Regulation of CCl-induced liver cirrhosis by hepatically differentiated human dental pulp stem cells.

Liver transplantation is the most effective treatment for treating liver cirrhosis. However, a limited number of donors, graft rejection, and other complications can undermine transplant success. It is considered that cell transplantation is an alternative approach of liver transplantation.

Regeneration of insulin-producing islets from dental pulp stem cells using a 3D culture system.

Aim: In this study, we aimed to establish the differentiation protocol of dental pulp stem cells (DPSCs) into pancreatic islets using a 3D structure.

Materials & Methods: DPSCs were differentiated in a 3D culture system using a stepwise protocol. Expression of β-cell markers, glucose-stimulated insulin secretion, and PI3K/AKT and WNT pathways were compared between monolayer-cultured pancreatic cells and islets.

Hydrogen sulfide enhances pancreatic β-cell differentiation from human tooth under normal and glucotoxic conditions.

Aim: Glucotoxicity obstructs pancreatic differentiation from adult stem cells. The aim was to develop a novel protocol for differentiation of dental pulp stem cells (DPSCs) into pancreatic β cells and determine the effect of HS on glucotoxicity.

Materials & Methods: DPSCs were differentiated with media containing 5.

Disruption of biomineralization pathways in spinal tissues of a mouse model of diffuse idiopathic skeletal hyperostosis.

Equilibrative nucleoside transporter 1 (ENT1) mediates passage of adenosine across the plasma membrane. We reported previously that mice lacking ENT1 (ENT1(-/-)) exhibit progressive ectopic mineralization of spinal tissues resembling diffuse idiopathic skeletal hyperostosis (DISH) in humans. Here, we investigated mechanisms underlying aberrant mineralization in ENT1(-/-) mice.

Loss of equilibrative nucleoside transporter 1 in mice leads to progressive ectopic mineralization of spinal tissues resembling diffuse idiopathic skeletal hyperostosis in humans.

Diffuse idiopathic skeletal hyperostosis (DISH) is a noninflammatory spondyloarthropathy, characterized by ectopic calcification of spinal tissues. Symptoms include spine pain and stiffness, and in severe cases dysphagia and spinal cord compression. The etiology of DISH is unknown and there are no specific treatments.

The role of p53 in an apoptotic process caused by an oral malodorous compound in periodontal tissues: a review.

Oral malodor is caused by volatile sulfur compounds (VSCs) composed mainly of hydrogen sulfide (H(2)S) and methyl mercaptan. In particular, H(2)S is an important compound, since it is a major component of physiologic halitosis. The toxicity of VSCs is similar to that of hydrogen cyanide, and is well investigated.

Hydrogen sulfide increases hepatic differentiation in tooth-pulp stem cells.

The toxicity of hydrogen sulfide (H(2)S), an oral malodorous compound, is well reported. We have recently established an experimental model of hepatic differentiation from human tooth-pulp stem cells (HTPC) using serum-free medium. The objective of the present study is to determine the effect of H(2)S on hepatic differentiation.

Standardization of clinical protocols in oral malodor research.

The objective of this study is to standardize protocols for clinical research into oral malodor caused by volatile sulfur compounds (VSCs). To detect VSCs, a gas chromatograph (GC) using a flame photometric detector equipped with a bandpass filter (at 393 nm) is the gold standard (sensitivity: 5 × 10(-11) gS s(-1)). The baselines of VSC concentrations in mouth air varied considerably over a week.

Hydrogen sulfide causes apoptosis in human pulp stem cells.

Introduction: Untreated dental caries will eventually lead to pulpal inflammation. Although much is known regarding the interaction of microbial antigens and the immunologic defense systems of pulp, many aspects of the pathogenesis of pulpitis are not fully understood. The relationship between human pulp stem cells (HPSCs) and the pathogenesis of pulpitis remains among the poorly understood areas.

Oral malodorous compound induces osteoclast differentiation without receptor activator of nuclear factor κB ligand.

Background: Hydrogen sulfide (H(2)S), the main component of halitosis, is one of the etiologic factors for periodontitis. We recently reported that H(2)S may induce pathologic changes in rat alveolar bone. The objective of this study is to determine the effect of H(2)S on osteoclast differentiation.

Effects of a composition containing lactoferrin and lactoperoxidase on oral malodor and salivary bacteria: a randomized, double-blind, crossover, placebo-controlled clinical trial.

We report a clinical trial of the effects of test tablets containing bovine lactoferrin and lactoperoxidase on oral malodor and salivary bacteria. Fifteen subjects with volatile sulfur compounds (VSCs) in mouth air above the olfactory threshold (H(2)S >1.5 or CH(3)SH >0.

Oral malodorous compound inhibits osteoblast proliferation.

Background: Oral malodorous compounds including hydrogen sulfide (H2S) are causative agents of periodontitis because the toxicities are similar to that of cyanate. Previous studies demonstrated that volatile sulfur compounds (VSCs) were highly toxic to periodontal tissues, causing a large reduction in the amount of collagen in human gingival fibroblasts and extracellular matrix as well as, for example, apoptosis, immunologic responses, and matrix metalloproteinase production. The objective of this study was to determine the effect of H2S on the proliferation of osteoblasts and a signaling transduction pathway through the mitogen-activated protein kinase (MAPK).

Oral malodorous compound activates mitochondrial pathway inducing apoptosis in human gingival fibroblasts.

Hydrogen sulfide (H(2)S) is a main cause of physiologic halitosis. H(2)S induces apoptosis in human gingival cells, which may play an important role in periodontal pathology. Recently, it has been reported that H(2)S induced apoptosis and DNA damage in human gingival fibroblasts (HGFs) by increasing the levels of reactive oxygen species.

A single application of hydrogen sulphide induces a transient osteoclast differentiation with RANKL expression in the rat model.

Objective: Oral malodor is mainly attributed to volatile sulphur compounds (VSCs) such as hydrogen sulphide (H(2)S), methyl mercaptan and dimethyl sulphide. VSC accelerate periodontal soft tissue destruction. However, there is little information about the potential role of H(2)S in alveolar bone loss.