Ablation of FAM20C caused short root defects via suppressing the BMP signaling pathway in mice.

Short root defects are prone to cause various periodontal diseases and lead to tooth loss in some serious cases. Studies about the mechanisms governing the development of the root are needed for a better understanding of the pathogenesis of short root defects. The protein family with sequence similarity 20 group C (FAM20C) is a Golgi casein kinase that has been well studied in the development of tooth crown formation. However, whether FAM20C plays a role in the development of tooth root is still unknown. Thus, we generated Sox2-Cre;Fam20cfl/fl (cKO) mice, in which Fam20c was ablated in both the dental epithelium and dental mesenchyme, and found that the cKO mice showed severe short root defects mainly by inhibiting the development of dental mesenchyme in the root region. In this investigation, we found morphological changes and differentiation defects, with reduced expression of dentin sialophosphoprotein (DSPP) in odontoblasts of the root region in cKO mice. Furthermore, the proliferation rate of apical papillary cells was reduced in the root of cKO mice. In addition, the levels of bone morphogenetic protein 4 (BMP4) and phospho-Smad1/5/8, and that of Osterix and Krüppel-like factor 4 (KLF4), two downstream target molecules of the BMP signaling pathway, were significantly reduced in the root of cKO mice. These results indicate that FAM20C plays an essential role in the development of the root by regulating the BMP signaling pathway.

Effects of different pretreatment agents on primary tooth dentin bonding durability / 口腔疾病防治

Objective@#To explore the effects of different pretreatment agents on primary tooth dentin bonding durability.@*Methods @#Forty-two retained primary molars were selected, 24 of which were cut along the mesial and distal directions; thus, 48 samples were obtained for shear bond strength tests, and the other 18 teeth were used for nanoleakage tests. According to different pretreatments, both experimental samples were divided randomly into three groups (Group A: distilled water pretreatment group; Group B: 2% chlorhexidine pretreatment group; Group C: 10 mg/mL resveratrol pretreatment group). The test specimens were prepared, the shear bond strength was tested, and interfacial nanoleakage evaluation and scanning electron microscope observation were performed to evaluate the effects of different pretreatment agents on the bonding interface immediately and after aging for one hour with 10% sodium hypochlorite aqueous solution.@*Results @#The immediate shear bond strength results showed that there was no significant difference among the three test groups. After aging, the shear bond strength of Group C was significantly higher than that of Group A and Group B (P<0.05). After aging, the shear bond strength of Group A was significantly lower than the immediate shear bond strength (P<0.05), whereas there was no significant difference in shear bond strength before and after aging in Group B and Group C (P>0.05). For Group C, there was no significant difference in interfacial nanoleakage before and after aging. In addition, among the three groups, Group C had the lowest interfacial nanoleakage (P<0.05).@*Conclusion@# Both chlorhexidine and resveratrol pretreatment can improve the adhesion durability of deciduous dentin, but the effects of resveratrol are better than those of chlorhexidine.

Identification and Validation of HOTAIRM1 as a Novel Biomarker for Oral Squamous Cell Carcinoma.

ORAL squamous cell carcinoma (OSCC) is a malignant tumor with the highest incidence among tumors involving the oral cavity maxillofacial region, and is notorious for its high recurrence and metastasis potential. Long non-coding RNAs (lncRNAs), which regulate the genesis and evolution of cancers, are potential prognostic biomarkers. This study identified HOTAIRM1 as a novel significantly upregulated lncRNA in OSCC, which is strongly associated with unfavorable prognosis of OSCC. Systematic bioinformatics analyses demonstrated that HOTAIRM1 was closely related to tumor stage, overall survival, genome instability, the tumor cell stemness, the tumor microenvironment, and immunocyte infiltration. Using biological function prediction methods, including Weighted gene co-expression network analysis (WGCNA), Gene set enrichment analysis (GSEA), and Gene set variation analysis (GSVA), HOTAIRM1 plays a pivotal role in OSCC cell proliferation, and is mainly involved in the regulation of the cell cycle. In vitro, cell loss-functional experiments confirmed that HOTAIRM1 knockdown significantly inhibited the proliferation of OSCC cells, and arrested the cell cycle in G1 phase. At the molecular level, PCNA and CyclinD1 were obviously reduced after HOTAIRM1 knockdown. The expression of p53 and p21 was upregulated while CDK4 and CDK6 expression was decreased by HOTAIRM1 knockdown. In vivo, knocking down HOTAIRM1 significantly inhibited tumor growth, including the tumor size, weight, volume, angiogenesis, and hardness, monitored by ultrasonic imaging and magnetic resonance imaging In summary, our study reports that HOTAIRM1 is closely associated with tumorigenesis of OSCC and promotes cell proliferation by regulating cell cycle. HOTAIRM1 could be a potential prognostic biomarker and a therapeutic target for OSCC.

