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Search Results: 1 - 10 of 241840 matches for " Alexandre R. Vieira "
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New Directions in Cariology Research 2011
Alexandre R. Vieira
International Journal of Dentistry , 2012, DOI: 10.1155/2012/392730
Abstract:
New Directions in Cariology Research
Alexandre R. Vieira
International Journal of Dentistry , 2010, DOI: 10.1155/2010/525417
Abstract:
New Directions in Cariology Research
Alexandre R. Vieira
International Journal of Dentistry , 2010, DOI: 10.1155/2010/525417
Abstract:
Explaining Gender Differences in Caries: A Multifactorial Approach to a Multifactorial Disease
Maria Ferraro,Alexandre R. Vieira
International Journal of Dentistry , 2010, DOI: 10.1155/2010/649643
Abstract: Many studies have demonstrated that caries rates are higher in women than in men. This review attempts to provide an explanation for this trend by examining each factor which contributes to caries and how the factor differs in men and women. Evidence has been provided to demonstrate that caries risk factors for women include a different salivary composition and flow rate, hormonal fluctuations, dietary habits, genetic variations, and particular social roles among their family. Systemic diseases that have been found to be associated with caries have also been found to have an association with the female gender. An extended exposure to the oral cavity or a more cariogenic oral microflora has not been proven to contribute to higher caries in women. Further research in these areas could be done in the future to explain their contribution, or lack thereof, to a higher caries rate in women. 1. Introduction The significant impact of caries on the world’s population makes the disease an important topic of understanding. The development of caries is multifactorial, depending on many interacting variables to promote its development. In particular, the presence of bacteria, a substrate for the bacteria (food/sugars), the host’s oral environment, as well as the passing of time are the main contributing factors in the formation of caries. Epidemiological and clinical studies, through the use of tools such as DMFT and DMFS scores, have revealed a consistent trend in caries development, with females having higher prevalence than males [1]. The mechanisms underlying the reasoning for this trend can possibly be explained by an investigation of the suggested factors involved in caries development. 2. Genetic Contributions: AMELX The underlying mechanisms of any genetic contributions to the increased prevalence of caries in females versus males can be speculated to reside in the sex chromosomes, exhibiting sex-linked modes of inheritance. Genes present on the X or Y chromosome whose function affects those factors which contribute to the development of caries can be investigated. Variations in these genes would alter the host’s oral environment and the host’s response to the initiation of caries. The Amelogenin (AMELX) gene resides on the p arm of the X chromosome. Its locus is Xp22.31-p22.1 [2]. This gene and its protein product contribute to enamel formation in the dentition. The amelogenin protein constitutes 90% of the enamel matrix [3]. A mutation/deletion in the AMELX gene results in X-linked amelogenesis imperfecta [2]. There is a possibility that a deficient
Elderly at Greater Risk for Root Caries: A Look at the Multifactorial Risks with Emphasis on Genetics Susceptibility
Daniel Gati,Alexandre R. Vieira
International Journal of Dentistry , 2011, DOI: 10.1155/2011/647168
Abstract: Root caries is one of the most significant dental problems among older adults today. Many studies have demonstrated that older adults are at greater risk for developing root caries. Here we examine what risk factors older adults are prone to and explain how they contribute to higher rates of oral disease, in particular root caries. The elderly are at risk for root caries due to dentures, lack of dexterity, a shift from complex to simple sugars, and poor oral hygiene. Decreased salivary flow and its manifestations with other social/behavioral and medical factors may provide a more comprehensive explanation to a higher frequency of root caries in older adults. 1. Introduction Due to increasing life expectancy of the dentition, older adults are experiencing root caries and gingival recession, putting them at even higher risk for periodontal disease. Root caries is the major cause of tooth loss in older adults, and tooth loss is the most significant oral health-related negative variable of quality of life for the elderly [1]. Nearly half of all individuals aged 75 and older have root caries [2]. One prominent goal of the dental profession is to preserve and maintain dentitions throughout life. Population projections suggest that the proportion of the population aged 65 years and older will nearly double between 2000 (12.6 percent) and 2030 (20.0 percent), and that the proportion of those aged 85 years and older will increase dramatically over the next 10 to 15 years [3]. This population trend coupled with compelling evidence that people are retaining their teeth into old age suggests that there will be an increased number of older adults with many more natural teeth in the years to come. There are known clinical and behavioral risk factors involved in the production and progression of root caries in the elderly. Risks are described in a number of levels, from socioeconomic status to salivary flow to presence of dentures. Data have shown correlations of dietary and oral habits and other variables on root caries [4]. Many risk factors can compromise an older adult’s systemic health such as sociodemographic variables, nutrition/diet, and weakened immune system [5]. This paper examines salivary hypofunction, the systemic and oral immune system (immunoglobulins found in saliva) in older adults, and their manifestations. These factors are strongly determined by individual genetic background. There are several indicators that provide insight into the incidence and prevalence of caries in healthy people and the medical or disability conditions that place
Edad materna y defectos del tubo neural: evidencia para un efecto mayor en espina bífida que anencefalia
