996 resultados para ORAL-CAVITY


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Diabetes has been implicated in the dryness of the mouth, loss of taste sensation, sialosis, and other disorders of the oral cavity, by impairment of the salivary glands. The aim of the present study was to examine the plasma membrane, microsomal, and homogenate Ca(2+)-ATPase activity in the rat submandibular and parotid salivary glands of streptozotocin-induced diabetes. We have also examined the influence of the acidosis state oil this parameter. Diabetes was induced by an intraperitoneal injection of streptozotocin and acidosis was induced by daily injection of NH(4)Cl. At 15 and 30 days after diabetes induction, the animals were euthanized and the submandibular and parotid salivary glands were removed and analyzed. Ca(2+)-ATPase (total, independent, and dependent) was determined in the homo-enate, microsomal, and plasma membranes of the salivary glands of diabetic and control rats. Calcium concentration was also determined in the glands and showed to be hi-her in the diabetic animals. Ca(2+)-ATPase activity was found to be reduced in all cell fractions studied in the diabetic animals compared with control. Similar results were obtained for the submandibular salivary glands of acidotic animals; however in the parotid salivary glands it was found an increase in the enzyme activity. Copyright (c) 2009 John Wiley & Sons, Ltd.

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Background: Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) is a Gram-negative bacterium present in the oral cavity and is usually associated with localized aggressive periodontitis. Isolated antigens from A. actinomycetemcomitans can activate innate immune cells through Toll-like receptors (TLRs), which are molecules that recognize structural components conserved among microorganisms. In this study, we evaluate the role of TLR2 in the recognition of A. actinomycetemcomitans. Methods: Macrophages and neutrophils from knockout mice with targeted disruption of TLR2 (TLR2(-/-) mice) and wild-type mice were collected and used for the subsequent assays. The production of cytokines and chemokines was evaluated by enzyme-linked immunosorbent assay (ELISA), and the presence of apoptotic cells was determined by flow cytometry. In addition, the mechanisms that modulate the outcome of A. actinomycetemcomitans-induced periodontal disease in TLR2(-/-) mice were examined. Results: The results show that TLR2-deficient mice developed more severe periodontitis after A. actinomycetemcomitans infection, characterized by significantly higher bone loss and inflammatory cell migration to periodontal tissues. The inflammatory cell influx into the peritoneal cavities of TLR2(-/-) mice was three-fold lower than that observed for the littermate controls. A significantly diminished production of the cytokines tumor necrosis factor-alpha and interleukin-1 beta as well as the chemokine CC-ligand-5 in the peritoneal cavities of TLR2(-/-) mice was observed. In addition, a high frequency of apoptotic cells in the inflammatory exudates from TLR2(-/-) mice was observed. Phagocytosis and nitric oxide production was diminished in cells from TLR2(-/-) mice, facilitating the dissemination of the pathogen to the spleen. Conclusion: The results of this study highlight the involvement of TLR2 in recognizing A. actinomycetemcomitans and its essential role in controlling A. actinomycetemcomitans infection. J Periodontot 2009,80:2070-2019.

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This study evaluated, by cross-sectional hardness (CSH), enamel maturation at different depths in sound human teeth at different posteruptive ages (12 per age group): unerupted (molars; control), 2-3 years (premolars), 4-10 years (premolars) and >10 years (molars). Cross-sectional Knoop hardness was measured at 10, 30, 50, 70, 90, 110, 220 and 330 mu m depth from the surface. The data were subjected to two-way ANOVA followed by Bonferroni`s pairwise tests (alpha = 0.05). The CSH significantly increased with posteruptive age, indicating that the time of exposure in the oral cavity might result in deep enamel maturation. Copyright (C) 2009 S. Karger AG, Basel

