Push-out Bond Strength of Fiber Posts Luted with Unfilled Resin Cement

Purpose: The study evaluates the behavior of different adhesive systems and resin cements in fiber post placement, with the intent to clarify the possible role of unfilled resin as a luting material for fiber posts. Materials and Methods: Two luting agents (Dual-Link and Unfilled Resin) for cementing fiber posts into root canals were applied either with All-Bond 2 or One-Step Plus, or without an adhesive system, and challenged with the push-out test. Slices of roots restored with posts were loaded until post segment extrusion in the apical-coronal direction. Failure modes were analyzed under SEM. Results: Push-out strength was significantly influenced by the luting agent (p < 0.05), but not by the bonding strategy (p > 0.05). The best results were obtained in combination with Unfilled Resin with One-Step Plus. Dual-Link groups failed mainly cohesively within the cement, while Unfilled Resin demonstrated more adhesive fracture at the post interface. Conclusion: The results of this study support the hypothesis that adhesive unfilled resin application is essential for achieving high bond strength to radicular dentin.

Microtensile vs Microshear Bond Strength of All-in-One Adhesives to Unground Enamel

Purpose To determine the bond strength to unground enamel of all in one adhesives in comparison with an etch and rinse system and to compare the reliability of microtensile and microshear methods in providing such measurements Materials and Methods The bonding procedure was performed on enamel of 64 extracted molars The tested all in one adhesives were Bond Force (Tokuyama), AdheSE One (Ivoclar Vivadent) and Xeno V (Dentsply) Prime&Bond NT (Dentsply) served as control Microtensile specimens were obtained from 4 teeth per group Twelve teeth per group were used for microshear testing Microtensile specimens that failed prior to testing were included in statistical calculations, they were assigned the lowest value measured in the respective group Failure modes were observed under light microscope and classified (cohesive within substrates, adhesive mixed) Statistically significant differences in bond strength were assessed among the adhesives within each testing method and between microshear and microtensile data for each adhesive Failure mode distributions were compared using the chi square test Results All in-one adhesives had similar microshear and microtensile bond strengths In both testing methods, the etch and rinse system achieved the strongest bond For all adhesives significantly higher bond strengths were measured with the microshear test In microtensile testing specimens bonded with the etch and rinse adhesive exhibited a significantly different distribution of failure modes The coefficients of variation were extremely high for microtensile bond strength data, particularly of all in one adhesives Conclusion The adhesive potential to intact enamel of recently introduced all in-one adhesives was inferior to that of an etch and rinse system When testing bond strength to enamel of all in one adhesives, microshear testing may be a more accurate method than microtensile

Role of the spinal cord heme oxygenase-carbon monoxide-cGMP pathway in the nociceptive response of rats

The aim of the present study was to investigate the role of the spinal cord heme oxygenase (HO)-carbon monoxide (CO)-soluble guanylate cyclase (sGC)-cGMP pathway in nociceptive response of rats to the formalin experimental nociceptive model. Animals were handled and adapted to the experimental environment for a few days before the formalin test was applied. For the formalin test 50 mu l of a 1% formalin solution was injected subcutaneously in the dorsal surface of the right hind paw. Following injections, animals were observed for I h and flinching behavior was measured as the nociceptive response. Thirty min before the test, rats were pretreated with intrathecal injections with the HO inhibitor, zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) or heme-lysinate, which is known to induce the HO pathway. Control animals were treated with vehicles. We observed a significant increase in nociceptive response of rats treated with ZnDPBG, and a drastic reduction of flinching nociceptive behavioral response in the heme-lysinate treated animals. Furthermore, the HO pathway seems to act via cGMP, since methylene blue (a sGC inhibitor) prevented the reduction of flinching nociceptive behavioral response caused by heme-lysinate. These findings strongly indicate that the HO pathway plays a spinal antinociceptive role during the formalin test, acting via cGMP. (C) 2007 Elsevier B.V. All rights reserved.

