Dental pulp stem cells (DPSCs), precursor cells of odontoblasts, are ideal seed cells for tooth tissue engineering and regeneration. Our previous study has demonstrated that stem cells exist in dental pulp with deep caries and are called carious dental pulp stem cells (CDPSCs). The results indicated that CDPSCs had a higher proliferative and stronger osteogenic differentiation potential than DPSCs. However, the molecular mechanisms responsible for the biological differences between DPSCs and CDPSCs are poorly understood. The aim of this study was to define the molecular features of DPSCs and CDPSCs by comparing the proteomic profiles using two-dimensional fluorescence difference gel electrophoresis (2-D DIGE) in combination with matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS). Our results revealed that there were 18 protein spots differentially expressed between DPSCs and CDPSCs in a narrow pH range of 4 to 7. These differently expressed proteins are mostly involved in the regulation of cell proliferation, differentiation, cell cytoskeleton and motility. In addition, our results suggested that CDPSCs had a higher expression of antioxidative proteins that might protect CDPSCs from oxidative stress. This study explores some potential proteins responsible for the biological differences between DPSCs and CDPSCs and expands our understanding on the molecular mechanisms of mineralization of DPSCs in the formation of the dentin-pulp complex.
Extracellular matrix (ECM) remodeling is accompanied by the continuous synthesis and degradation of the ECM components. This dynamic process plays an important role in guiding cell adhesion, migration, proliferation, and differentiation, as well as in tissue development, body repair, and maintenance of homeostasis. Nanomaterials, due to their photoelectric and catalytic properties and special structure, have garnered much attention in biomedical fields for use in processes such as tissue engineering and disease treatment. Nanomaterials can reshape the cell microenvironment by changing the synthesis and degradation of ECM-related proteins, thereby indirectly changing the behavior of the surrounding cells. This review focuses on the regulatory role of nanomaterials in the process of cell synthesis of different ECM-related proteins and extracellular protease. We discuss influencing factors and possible related mechanisms of nanomaterials in ECM remodeling, which may provide different insights into the design and development of nanomaterials for the treatment of ECM disorder-related diseases.
This study is aimed at comparing the efficacy of heat softening and ultrasonic removal of root-end gutta-percha during retrograde preparation for root apical microsurgery. Recently extracted single-rooted premolars (n = 40) were prepared with standardized endodontically treated and root-end resection and then randomly divided into four groups that received root-end cavity preparation using four different instruments: a diamond-coated ultrasonic tip (AS3D; SACTEON, Paris, France), AS3D with the modified plugger of cordless heat carrier (MSE; B&L Biotech, Bala Cynwyd, PA, USA), stainless steel ultrasonic tip (Jetip-2; B&L Biotech, Bala Cynwyd, PA, USA), or Jetip-2 with MSE. The time required for root-end preparation was recorded. The root apex samples were examined by scanning electron microscopy to assess root surface microcracks and marginal integrity. The remnants of gutta-percha on the cavity walls were evaluated using a stereomicroscope. Statistical analysis was performed using Student's t-test and Wilcoxon rank-sum test (P < 0.05). Usage of MSE with Jetip-2 significantly reduced preparation time from 99.8 ± 6.8 s to 32.4 ± 1.0 s (P = 0.009), the number of microcracks from 42 to 13 (P = 0.036), and the remnants of gutta-percha from 80% to 20% (P = 0.041). Similar results were observed for AS3D with MSE. The heat softening of MSE was effective in cleaning gutta-percha, thus greatly improving the efficiency of the root-end preparation, thereby producing a root-end cavity with fewer microcracks and better marginal integrity.
AIM: To construct a RgpAc knockout strain of Streptococcus mutans.METHODS: The upstream and downstream sequences of RgpAc gene were amplified by polymerase chain reaction(PCR),and were then inserted into 2 multiple clone enzyme cutting sites of pFW5 vector.The reconstructed plasmid was transformed into Streptococcus mutans UA159 by homologous recombination to get the RgpAc gene knock-out mutant.RESULTS: PCR and fluorescence quantitative PCR results showed that the RgpAc gene was replaced.CONCLUSION: Streptococcus mutans RgpAc knockout mutant strain was successfully constructed.
To evaluate the clinical success of the treatment of maxillary anterior primary incisors caries with composite resin strip crowns.Children who presented with severe early childhood caries and were treated comprehensive caries under general anesthesia from January to December 2016 were enrolled in this study. Composite crowns using preformed celluloid crown (3M ESPE, USA) called as "strip crown technique" were applied to treat vital primary incisors with two or multiple surface cavities. Selective etchings of enamel, Universal Bond adhesive and 3M Z350 resin were used to make strip crowns. The patients returned at the end of 6, 12 and 18 months and received clinical and radiologic examinations. Dentists who did not attend the treatment evaluated the strip crowns clinically by modified United States Public Health Service (USPHS) criteria.Four hundred eighteen restorations, placed in 127 children aged 1.17-5.75 years (average of 3.22), were evaluated. The overall retention rate was 97.8% at the end of 6 months, 93.6% at 12 months and 89.2% at 18 months. After 18 months, 28 restorations (6.7%) were totally lost and 4.1% were rated as having lost some resin material. Only four teeth (1.0%) had secondary caries at the end of 18 months and 1.4% teeth had pulpal pathology requiring root canal treatment. Composite crowns had good performance in contour and adjacent contact and improved aesthetics significantly. Twenty-nine teeth (6.9%) showed mild gingivitis and 93.1% showed healthy gingival. 11.2% of the teeth demonstrated color change because plaque accumulation and the polish could remove the stains. The complete loss of strip crowns was mainly related to eating bites.Strip crowns performed well for restoring primary incisors with large or multisurface caries for periods of over 18 months. The strip crowns can be a durable and aesthetic restoration for vital carious primary incisors with adequate tooth structure after caries removal. Functional movement is an important cause of complete loss. Because of the high technical sensitivity and its requirement of the cooperation of children, strip crowns are more suitable for older and cooperative children as well as children receiving dental treatment under sedation or general anesthesia.