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Schistosoma mansoni masks its surface with adsorbed host proteins including erythrocyte antigens, immunoglobulins, major histocompatibility complex class I, and beta (2)-microglobulin (beta (2)m), presumably as a means of avoiding host immune responses, How this is accomplished has not been explained. To identify surface receptors for host proteins, we biotinylated the tegument of live S, mansoni adults and mechanically transformed schistosomula and then removed the parasite surface with detergent, Incubation of biotinylated schistosome surface extracts witt l human immunoglobulin G (IgG) Fc-Sepharose resulted in purification of a 97-kDa protein that was subsequently identified as paramyosin (Pmy), using antiserum specific for recombinant Pmy, Fc also bound recombinant S. mansoni Pmy and native S. japonicum Pmy, Antiserum to Pmy decreased the binding of Pmy to Fc-Sepharose, and no proteins bound after removal of Pmy from extracts. Fluoresceinated human Fe bound to the surface, vestigial penetration glands, and nascent oral cavity of mechanically transformed schistosomula, and rabbit anti-Pmy Fab fragments ablated the binding of Fc to the schistosome surface, Pmy coprecipitated with host IgG from parasite surface extracts, indicating that complexes formed on the parasite surface as well as in vitro. Binding of Pmy to Fe was not inhibited by soluble protein A, suggesting that Pmy does not bind to the region between the CH2 and CH3 domains used by many other Fc-binding proteins. beta (2)m did not bind to the schistosome Fc receptor (Pmy), a finding that contradicts reports from earlier workers but did bind to a heteromultimer of labeled schistosomula surface proteins, This is the first report of the molecular identity of a schistosome Fc receptor; moreover it demonstrates an additional aspect of the unusual and multifunctional properties of Pmy from schistosomes and other parasitic flatworms.

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Disturbances of the dental development may result in anomalies, which may be apparent as soon as the child is born. Eruption cysts are rarely observed in neonates considering that at this stage of the child`s life teeth eruption is uncommon. Thus, the aim of this report is to describe a case of eruption cysts in a neonate. A male neonate was brought to the emergency service with the chief complaint of an elevated area on the anterior region of the inferior alveolar ridge. The lesion was clinically characterized as a compressive and floating swelling. Through a radiographic exam two mandibular primary incisors could be seen superficially located. Due to the patient`s age and the initial diagnosis of eruption cysts the conduct adopted was clinical surveillance. Forty-five days after the first visit the lesions had significantly decreased in size, and completely disappeared after 4 months. at that age, both mandibular central incisors were already in the oral cavity exhibiting small hypoplastic areas in the incisal edges. The clinical and radiographic follow-up of eruption cysts in neonates appears to be an adequate conduct without differing from that recommended for older children.

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For the purposes of this report, ""systemic disease"" will be interpreted as conditions that are spread out within the body rather than localized strictly to the tissues of the oral cavity. Since it would take many volumes to review all such conditions, the intent of the authors is to review a few examples of conditions where initial panoramic radiographic findings suggested widespread disease of significance enough to affect the quality of life and longevity of the patient.

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This study investigated whether sodium bicarbonate solution, applied on enamel previously exposed to a simulated intrinsic acid, can control dental erosion. Volunteers wore palatal devices containing enamel slabs, which were exposed twice daily extra-orally to hydrochloric acid (0.01 M, pH 2) for 2 min. Immediately afterwards, the palatal devices were re-inserted in the mouth and volunteers rinsed their oral cavity with a sodium bicarbonate solution or deionized water for 60 s. After the washout period, the palatal devices were refilled with a new set of specimens and participants were crossed over to receive the alternate rinse solution. The surface loss and surface microhardness (SMH) of specimens were assessed. The surface loss of eroded enamel rinsed with a sodium bicarbonate solution was significantly lower than the surface loss of eroded enamel rinsed with deionized water. There were no differences between treatments with sodium bicarbonate and deionized water for SMH measurements. Regardless of the solution used as an oral rinse, eroded enamel showed lower SMH than uneroded specimens. Rinsing with a sodium bicarbonate solution after simulated endogenous erosive challenge controlled enamel surface loss but did not alter the microhardness.

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Purpose: To assess, by a crossover 2 x 2 in situ study, the speculated protective role of a sodium bicarbonate-containing toothpaste in controlling erosive lesions. Methods: Bovine enamel slabs were sterilized, and submitted to baseline Knoop microhardness measurements. After a 3-day lead-in period, 14 volunteers wore palatal acrylic appliances containing six enamel slabs (three on each side), for 4 consecutive days. On the first day, appliances with contained specimens were placed in the oral cavity to allow salivary pellicle formation. On the subsequent days, half of the enamel slabs were immersed extraorally in a lemonade-like soft drink for 90 seconds, twice daily. On both of these occasions, the appliance was dipped in toothpaste slurry of either a sodium bicarbonate-containing toothpaste or a regular counterpart for 60 seconds. Following a 3-day washout period, a new set of enamel slabs were mounted and the volunteers started the second period using the alternate dentifrice. Results: ANOVA (alpha = 0.05) showed no statistically significant difference between enamel treated with regular and sodium bicarbonate-based dentifrices, regardless of whether specimens were eroded or not (P=0.8430). Acid-challenged specimens revealed lower microhardness values than uneroded samples. (Am J Dent 2008;21:300-302).

