999 resultados para tooth pulp disease
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In order to determine the age of adult wild dogs, we compared two methods ( that of Thomson and Rose (TR method) and that of Knowlton and Whittemore (KW method)) of measuring and calculating pulp cavity : tooth width ratios on upper and lower canine teeth from 68 mixed-sex, known-age wild dogs of 9 months to 13 years of age reared at two localities. Although significant relationships ( P = 0.0001) were found between age and pulp cavity ratios by both methods, the TR ratio calculation and measurement showed heteroscedasity in error variance whereas the KW ratios had a more stable error variance and were normally distributed. The KW method also found significant differences between pulp cavity ratios between teeth of the upper and lower jaws ( P < 0.0001) and sex ( P = 0.01) but not geographic origin ( P = 0.1). Regressions and formulae for fitted curves are presented separately for male and female wild dogs. Males show greater variability in pulp cavity decrements with age than do females, suggesting a physiological difference between the sexes. We conclude that the KW method of using pulp cavity as a proportion of tooth width, measured 15 mm from the root tip and averaged over both upper canines, is the more accurate method of estimating the age of adult wild dogs.
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Thesis (Ph.D.)--University of Washington, 2016-07
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Background: Mutations of GDAP1 gene cause autosomal dominant and autosomal recessive Charcot-Marie-Tooth disease and more than 40 different mutations have been reported. The recessive Q163X mutation has been described in patients of Spanish ancestry, and a founder mutation in South American patients, originating in Spain has been demonstrated. Objective: We describe physical and histological features, and the molecular impact of mutation Q163X in a Colombian family. Methods: We report two female patients, daughters of consanguineous parents, with onset of symptoms within the first two years of life, developing severe functional impairment, without evidence of dysmorphic features, hoarseness or diaphragmatic paralysis. Electrophysiology tests showed a sensory and motor neuropathy with axonal pattern. Sequencing of GDAP1 gene was requested and the study identified a homozygous point mutation (c.487 C>T) in exon 4, resulting in a premature stop codon (p.Q163X). This result confirms the diagnosis of Charcot-Marie-Tooth disease, type 4A. Results: The patients were referred to Physical Medicine and Rehabilitation service, in order to be evaluated for ambulation assistance. They have been followed by Pulmonology service, for pulmonary function assessment and diaphragmatic paralysis evaluation. Genetic counseling was offered. The study of the genealogy of the patient, phenotypic features, and electrophysiological findings must be included as valuable tools in the clinical approach of the patient with Charcot-Marie-Tooth disease, in order to define a causative mutation. In patients of South American origin, the presence of GDAP1 gene mutations should be considered, especially the Q163X mutation, as the cause of CMT4A disease.
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Background: Mutations of GDAP1 gene cause autosomal dominant and autosomal recessive Charcot-Marie-Tooth disease and more than 40 different mutations have been reported. The recessive Q163X mutation has been described in patients of Spanish ancestry, and a founder mutation in South American patients, originating in Spain has been demonstrated. Objective: we describe physical and histological features, and the molecular impact of mutation Q163X in a Colombian family. Methods: We report two female patients, daughters of consanguineous parents, with onset of symptoms within the first two years of life, developing severe functional impairment, without evidence of dysmorphic features, hoarseness or diaphragmatic paralysis. Electrophysiology tests showed a sensory and motor neuropathy with axonal pattern. Sequencing of GDAP1 gene was requested and the study identified a homozygous point mutation (c.487 C>T) in exon 4, resulting in a premature stop codon (p.Q163X). This result confirms the diagnosis of Charcot-Marie-Tooth disease, type 4A. Results: The patients were referred to Physical Medicine and Rehabilitation service, in order to be evaluated for ambulation assistance. They have been followed by Pulmonology service, for pulmonary function assessment and diaphragmatic paralysis evaluation. Genetic counseling was offered. The study of the genealogy of the patient, phenotypic features, and electrophysiological findings must be included as valuable tools in the clinical approach of the patient with Charcot-Marie-Tooth disease, in order to define a causative mutation. In patients of South American origin, the presence of GDAP1 gene mutations should be considered, especially the Q163X mutation, as the cause of CMT4A disease.
