Human calculus adhesive-induced periodontitis model recapitulating human periodontitis microbiota in rats.

Background: Periodontitis is a chronic inflammatory condition characterized by oral dysbiosis. Current animal models of periodontitis using ligation and pathogen inoculation are time-consuming and do not reflect the chronic characteristics of human periodontitis. One of the significant differences is the difference between the current experimental animal periodontitis microbiome and human periodontitis microbiome.

Intracanal nickel element distribution after root canal preparation using five nickel-titanium instruments and its cytotoxicity on dental pulp cells.

Objectives: This study investigated the distribution of nickel elements in root canals after root canal preparation using five different nickel-titanium instruments, as well as its cytotoxicity on dental pulp cells.

Materials And Methods: Root canal preparations were performed on extracted dental slices using five nickel-titanium instruments. The distribution of nickel within the root canal was analyzed using Inductively Coupled Plasma Mass Spectrometry (ICP-MS) and Field Emission Electron Probe Micro-Analyzer (EPMA).

C166 EVs potentiate miR cardiac reprogramming via miR-148a-3p.

We have demonstrated that directly reprogramming cardiac fibroblasts into new cardiomyocytes via miR combo improves cardiac function in the infarcted heart. However, major challenges exist with delivery and efficacy. During a screening based approach to improve delivery, we discovered that C166-derived EVs were effective delivery agents for miR combo both in vitro and in vivo.

Advances in exercise-induced vascular adaptation: mechanisms, models, and methods.

Insufficient physical activity poses a significant risk factor for cardiovascular diseases. Exercise plays a crucial role in influencing the vascular system and is essential for maintaining vascular health. Hemodynamic stimuli generated by exercise, such as shear stress and circumferential stress, directly impact vascular structure and function, resulting in adaptive changes.

Maternal exercise represses Nox4 via SIRT1 to prevent vascular oxidative stress and endothelial dysfunction in SHR offspring.

Maternal exercise during pregnancy has emerged as a potentially promising approach to protect offspring from cardiovascular disease, including hypertension. Although endothelial dysfunction is involved in the pathophysiology of hypertension, limited studies have characterized how maternal exercise influences endothelial function of hypertensive offspring. In this study, pregnant spontaneously hypertensive rats and Wistar-Kyoto rats were assigned either to a sedentary lifestyle or to swimming training daily, and fetal histone deacetylase-mediated epigenetic modification and offspring vascular function of mesenteric arteries were analyzed.

Neonatal and adult cardiac fibroblasts exhibit inherent differences in cardiac regenerative capacity.

Directly reprogramming fibroblasts into cardiomyocytes improves cardiac function in the infarcted heart. However, the low efficacy of this approach hinders clinical applications. Unlike the adult mammalian heart, the neonatal heart has an intrinsic regenerative capacity.

DNA damage-inducible transcript 3 restrains osteoclast differentiation and function.

DNA damage-inducible transcript 3 (DDIT3), a member of the CCAAT/enhancer-binding protein (C/EBP) family, is involved in cellular apoptosis and differentiation. DDIT3 participates in the regulation of adipogenesis and osteogenesis in vitro and in vivo. However, the role of DDIT3 in osteoclastogenesis is not yet known.

CRISPR/Cas9 Mediated Deletion of the Angiotensinogen Gene Reduces Hypertension: A Potential for Cure?

[Figure: see text].

Sequential paracrine mechanisms are necessary for the therapeutic benefits of stem cell therapy.

Stem cell injections are an attractive therapeutic tool. It has been demonstrated that injected stem cells promote tissue repair and regeneration via paracrine mechanisms. However, the effects of injected stem cells continue for far longer than they are present.

Intramembranous Ossification Imitation Scaffold with the Function of Macrophage Polarization for Promoting Critical Bone Defect Repair.

The regeneration of craniofacial bone defects remains a crucial clinical challenge. To date, numerous biomaterials are applied in this field. However, current strategies have ignored the importance of intramembranous ossification and the vital role of macrophages in regulating osteogenesis.

Yes-associated protein promotes tumour necrosis factor α-treated cementoblast mineralization partly by inactivating NF-κB pathway.

Cementum regeneration, as one of the most difficult challenges of periodontal regeneration, is influenced by inflammatory factors. Inflammation may hamper or promote periodontal tissue repair under different circumstances, as it is found to do in dentin-pulp complex and bone tissue. Our team demonstrated that YAP promotes mineralization of OCCM, a cementoblast cell line.

YAP1 inhibits the induction of TNF-α-stimulated bone-resorbing mediators by suppressing the NF-κB signaling pathway in MC3T3-E1 cells.

Yes-associated protein 1 (YAP1), the core downstream effector of the Hippo signaling cascade, was involved in the regulation of osteoblast and osteoclast differentiation and in bone metabolism. However, the regulatory effects and mechanisms of YAP1 on bone-remodeling molecules in osteoblasts under inflammation remain unknown. In this study, YAP1 expression level was downregulated after treatment with inflammatory cytokine tumor necrosis factor-α (TNF-α) in MC3T3-E1 cells.

MicroRNA-181b-5p modulates tumor necrosis factor-α-induced inflammatory responses by targeting interleukin-6 in cementoblasts.

Tooth cementum is a bone-like mineralized tissue and serves as a microbial barrier against invasion and destruction. Cementum is also responsible for tooth stability and defending pulp from outside stimuli, which is formed by cementoblasts. Although it is crucial for periodontal and periapical diseases, the mechanisms underlying the pathophysiological changes of cementoblasts and their inflammatory responses remain unclear.

Downregulation of angiopoietin-like protein 2 inhibits cementoblast differentiation partially by activating the ERK1/2 signaling pathway.