Involvement of the heme oxygenase-carbon monoxide-cGMP pathway in the nociception induced by acute painful stimulus in rats

Heme oxygenase-carbon monoxide-cGMP (HO-CO-cGMP) pathway has been reported to be involved in peripheral and spinal modulation of inflammatory pain. However, the involvement of this pathway in the modulation of acute painful stimulus in the absence of inflammation remains unknown. Thus, we evaluated the involvement of the HO-CO-cGMP pathway in nociception by means the of analgesia index (AI) in the tail flick test. Rats underwent surgery for implantation of unilateral guide cannula directed toward the lateral ventricle and after the recovery period (5-7 days) were subjected to the measures of baseline tail flick test Animals were divided into groups to assess the effect of intracerebroventricular administration (i.c.v.) of the following compounds: ZnDPBG (HO inhibitor) or vehicle (Na(2)CO(3)), heme-lysinate (substrate overload) or vehicle (L-lysine), or the selective inhibitor of soluble guanilate cyclase ODQ or vehicle (DMSO 1%) following the administration of heme-lysinate or vehicle. Heme overload increased AI, indicating an antinociceptive role of the pathway. This response was attenuated by i.c.v. pretreatment with the HO inhibitor ZnDPBG. In addition, this effect was dependent on cGMP activity, since the pretreatment with ODQ blocked the increase in the AI. Because CO produces most of its actions via cGMP, these data strongly imply that CO is the HO product involved in the antinociceptive response. This modulation seems to be phasic rather than tonic, since i.c.v. treatment with ZnDPBG or ODQ did not alter the AI. Therefore, we provide evidence consistent with the notion that HO-CO-cGMP pathway plays a key phasic antinociceptive role modulating noninflammatory acute pain. (C) 2011 Elsevier B.V. All rights reserved.

GABAergic antagonist blocks the reduction of tonic immobility behavior induced by activation of 5-HT(2) receptors in the basolateral nucleus of the amygdala in guinea pigs

Tonic immobility (TI) is a temporary state of profound motor inhibition induced by situations that generate intense fear, with the objective of protecting an animal from attacks by predators. A preliminary study by our group demonstrated that microinjection into the basolateral nucleus of the amygdala (BLA) of an agonist to 5-HT(1A) and 5-HT(2) receptors promoted a decrease in TI duration. In the current study, the effects of GABAergic stimulation of the BLA and the possible interaction between GABA(A) and 5-HT(2) receptors on TI modulation were investigated. Observation revealed that GABAergic agonist muscimol (0.26 nmol) reduced the duration of TI episodes, while microinjection of the GABAergic antagonist bicuculline (1 nmol) increased TI duration. Additionally, microinjection of 5-HT(2) agonist receptors (alpha-methyl-5-HT, 0.32 nmol) into the BLA decreased TI duration, an effect reversed by pretreatment with bicuculline (at the dose that had no effect per se, 0.2 nmol). Moreover, the activation of GABA(A) and 5-HT(2) receptors in the BLA did not alter the spontaneous motor activity in the open field test. These experiments demonstrated that the activation of GABA(A) and 5-HT(2) receptors of the BLA possibly produce a reduction in unconditioned fear that decreases the TI duration in guinea pigs, but this is not due to increased spontaneous motor activity, which could affect a TI episode nonspecifically. Furthermore, these results suggest an interaction between GABAergic and serotoninergic mechanisms mediated by GABA(A) and 5-HT(2) receptors. In addition, the GABAergic circuit of the BLA presents a tonic inhibitory influence on TI duration. (C) 2009 Elsevier Inc. All rights reserved.

Effects of short-term acetaminophen and celecoxib treatment on orthodontic tooth movement and neuronal activation in rat

