Force Eruption of Mandibular Second Incisor in an 11- Year Old Boy: A Technical Report

There is a great challenge in the treatment of deeply fractured and un-restorable teeth among dentists. Orthodontic force eruption is a method of treatment for these teeth to preserve natural root system and periodontal structures. This technical report is a new modification of this procedure presented in an 11- year old boy with deeply fractured left second mandibular incisor. The fractured teeth were treated with root canal therapy and a file #80 was modified to become a hook cemented into the fractured tooth. Anterior teeth were splinted and used as anchorage to help the root extrusion. 1-year follow up of the tooth showed the convenience of the treatment. This simple and low-cost method can be an acceptable alternative to the current high cost techniques, achieving the same results

Comparison of the Push-Out Bond Strength of 5th, 6th, 7th and 8th Generation Bonding Agents to Intracanal Dentin of Primary Anterior Teeth

Background and Objective: Due to the importance of primary anterior teeth in chewing, pronunciation of words, self-confidence, facial appearance of children, efforts to preserve these teeth continue. The aim of the present study was to evaluate the push-out bond strength of 5th, 6th, 7th, and 8th generation bonding agents to intracanal dentin of primary anterior teeth which are reconstructed with the composite posts. Methods: The present experimental in vitro study was conducted on 60 extracted primary anterior teeth with at least two-thirds of the root length remaining. The teeth were randomly divided into five groups: 5th generation (3M Adper single bond 2 Adhesive-USA), 6th generation (clearfil SE bond, Japan), 7th generation (kerr-optibond all in one Adhesive-Italy), and 8th generation total-etch and 8th generation self-etch (GC-G permio bond-Japan) bonding agents. After root canal preparation, prepared canals were filled with Metapex. The coronal 3mm of the canals was etched and impregnated with the dentin bonding agents. Then, they were restored with composite. The push-out test was performed to evaluate the bond strength of adhesives. Accordingly, by a light microscope the failure modes were determined. Findings: The mean bond strength of 5th, 6th, 7th, and 8th generation (self-etch, total-etch) bonding agents was 4.36±2.15, 3.88±1.55, 4.29±2.02, 12.84±3.62, and 7.77±3.81 MPa, respectively. The push-out bond strength of the 8th generation bonding agent using both self-etch (p=0.000) and total-etch techniques was higher than the 5th, 6th, and 7th generation bonding agents (p=0.032, 0.01, 0.027, respectively). No significant difference was found between the bond strength of the 5th, 6th, and 7th generation bonding agents. Conclusion: The push-out bond strength of the 8th generation bonding system was higher than the other groups. Therefore, the 8th generation bonding agents can be used to bond composite posts to intracanal dentin of primary anterior teeth. Also, self-etch (8th generation) has higher bond strength compared to the total-etch technique

Signaling pathways downstream of P2 receptors in human neutrophils

Extracellular nucleotides stimulate human neutrophils by activating the purinergic P2Y2 receptor. However, it is not completely understood which types of G proteins are activated downstream of this P2 receptor subtype. We investigated the G-protein coupling to P2Y2 receptors and several subsequent signaling events. Treatment of neutrophils with pertussis toxin (PTX), a Gi protein inhibitor, caused only ∼75% loss of nucleotide-induced Ca2+ mobilization indicating that nucleotides cause Ca2+ mobilization both through Gi-dependent and Gi-independent pathways. However, the PLC inhibitor U73122 almost completely inhibited Ca2+ mobilization in both nucleotide- and fMLP-stimulated neutrophils, strongly supporting the view that both the PTX-sensitive and the PTX-insensitive mechanism of Ca2+ increase require activation of PLC. We investigated the dependence of ERK phosphorylation on the Gi pathway. Treatment of neutrophils with PTX caused almost complete inhibition of ERK phosphorylation in nucleotide or fMLP activated neutrophils. U73122 caused inhibition of nucleotide- or fMLP-stimulated ERK phosphorylation, suggesting that although pertussis toxin-insensitive pathways cause measurable Ca2+ mobilization, they are not sufficient for causing ERK phosphorylation. Since PLC activation leads to intracellular Ca2+ increase and PKC activation, we investigated if these intracellular events are necessary for ERK phosphorylation. Exposure of cells to the Ca2+ chelator BAPTA had no effect on nucleotide- or fMLP-induced ERK phosphorylation. However, the PKC inhibitor GF109203X was able to almost completely inhibit nucleotide- or fMLP-induced ERK phosphorylation. We conclude that the P2Y2 receptor can cause Ca2+ mobilization through a PTX-insensitive but PLC-dependent pathway and ERK phosphorylation is highly dependent on activation of the Gi proteins

The priming effect of extracellular UTP on human neutrophils: Role of calcium released from thapsigargin-sensitive intracellular stores

P2Y2 receptors, which are equally responsive to ATP and UTP, can trigger intracellular signaling events, such as intracellular calcium mobilization and mitogen-activated protein (MAP) kinase phosphorylation in polymorphonuclear leukocytes (PMN). Moreover, extracellular nucleotides have been shown to prime chemoattractant-induced superoxide production. The aim of our study was to investigate the mechanism responsible for the priming effect of extracellular nucleotides on reactive oxygen species (ROS) production induced in human neutrophils by two different chemoattractants: formyl-methionyl-leucyl-phenylalanine (fMLP) and interleukin-8 (IL-8). Nucleotide-induced priming of ROS production was concentration- and time-dependent. When UTP was added to neutrophil suspensions prior to chemoattractant, the increase of the response reached the maximum at 1 min of pre-incubation with the nucleotide. UTP potentiated the phosphorylation of p44/42 and p38 MAP kinases induced by chemoattractants, however the P2 receptor-mediated potentiation of ROS production was still detectable in the presence of a SB203580 or U0126, supporting the view that MAP kinases do not play a major role in regulating the nucleotide-induced effect. In the presence of thapsigargin, an inhibitor of the ubiquitous sarco-endoplasmic reticulum Ca2+-ATPases in mammalian cells, the effect of fMLP was not affected, but UTP-induced priming was abolished, suggesting that the release of calcium from thapsigargin-sensitive intracellular stores is essential for nucleotide-induced priming in human neutrophils

