QUANTIFICAÇÃO DE COMPOSTOS FENÓLICOS PRESENTES NA CAGAITA (Eugenia dysenterica DC.), A PARTIR DOS EXTRATOS ETÉREO, ETANÓLICO E AQUOSO

O Centro-Oeste é dominado pelo bioma Cerrado, no qual possui diversas espécies frutíferas nativas, dentre elas, a cagaiteira. A cagaiteira cujo fruto é a cagaita (Eugenia dysenterica DC.) pertence à família das Mirtáceas, seus frutos são ligeiramente ácidos de cor amarelo-clara. Na maioria dos vegetais, os compostos fenólicos constituem os antioxidantes mais abundantes1, desempenhando papel importante nos processos de inibição do risco das doenças cardiovasculares e atuando sobre o estresse oxidativo2. Desta forma, este trabalho teve como objetivo quantificar o teor de compostos fenólicos presentes na cagaita, através dos extratos etéreo, etanólico e aquoso. Os frutos foram coletados no município de Abadia-GO, e as análises foram realizadas na Faculdade de Farmácia/UFG. O teor de compostos fenólicos, nos três extratos foram determinados em espectrofotômetro, a 750 nm, utilizando o reagente Folin-Ciocalteau, segundo Waterhouse (2002). A quantificação foi baseada no estabelecimento da curva padrão de ácido gálico (EAG), na faixa de 5 a 50 mg.L-1. Os resultados foram expressos em mg de (EAG)/100g de amostra. Nos três extratos foram avaliados os teores de compostos fenólicos na cagaita verde (colhida 10 dias após antese) e na cagaita madura (37 dias após antese). No extrato étereo a quantidade de compostos fenólicos aumentou 11,398 mg de (EAG)/100g de amostra do fruto verde para o maduro. Já nos extratos etanólico e aquoso, os compostos fenólicos tiveram redução de 17,934 e 14,204 mg de (EAG)/100g de amostra, porém o extrato etanólico extraiu a maior quantidade de compostos fenólicos, 382,178 mg de (EAG)/100g de amostra. Conclui-se que a cagaita apresenta satisfatória quantidade de compostos fenólicos quando o fruto ainda está verde, visto que o extrato etanólico extraiu maior quantidade deste composto com o fruto colhido com 10 dias

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p = 0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p = 0.006) and TUIP11 (p = 0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity. © 2012 Shimizu et al

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

Abstract There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p = 0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p = 0.006) and TUIP11 (p = 0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity

Different contribution of BRINP3 gene in chronic periodontitis and peri-implantitis: A cross-sectional study

Background: Peri-implantitis is a chronic inflammation, resulting in loss of supporting bone around implants. Chronic periodontitis is a risk indicator for implant failure. Both diseases have a common etiology regarding inflammatory destructive response. BRINP3 gene is associated with aggressive periodontitis. However, is still unclear if chronic periodontitis and peri-implantitis have the same genetic background. The aim of this work was to investigate the association between BRINP3 genetic variation (rs1342913 and rs1935881) and expression and susceptibility to both diseases. Methods: Periodontal and peri-implant examinations were performed in 215 subjects, divided into: healthy (without chronic periodontitis and peri-implantitis, n = 93); diseased (with chronic periodontitis and peri-implantitis, n = 52); chronic periodontitis only (n = 36), and peri-implantitis only (n = 34). A replication sample of 92 subjects who lost implants and 185 subjects successfully treated with implants were tested. DNA was extracted from buccal cells. Two genetic markers of BRINP3 (rs1342913 and rs1935881) were genotyped using TaqMan chemistry. Chi-square (p<0.05) compared genotype and allele frequency between groups. A subset of subjects (n = 31) had gingival biopsies harvested. The BRINP3 mRNA levels were studied by CT method (2δδCT). Mann-Whitney test correlated the levels of BRINP3 in each group (p<0.05). Results: Statistically significant association between BRINP3 rs1342913 and peri-implantitis was found in both studied groups (p<0.04). The levels of BRINP3 mRNA were significantly higher in diseased subjects compared to healthy individuals (p<0.01). Conclusion: This study provides evidence that the BRINP3 polymorphic variant rs1342913 and low level of BRINP3 expression are associated with peri-implantitis, independently from the presence of chronic periodontitis