Non-steroidal anti-inflammatory drugs (NSAIDs) have been used for pain relief in orthodontics, but clinical studies reported that they may reduce tooth movement (TM). By other side, TM seems to activate brain structures related to nociception, but the effects of NSAIDs in this activation have not been studied yet. We analyzed the effect of short-term treatment with acetaminophen or celecoxib in the separation of rat upper incisors, as well as in neuronal activation of the spinal trigeminal nucleus, following tooth movement. Thirty rats (400-420 g) were pretreated through oral gavage (1 ml/dose)with acetaminophen (200 mg/kg), celecoxib (50 mg/kg) or vehicle (carboxymethylcellulose 0.4%). After 30 min, they received an activated (30 g) orthodontic appliance for TM. In controls, this appliance was immediately removed after its introduction. Rats received ground food, and every 12 h, one of the drugs or vehicle. After 48 h, they were anesthetized, maxilla was radiographed, and were perfused with 4% paraformaldehyde. Brains were further processed for Fos immunohistochemistry. TM induced incisor distalization (p < 0.05) and neuronal activation of the spinal trigeminal nucleus. Treatment with both drugs did not affect tooth movement, but reduced c-fos expression in the caudalis subnucleus. No changes in c-fos expression were seen in the oralis and interpolaris subnuclei. We conclude that neither celecoxib nor acetaminophen seems to affect tooth movement, when used for 2 days, but both drugs are able to reduce the activation of brain structures related to nociception. Short-term treatment with celecoxib, thus, may be a therapeutic alternative to acetaminophen when the latter is contra indicated. (C) 2009 Elsevier Inc. All rights reserved.

Blocking systemic nitric oxide production alters neuronal activation in brain structures involved in cardiovascular regulation during polymicrobial sepsis

In a previous study, we concluded that overproduction of nitric oxide (NO) by inducible nitric Oxide synthase (iNOS) in the late phase of sepsis prevents hypothalamic activation, blunts vasopressin secretion and contributes to hypotension, irreversible shock and death. The aim of this follow-up study was to evaluate if the same neuronal activation pattern happens in brain structures related to cardiovascular functions. Male Wistar rats received intraperitoneal injections of aminoguanidine, an iNOS inhibitor, or saline 30 min before cecal ligation and puncture (CLP) or sham surgeries. The animals were perfused 6 or 24 h after the surgeries and the brains were removed and processed for Fos immunocytochemistry We observed an increase (P < 0.001) in c-fos expression 6 h after CLP in the area postrema (AP), nucleus of he tractus solitarius (NTS), ventral lateral medulla (VLM), locus coeruleus (LC) and parabrachial nucleus (PB). At 24 h after CLP, however, c-fos expression was strongly decreased in all these nuclei (P < 0.05), except for the VLM. Aminoguanidine reduced c-fos expression in the AP and NTS at 6 h after CLR but showed an opposite effect at 24 h, with an increase in the AP, NTS, and also in the VLM. No such effect was observed in the LC and PB at 6 or 24 h. In all control animals, c-fos expression was minimal or absent. We conclude that in the early phase of sepsis iNOS-derived NO may be partially responsible for the activation of brain structures related to cardiovascular regulation. During the late phase, however, this activation is reduced or abolished. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Rapid maxillary expansion causes neuronal activation in brain structures of rats

A correlation between pain sensation and neuronal c-fos expression has been analyzed following experimental rapid maxillar expansion (RME). Adult male Wistar rats were anaesthetized and divided into three groups: animals that received an orthodontic apparatus, which was immediately removed after the insertion (control), animals that received an inactivated orthodontic apparatus (without force), and animals that received an orthodontic apparatus previously activated (140 g force). After 6, 24, 48, or 72 h, the animals were re-anaesthetized, and perfused with 4% paraformaldehyde. The brains were removed, fixed, and sections containing brain structures related to nociception were processed for Fos protein immunohistochemistry (IHC). The insertion of the orthodontic apparatus with 140 g was able to cause RME that could be seen by radiography. The IHC results showed that the number of activated neurons in the different nuclei changed according to the duration of appliance insertion and followed a temporal pattern similar to that of sensations described in clinics. The animals that received the orthodontic apparatus without force did not show RME but a smaller c-fos expression in the same brain structures. In conclusion, we demonstrate that orthodontic force used for palate disjunction activates brain structures that are related to nociception, and that this activation is related to the pain sensation described during orthodontic treatment. (c) 2008 Elsevier Inc. All rights reserved.

