Aquaporin 5 Interacts with Fluoride and Possibly Protects Against Caries

Aquaporins (AQP) are water channel proteins and the genes coding for AQP2, AQP5, and AQP6 are clustered in 12q13. Since AQP5 is expressed in serous acinar cells of salivary glands, we investigated its involvement in caries. DNA samples from 1,383 individuals from six groups were studied. Genotypes of eight single nucleotide polymorphisms covering the aquaporin locus were tested for association with caries experience. Interaction with genes involved in enamel formation was tested. The association between enamel microhardness at baseline, after creation of artificial caries lesion, and after exposure to fluoride and the genetic markers in AQP5 was tested. Finally, AQP5 expression in human whole saliva, after exposure to fluoride in a mammary gland cell line, which is known to express AQP5, and in Wistar rats was also verified. Nominal associations were found between caries experience and markers in the AQP5 locus. Since these associations suggested that AQP5 may be inhibited by levels of fluoride in the drinking water that cause fluorosis, we showed that fluoride levels above optimal levels change AQP5 expression in humans, cell lines, and rats. We have shown that AQP5 is involved in the pathogenesis of caries and likely interact with fluoride.Fil: Anjomshoaa, Ida. University of Pittsburgh; Estados UnidosFil: Briseño Ruiz, Jessica. University of Pittsburgh; Estados UnidosFil: Deeley, Kathleen. University of Pittsburgh; Estados UnidosFil: Poletta, Fernando Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas "Norberto Quirno". CEMIC-CONICET.; ArgentinaFil: Mereb, Juan C.. Provincia de Río Negro. Ministerio de Salud. Hospital de Área El Bolsón ; ArgentinaFil: Leite, Aline L.. Universidade de Sao Paulo; BrasilFil: Barreta, Priscila A. T.. Universidade de Sao Paulo; BrasilFil: Silva, Thelma L.. Universidade de Sao Paulo; BrasilFil: Dizak, Piper. University of Pittsburgh; Estados UnidosFil: Ruff, Timothy. University of Pittsburgh; Estados UnidosFil: Patir, Asli. İstanbul Medipol Üniversitesi; TurquíaFil: Koruyucu, Mine. İstanbul Üniversitesi; TurquíaFil: Abbasoğlu, Zerrin. Yeditepe Üniversitesi; TurquíaFil: Casado, Priscila L.. Universidade Federal Fluminense; BrasilFil: Brown, Andrew. University of Pittsburgh; Estados UnidosFil: Zaky, Samer H.. University of Pittsburgh; Estados UnidosFil: Bayram, Merve. İstanbul Medipol Üniversitesi; TurquíaFil: Küchler, Erika C.. University of Pittsburgh; Estados UnidosFil: Cooper, Margaret E.. University of Pittsburgh; Estados UnidosFil: Liu, Kai. University of Pittsburgh; Estados UnidosFil: Marazita, Mary L.. University of Pittsburgh; Estados UnidosFil: Tanboğa, İlknur. Marmara Üniversitesi; TurquíaFil: Granjeiro, José M.. Universidade Federal Fluminense; Brasil. Instituto Nacional de Metrologia, Qualidade e Tecnologia; BrasilFil: Seymen, Figen. İstanbul Üniversitesi; TurquíaFil: Castilla, Eduardo Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas "Norberto Quirno". CEMIC-CONICET.; Argentina. Fundación Oswaldo Cruz; BrasilFil: Orioli, Iêda M.. Universidade Federal do Rio de Janeiro; BrasilFil: Sfeir, Charles. University of Pittsburgh; Estados UnidosFil: Owyang, Hongjiao. Marmara Üniversitesi; TurquíaFil: Rabelo Buzalaf, Marilia Afonso. Universidade de Sao Paulo; BrasilFil: Vieira, Alexandre R.. University of Pittsburgh; Estados Unido

Role of estrogen related receptor beta (ESRRB) in DFN35B hearing impairment and dental decay

