MMP inhibition, marginal integrity and cytotoxicity of zinc-releasing GIC.

Objectives: The degradation of the restorative-dentin interface due to endogenous dentin enzymes, such as matrix metalloproteinases (MMPs), is a significant issue that accelerates the deterioration of the dentin matrix and leads to the failure of restorative treatments. Caredyne Restore (CR), a novel glass ionomer cement (GIC) with zinc ions in its formulation, represents the latest effort to mitigate this issue. This investigation aimed to evaluate the MMPs inhibitory effect, marginal integrity, and cytotoxicity of CR compared to a conventional GIC, Fuji IX (FIX).

Effects of Capsaicin on Migration and Alkaline Phosphatase Activity of Dental Pulp Cells.

Objectives:  Dental pulp, a specialized mesenchymal tissue within teeth, is pivotal in dental health and tissue repair. Capsaicin, the primary pungent component of chili peppers, is known for its diverse pharmacological properties. While capsaicin's effects on various cell types have been studied, its impact on dental pulp cells remains relatively unexplored.

Evaluation of a hydroxyapatite-crosslinked fish gelatin membranes.

Background/purpose: Porcine collagen is widely used in regenerative therapies to generate membranes for bone augmentation. However, porcine or bovine gelatin or collagen is often not appropriate for patients with creed and religious beliefs or for allergic reasons. In this study, we evaluated the potential of fish gelatin to generate membranes.

Correction: Lu et al. Periodontal Pathogen Adhesion, Cytotoxicity, and Surface Free Energy of Different Materials for an Implant Prosthesis Screw Access Hole. 2022, , 329.

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An In Vitro Evaluation of Selenium Nanoparticles on Osteoblastic Differentiation and Antimicrobial Properties against .

Despite numerous treatment methods, there is no gold standard for the treatment of peri-implantitis-an infectious peri-implant disease. Here, we examined selenium nanoparticles (SeNPs) at a wide range of concentrations to investigate their cytotoxicity, regulation of osteoblastic differentiation, and assessed the antibacterial effect against . SeNPs (mean size: 70 nm; shape: near-spherical; concentration: 0-2048 ppm) were tested against the MC3T3-E1 osteoblast precursor cell line and red complex pathogen.

Periodontal Pathogen Adhesion, Cytotoxicity, and Surface Free Energy of Different Materials for an Implant Prosthesis Screw Access Hole.

: Oral implant restorations are an excellent treatment option for edentulous patients; however, periodontopathogenic bacteria have been found in the microgaps between implant-abutment junctions. Implant designs to limit the microgaps have been extensively studied. However, studies have shown microgaps continue to exist, allowing for the leakage of bacteria into the implant system.

Bone morphogenetic protein induces bone invasion of melanoma by epithelial-mesenchymal transition via the Smad1/5 signaling pathway.

Oral malignant melanoma, which frequently invades the hard palate or maxillary bone, is extremely rare and has a poor prognosis. Bone morphogenetic protein (BMP) is abundantly expressed in bone matrix and is highly expressed in malignant melanoma, inducing an aggressive phenotype. We examined the role of BMP signaling in the acquisition of an aggressive phenotype in melanoma cells in vitro and in vivo.

The effect of reduced glutathione on the toxicity of silver diamine fluoride in rat pulpal cells.

Introduction: Due to its ability to arrest untreated dental caries, silver diamine fluoride (SDF) has been advocated for indirect pulp capping procedures. However, the high concentrations of silver and fluoride in SDF raise concerns about its biocompatibility to pulpal tissues.

Objectives: This study aimed to investigate the effect of SDF on the viability, alkaline phosphatase (ALP) activity, and morphology of pulpal-like cells (RPC-C2A) and to evaluate the influence of reduced glutathione (GSH) on SDF-induced cytotoxicity and deposit formation on dentin.

The effect of surface pre-reacted glass-ionomer filler eluate on dental pulp cells and mineral deposition on dentin: In vitro study.

The effects of surface pre-reacted glass-ionomer (S-PRG) filler on pulpal cells and on the composition of dentinal deposits were investigated. Proliferation (CCK-8), cytotoxicity (LDH), and differentiation activity (ALP) tests, along with cell morphology observations, were conducted at 6 and 24 h after treatment of pulpal cells with different S-PRG filler eluate concentrations. Dentinal surfaces were immersed in deionized water or S-PRG filler eluate followed by immersion in deionized water or simulated body fluid and observed under scanning electron microscope and elemental analysis using energy dispersive x-ray spectrometer.

In Vitro Mitigation of Arsenic-Induced Toxicity by Reduced Glutathione in Rat Pulp Cells.

Objective: Despite the controversial results regarding the amount of arsenic (As) in mineral trioxide aggregate (MTA) and MTA-like cements, it is prudent to assess the effect of this heavy metal on pulpal cells and search for methods to attenuate its toxicity. This study investigated the toxic effect of As on pulpal-like cells and evaluated the influence of reduced glutathione (GSH) on As-induced toxicity.