Role of locus coeruleus heme oxygenase-carbon monoxide-cGMP pathway during hypothermic response to restraint

Central heme oxigenase-carbon monoxide (HO-CO) pathway has been shown to play a pyretic role in the thermoregulatory response to restraint. However, the specific site in the central nervous system where CO may act modulating this response remains unclear. LC is rich not only in sGC but also in heme oxygenase (HO; the enzyme that catalyses the metabolism of heme to CO, along with biliverdin and free iron). Therefore, the possible role of the HO-CO-cGMP pathway in the restraint-induced-hypothermia by LC neurons was investigated. Body temperature dropped about 0.7 degrees C during restraint. ZnDPBG (a HO inhibitor; 5 nmol, intra-LC) prevented the hypothermic response during restraint. Conversely, induction of the HO pathway in the LC with heme-lysinate (7.6 nmol, intra-LC) intensified the hypothermic response to restraint, and this effect was prevented by pretreatment with ODQ (a sGC inhibitor; given intracerebroventricularly, 1.3 nmol). Taken together, these data suggest that CO in the LC produced by the HO pathway and acting via cGMP is implicated in thermal responses to restraint. (C) 2007 Elsevier Inc. All rights reserved.

Bond Strength of Fiber Posts to Weakened Roots After Resin Restoration With Different Light-Curing Times

Introduction: This study evaluated the bond strength of translucent fiber posts to experimentally weakened radicular dentin restored with composite resin and polymerized with different light-exposure time. Methods: Roots of 60 maxillary incisors were used. Twenty-four hours after obturation, the filling materials of root canals were removed to a depth of 12 mm, and 4 groups were randomly formed. In 3 groups, root dentin was flared to produce a space between fiber post and canal walls. In the control group, the roots were not experimentally weakened. The flared roots were bulk restored with composite resin, which was light-activated through the translucent post for 40, 80, or 120 seconds. Posts were cemented, and after 24 hours, all roots were sectioned transversely in the coronal, middle, and apical regions, producing 1-mm-thick slices. Push-out test was performed, and failure modes were observed. Results The quantitative analysis showed significant statistical difference only among groups (P <.001). Comparing the weakened/restored groups, composite light-exposure time did not influence the results. Overall, adhesive failures occurred more frequently than other types of failures. Cohesive failures occurred only in the weakened/restored roots. Conclusions Intracanal root restoration with composite resin and translucent fiber posts provided similar or higher bond strength to dentin than the control group, regardless of the light-exposure time used for polymerization. (J Endod 2009;35:1034-1039)

Bond Strength of Epiphany Sealer Prepared with Resinous Solvent

This study evaluated in vitro the bond strength of Epiphany sealer prepared with resinous solvent of Epiphany system (Thinning resin) by using a push-out test. Forty maxillary canines were sectioned transversally below the cementoenamel junction to provide 4-mm-thick dentin disks that were centered in aluminum rings and embedded in acrylic resin. Root canals were prepared with tapered diamond bur. Intraradicular dentin was treated with 1% NaOCl for 30 minutes, 17% ethylenediaminetetraacetic acid for 5 minutes, and flushed with distilled water for 1 minute. The specimens were randomly distributed into 4 groups (n = 10) according to the filling material: GI, Epiphany without photoactivation; GII, Epiphany prepared with solvent without photoactivation; Gill, Epiphany followed by photoactivation; and GIV, Epiphany prepared with solvent followed by photoactivation. After the setting time, the specimens were submitted to the push-out test. The highest mean value (14.91 +/- 2.82 MPa) was obtained with Epiphany prepared with solvent followed by photoactivation (GIV), which was statistically different (P < .01) from the other groups. Groups I (8.15 +/- 2.47 MPa), II (9.46 +/- 2.38 MPa), and III (9.80 +/- 2.51 MPa) had inferior bond strength values and were statistically similar among themselves (P > .01). The resinous solvent of Epiphany system increased the bond strength of Epiphany sealer to dentin walls when followed by photoactivation. (J Endod 2009;35: 251-255)

Bond strength of AH Plus and Epiphany sealers on root dentine irradiated with 980 nm diode laser