BACKGROUND Parathyroid hormone (PTH) is an effective anti-osteoporosis agent, after binding to its receptor PTHR1, several signaling pathways, including cAMP/protein kinase A (PKA) and phospholipase C (PLC)/protein kinase C (PKC), are initiated through G proteins; with the cAMP/PKA pathway as the major pathway. Earlier studies have reported that PTHR1 might also activate PKC via a PLC-independent mechanism, but this pathway remains unclear. MATERIAL AND METHODS In HEK293 cells, cAMP accumulation was measured with ELISA and PKC was measured with fluorescence resonance energy transfer (FRET) analysis using CKAR plasmid. In MC3T3-E1 cells, real-time PCR was performed to examine gene expressions. Then assays for cell apoptosis, cell differentiation, alkaline phosphatase activity, and mineralization were performed. RESULTS The FRET analysis found that PTH(1-34), [G1,R19]PTH(1-34) (GR(1-34), and [G1,R19]PTH(1-28) (GR(1-28) were all activated by PKC. The PKC activation ability of GR(1-28) was blocked by cAMP inhibitor (Rp-cAMP) and rescued with the addition of active PKA-α and PKA-β. The PKC activation ability of GR(1-34) was partially inhibited by Rp-cAMP. In MC3T3-E1 cells, gene expressions of ALP, CITED1, NR4a2, and OSX that was regulated by GR(1-28) were significantly changed by the pan-PKC inhibitor Go6983. After pretreatment with Rp-cAMP, the gene expressions of ALP, CITED1, and OPG were differentially regulated by GR(1-28) or GR(1-34), and the difference was blunted by Go6983. PTH(1-34), GR(1-28), and GR(1-34) significantly decreased early apoptosis and augmented osteoblastic differentiation in accordance with the activities of PKA and PKC. CONCLUSIONS PLC-independent PKC activation induced by PTH could be divided into two potential mechanisms: one was PKA-dependent and associated with PTH(1-28); the other was PKA-independent and associated with PTH(29-34). We also found that PTH could activate PLC-independent PKC via PKA-dependent mechanisms.
Tooth formation is tightly regulated by epithelial‐mesenchymal interactions via hierarchic cascades of signaling molecules. The glycosaminoglycan ( GAG ) chains covalently attached to the core protein of proteoglycans ( PG s) provide docking sites for signaling molecules and their receptors during the morphogenesis of tissues and organs. Although PG s are believed to play important roles in tooth formation, little is known about their exact functions in this developmental process and the relevant molecular basis. Family with sequence similarity member 20‐B ( FAM 20B) is a newly identified kinase that phosphorylates the xylose in the common linkage region connecting the GAG with the protein core of PG s. The phosphorylation of xylose is essential for elongation of the common linkage region and the subsequent GAG assembly. In this study, we generated a Fam20B ‐floxed allele in mice and found that inactivating Fam20B in the dental epithelium leads to supernumerary maxillary and mandibular incisors. This finding highlights the pivotal role of PG s in tooth morphogenesis and opens a new window for understanding the regulatory mechanism of PG ‐mediated signaling cascades during tooth formation.
The neutralisation ability of homologous and heterologous booster vaccinations against the KP.2 variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is unknown. We evaluated Omicron variants (XBB.1, JN.1, and KP.2) neutralisation in participants vaccinated with heterologous versus homologous boosters. In 38 participants each from homologous and heter-ologous booster groups over 690 days, serum pseudovirus neutralisation was tested against the prototype, XBB.1, JN.1, and KP.2 variants to detect neutralisation titres. Total concentration of neutralising antibodies against SARS-CoV-2 receptor-binding domain was measured by en-zyme-linked immunosorbent assay. On throat swab samples, reverse transcription polymerase chain reaction was used to verify breakthrough SARS-CoV-2 infections in participants. Geometric mean neutralising titres against the prototype, total, XBB.1, JN.1, and KP.2 variants were 488.3, 54.5, 42.9, 39.7, and 39.8, respectively. Neutralisation assays revealed 12.3-, 12.3-, and 11.4-fold reduc-tions against JN.1, KP.2, and XBB.1 variants, respectively, compared with the prototype. No sig-nificant difference occurred in neutralising antibody titres among JN.1, KP.2, and XBB.1 Omicron variants. Homologous booster group and males produced fewer neutralising antibodies than heterologous booster group and females, respectively. KP.2 Omicron variant exhibited compa-rable immune evasion properties with other variants. A second different-type or broad-spectrum booster may improve neutralisation against Omicron variants KP.2.
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