Methods: The cytotoxicity of 50 µm As, 50 µm As+50 µM GSH, 50µm As+500 µM GSH or 50 µm As+5000 µM GSH on rat pulpal cells (RPC-C2A) was evaluated at 24 hours and 72 hours.

The Hormetic Effect of Arsenic Trioxide on Rat Pulpal Cells: An In Vitro Preliminary Study.

Objectives:  Despite the agreement that there is no longer any indication for arsenic use in modern endodontics, some concerns are surfacing about the minute amount of arsenic trioxide (AsO) released from Portland cement-based materials. The present study investigated the effect of different concentrations of AsO on rat pulpal cells and the efficacy of -acetylcysteine (NAC) in preventing AsO-mediated toxicity.

Materials And Methods:  Cytotoxicities of 50, 10, or 5 µm AsO and the effect of cells co-treatment with 50 µm AsO and 5,000 µm NAC or 500 µm NAC were tested at 24 hours or 3 days.

Bif-1/Endophilin B1/SH3GLB1 regulates bone homeostasis.

Skeletal tissue homeostasis is maintained via the balance of osteoclastic bone resorption and osteoblastic bone formation. Autophagy and apoptosis are essential for the maintenance of homeostasis and normal development in cells and tissues. We found that Bax-interacting factor 1 (Bif-1/Endophillin B1/SH3GLB1), involving in autophagy and apoptosis, was upregulated during osteoclastogenesis.

The induction of RANKL molecule clustering could stimulate early osteoblast differentiation.

We recently found that the membrane-bound receptor activator of NF-κB ligand (RANKL) on osteoblasts works as a receptor to stimulate osteoblast differentiation, however, the reason why the RANKL-binding molecules stimulate osteoblast differentiation has not been well clarified. Since the induction of cell-surface receptor clustering is known to lead to cell activation, we hypothesized that the induction of membrane-RANKL clustering on osteoblasts might stimulate osteoblast differentiation. Immunoblotting showed that the amount of RANKL on the membrane was increased by the RANKL-binding peptide OP3-4, but not by osteoprotegerin (OPG), the other RANKL-binding molecule, in Gfp-Rankl-transfected ST2 cells.

Bacterial Inhibition and Osteoblast Adhesion on Ti Alloy Surfaces Modified by Poly(PEGMA- r-Phosmer) Coating.

We have synthesized and immobilized PEGMA-Phosmer to Ti6Al4V surfaces by a simple procedure to reduce bacteria-associated infection without degrading the cell response. Adhered bacteria coverage was lessened to 1% on polymer-coated surfaces when exposed to Escherichia coli, Staphylococcus epidermidis, and Streptococcus mutans. Moreover, PEGMA-Phosmer and homoPhosmer coatings presented better responses to MC3T3-E1 preosteoblast cells when compared with the results for PEGMA-Phosmer-coated and raw Ti alloy surfaces.

A peptide that blocks the interaction of NF-κB p65 subunit with Smad4 enhances BMP2-induced osteogenesis.

Bone morphogenetic protein (BMP) potentiates bone formation through the Smad signaling pathway in vitro and in vivo. The transcription factor nuclear factor κB (NF-κB) suppresses BMP-induced osteoblast differentiation. Recently, we identified that the transactivation (TA) 2 domain of p65, a main subunit of NF-κB, interacts with the mad homology (MH) 1 domain of Smad4 to inhibit BMP signaling.

Low-level ultrahigh-frequency and ultrashort-pulse blue laser irradiation enhances osteoblast extracellular calcification by upregulating proliferation and differentiation via transient receptor potential vanilloid 1.

Background And Objective: Low-level laser irradiation (LLLI) exerts various biostimulative effects, including promotion of wound healing and bone formation; however, few studies have examined biostimulation using blue lasers. The purpose of this study was to investigate the effects of low-level ultrahigh-frequency (UHF) and ultrashort-pulse (USP) blue laser irradiation on osteoblasts.

Study Design/ Materials And Methods: The MC3T3-E1 osteoblast cell line was used in this study.

The intra-articular injection of RANKL-binding peptides inhibits cartilage degeneration in a murine model of osteoarthritis.

We recently found that the receptor activator of NF-κB ligand (RANKL)-binding peptide, OP3-4 stimulated the differentiation of both chondrocytes and osteoblasts. OP3-4 is also shown to inhibit cartilage degeneration. To clarify whether the peptide can inhibit cartilage degeneration without stimulating bone formation, we first performed a proliferation assay using C3H10T1/2 (the murine mesenchymal stem cell line), which is the common origin of both chondrocytes and osteoblasts.

The inhibitory effects of a RANKL-binding peptide on articular and periarticular bone loss in a murine model of collagen-induced arthritis: a bone histomorphometric study.

