6 resultados para TOOTH ENAMEL

em Bioline International


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Optimum fluoride intake plays an essential role in the prevention of dental caries while fluoride consumption above recommended level interferes with the normal formation of tooth enamel and bones and may increase risk of dental and skeletal fluorosis. The knowledge and practices of endemic communities on etiology of fluorosis will help in its mitigation and prevention. The objective of this study was to investigate the knowledge, attitude and practices of endemic community on fluoride contamination, fluorosis and prevention practices in order to devise coordinated and targeted prevention mechanisms. Focus group discussions (FGD) and key-informant interview were conducted in three dietary areas to collect knowledge, attitude and practices (KAP) of the endemic community in July 2013.The results indicated that health consequences of fluoride contaminated water are fairly understood. None of the discussants mentioned the word “fluoride”. The knowledge and perception of the community on fluoride ingestion is poor. Health extension workers (HEWs) did not teach about fluoride and related health consequences. Dental fluorosis was reported to start at early ages and not commonly perceived as a major problem. However, adolescents worried and felt that they might be singled out when going to other areas. Older people have a skeletal fluorosis, which interferes with their day to day activities. In severely affected people, the teeth were weak and fragile and thus create difficulty in chewing hard foods like unfermented dry flat bread, sugar cane and toasted grains. People prefer rain water rather than water from borehole because of the inconvenient taste of the latter. The endemic communities have no sufficient knowledge and skills on potential sources of fluoride intake, the debilitating effect of high fluoride ingestion, and preventive and mitigatory measures to reduce fluoride intake. The effect of fluoride contamination and mitigatory methods should get sufficient attention by the community, health workers and concerned governmental bodies. The trend of harvesting and using rain water should be encouraged as it reduces fluoride intake. Future studies should focus on information communication on possible fluoride risks, intervention and evaluation studies on defluoridation, rain water harvesting and mitigatory techniques.

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Aim: To evaluate the effect of different in-office bleaching agents on the permeability, roughness and surface microhardness of human enamel. Methods: For evaluation of roughness and microhardness, 40 hemi-faces of 20 premolars were subjected to initial roughness (Ra parameter) and microhardness (VHN) measurements. Thirty-two premolar’s crowns were used for permeability test. Then, all specimens were randomly divided into four groups: C - without bleaching (control), HP35 - bleaching with 35% hydrogen peroxide (HP), HPF38 - 38% HP+fluoride, HPC35 - 35% HP+calcium. Final roughness (FR) and microhardness (FM) measurements were evaluated. For permeability, the 32 crowns were immersed in 1% sodium hypochlorite (20 min) and silver nitrate solutions (2 h) and subjected to developing solution under fluorescent light (16 h). Three sections from the crowns were analyzed in light microscope (100x) to evaluate the scores of permeability: Score 0 - no tracer agent penetration; Score 1 - less than half the thickness of enamel penetration; Score 2 - tracer agent reaching half the enamel thickness; Score 3 - entire enamel depth penetration, without reaching dentin and Score 4 - tracer agent reaching dentin. For roughness and microhardness evaluation were used one-way ANOVA and Dunnet post-test for independent samples, and t test for paired samples. For permeability, the data were analyzed by Kruskal Wallis and Dunn tests. Results: A significantly higher permeability and surface roughness were observed in groups HP35, HPF38 and HPC35 compared to the C group, as well as decreased microhardness (p<0.05). Conclusions: All bleaching agents increased permeability and surface roughness, and decreased microhardness of human enamel; thus, the addition of fluoride or calcium was not beneficial.

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Aim: This prospective cohort study was to evaluate the independent and mutual effects of socioeconomic, oral health behaviors and individual clinical factors, including enamel hypomineralization, as possible risk factors for increase in caries experience in second primary molar (SPM) over a period of 2-years. Methods: Children (n=216) aged 4-6 years were examined for hypomineralized second primary molar (HSPM) and dental caries in school settings and were recalled every 6 months. The caregivers filled out a semi-structured questionnaire about their socio-demographic and oral health-related behaviors. Data analysis was performed using a hierarchical model with three levels. Multiple analyses were performed at each level and variables with p<0.20 were tested by stepwise multiple Generalized Estimating Equation. Results: At final examination, 33.3% of the children had developed new caries lesions in SPM. The model showed that the number of years of mother’s schooling and the caregiver´s perception about their children’s caries experience played a protective role in the incidence of dental caries. Children who had white spot lesions were more likely to develop new carious lesions in SPM. Children with HSPM showed no higher incidence of caries in their SPM than those without HSPM. Conclusions: Clinical, socioeconomic and behavioral factors impacted on caries development in primary second molars. However, further studies are required to better understand the role of HSPM in caries development in other age groups.

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Aim: To determine if the prevalence of enamel hypoplasia, molar-incisor hypomineralisation (MIH) and deciduous molar hypomineralisation (DMH) is associated with the socioeconomic status of the child and to determine the prevalence of enamel hypoplasia and MIH/DMH comorbidity in the study population. Methods: Information was collected on the sex and socioeconomic status of the 1,169 study participants’ resident in Ile-Ife, Nigeria, recruited through a household survey. The children were clinically examined to assess for the presence of enamel hypoplasia, MIH and DMH. Associations between sex, socioeconomic status and the prevalence of enamel hypoplasia, MIH and DMH were determined. The proportion of children with enamel hypoplasia and MIH/DMH co-morbidity was also determined. Results: Among the 1,169 study participants, 47(4.0%) had MIH, 15 (1.3%) had DMH and 161 (13.8%) had enamel hypoplasia. One (0.09%) study participant had MIH/DMH co-morbidity, 12 (1.0%) had DMH/enamel hypoplasia co-morbidity, and 9 (0.8%) had MIH/hypoplasia co-morbidity. There was no significant association between the socioeconomic status and presence of enamel hypoplasia (p=0.22), MIH (p=0.78) or DMH (p=1.00). Conclusions: The socioeconomic status cannot be used as a distinguishing factor for enamel hypoplasia, MIH and DMH. The possibility of co-existence of enamel hypoplasia and MIH/DMH makes it imperative to find ways to distinguish between the lesions.

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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.