Histopathological changes in rabbit craniomandibular joint associated with experimentally induced anterior disk displacement (ADD)

Several studies have shown that anterior disk displacement (ADD) of human temporomandibular joint (TMJ) can lead to cellular and extracellular alterations in the disk proper, bilaminar zone (BZ), condyle, articular eminence and synovial membrane. Due to lack of an animal model for this disease, it is not known whether the mechanical displacement of the disk could lead to the observed histopathological changes. The purpose of this experiment was to investigate the histopathological changes that occur in the rabbit craniomandibular joint (CMJ) following surgical induction of ADD. The right CMJ was exposed surgically and the discal attachments were severed except for the BZ attachments. Then the disk was displaced anteriorly and sutured to the zygomatic arch. The left joint served as surgical control. The CMJs were removed after 24 h, 1 week, 2 weeks or 6 weeks and stained with H&E or modified Masson stain. The results showed neovascularization, cell clustering and fibrillation of the displaced disk. The BZ showed marked fibrosis. The condyle showed subchondral hemorrhage and fibrosis followed by osteoarthritic changes in the articular cartilage. The articular eminence showed chondrocytic clustering and an increase in the amount of chon-droid bone. Synovial membrane exhibited marked hyperplasia. We concluded that surgical induction of ADD in the rabbit CMJ leads to cellular and extracellular alterations in the disk proper, BZ, condyle, articular eminence and synovial membrane similar to those described previously in human ADD. It appears that the mechanical trauma resulting from ADD could lead to a cascade of reparative and degenerative changes of the affected joints similar to those described for osteoarthritis.     

Effect of Aluminum Oxide Addition on the Flexural Strength and Thermal Diffusivity of Heat-Polymerized Acrylic Resin

Purpose: This work was undertaken to investigate the effect of adding from 5% to 20% by weight aluminum oxide powder on the flexural strength and thermal diffusivity of heat‐polymerized acrylic resin. Materials and Methods: Seventy‐five specimens of heat‐polymerized acrylic resin were fabricated. The specimens were divided into five groups (n = 15) coded A to E. Group A was the control group (i.e., unmodified acrylic resin specimens). The specimens of the remaining four groups were reinforced with aluminum oxide (Al₂O₃) powder to achieve loadings of 5%, 10%, 15%, and 20% by weight. Specimens were stored in distilled water at 37°C for 1 week before flexural strength testing to failure (5 mm/min crosshead speed) in a universal testing machine. Results were analyzed by one‐way analysis of variance and post hoc Tukey paired group comparison tests (p < 0.05). Weibull analysis was used to calculate the Weibull modulus, characteristic strength, and the required stress for 1% and 5% probabilities of failure. Cylindrical test specimens (5 specimens/group) containing an embedded thermocouple were used to determine thermal diffusivity over a physiologic temperature range (0 to 70°C). Results: The mean flexural strength values of the heat‐polymerized acrylic resin were (in MPa) 99.45, 119.92, 121.19, 130.08, and 127.60 for groups A, B, C, D, and E, respectively. The flexural strength increased significantly after incorporation of 10% Al₂O₃. The mean thermal diffusivity values of the heat‐polymerized acrylic resin (in m²/sec) were 6.8, 7.2, 8.0, 8.5, and 9.3 for groups A, B, C, D, and E, respectively. Thermal diffusivities of the composites were found to be significantly higher than the unmodified acrylic resin. Thermal diffusivity was found to increase in proportion to the weight percentage of alumina filler, which suggested that the proper distribution of alumina powders through the insulating polymer matrix might form a pathway for heat conduction. Conclusion: Al₂O₃ fillers have potential as added components in denture bases to provide increased flexural strength and thermal diffusivity. Increasing the flexural strength and heat transfer characteristics of the acrylic resin base material could lead to more patient satisfaction.     

Effect of titanium tetrafluoride addition on the physicochemical and antibacterial properties of Biodentine as intraorfice barrier

Objective

To evaluate the influence of titanium tetrafluoride (TiF₄) incorporation on the physicochemical and antibacterial properties of Biodentine (BD; Septodont, Saint Maur des Faussés, France) as an intraorfice barrier material.

Apoptosis is the most efficient death-pathway in tumor cells after topoisomerase II inhibition

OBJECTIVE: To compare the efficiency of apoptosis and other modes of cell death in killing tumor cells after the induction of DNA damage by topoisomerase inhibitors like etoposide. METHODS: This study was carried out in the Tumor Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt, from September 2005 to August 2007. The breast cancer MCF7, the cervix carcinoma, human cervical adenocarcinoma Hela, and the brain tumor U251 cell lines were exposed to etoposide. Apoptosis was detected using the flow cytometry and the DNA ladder formation methods. Cell viability was determined by a colorimetric assay, and the residual DNA double-strand breaks dsb were measured by gel electrophoresis. RESULTS: The Hela cells were the most, the MCF7's were moderately, whereas the U251's were the least sensitive to etoposide. Apoptosis was detected only in Hela cells whereas the other 2 cell lines showed a very low level of apoptosis only 3% increase above the control cells. At equitoxic drug concentrations namely IC50, the Hela cells showed the lowest amount of non-repaired DNA dsb, and the MCF7's showed the highest amount, whereas the U251 cells showed a moderate amount. CONCLUSION: These results indicate that although other modes of cell death exist, apoptosis is the most efficient and requires lower drug concentrations and fewer numbers of non-repaired dsb to give the same killing effect. Clinically, this means that tumors that can execute apoptosis may require lower doses of topoisomerase inhibitors than those that lost the ability to exercise apoptosis.     