Substance P Induces Rapid and Transient Membrane Blebbing in U373MG Cells in a p21-Activated Kinase-Dependent Manner

U373MG astrocytoma cells endogenously express the full-length neurokinin 1 receptor (NK1R). Substance P (SP), the natural ligand for NK1R, triggers rapid and transient membrane blebbing and we report that these morphological changes have different dynamics and intracellular signaling as compared to the changes that we have previously described in HEK293-NK1R cells. In both cell lines, the SP-induced morphological changes are Gq-independent, and they require the Rho, Rho-associated coiled-coil kinase (ROCK) signaling pathway. Using confocal microscopy we have demonstrated that tubulin is phosphorylated subsequent to cell stimulation with SP and that tubulin accumulates inside the blebs. Colchicine, a tubulin polymerization inhibitor, blocked SP-induced blebbing in U373MG but not in HEK293-NK1R cells. Although p21-activated kinase (PAK) is expressed in both cell lines, SP induced rapid phosphorylation of PAK in U373MG, but failed to phosphorylate PAK in HEK293-NK1R cells. The cell-permeable Rho inhibitor C3 transferase inhibited SP-induced PAK phosphorylation, but the ROCK inhibitor Y27632 had no effect on PAK phosphorylation, suggesting that Rho activates PAK in a ROCK-independent manner. Our study demonstrates that SP triggers rapid changes in cell morphology mediated by distinct intracellular signaling mechanisms in U373MG versus HEK293-NK1R cells

Integration of P2Y receptor-activated signal transduction pathways in G protein-dependent signalling networks

The role of nucleotides in intracellular energy provision and nucleic acid synthesis has been known for a long time. In the past decade, evidence has been presented that, in addition to these functions, nucleotides are also autocrine and paracrine messenger molecules that initiate and regulate a large number of biological processes. The actions of extracellular nucleotides are mediated by ionotropic P2X and metabotropic P2Y receptors, while hydrolysis by ecto-enzymes modulates the initial signal. An increasing number of studies have been performed to obtain information on the signal transduction pathways activated by nucleotide receptors. The development of specific and stable purinergic receptor agonists and antagonists with therapeutical potential largely contributed to the identification of receptors responsible for nucleotide-activated pathways. This article reviews the signal transduction pathways activated by P2Y receptors, the involved second messenger systems, GTPases and protein kinases, as well as recent findings concerning P2Y receptor signalling in C6 glioma cells. Besides vertical signal transduction, lateral cross-talks with pathways activated by other G protein-coupled receptors and growth factor receptors are discussed

The Fatigue Behavior of Restorations Used Under the Rest of Removable Partial Denture

Statement of Problem: The question about resistance of resin composites under rest in removable partial denture (RPD) is still unanswered. It is important to find the strongest material that withstands the applied stresses when used under RPD components. Objectives: To evaluate and compare the fatigue behavior of amalgam and composite restorations used under the rest of the removable partial denture. Materials and Methods: Forty-five permanent human upper premolars were prepared with standard class II DO cavities and divided into 3 groups of specimens (n=15 for each group). Group I was filled with amalgam (Dispersalloy), group II and III were filled with resin composite (Flitek Z250 and Tetric ceram, respectively). The teeth were stored in distilled water for 14 days before testing. After thermocycling, the “staircase” approach was used to determine the flexural fatigue limits (FFL). The mean differences were evaluated using One-Way ANOVA and post hoc test. Results: A strong significant differences of flexural fatigue strength have been found between amalgam and composite groups (P<0.001). There was no significant difference between two groups of resin composite (P=0.1). Conclusions: To achieve more flexural fatigue strength in the rest seats, the use of resin composite in comparison with amalgam is recommended

Activation of human neutrophils by oleic acid involves the production of reactive oxygen species and a rise in cytosolic calcium concentration: a comparison with N-6 polyunsaturated fatty acids

Contains fulltext : 95617.pdf (publisher's version ) (Open Access)BACKGROUND: There is a growing body of evidence showing that dietary constituents and lipids in particular, influence the function of the human immune system. However, although the beneficial effects of oleic acid (OA) are clear, its mechanism of action at the molecular level is poorly understood. AIMS: To evaluate neutrophil activation under the influence of OA and compare this with several n-6 PUFAs. METHODS: Two key aspects of neutrophil activation were investigated: oxygen radical (ROS) production and intracellular Ca(2+) signaling. RESULTS: OA and the n-6 PUFA arachidonic acid (AA) both induced ROS production in a dose-dependent manner, although AA was the more potent stimulus. When looking for the mechanisms behind these effects, we found that both FA induce increases in cytosolic calcium concentration [Ca(2+)](i)), but whereas OA-induced ROS production is totally mediated through Ca2+ signaling, this is not the case for AA since ROS generation by AA is only partly inhibited in BAPTA-treated cells. We also found evidence for the involvement of protein kinase C (PKC) in the OA-induced ROS generation; by contrast, other enzymes apart from PKC seem to be implicated in n-6 PUFA-induced ROS production. In addition, our results argue against the involvement of a pertussis toxin-sensitive receptor activated by OA. CONCLUSIONS: OA differs from the n-6 PUFA AA in the activation of human neutrophils and these differences may be related to their distinct inmunomodulatory properties