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SHED (stem cells from human exfoliated deciduous teeth) represent a population of postnatal stem cells capable of extensive proliferation and multipotential differentiation. Primary teeth may be an ideal source of postnatal stem cells to regenerate tooth structures and bone, and possibly to treat neural tissue injury or degenerative diseases. SHED are highly proliferative cells derived from an accessible tissue source, and therefore hold potential for providing enough cells for clinical applications. In this review, we describe the current knowledge about dental pulp stem cells and discuss tissue engineering approaches that use SHED to replace irreversibly inflamed or necrotic pulps with a healthy and functionally competent tissue that is capable of forming new dentin.
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This study evaluated in vitro the pulp chamber temperature rise induced by the light-activated dental bleaching technique using different light sources. The root portions of 78 extracted sound human mandibular incisors were sectioned approximately 2 mm below the cementoenamel junction. The root cavities of the crowns were enlarged to facilitate the correct placing of the sensor into the pulp chamber. Half of specimens (n=39) was assigned to receive a 35% hydrogen peroxide gel on the buccal surface and the other halt (n=39) not to receive the bleaching agent. Three groups (n=13) were formed for each condition (bleach or no bleach) according to the use of 3 light sources recommended for dental bleaching: a light-emitting diode (LED)laser system, a LED unit and a conventional halogen light. The light sources were positioned perpendicular to the buccal surface at a distance of 5 mm and activated during 30 s. The differences between the initial and the highest temperature readings for each specimen were obtained, and, from the temperature changes, the means for each specimen and each group were calculated. The values of temperature rise were compared using Kruskal-Wallis test at 1% significance level. Temperature rise varied significantly depending on the light-curing unit, with statistically significant differences (p<0.01) among the groups. When the bleaching agent was not applied, the halogen light induced the highest temperature rise (2.38±0.66ºC). The LED unit produced the lowest temperature increase (0.29±0.13ºC); but there was no significant difference between LED unit and LED-laser system (0.35±0.15ºC) (p>0.01). When the bleaching agent was applied, there were significant differences among groups (p<0.01): halogen light induced the highest temperature rise (1.41±0.64ºC), and LED-laser system the lowest (0.33±0.12ºC); however, there was no difference between LED-laser system and LED unit (0.44±0.11ºC). LED and LED-laser system did not differ significantly from each other regardless the temperature rise occurred with or without bleaching agent application. It may be concluded that during light-activated tooth bleaching, with or without the bleaching agent, halogen light promoted higher pulp chamber temperature rise than LED unit and LED-laser system. The tested light-curing units provided increases in the pulp chamber temperature that were compatible with pulpal health.
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Objectives: To describe the microscopic pulpal reactions resulting from orthodontically induced tooth movement associated with low-level laser therapy (LLLT) in rats. Materials and Methods: Forty-five young male Wistar rats were randomly assigned to three groups. In group I (n = 20), the maxillary right first molars were submitted to orthodontic movement with placement of a coil spring. In group II (n = 20), the teeth were submitted to orthodontic movement plus LLLT at 4 seconds per point (buccal, palatal, and mesial) with a GaAlAs diode laser source (830 nm, 100 mW, 18 J/cm(2)). Group III (n = 5) served as a control (no orthodontic movement or LLLT). Groups I and 11 were divided into four subgroups according to the time elapsed between the start of tooth movement and sacrifice (12 hours, 24 hours, 3 days, and 7 days). Results: Up until the 3-day period, the specimens in group I presented a thicker odontoblastic layer, no cell-free zone of Weil, pulp core with differentiated mesenchymal and defense cells, and a high concentration of blood vessels. In group II, at the 12- and 24-hour time points, the odontoblastic layer was disorganized and the cell-free zone of Weil was absent, presenting undifferentiated cells, intensive vascularization with congested capillaries, and scarce defense cells in the cell-rich zone. In groups I and II, pulpal responses to the stimuli were more intense in the area underneath the region of application of the force or force/laser. Conclusions: The orthodontic-induced tooth movement and LLLT association showed reversible hyperemia as a tissue response to the stimulus. LLLT leads to a faster repair of the pulpal tissue due to orthodontic movement. (Angle Orthod. 2010;80:116-122.)