Vieira,Alexandre R.; Castillo Taucher,Silvia;
Revista médica de Chile , 2005, DOI: 10.4067/S0034-98872005000100008
Abstract: background: recent evidence from birth order data suggest that maternal factors can differently influence anencephaly and spina bifida. aim: to study the influence of maternal age on the risk for neural tube defects. material and methods: a meta-analysis of published data on neural tube defects (ntds) was carried out to determine whether there is an increased risk to have a child with ntds for younger and older mothers and if this risk differs depending on the type of ntd. all data available with information regarding the frequency of live births and ntds cases by maternal age (five- or ten-year intervals) were included in the analysis. effect sizes calculations were performed. results: the analysis supports the hypothesis that there is an increased risk of having an offspring with ntds for mothers 40 years of age or older. however, this effect is stronger for spina bifida than for anencephaly. there is also evidence that mothers 19 years old or younger have a higher risk for having a child with spina bifida. conclusions: maternal age influences the risk of having an offspring with neural tube defects (rev méd chile 2005; 133: 62-70)
Edad materna y defectos del tubo neural: evidencia para un efecto mayor en espina bífida que anencefalia Influence of maternal age on the risk for neural tube defects, a meta analysis
Alexandre R. Vieira,Silvia Castillo Taucher
Revista médica de Chile , 2005,
Abstract: Background: Recent evidence from birth order data suggest that maternal factors can differently influence anencephaly and spina bifida. Aim: To study the influence of maternal age on the risk for neural tube defects. Material and methods: A meta-analysis of published data on neural tube defects (NTDs) was carried out to determine whether there is an increased risk to have a child with NTDs for younger and older mothers and if this risk differs depending on the type of NTD. All data available with information regarding the frequency of live births and NTDs cases by maternal age (five- or ten-year intervals) were included in the analysis. Effect sizes calculations were performed. Results: The analysis supports the hypothesis that there is an increased risk of having an offspring with NTDs for mothers 40 years of age or older. However, this effect is stronger for spina bifida than for anencephaly. There is also evidence that mothers 19 years old or younger have a higher risk for having a child with spina bifida. Conclusions: Maternal age influences the risk of having an offspring with neural tube defects (Rev Méd Chile 2005; 133: 62-70)
Failure to Control Caries in an AIDS-Affected Individual: A Case Report
Karen A. Nedwick-Castro,Alexandre R. Vieira
Case Reports in Dentistry , 2012, DOI: 10.1155/2012/643436
Abstract: Many patients today are living longer with certain health issues like human immunodeficiency virus (HIV). These patients take numerous medications (HAART: highly active antiretroviral therapy) that cause xerostomia, which increases caries risk. There are particular challenges when treating HIV-positive patients with decreased immune systems, which can also accelerate the progression of periodontal disease. This paper discusses one such case that was followed from 2002 to 2010 at the University of Pittsburgh School of Dental Medicine, where an HIV patient lost all his teeth despite investing thousands of dollars. It is also common sense that just performing restorations to decayed teeth is not enough to control the disease, but recommending a personalized preventive maintenance program to the patient is a must.
Estudio genético de una familia chilena con tres fenotipos dentales diferentes
Andrea Pardo V,Rosa; Castillo T,Silvia; R Vieira,Alexandre;
Revista médica de Chile , 2006, DOI: 10.4067/S0034-98872006001200008
Abstract: background: congenital dental anomalies can affect up to 25% of the population. aim: to report the genetic study of a family with dental anomalies. material and methods: we studied a chilean family presenting with three independent dental phenotypes: third molar agenesis, supernumerary teeth, and dentinal dysplasia type i. we searched for mutations in candidate genes proposed for tooth agenesis and supernumerary teeth: irf6, fgfr1, msx1, msx2, pax9, prdm16 and tgfa. we also studied dspp as a candidate gene for dentinal dysplasia type i. results: we did not find mutations in fgfr1, msx2, pax9, prdm16, or tgfa. we found a msx1 mutation (g16d) in both affected and unaffected family members. also, we found a genetic variation not described before in irf6 in the dentinal dysplasia type i case. conclusions: further investigation is necessary to evaluate if these variants are functional in nature. finally, we are reporting a mutation in dspp in an asymptomatic 2-year-old child, which illustrates the ethical pitfalls of interpreting molecular data for genetic counseling of young and/or asymtomatic individuals
Análisis mutacional del gen Homeobox de segmento muscular 1 (MSX1) en chilenos con fisuras orales Mutational analysis of the muscle segment homeobox gene 1 (MSX1) in Chilean patients with cleft lip/palate
Alexandre R Vieira,Silvia Castillo Taucher,Teresa Aravena,Carmen Astete
Revista médica de Chile , 2004,
Abstract: Background: Mutations of the MSX1 gene may contribute to nonsyndromic forms of cleft lip and/or cleft palate. Aim: To search for mutations of MSX1 coding regions, including one highly conserved non-coding region in the single intron, among Chilean patients with cleft lip/palate. Patients and Methods: We studied 45 patients with cleft lip/palate and their parents. Oral mucosa samples were obtained with a swab. DNA was extracted and amplified by PCR. Results: Two missense mutations (G16D and G34A) were identified in this study that may be useful for future admixture studies. The G16D mutation appears to disrupt a possible splicing site and may contribute to clefting in this population. Conclusions: Rare MSX1 mutations are found in some cases of cleft lip and/or cleft palate but others remain to be found most likely in other regulatory regions of the gene (Rev Méd Chile 2004; 132: 816-22)
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