Effect of dentin surface treatments on the bond strength of resin-modified glass ionomer cement / 口腔疾病防治

@#Resin-modified glass ionomer cement (RMGIC) has good physical, chemical and biological properties and is suitable for the treatment of deciduous caries, aged root surface caries and wedge-shaped defects. Surface treatment is a common method to improve bonding strength, which can improve physical and chemical retention between different components. This paper mainly introduces the current research status of the influence of different dentin surface treatment methods on the bonding strength of RMGIC. At present, the common dentin surface treatment methods are pretreatment, acid etching, laser treatment, etc. The pretreatment agent can improve the bond strength of RMGIC by increasing the surface area and porosity of dentin. The bond strength of RMGIC could be effectively improved after the dentin was treated by an acid-etching bonding system. The dentin was treated with a laser to obtain a higher bonding strength. However, whether the use of resin adhesives will affect the release of fluoride ions in RMGIC into the deep dentin and thus affect the repair effect also needs further research.

Effect of two hemostatic agents on the bonding strength of total-etch and self-etch adhesive systems in primary tooth dentin / 口腔疾病防治

Objective @#To explore the effects of two hemostatic agents on the bonding strength of different bonding systems in primary tooth dentin.@*Methods @# Seventy-two retained deciduous teeth were randomly selected. Forty-eight teeth were used to construct the microleakage model, the other 24 teeth were cut along the mesial and distal directions and 48 samples were obtained to construct the shear bond strength model. The two experiments were divided into 2 groups. Group A was the total-etch group: A1 (ViscoStat + Spectrum Bond NT); A2 (ViscoStat Clear + Spectrum Bond NT); and A3 (Non + Spectrum Bond NT); Group B was the self-etch group: B1 (ViscoStat + Single bond Universal Adhesive); B2 (ViscoStat Clear + Single bond Universal Adhesive); and B3 (Non + Single bond Universal Adhesive). Microleakage experiments and shear bond strength experiments were carried out respectively and the morphology of the fracture surface was observed by scanning electron microscopy.@* Results @#There was no significant difference in microleakage among groups A1, A2, and A3 (P > 0.05). There was no significant difference in microleakage among groups B1, B2, and B3 (P > 0.05). There was no significant difference in the shear bond strength among groups A1, A2 and A3 (P > 0.05). The shear bond strength of groups B1 and B2 was significantly lower than that of group B3 (P < 0.05). There was no significant difference between groups B1 and B2 (P > 0.05). @*Conclusion@#ViscoStat and ViscoStat Clear had no effect on the marginal integrity of deciduous tooth dentin under the different bonding systems. The two hemostatic agents reduced the shear bonding strength of deciduous tooth dentin under the self-etch adhesive system, but had no effect on the shear bonding strength of deciduous tooth dentin under the total-etch adhesive system.

[Effects of protein kinase C and motigen-activated protein kinase kinase/extracellular regulated protein kinases signaling pathway on mRNA level of inducible nitric oxide synthase in Tca8113 cells].

OBJECTIVE: To explore the regulatory mechanism of inducible nitric oxide synthase (NOS-2) expression related to proliferation of Tca8113 cells. METHODS: RNAi mediated by short hairpin RNAs was utilized to knock down NOS-2, protein kinase C (PKC)-α, PKC-ß and PKC-δ. Griess Reagent played a significant role on the detection of NO product after NOS-2 silence. The cell proliferation was determined by CCK8 method. Quantitative real-time polymerase chain reaction (q-PCR) was recruited to check the mRNA level of NOS-2, PKC-α, PKC-ß and PKC-δ after treated by a variety of ways. Eventually, the measure of phosphorylation of extracellular regulated protein kinases (ERK)1/2 was performed by Western blotting in PMA-treated Tca8113 cells. RESULTS: The cell viability of Tca8113 decreased obviously after transfected with NOS-2 siRNA (P<0.01). PKC reduced the expression level of NOS-2 mRNA (P<0.05). PKC-α, PKC-ß and PKC-δ worked together to regulate the level of NOS-2 mRNA (P<0.01). Motigen-activated protein kinase kinase (MEK)/ERK signaling pathway regulated the level of NOS-2 mRNA negatively (P<0.05). PKC down regulated the level of NOS-2 mRNA through MEK/ERK signaling pathway (P<0.05). CONCLUSIONS: PKC regulates the mRNA level of NOS-2 related to proliferation through MEK/ERK signaling pathway in Tca8113 cells.

Distinctive pathways characterize A. actinomycetemcomitans and P. gingivalis.