Aim To evaluate the bond strength of AH Plus and Epiphany sealers to human root canal dentine irradiated with a 980 nm diode laser at different power and frequency parameters, using the push-out test. Methodology Sixty canine roots were sectioned below the cementoenamel junction to provide 4-mm-thick dentine discs that had their root canals prepared with a tapered bur and irrigated with sodium hypochlorite, ethylenediaminetetraacetic acid and distilled water. The specimens were assigned to five groups (n = 12): one control (no laser) and four experimental groups that were submitted to 980 nm diode laser irradiation at different power (1.5 and 3.0 W) and frequency (continuous wave and 100 Hz) parameters. Half of specimens in each group had their canals filled with AH Plus sealer and half with Epiphany. The push-out test was performed and data (MPa) were analysed statistically by ANOVA and Tukey`s test (P < 0.05). The specimens were split longitudinally and examined under SEM to assess the failure modes after sealer displacement. Results The specimens irradiated with the diode laser and filled with AH Plus had significantly higher bond strength values (8.69 +/- 2.44) than those irradiated and filled with Epiphany (3.28 +/- 1.58) and the nonirradiated controls (3.86 +/- 0.60). The specimens filled with Epiphany did not differ significantly to each other or to the control (1.75 +/- 0.69). There was a predominance of adhesive failures at Epiphany-dentine interface (77%) and mixed failures at AH Plus-dentine interface (67%). Conclusions The 980 nm diode laser irradiation of root canal dentine increased the bond strength of AH Plus sealer, but did not affect the adhesion of Epiphany sealer.

Shear Bond Strength of A Sealant to Contaminated-Enamel Surface: Influence of Erbium : Yttrium-Aluminum-Garnet Laser Pretreatment

Salivary contamination is one of the factors that can disturb the sealing process and interfere in the longevity of pit and fissure sealants. Erbium : yttrium-aluminum-garnet (Er : YAG) laser could influence the bond strength of enamel and increase the acid resistance. To evaluate the influence of Er : YAG laser on the shear bond strength of a sealant to a salivary contaminated enamel surface. Twenty-four third molars had the roots sectioned 2 mm coronal to the cementoenamel junction. The crowns were mesiodistally sectioned providing 48 halves that were embedded in polyester resin. Enamel was flattened and a 2-mm diameter bonding area was demarcated. Specimens were randomly assigned to two groups according to the superficial pretreatment-37% phosphoric acid (A) and Er : YAG laser (80 mJ/2 Hz) + phosphoric acid (L), which were subdivided into two groups (N = 12), without salivary contamination (C) and with salivary contamination (SC). To contaminate the specimens, 0.25 mL of human fresh saliva was applied for 20 seconds and then dried. Fluroshield sealant was applied in all specimens. After storage, shear bond strength of samples were tested in a universal testing machine. Means in MPa were: AC-14.61 (+/- 2.52); ASC-6.66 (+/- 2.34); LC-11.91 (+/- 1.34); and LSC-2.22 (+/- 0.66). Statistical analysis revealed that surfaces without salivary contamination and with acid treatment had the highest mean (p < 0.05). The group with salivary contamination treated by Er : YAG laser followed by phosphoric acid application presented the lowest bond values (p < 0.05). The phosphoric acid etching under dry condition yielded better bonding performance. Er : YAG laser was not able to increase the effectiveness of conventional acid etching of enamel in the bond of sealants in both dry and wet conditions. Under the conditions of this study, the conventional etching protocol (phosphoric acid without salivary contamination) is still preferable to laser-conditioning enamel surface prior to sealant application.

Cdc25-dependent activation of cyclin A/cdk2 is blocked in G2 phase arrested cells independently of ATM/ATR

Cyclin A/cdk2 is active during S and G2 phases of the cell cycle, but its regulation and function during G2 phase is poorly understood. In this study we have examined the regulation of cyclin A/cdk2 activity during normal G2 phase progression and in genotoxin-induced G2 arrest. We show that cyclin A/cdk2 is activated in early G2 phase by a cdc25 activity. In the G2 phase checkpoint arrest initiated in response to various forms of DNA damage, the cdc25-dependent activation of both cyclin A/cdk2 and cyclin B1/cdc2 is blocked. Ectopic expression of cdc25B, but not cdc25C, in G2 phase arrested cells efficiently activated both cyclin A/cdk2 and cyclin B1/cdc2. Finally, we demonstrate that the block in cyclin A/cdk2 activation in the G2 checkpoint arrest is independent of ATM/ATR. We speculate that the ATM/ ATR-independent block in G2 phase cyclin A/cdk2 activation may act as a further layer of checkpoint control, and that blocking G2 phase cyclin A/cdk2 activation contributes to the G2 phase checkpoint arrest.