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Mutations of the mitofusin 2 (MFN2) gene have been reported to be the most common cause of the axonal form of Charcot Marie Tooth disease (CMT). The aim of this study was to describe a de novo MFN2 p.R104W mutation and characterize the associated phenotype. We screened the entire coding region of MFN2 gene and characterized its clinical phenotype, nerve conduction studies and sural nerve biopsy. Neuropsychological tests and brain MRI were also performed. A de nova mutation was found in exon 4 (c.310C > T; p.R104W). In addition to a severe and early onset axonal neuropathy, the patient presented learning problems, obesity, glucose intolerance, leukoencephalopathy, brain atrophy and evidence of myelin involvement and mitochondrial structural changes on sural nerve biopsy. These results suggest that MFN2 p.R104W mutation is as a hot-spot for MFN2 gene associated to a large and complex range of phenotypes. (C) 2011 Elsevier B.V. All rights reserved.
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Causes of dental infections can be related to failed dental eruption, malocclusion, abrasion, fractures with or without exposure of the dental pulp, and periodontal disease. Reports of oral myiasis in megavertebrates in captivity air infrequent, perhaps due to the difficulty in observing the oral cavity in such species. This report describes a case of oral myiasis in an adult male hippopotamus in the gingival area and alveolar mucosa of the left mandibular canine tooth. J Vet Dent 26 (3); 168 170,2009
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Diabetes can interfere in tissue nutrition and can impair dental pulp metabolism. This disease causes oxidative stress in cells and tissues. However, little is known about the antioxidant system in the dental pulp of diabetics. Thus, it would be of importance to study this system in this tissue in order to verify possible alterations indicative of oxidative stress. The aim of this study was to evaluate some parameters of antioxidant system of the dental pulp of healthy (n = 8) and diabetic rats (n = 8). Diabetes was induced by streptozotocin in rats. Six weeks after diabetes induction, a pool of the dental pulp of the 4 incisors of each rat (healthy and diabetic) was used for the determination of total protein and sialic acid concentrations and catalase and peroxidase activities. Data were compared by a Student t test (p <= 0.05). Dental pulps from both groups presented similar total protein concentrations and peroxidase activity. Dental pulps of diabetic rats exhibited significantly lower free, conjugated, and total sialic acid concentrations than those of control tissues. Catalase activity in diabetic dental pulps was significantly enhanced in comparison with that of control pulps. The result of the present study is indicative of oxidative stress in the dental pulp caused by diabetes. The increase of catalase activity and the reduction of sialic acid could be resultant of reactive oxygen species production.
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Aim To evaluate the use of pulse oximetry as a test for pulp vitality, by comparing in the same patient, the levels of oxygen saturation of the index finger and of the maxillary central incisor and canine teeth without clinically detectable pulp inflammation. Methodology Seventeen male and female patients aged between 26 and 38 years participated and a total of 32 maxillary central incisor and 32 canine teeth were analysed. Selection criteria required the teeth to have healthy crowns, or with restorations no more than 2 mm in diameter and no clinical and radiographical signs or symptoms of pulp or periapical inflammatory changes. The negative control group consisted of 10 root filled teeth. Measurements were first taken from the index finger of patients. Their teeth were then subjected to a thermal test with refrigerant gas and then to a vitality test with pulse oximetry. Data were analysed by Pearson`s and paired t-tests. Results There were no significant statistical correlations between blood oxygen levels in the index finger and in the teeth of the patient (P > 0.05). There was a statistically significant difference in the oxygen levels between the two tooth groups studied and the index finger (P <= 0.002). Mean oxygen values in the index finger of patients were 95% (SD = 1.6), oxygen values in the maxillary central incisor were 91.29% (SD = 2.61) and mean oxygen values in maxillary canine were 90.69% (SD = 2.71). Conclusion The method determined consistently the level of blood oxygen saturation of the pulp in maxillary central incisor and canine teeth and can therefore be used for pulp vitality testing. Further studies are required to assess the effectiveness and validity of pulse oximetry in determining pulp vitality in traumatized teeth.