Dibromoacetonitrile-induced protein oxidation and inhibition of proteasomal activity in rat glioma cells

Dibromoacetonitrile (DBAN) is a disinfection byproduct of water chlorination. The present study was designed to investigate the potential oxidative protein modifications and alterations in proteasomal activity induced by DBAN in C6 glioma cells (C6 cells). Cells were exposed to 50-400 ppb DBAN for 24 h or 48 h. Cellular viability and lactate dehydrogenase (LDH) leakage were unaffected at 24 h. However, at 48 h after exposure to high concentrations of DBAN, there was a significant decrease in cell viability accompanied by a significant increase in LDH leakage. Exposure to DBAN for 48 h significantly enhanced formation of reactive oxygen species (ROS) in a concentration-related manner. Incubation of C6 cells for 24h or 48 h caused 1.3-2.4-fold increase in levels of lipid peroxidation as indicated by malondialdehyde (MDA)+4-hydroxy-2(e)-nonenal (4-HNE). Further, DBAN induced a concentration and time-dependent increase (1.6-6-folds) in the levels of protein carbonylation. At 48 h, proteasomal activities were found to decrease to 80%, 72%, 46%, and 34% of control with 50 ppb, 100 ppb, 200 ppb, 400 ppb DBAN, respectively. In conclusion, the present study indicates that exposure of C6 cells to DBAN results in generation of ROS, lipid peroxidation, accumulation of oxidized proteins and inhibition of proteasomal activity.     

Gastrointestinal nematode infection increases organophosphate toxicity in rats

Serum paraoxonase-1 (PON1) is an esterase associated with high-density lipoproteins in plasma and is involved in the detoxification of organophosphates (OP). We have previously reported a significant decrease in serum PON1 activity following Nippostrongylus brasiliensis infection in Wistar rats. In the present study we investigated the effects of decreased serum PON1 activity due to N. brasiliensis infection on acute toxicity induced by chlorpyrifos oxon (CPO) and paraoxon (PO) in rats. CPO and PO were dermally applied at doses of 8 mg/kg and 0.2 mg/kg body weight, respectively, to infected (on day 7 post-infection) and uninfected rats, after which acetylcholinesterase (AChE) activity was measured within the brain, diaphragm, plasma, and red blood cells, 4h after administration as a measure of toxicity. In addition, serum PON1 activity was measured immediately prior to administration of CPO and PO. N. brasiliensis infection significantly increased the degree of inhibition of AChE in the brain and diaphragm after treatment with CPO and PO in association with a significant reduction in PON1 activity. Likewise, similar findings were observed in the blood (plasma and RBCs) ChE activity after treatment with PO, but not CPO. These results indicate that N. brasiliensis infection makes rats more susceptible to CPO and PO toxicity, suggesting that gastrointestinal nematode infection might be a potential factor affecting OP toxicity.     

Synaptic vesicle pools at diaphragm neuromuscular junctions vary with motoneuron soma, not axon terminal, inactivity

Both spinal hemisection (SH) at C2 and tetrodotoxin (TTX) phrenic nerve blockade result in diaphragm muscle paralysis and inactivity of the phrenic axon terminals. However, phrenic motoneuron somata are inactive with SH but remain active with TTX phrenic nerve blockade. Neuromuscular transmission failure with repeated activation decreases following SH and increases following TTX phrenic nerve blockade, suggesting that matching (or mismatching) of somal and synaptic inactivities of phrenic motoneurons differentially regulates synaptic vesicle pools at diaphragm neuromuscular junctions. At individual type-identified rat diaphragm presynaptic terminals, the size of the releasable pool of synaptic vesicles was analyzed by fluorescence confocal microscopy of N-(3-triethylammoniumpropyl)-4-(6-(4-(diethylamino)phenyl)hexatrienyl) pyridinium dibromide (FM4-64) uptake and synaptic vesicle density at active zones was determined using transmission electron microscopy. After 14 days of SH and TTX-induced diaphragm muscle inactivity, neuromuscular junction size was not different at type I or IIa fibers, but increased at type IIx and/or IIb fibers (by 51% in SH and 35% in TTX) compared with control. With SH, synaptic vesicle pool size and density increased at presynaptic terminals innervating type I or IIa fibers (17 and 63%, respectively; P<0.001) and type IIx and/or IIb fibers (41 and 31%, respectively; P<0.001) when compared with controls. Following TTX, synaptic vesicle pool size and density decreased by 64 and 17%, respectively, at presynaptic terminals innervating type I or IIa fibers, and by 50 and 36%, respectively, at type IIx and/or IIb fibers (P<0.001, for all comparisons). Thus, matching motoneuron soma and axon terminal inactivity (SH) increases the size and density of releasable synaptic vesicle pools at adult rat diaphragm neuromuscular junctions. Mismatching motoneuron soma and axon terminal inactivities (TTX) results in converse presynaptic adaptations. Inactivity-induced neuromuscular plasticity reflects specific adaptations in the size and density of synaptic vesicle pools that depend on motoneuron soma rather than axon terminal (or muscle fiber) inactivity.