Introduction: We designed OP3-4 (YCEIEFCYLIR), a cyclic peptide, to mimic the soluble osteoprotegerin (OPG), and was proven to bind to RANKL (receptor activator of NF-κB ligand), thereby inhibiting osteoclastogenesis. We recently found that another RANKL binding peptide, W9, could accelerate bone formation by affecting RANKL signaling in osteoblasts. We herein demonstrate the effects of OP3-4 on bone formation and bone loss in a murine model of rheumatoid arthritis.

Nanogel-crosslinked nanoparticles increase the inhibitory effects of W9 synthetic peptide on bone loss in a murine bone resorption model.

We investigated the biological activity of W9, a bone resorption inhibitor peptide, using NanoClik nanoparticles as an injectable carrier, where acryloyl group-modified cholesterol-bearing pullulan (CHPOA) nanogels were crosslinked by pentaerythritol tetra (mercaptoethyl) polyoxyethylene. Thirty 5-week-old male C57BL/6J mice were fed a low calcium diet and received once-daily subcutaneous injections of the carrier alone, W9 24 mg/kg/day alone, W9 24 mg/kg/day incorporated in cholesterol bearing pullulan (CHP) nanogels, or W9 (8 and 24 mg/kg/day) incorporated in NanoClik nanoparticles for 4 days (n=5). Mice that received a normal calcium diet with NanoClik nanoparticle injections without W9 were used as a control group.

Phytic acid: an alternative root canal chelating agent.

Introduction: The objectives of this study were to investigate the effect of phytic acid, inositol hexakisphosphate (IP6), as a final rinse on the surface of instrumented root canals and smear-layered flat dentin surfaces treated with sodium hypochlorite (NaOCl) and to evaluate its effect on the viability and alkaline phosphatase activity of osteoblast-like cells (MC3T3-E1).

Methods: The universally accepted chelating agent EDTA was used as the control in all conducted experiments. Root canals of human canines were instrumented with rotary files and irrigated with 5% NaOCl, followed by a final rinse of 17% EDTA (1 minute), 1% IP6 (1 minute or 30 seconds), or distilled water.

The inhibition effect of non-protein thiols on dentinal matrix metalloproteinase activity and HEMA cytotoxicity.

Objectives: Phosphoric acid (PA) etching used in etch-and-rinse adhesives is known to activate host-derived dentinal matrix-metalloproteinases (MMPs) and increase dentinal permeability. These two phenomena will result, respectively; in degradation of dentine-adhesive bond and leaching of some monomers especially 2-hydroxyethyl methacrylate (HEMA) into the pulp that would negatively affect the viability of pulpal cells. This study is the first to investigate the inhibitory effect of non-protein thiols (NPSH); namely reduced glutathione (GSH) and N-acetylcysteine (NAC) on dentinal MMPs and compare their effects on HEMA cytotoxicity.

Effect of phytic acid used as etchant on bond strength, smear layer, and pulpal cells.

This study aimed to evaluate the effect of phytic acid (IP6), used as etchant, on resin-dentin bond strength, smear layer removal, and the viability of pulpal cells. Flat dentin surfaces with smear layer were etched with 1% IP6 for 60, 30, or 15 s; in the control group 37% phosphoric acid (PA) was used. Dentin surfaces were rinsed, blot-dried, and bonded with an etch-and-rinse adhesive, followed by composite build-ups.

p130Cas, Crk-associated substrate, plays important roles in osteoclastic bone resorption.

p130Cas, Crk-associated substrate (Cas), is an adaptor/scaffold protein that plays a central role in actin cytoskeletal reorganization. We previously reported that p130Cas is not tyrosine-phosphorylated in osteoclasts derived from Src-deficient mice, which are congenitally osteopetrotic, suggesting that p130Cas serves as a downstream molecule of c-Src and is involved in osteoclastic bone resorption. However, the physiological role of p130Cas in osteoclasts has not yet been confirmed because the p130Cas-deficient mice displayed embryonic lethality.

Cytotoxicity of 45S5 bioglass paste used for dentine hypersensitivity treatment.

Objectives: 45S5 bioglass mixed with 50% phosphoric acid has been suggested to treat dentine hypersensitivity and incipient enamel caries. This study is going to evaluate the biocompatibility of using the aforementioned technique with the rat pulpal cells.

Methods: The relative cytotoxicity of 45S5 bioglass on rat dental pulp cells was compared to the cytotoxicity of a temporary filling material (Caviton; GC, Japan), Type 1 glass ionomer cement (Fuji I; GC, Tokyo, Japan) and commercial desensitising agent (SuperSeal; Phoenix Dental, Fenton, MI, USA) using a transwell insert model.

The tumor necrosis factor type 2 receptor plays a protective role in tumor necrosis factor-α-induced bone resorption lacunae on mouse calvariae.

Tumor necrosis factor (TNF)-α exerts its biological function via TNF type 1 and type 2 receptors (TNFR1 and TNFR2). We have previously reported that bone resorption induced by lipopolysaccharide (LPS) in TNFR2-deficient mice is accelerated compared to that in wild-type (WT) mice. Although these results suggested that TNFR2 might have a protective role in bone resorption, we could not exclude the possibility that TNFR2 has no role in bone resorption.