Enamel Formation Genes Influence Enamel Microhardness Before and After Cariogenic Challenge

There is evidence for a genetic component in caries susceptibility, and studies in humans have suggested that variation in enamel formation genes may contribute to caries. For the present study, we used DNA samples collected from 1,831 individuals from various population data sets. Single nucleotide polymorphism markers were genotyped in selected genes (ameloblastin, amelogenin, enamelin, tuftelin, and tuftelin interacting protein 11) that influence enamel formation. Allele and genotype frequencies were compared between groups with distinct caries experience. Associations with caries experience can be detected but they are not necessarily replicated in all population groups and the most expressive results was for a marker in AMELX (p = 0.0007). To help interpret these results, we evaluated if enamel microhardness changes under simulated cariogenic challenges are associated with genetic variations in these same genes. After creating an artificial caries lesion, associations could be seen between genetic variation in TUFT1 (p = 0.006) and TUIP11 (p = 0.0006) with enamel microhardness. Our results suggest that the influence of genetic variation of enamel formation genes may influence the dynamic interactions between the enamel surface and the oral cavity

Role of TRAV Locus in Low Caries Experience

Submitted by sandra infurna ([email protected]) on 2016-01-14T10:57:58Z No. of bitstreams: 1 eduardo_castilla3_etal_IOC_2013.pdf: 1589582 bytes, checksum: da12596860deef9b52fce978ae3bf565 (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-01-14T12:11:08Z (GMT) No. of bitstreams: 1 eduardo_castilla3_etal_IOC_2013.pdf: 1589582 bytes, checksum: da12596860deef9b52fce978ae3bf565 (MD5)Made available in DSpace on 2016-01-14T12:11:08Z (GMT). No. of bitstreams: 1 eduardo_castilla3_etal_IOC_2013.pdf: 1589582 bytes, checksum: da12596860deef9b52fce978ae3bf565 (MD5) Previous issue date: 2013University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.Nihon University of Dentistry at Matsudo. Department of Pediatric Dentistry. Matsudo Chiba, Japan.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.ECLAMC (Latin American Collaborative Study of Congenital Malformations). CEMIC (Center for Medical Education and Clinical Research), Buenos Aires, Argentina / ECLAMC at INAGEMP-CNPq (National Institute of Population Medical Genetics) . Fundação Oswaldo Cruz. Departamento de Genética. Rio de Janeiro, RJ, Brasil.Pontifícia Universidade Católica do Paraná (PUCPR). Centro de Ciências Biológicas e da Saúde. Curitiba, PR, Brasil.Pontifícia Universidade Católica do Paraná (PUCPR). Centro de Ciências Biológicas e da Saúde. Curitiba, PR, Brasil.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.Universidade Federal do Rio de Janeiro. Departamento de Odontologia Pediátrica e Ortodontia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Unidade de Pesquisa Clínica. Niterói, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Unidade de Pesquisa Clínica. Niterói, RJ, Brasil.Istanbul Medipol University. Department of Pedodontics. Istanbul, Turkey.Istanbul University. Department of Pedodontics. Istanbul, Turkey.ECLAMC at Hospital de Area El Bolsón. Río Negro, Argentina.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.University of Texas Health Science Center. Medical School. Pediatric Research Center. School of Dentistry. Department of Endodontics. Houston, Texas, USA.University of Texas Health Science Center. Medical School. Pediatric Research Center. School of Dentistry. Department of Endodontics. Houston, Texas, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA.Istanbul University. Department of Pedodontics. Istanbul, Turkey.Universidade Federal do Rio de Janeiro. Departamento de Odontologia Pediátrica e Ortodontia. Rio de Janeiro, RJ, Brasil.Universidade Federal Fluminense. Instituto de Biologia. Unidade de Pesquisa Clínica. Niterói, RJ, Brasil / INMETRo. Duque