Alterations to Titanium Surface Depending on the Fluorides and Abrasives in Toothpaste.

Fluoride and abrasives in toothpastes may cause corrosion and deterioration of the titanium used for implants and other prostheses. The purpose of this study was to investigate how the presence or absence and types of fluoride and abrasives affected the titanium surface texture. Brushing with toothpastes was performed on pure-titanium discs using an abrasive testing machine.

Porcine Dental Epithelial Cells Differentiated in a Cell Sheet Constructed by Magnetic Nanotechnology.

Magnetic nanoparticles (MNPs) are widely used in medical examinations, treatments, and basic research, including magnetic resonance imaging, drug delivery systems, and tissue engineering. In this study, MNPs with magnetic force were applied to tissue engineering for dental enamel regeneration. The internalization of MNPs into the odontogenic cells was observed by transmission electron microscopy.

Soluble RANKL Cleaved from Activated Lymphocytes by TNF-α-Converting Enzyme Contributes to Osteoclastogenesis in Periodontitis.

Host immune responses play a key role in promoting bone resorption in periodontitis via receptor activator of NF-κB ligand (RANKL)-dependent osteoclastogenesis. Both membrane-bound RANKL (mRANKL) expressed on lymphocytes and soluble RANKL (sRANKL) are found in periodontal lesions. However, the underlying mechanism and cellular source of sRANKL release and its biological role in periodontitis are unclear.

A-Disintegrin and Metalloproteinase (ADAM) 17 Enzymatically Degrades Interferon-gamma.

Interferon-gamma (IFN-γ) is a pleiotropic cytokine that exerts anti-tumor and anti-osteoclastogenic effects. Although transcriptional and post-transcriptional regulation of IFN-γ is well understood, subsequent modifications of secreted IFN-γ are not fully elucidated. Previous research indicates that some cancer cells escape immune surveillance and metastasize into bone tissue by inducing osteoclastic bone resorption.

Increase in receptor activator of nuclear factor κB ligand/osteoprotegerin ratio in peri-implant gingiva exposed to lipopolysaccharide.

Background/purpose: The prevalence of peri-implant diseases, including peri-implant mucositis and peri-implantitis, is increasing. The aim of this study was to elucidate the pathological mechanisms of inflammation and alveolar bone resorption in peri-implant tissues. To do this, we fabricated inflamed gingiva around mini-implants in the palatine processes of rats using lipopolysaccharide derived from (-LPS).

Inhibition of RANKL-dependent cellular fusion in pre-osteoclasts by amiloride and a NHE10-specific monoclonal antibody.

The functions of Na(+) /H(+) exchangers (NHEs) during osteoclastic differentiation were investigated using the NHE inhibitor amiloride and a monoclonal antibody (MAb). Compared with sRANKL-stimulated control cells, amiloride decreased the number of large TRAP-positive osteoclast cells (OCs) with ≥10 nuclei and increased the number of small TRAP-positive OCs with ≤10 nuclei during sRANKL-dependent osteoclastic differentiation of RAW264.7 cells.

Release of titanium ions from an implant surface and their effect on cytokine production related to alveolar bone resorption.

Although interest in peri-implant mucositis and peri-implantitis has recently been increasing, the mechanisms driving these diseases remain unknown. Here, the effects of titanium ions on the inflammation and bone resorption around an implant were investigated. First, the accumulated amount of Ti ions released into gingival and bone tissues from an implant exposed to sodium fluoride solution was measured using inductively coupled plasma mass spectrometry.

Involvement of ERK and p38 MAPK pathways on Interleukin-33-induced RANKL expression in osteoblastic cells.

The receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG) system is a well-known key factor in osteoclast differentiation, and osteoblastic lineage cells are the major sources of RANKL and OPG in local bone tissue. Recently, a new molecule from the interleukin (IL)-1 family, IL-33, was identified. Here, we report the possible involvement of IL-33 in RANKL and OPG expression, and the signaling pathways that are required for maximal IL-33-induced RANKL expression in MC3T3-E1 osteoblastic cells.

Blocking of sodium and potassium ion-dependent adenosine triphosphatase-α1 with ouabain and vanadate suppresses cell-cell fusion during RANKL-mediated osteoclastogenesis.

To examine the possible enrolment of Na(+)/K(+)-ATPase during osteoclast differentiation, Na(+)/K(+)-ATPase inhibitors, including ouabain and vanadate, were used in this study. These inhibitors significantly inhibited cell-cell fusion of RAW264.7 cells and bone marrow cells induced by RANKL.

Evaluation of trabecular bone formation in a canine model surrounding a dental implant fixture immobilized with an antimicrobial peptide derived from histatin.

JH8194 induces osteoblast differentiation, although it was originally designed to improve antifungal activity. This suggests that JH8194 is useful for implant treatment. Therefore, the aim of this study was to evaluate the osseointegration capacity of JH8194-modified titanium dental implant fixtures (JH8194-Fi).

Bovine milk fermented with Lactobacillus rhamnosus L8020 decreases the oral carriage of mutans streptococci and the burden of periodontal pathogens.

Aim:   The aim of this study was to find the oral isolate of lactobacilli, which has the potential to inhibit either periodontal, cariogenic, or fungal pathogens in vitro, and to examine the effects of bovine milk fermented with the isolate on the oral carriage of cariogenic and periodontal pathogens.