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Our long-term objective is to devise reliable methods to generate biological replacement teeth exhibiting the physical properties and functions of naturally formed human teeth. Previously, we demonstrated the successful use of tissue engineering approaches to generate small, bioengineered tooth crowns from harvested pig and rat postnatal dental stem cells (DSCs). To facilitate characterizations of human DSCs, we have developed a novel radiographic staging system to accurately correlate human third molar tooth developmental stage with anticipated harvested DSC yield. Our results demonstrated that DSC yields were higher in less developed teeth (Stages 1 and 2), and lower in more developed teeth (Stages 3, 4, and 5). The greatest cell yields and colony-forming units (CFUs) capability was obtained from Stages 1 and 2 tooth dental pulp. We conclude that radiographic developmental staging can be used to accurately assess the utility of harvested human teeth for future dental tissue engineering applications.
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Objective: The present study evaluated the relationship between periodontal disease and its clinical variables in Brazilian non-diabetic pregnant women (C), gestational diabetes mellitus (GDM), or type 1 diabetes mellitus (T1DM). Subjects and methods: A periodontal exam was performed in one hundred and sixty-one pregnant women (GDM:80; T1DM:31; C:50) by a single-blinded calibrated examiner who recorded plaque index (PI), gingival index (GI), bleeding index (BI), gingival margin location (GM), probing depth (PD), clinical attachment level (CAL), bleeding on probing (BOP), and tooth mobility index (MI). The medical variables were age, pregestational body mass index (pre-BMI), fasting plasma glucose (FPG), and glycated hemoglobin (HbA(1c)). Results: The GI, GM, PD, CAL, BOP, and MI were significantly higher (P < 0.01) among GDM and T1DM than for C. The PI was higher in GDM and similar between C and T1DM. The Adjusted Final Model for medical variables to evaluate the effects of groups on periodontal parameters confirmed these results. Conclusions: The presence of periodontal disease was significantly higher in Brazilian diabetic pregnancies (GDM and T1DM) when compared to non-diabetic pregnant women (C). The degree of periodontal disease was similar between the GDM and T1DM groups. Age, pregestational BMI, and HbA(1c) were factors related to CAL development in these two types of diabetes mellitus.
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P>Aim The aim of this study was to investigate the possible associations between isolated growth hormone deficiency (IGHD) and periodontal attachment loss (PAL) in adults affected by congenital IGHD. Materials and methods Forty-five previously identified IGHD subjects were eligible for this study. The final study sample comprised 32 cases (gender:20M/12F; age:44.8 +/- 17.5) matched for age, gender, diabetes, smoking status and income to 32 controls (non-IGHD subjects). Participants were submitted to a full-mouth clinical examination of six sites per tooth and were interviewed using a structured, written questionnaire. Periodontitis was defined as proximal PAL >= 5 mm affecting >= 30% of teeth. Results No significant differences were observed in the percentage of sites with visible plaque between IGHD and non-IGHD subjects (59.4% versus 46.9%, p=0.32). IGHD subjects had significant less supragingival calculus (31.3% versus 59.4%, p=0.02) and more bleeding on probing (71.9% versus 18.8%, p < 0.01) than controls. PAL >= 5 mm was significantly more prevalent (100% versus 71.9%, p < 0.01) and affected more teeth (30.5% versus 6.7%, p < 0.01) in cases than in controls. After adjusting for supragingival calculus, IGHD cases had a higher likelihood of having periodontitis than controls (OR=17.4-17.8, 95% CI=2.3-134.9, p=0.004-0.005). Conclusion Congenital IGHD subjects have a greater chance of having PAL.
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Introduction: Collagen-degrading matrix metalloproteinases (MMPs) are expressed by odontoblasts and present in dentin. We hypothesized that odontoblasts express other collagen-degrading enzymes such as cysteine cathepsins, and their activity would be present in dentin, because odontoblasts are known to express at least cathepsin D. Effect of transforming growth factor beta (TGF-beta) on cathepsin expression was also analyzed. Methods: Human odontoblasts and pulp tissue were cultured with and without TGF-beta, and cathepsin gene expression was analyzed with DNA microarrays. Dentin cathepsin and MMP activities were analyzed by degradation of respective specific fluorogenic substrates. Results: Both odontoblasts and pulp tissue demonstrated a wide range of cysteine cathepsin expression that gave minor responses to TGF-beta. Cathepsin and MMP activities were observed in all dentin samples, with significant negative correlations in their activities with tooth age. Conclusions: These results demonstrate for the first time the presence of cysteine cathepsins in dentin and suggest their role, along with MMPs, in dentin modification with aging. (J Endod 2010;36:475-481)