Angiopoietin-like protein 2 (ANGPTL2) is abundantly expressed in adipose tissue, is associated with tissue homeostasis, and promotes osteoblast and chondrocyte differentiation. In teeth, cementum, a thin layer of mineralized tissue that is formed by cementoblasts, covers the entire root surface and is a vital component of periodontium. The cementoblasts regulate the deposition and mineralization of the cementum matrix.

YAP1 influences differentiation of osteoblastic MC3T3-E1 cells through the regulation of ID1.

Yes-associated protein 1 (YAP1) transcriptional coactivator has recently been identified to regulate skeletal lineage cell differentiation and bone development. However, the role and molecular mechanisms of YAP1 in the regulation of osteoblastic differentiation remains to be elucidated. In this study, we demonstrated that YAP1 expression was increased during osteogenic differentiation of rat bone mesenchymal stem cells and MC3T3-E1.

DDIT3 regulates cementoblast mineralization by isocitrate dehydrogenase 1 through nuclear factor-κB pathway.

DDIT3 is of great importance in endoplasmic reticulum stress and is involved in many inflammatory diseases and mineralization processes. The cementum protects teeth from periodontitis and provides attachment for Sharpey's fibers of the periodontal ligament. However, the effect of DDIT3 on cementoblast differentiation remains largely unknown.

SIRT6 overexpression inhibits cementogenesis by suppressing glucose transporter 1.

Cementum, which shares common features with bone in terms of biochemical composition, is important for the homeostasis of periodontium during periodontitis and orthodontic treatment. Sirtuin 6 (SIRT6), as a member of the sirtuin family, plays key roles in the osteogenic differentiation of bone marrow mesenchymal stem cells. However, the involvement of SIRT6 in cementoblast differentiation and mineralization and the underlying mechanisms remain unknown.

IRX5 promotes NF-κB signalling to increase proliferation, migration and invasion via OPN in tongue squamous cell carcinoma.

Iroquois homeobox gene 5 (Irx5) is a highly conserved member of the Iroquois homeobox gene family. Members of this family play distinct and overlapping roles in normal embryonic cell patterning and development of malignancies. In this study, we observed that IRX5 was abnormally abundant in tongue squamous cell carcinoma (TSCC) tissues and cell lines.

Application of electrophoretic deposition to occlude dentinal tubules in vitro.

Objectives: This study aims to apply electrophoretic deposition (EPD) for occlusion of dentinal tubules in vitro and investigate its effect on tubule occlusion and shear bond strength (SBS).

Methods: Charged mesoporous silica nanoparticles (MSNs) were synthesized and characterized through field-emission scanning electron microscopy (FESEM), transmission electron microscopy (TEM), dynamic light scattering (DLS), and Fourier transform infrared (FT-IR) spectroscopy analyses. Thirty-nine sensitive dentin specimens were modeled and assigned randomly to three groups with different treatments (n = 13 each): group 1, immersion in the MSN suspension; and groups 2 and 3, anodic EPD with the specimen on the negative and positive electrode respectively.

The Role of Pannexin3-Modified Human Dental Pulp-Derived Mesenchymal Stromal Cells in Repairing Rat Cranial Critical-Sized Bone Defects.

Background/aims: Human dental pulp-derived mesenchymal stromal cells (hDPSCs) are promising seed cells for tissue engineering due to their easy accessibility and multi-lineage differentiation. Pannexin3 (Panx3) plays crucial roles during bone development and differentiation. The aim of the present study was to investigate the effect of Panx3 on osteogenesis of hDPSCs and the underlying mechanism.

Yes-associated protein 1 promotes the differentiation and mineralization of cementoblast.

Yes-associated protein 1 (YAP1) transcriptional coactivator is a mediator of mechanosensitive signaling. Cementum, which covers the tooth root surface, continuously senses external mechanical stimulation. Cementoblasts are responsible for the mineralization and maturation of the cementum.

YAP1 negatively regulates chondrocyte differentiation partly by activating the β-catenin signaling pathway.

YAP1 (Yes-associated protein 1) transcriptional coactivator is a downstream gene of the Hippo signaling pathway, which controls cell proliferation and differentiation. YAP1 plays a significant role in the regulation of cartilage and bone development. However, the molecular mechanism by which YAP1 regulates chondrocyte differentiation remains to be elucidated.

Effect of silane pretreatment on the immediate bonding of universal adhesives to computer-aided design/computer-aided manufacturing lithium disilicate glass ceramics.

The aim of this study was to investigate the effect of silane pretreatment on the universal adhesive bonding between lithium disilicate glass ceramic and composite resin. IPS e.max ceramic blocks etched with hydrofluoric acid were randomly assigned to one of eight groups treated with one of four universal adhesives (two silane-free adhesives and two silane-containing adhesives), each with or without silane pretreatment.

Ddit3 suppresses the differentiation of mouse chondroprogenitor cells.

Endochondral ossification is an essential skeletal development process which is strongly linked to chondrocyte differentiation. DNA damage-inducible transcript 3 (Ddit3), a member of the CCAAT/enhancer-binding protein family of transcription factors, is highly expressed in the cartilage plate. However, the role of DNA damage-inducible transcript 3 in chondrocyte differentiation remains to be investigated.

Pannexin3 inhibits TNF-α-induced inflammatory response by suppressing NF-κB signalling pathway in human dental pulp cells.

Human dental pulp cells (HDPCs) play a crucial role in dental pulp inflammation. Pannexin 3 (Panx3), a member of Panxs (Pannexins), has been recently found to be involved in inflammation. However, the mechanism of Panx3 in human dental pulp inflammation remains unclear.