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Purpose: The aims of this randomized controlled trial were to determine whether there were differences in the disease-free survival (DFS) and toxicity between conventional radiotherapy (CRT) and a continuous 3 week accelerated radiotherapy regimen (ART) in stage III and IV squamous cell carcinoma of the oral cavity, oropharynx, larynx and hypopharynx. Patients and methods: Patients from 14 centres throughout Australia and New Zealand were randomly assigned to either CRT, using a single 2 Gy/day to a dose of 70 Gy in 35 fractions in 49 days or to ART, using 1.8 Gy twice a day to a dose of 59.4 Gy in 33 fractions in 24 days. Treatment allocation was stratified for site and stage. The accrual began in 1991 and the trial was closed in 1998 when the target of 350 patients was reached. Results: The median potential follow-up time was 53 months (range, 14-101). The DFS at 5 years was 41% (95% CI, 33-50%) for ART and 35% (95% CI, 27-43%) for CRT (P = 0.323) and the hazard ratio was 0.87 in favour of ART (95% CI, 0.66-1.15). The 5-year disease-specific survival rates were 40% for CRT and 46% for ART (P = 0.398) and the loco-regional control was 47% for CRT vs. 52% for ART (P = 0.300). The respective hazard ratios were 0.88 (95% CI, 0.65-1.2) and 0.85 (0.62-1.16), favouring the accelerated arm. In the ART arm, confluent mucositis was more severe (94 vs. 71%; P < 0.001) and peaked about 3 weeks earlier than in the CRT arm, but healing appeared complete in all cases. There were statistically significant reductions in the probability of grade 2 or greater late soft tissue effects over time in the ART arm (P < 0.05), except for the mucous membrane where late effects were similar in both arms. Conclusions: Differences in DFS, disease-specific survival and loco-regional control have not been demonstrated. ART resulted in more acute mucosal toxicity, but this did not result in greater prolongation of the treatment time compared with the CRT arm. There were less late effects in the ART arm, with the exception of late mucosal effects. This trial has confirmed that tumour cell repopulation occurs during conventionally fractionated radiotherapy for head and neck cancer. However, it has also provided additional evidence that overall improvements in the therapeutic ratio using accelerated fractionation strategies are seriously constrained by the need to limit total doses to levels that do not exceed acute mucosal tolerance. The accelerated schedule tested has been shown in this trial to be an acceptable alternative to conventionally fractionated irradiation to 70 Gy. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

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It has been recognised that in order to study the displacement, timing and co-ordination of articulatory components (i.e., tongue. lips, jaw) in speech production it is desirable to obtain high-resolution movement data on multiple structures inside and outside the vocal tract. Until recently, with the exception of X-ray techniques such as cineradiography, the study 0. speech movements has been hindered by the inaccessibility of the oral cavity during speech. X-ray techniques are generally not used because of unacceptable radiation exposure. The aim of the present study was to demonstrate the use of a new physiological device, the electromagnetic articulograph, for assessing articulatory dysfunction subsequent to traumatic brain injury. The components of the device together with the measuring principle are described and data collected from a single case presented. A 19 year-old male who exhibited dysarthria subsequent to a traumatic brain injury was fitted wit 2 the electromagnetic articulograph (Carstens AG-100) and a kinematic analysis of his tongue movements during production of the lingual consonants it, s, k/ within single syllable words was performed. Examination of kinematic parameters including movemmt trajectories, velocity, and acceleration revealed differences in the speed and accuracy of his tongue movements compared to those produced by a non-neurologically impaired adult male. It was concluded that the articulograph is a useful device for diagnosing speed and accuracy disorders in tongue movements during speech and that the device has potential for incorporation into physiologically based rehabilitation programs as a real-time biofeedback instrument.