Methods:   The inhibitory effects of the supernatant of Man-Rogosa-Sharpe broth, in which each of 42 oral isolates of lactobacilli grown, was examined. One isolate, Lactobacillus rhamnosus L8020, that showed the potential to inhibit either periodontal, cariogenic, or fungal pathogens in vitro, was used to examine the effects of fermented milk on the oral carriage of cariogenic and periodontal pathogens, which was examined by a placebo-controlled and cohort trial using 50 participants.

Aggregatibacter actinomycetemcomitans Omp29 is associated with bacterial entry to gingival epithelial cells by F-actin rearrangement.

The onset and progressive pathogenesis of periodontal disease is thought to be initiated by the entry of Aggregatibacter actinomycetemcomitans (Aa) into periodontal tissue, especially gingival epithelium. Nonetheless, the mechanism underlying such bacterial entry remains to be clarified. Therefore, this study aimed to investigate the possible role of Aa outer membrane protein 29 kD (Omp29), a homologue of E.

Titanium ion induces necrosis and sensitivity to lipopolysaccharide in gingival epithelial-like cells.

Gingival epithelial-like cells (GE-1) were cultured and used to examine the cellular responses of gingival tissues to varying concentrations of titanium (Ti) ions. Titanium ions at concentrations of more than 13 ppm significantly decreased the viability of GE-1 cells and increased LDH release from the cells into the supernatant, but had no significant effect on their caspase 3 activity. These data suggest that a high concentration of Ti ions induced necrosis of the GE-1 cells.

Titanium immobilized with an antimicrobial peptide derived from histatin accelerates the differentiation of osteoblastic cell line, MC3T3-E1.

The objective of this study was to evaluate the effect of titanium immobilized with a cationic antimicrobial peptide (JH8194) derived from histatin on the biofilm formation of Porphyromonas gingivalis and differentiation of osteoblastic cells (MC3T3-E1). The titanium specimens (Ti) were immobilized with JH8194, according to the method previously described. The colonization of P.

Immobilized-OPG-Fc on a titanium surface inhibits RANKL-dependent osteoclast differentiation in vitro.

The purpose of the present study was to examine the effect of osteoprotegerin (OPG)-Fc fusion protein immobilized on a titanium surface on the initial differentiation of osteoclast precursor RAW264.7 cells. These cells were cultured on titanium specimens over which OPG-Fc was immobilized.

Impact of titanium ions on osteoblast-, osteoclast- and gingival epithelial-like cells.

Purpose: To investigate the effects of titanium (Ti) ions on the cell viability, the cell differentiation and the gene expressions related to bone resorption including Receptor Activator of NF-kappaB Ligand (RANKL) and Osteoprotegerin (OPG) in the tissues around dental implants, the osteoblast-, osteoclast-, and gingival epithelial-like cells were exposed to Ti ions.

Methods: An MTS assay was carried out to evaluate the viabilities of osteoblast-like MC3T3-E1, osteoclast-like RAW264.7 and epithelial cell-like GE-1 cells.

[Functional model of the middle ear ossicles].

In students' dissection practice, it is very difficult to teach students the structures and functions of the middle ear ossicles. The middle ear ossicles are too small to explain their structures and functions. Models are useful in explaining these points, but there have been no models that accurately explain the movements of the middle ear ossicles and the functions of the muscles in the middle ear.

Research projects related to complete dentures published in 2008 by members of the Japan Prosthodontic Society.

This article reviews the findings of the original papers related to complete dentures published in the Journal of the Japan Prosthodontic Society (Nippon Hotetsu Shika Gakkai Zasshi), Vol. 52, 2008. A total of six articles focused on complete dentures or materials related to complete dentures were selected and summarized.

[Model for the functional instruction of swallowing].

It is difficult to teach students about the mechanism of swallowing. There are three phases of swallowing; oral phase, pharyngeal phase and esophageal phase. The bolus of food is propelled to back of mouth by the tongue and the swallowing reflex happens.

Impact of the microgravity environment in a 3-dimensional clinostat on osteoblast- and osteoclast-like cells.

Mechanical unloading conditions result in decreases in bone mineral density and quantity, which may be partly attributed to an imbalance in bone formation and resorption. To investigate the effect of mechanical unloading on osteoblast and osteoclast differentiation, and the expression of RANKL and OPG genes in osteoblasts, we used a three-dimensional (3D) clinostat system simulating microgravity to culture MC3T3-E1 and RAW264.7 cells.

Titanium surface roughness accelerates RANKL-dependent differentiation in the osteoclast precursor cell line, RAW264.7.

The present study was a molecular analysis of the initial differentiation of osteoclast precursor RAW264.7 cells on titanium specimens. RAW264.

B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease.

Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues.

[A case of complete dentures with improvement of mandibular position].

Patient: A patient visited our hospital for fabrication of functional complete dentures to resolve masticatory disturbance. The case was diagnosed as edentulous jaws with inadequate mandibular position and movement. Therefore, new complete dentures were fabricated and set without reference to the old dentures.

In vitro mechanisms of interleukin-8-mediated responses of human gingival epithelial cells to Candida albicans infection.

Oral epithelial cells significantly influence host inflammatory responses against Candida albicans in oropharyngeal candidiasis. We sought to elucidate the pattern of interleukin-8 (IL-8) expression by oral epithelial cells, which may function as an early innate immune system mediator during C. albicans infection.