The study aimed to compare the molecular mechanism of Porphuromonas gingivalis (P. gingivalis) and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans). With microarray dataset (GSE9723) from Gene Expression Omnibus, differentially expressed genes (DEGs) were identified comparing normal cell samples with A. actinomycetemcomitans-infected and P. gingivalis-infected periodontitis cell samples, respectively (|logFC| > 1, p value <0.01), followed by hierarchical cluster analysis using Cluster software. Network topological features of A. actinomycetemcomitans-related and P. gingivalis-related protein-protein interaction networks, and background network, which included average shortest path length (ASPL), degree, closeness centrality (CC), eccentricity (EC), betweenness centrality (BC) and topological coefficient (TC) were compared using network analysis plugin of Cytoscape, followed by pathway enrichment analysis (p value <0.05) using FISHER hyper-geometric algorithm and calculation of pathway alter scores using LIMMA. Totally, 839 DEGs and 251 DEGs were screened for A. actinomycetemcomitans and P. gingivalis, respectively. A. actinomycetemcomitans-related network had lower ASPL, degree and EC but higher CC and TC (p < 0.01), while P. gingivalis-related network had lower EC but higher CC and BC (p < 0.01) compared to background network. P. gingivalis-related network had lower ASPL, degree and EC, but higher CC than the A. actinomycetemcomitans-related network (p < 0.05). A. actinomycetemcomitans was associated with the pathways relating to endothelial cells function, while neuroactive ligand-receptor interaction and MAPK pathways were important for P. gingivalis, which had higher alter scores in hematopoietic cell lineage, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy pathways than A. actinomycetemcomitans. Genes and pathways of the two pathogens were distinctive. The findings aided in preventing and treating relevant diseases.

Improved blood compatibility of Mg-1.0Zn-1.0Ca alloy by micro-arc oxidation.

Magnesium and its alloys have been used in the recent development of lightweight, biodegradeable implant materials. However, the corrosion properties of magnesium limit its usefulness. In a previous study, a micro-arc oxidation (MAO) method was used to modify a Mg-1.0 wt % Zn-1.0 wt % Ca alloy surface, with the purpose of improving the corrosion resistance of Mg alloys. However, the blood compatibility of MAO-treated Mg alloy is unknown. Results of cytotoxicity assays with bone marrow-derived mesenchymal stem cells showed that extracts of MAO-treated alloy significantly decreased cytotoxicity compared to titanium alloy extract. Results of blood compatibility tests showed that the MAO group had a decreased hemolytic ratio (2.25%) compared to the untreated Mg alloy group (24.58%) (p < 0.001). The MAO group showed significantly shorter prothrombin and thrombin times and significantly longer activated partial thromboplastin time than the untreated Mg alloy group. Arachidonic acid- and adenosine diphosphate-induced platelet aggregations were significantly decreased by the untreated Mg alloy extract, and they were less affected by extract of MAO-treated Mg alloy. In conclusion, MAO-treated Mg-1.0 wt % Zn-1.0 wt % Ca alloy exhibits favorable blood compatibility characteristics and may be useful in the development of magnesium implant materials.

Doubly hydrophilic multiarm hyperbranched polymers with acylhydrazone linkages as acid-sensitive drug carriers.

A novel type of drug carrier capable of controlled drug release is proposed. It consists of an acid-sensitive doubly hydrophilic multiarm hyperbranched copolymer with a hyperbranched polyamidoamine core and many linear poly(ethylene glycol) arms. Using pH-sensitive acylhydrazone linkages, the polymer forms unimolecular micelles that can encapsulate hydrophobic drugs. Due to their amphiphilicity, the drug-loaded unimolecular micelles can self-assemble into multimolecular micelles that show acid-triggered intracellular delivery of the hydrophobic drugs.

Analysis of mutation in exon 17 of PTCH in patients with nevoid basal cell carcinoma syndrome.

Abnormalities in sonic hedgehog (SHH) signaling pathway components are major contributing factors in the development of nevoid basal cell carcinoma syndromes (NBCCS) that include SHH, PTCH, SMO and GLI. The novel patched homologue (PTCH) mutation and clinical manifestations with NBCCS links PTCH haplosufficiency and aberrant activation of the sonic hedgehog/Patched/smoothened pathway. To investigate further the molecular genetics of NBCCS, we performed mutation analysis of PTCH gene in a family case with five affected members. These clinical manifestations might be associated with a novel constitutional mutation of the PTCH gene, 3146A-->T (1049N-->I), in exon 17. The analyzed results of tumor tissue show a high expression of GLI. Our findings suggested that the mutation of 3146A-->T may be the cause of high expression of GLI and permit SMO to transmit signal to the nucleus through SHH/PTCH/SMO pathway.