de Caxias, RJ, Brasil.Pontifícia Universidade Católica do Paraná (PUCPR). Centro de Ciências Biológicas e da Saúde. Curitiba, PR, Brasil.ECLAMC at INAGEMP-CNPq (National Institute of Population Medical Genetics) in. Universidade Federal do Rio de Janeiro. Centro de Ciências da Saúde. Instituto de Biologia. Departamento de Genética. Rio de Janeiro, RJ, Brasil.ECLAMC (Latin American Collaborative Study of Congenital Malformations). CEMIC (Center for Medical Education and Clinical Research), Buenos Aires, Argentina / ECLAMC at INAGEMP-CNPq (National Institute of Population Medical Genetics) . Fundação Oswaldo Cruz. Departamento de Genética. Rio de Janeiro, RJ, Brasil.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA / University of Pittsburgh. Department of Human Genetics, and Clinical and Translational Science. Center for Craniofacial and Dental Genetics. Pittsburgh, PA, USA.University of Pittsburgh. Department of Oral Biology. Pittsburgh, PA, USA / University of Pittsburgh. School of Dental Medicine, and Clinical and Translational Science. Department of Pediatric Dentistry. Center for Craniofacial and Dental Genetics. Pittsburgh, PA, USA.Caries is the most common chronic, multifactorial disease in the world today; and little is still known about the genetic factors influencing susceptibility. Our previous genome- wide linkage scan has identified five loci related to caries susceptibility: 5q13.3, 13q31.1, 14q11.2, 14q 24.3, and Xq27. In the present study, we fine mapped the 14q11.2 locus in order to identify genetic contributors to caries susceptibility. Four hundred seventy-seven subjects from 72 pedigrees with similar cultural and behavioral habits and limited access to dental care living in the Philippines were studied. An additional 387 DNA samples from unrelated individuals were used to determine allele frequencies. For replication purposes, a total of 1,446 independent subjects from four different populations were analyzed based on their caries experience (low versus high). Fortyeight markers in 14q11.2 were genotyped using TaqMan chemistry. Transmission disequilibrium test was used to detect overtransmission of alleles in the Filipino families, and chi-square, Fisher’s exact and logistic regression were used to test for association between low caries experience and variant alleles in the replication data sets. We finally assessed the mRNA expression of TRAV4 in the saliva of 143 study subjects. In the Filipino families, statistically significant associations were found between low caries experience and markers in TRAV4. We were able to replicate these results in the populations studied that were characteristically from underserved areas. Direct sequencing of 22 subjects carrying the associated alleles detect one missense mutation (Y30R) that is predicted to be probably damaging. Finally, we observed higher expression in children and teenagers with low caries experience, correlating with specific alleles in TRAV4. Our results suggest TRAV4 may have a role in protecting against caries

Definitions of caries experience based on age and DMFT (Decayed, Missing due to caries, Filled Teeth) scores used in the Filipino families.

a<p>DMFT cut-offs were modified from the World Health Organization (World Health Organization, 2003),</p>b<p>Standard deviation.</p

Single marker association results for enamel microhardness.

<p>p-values <0.05 are presented in bold font.</p>*<p>Samples from buccal and lingual surfafes were analyzed together.</p><p>Artificial Caries/Baseline; The ratio of change for microhardness after creation of artificial caries.</p><p>Fluoride/Artificial Caries; The ratio of change for microhardness after fluoride treatment.</p><p>pH-cycling/Fluoride; The ratio of change for microhardness after pH-cycling treatment.</p

Previously reported associations between enamel formation genes and caries susceptibility.

*<p>In the presence of <i>Streptococcus mutans</i>.</p>#<p>Only is less severely affected cases.</p