, the effect of iron homeostasis on the pathogenicity of E. faecalis and the research progress of inhibiting E. Faecalis by regulating iron homeostasis were reviewed, to provide theoretical basis for the prevention and treatment of infectious diseases such as periapical periodontitis.