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Increasingly, electropalatography (EPG) is being used in speech pathology research to identify and describe speech disorders of neurological origin. However, limited data currently exists that describes normal articulatory segment timing and the degree of variability exhibited by normal speakers when assessed with EPG. Therefore, the purpose of the current investigation was to use the Reading EPG3 system to quantify segmental timing values and examine articulatory timing variability for three English consonants. Ten normal subjects repeated ten repetitions of CV words containing the target consonants /t/, /l/, and /s/ while wearing an artificial palate. The target consonants were followed by the /i/ vowel and were contained in the carrier phrase 'I saw a __'. Mean duration of the approach, closure/constriction, and release phases of consonant articulation were calculated. In addition, inter-subject articulatory timing variability was investigated using descriptive graphs and intra-subject articulatory timing variability was investigated using a coefficient of variation. Results revealed the existence of intersubject variability for mean segment timing values. This could be attributed to individual differences in the suprasegmental features of speech and individual differences in oral cavity size and structure. No significant differences were reported for degree of intra-subject variability between the three sounds for these same phases of articulation. However, when this data set was collapsed, results revealed that the closure/constriction phase of consonant articulation exhibited significantly less intra-subject variability than both the approach and release phases. The stabilization of the tongue against the fixed structure of the hard palate during the closure phase of articulation may have reduced the levels of intra-subject variability.

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Genomic damage is probably the most important fundamental cause of development and degenerative disease. It is also well established that genomic damage is produced by environmental exposure to genotoxins, medical procedures (e.g. radiation and chemicals), micronutrient deficiency (e.g. folate), lifestyle factors (e.g. alcohol, smoking, drugs and stress), and genetic factors such as inherited defects in DNA metabolism and/or repair. Tobacco smoke has been associated to a higher risk of development of cancer, especially in the oral cavity, larynx and lungs, as these are places of direct contact with many carcinogenic tobacco’s compounds. Alcohol is definitely a recognized agent that influence cells in a genotoxic form, been citied as a strong agent with potential in the development of carcinogenic lesions. Epidemiological evidence points to a strong synergistic effect between cigarette smoking and alcohol consumption in the induction of cancers in the oral cavity. Approximately 90% of human cancers originate from epithelial cells. Therefore, it could be argued that oral epithelial cells represent a preferred target site for early genotoxic events induced by carcinogenic agents entering the body via inhalation and ingestion. The MN assay in buccal cells was also used to study cancerous and precancerous lesions and to monitor the effects of a number of chemopreventive agents.

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Formaldehyde (FA) is a colour less gas widely used in the industry and hospitals as an aqueous solution, formalin. It is extremely reactive and induces various genotoxic effects in proliferating cultured mammalian cells. Tobacco smoke has been epidemiologically associated to a higher risk of development of cancer, especially in the oral cavity, larynx and lungs, as these are places of direct contact with many carcinogenic tobacco’s compounds. Approximately 90% of human cancers originate from epithelial cells. Therefore, it could be argued that oral epithelial cells represent a preferred target site for early genotoxic events induced by carcinogenic agents entering the body via inhalation and ingestion. The cytokinesis-blocked micronucleus assay (CBMN) in human lymphocytes is one of the most commonly used methods for measuring DNA damage, namely the detection of micronucleus, nucleoplasmic bridges, and nuclear buds.

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Formaldehyde (FA) is a colourless gas widely used in the industry and hospitals as an aqueous solution, formalin. It is extremely reactive and induces various genotoxic effects in proliferating cultured mammalian cells. Tobacco smoke has been epidemiologically associated to a higher risk of development of cancer, especially in the oral cavity, larynx and lungs, as these are places of direct contact with many carcinogenic tobacco’s compounds. Genetic polymorphisms in enzymes involved in the metabolism are very important and can make changes in the individual susceptibility to disease. Alcohol dehydrogenase class 3 (ADH3), also known as formaldehyde dehydrogenase dependent of glutathione, is the major enzyme involved in the formaldehyde oxidation, especially in the buccal mucosa. The polymorphism in study is a substitution of an isoleucine for a valine in codon 349. The cytokinesis-blocked micronucleus assay (CBMN) in human lymphocytes is one of the most commonly used methods for measuring DNA damage, namely the detection of micronucleus, nucleoplasmic bridges, and nuclear buds, classified as genotoxicity biomarkers.

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Formaldehyde is classified by IARC as carcinogenic to humans (nasopharyngeal cancer). Tobacco smoke has been epidemiologically associated to a higher risk of development of cancer, especially in the oral cavity, larynx and lungs, as these are places of direct contact with many carcinogenic tobacco’s compounds. XRCC3 is involved in homologous recombination repair of cross-links and chromosomal double-strand breaks (Thr241Met polymorphism). The aim of the study is to determine whether there is an in vivo association between genetic polymorphism of the gene XRCC3 and the frequency of genotoxicity biomarkers in subjects exposed or not to formaldehyde and with or without tobacco consumption.