BACKGROUND: Congenital forms of hearing impairment can be caused by mutations in the estrogen related receptor beta (ESRRB) gene. Our initial linkage studies suggested the ESRRB locus is linked to high caries experience in humans. METHODS: We tested for association between the ESRRB locus and dental caries in 1,731 subjects, if ESRRB was expressed in whole saliva, if ESRRB was associated with the microhardness of the dental enamel, and if ESRRB was expressed during enamel development of mice. RESULTS: Two families with recessive ESRRB mutations and DFNB35 hearing impairment showed more extensive dental destruction by caries. Expression levels of ESRRB in whole saliva samples showed differences depending on sex and dental caries experience. CONCLUSIONS: The common etiology of dental caries and hearing impairment provides a venue to assist in the identification of individuals at risk to either condition and provides options for the development of new caries prevention strategies, if the associated ESRRB genetic variants are correlated with efficacy.Fil: Weber, Megan L.. University of Pittsburgh; Estados UnidosFil: Hsin, Hong Yuan. University of Pittsburgh; Estados UnidosFil: Kalay, Ersan. Karadeniz Technical University; TurquíaFil: Brožková, Dana Š. Charles University; República Checa. University Hospital Motol; República ChecaFil: Shimizu, Takehiko. Nihon University. School of Dentistry; JapónFil: Bayram, Merve. Medipol Istanbul University; TurquíaFil: Deeley, Kathleen. University of Pittsburgh; Estados UnidosFil: Küchler, Erika C.. University of Pittsburgh; Estados UnidosFil: Forella, Jessalyn. University of Pittsburgh; Estados UnidosFil: Ruff, Timothy D.. University of Pittsburgh; Estados UnidosFil: Trombetta, Vanessa M.. University of Pittsburgh; Estados UnidosFil: Sencak, Regina C.. University of Pittsburgh; Estados UnidosFil: Hummel, Michael. University of Pittsburgh; Estados UnidosFil: Briseño Ruiz, Jessica. University of Pittsburgh; Estados UnidosFil: Revu, Shankar K.. University of Pittsburgh; Estados UnidosFil: Granjeiro, José M.. Universidade Federal Fluminense; BrasilFil: Antunes, Leonardo S.. Universidade Federal Fluminense; BrasilFil: Antunes, Livia A.. Universidade Federal Fluminense; BrasilFil: Abreu, Fernanda V.. Universidade Federal Fluminense; BrasilFil: Costabel, Marcelo C.. Universidade Federal do Rio de Janeiro; BrasilFil: Tannure, Patricia N.. Veiga de Almeida University; Brasil. Salgado de Oliveira University; BrasilFil: Koruyucu, Mine. Istanbul University; TurquíaFil: Patir, Asli. Medipol Istanbul University; TurquíaFil: Poletta, Fernando Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Mereb, Juan C.. Estudio Colaborativo Latino Americano de Malformaciones Congénitas; ArgentinaFil: Castilla, Eduardo Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. CEMIC-CONICET. Centro de Educaciones Médicas e Investigaciones Clínicas ; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Orioli, Iêda M.. Universidade Federal do Rio de Janeiro; BrasilFil: Marazita, Mary L.. University of Pittsburgh; Estados UnidosFil: Ouyang, Hongjiao. University of Pittsburgh; Estados UnidosFil: Jayaraman, Thottala. University of Pittsburgh; Estados UnidosFil: Seymen, Figen. Istanbul University; TurquíaFil: Vieira, Alexandre R.. University of Pittsburgh; Estados Unido

Detection of Streptococcus mutans Genomic DNA in Human DNA Samples Extracted from Saliva and Blood

Caries is a multifactorial disease, and studies aiming to unravel the factors modulating its etiology must consider all known predisposing factors. One major factor is bacterial colonization, and Streptococcus mutans is the main microorganism associated with the initiation of the disease. In our studies, we have access to DNA samples extracted from human saliva and blood. In this report, we tested a real-time PCR assay developed to detect copies of genomic DNA from Streptococcus mutans in 1,424 DNA samples from humans. Our results suggest that we can determine the presence of genomic DNA copies of Streptococcus mutans in both DNA samples from caries-free and caries-affected individuals. However, we were not able to detect the presence of genomic DNA copies of Streptococcus mutans in any DNA samples extracted from peripheral blood, which suggests the assay may not be sensitive enough for this goal. Values of the threshold cycle of the real-time PCR reaction correlate with higher levels of caries experience in children, but this correlation could not be detected for adults

Detection of Streptococcus mutans Genomic DNA in Human DNA Samples Extracted from Saliva and Blood

Caries is a multifactorial disease, and studies aiming to unravel the factors modulating its etiology must consider all known predisposing factors. One major factor is bacterial colonization, and Streptococcus mutans is the main microorganism associated with the initiation of the disease. In our studies, we have access to DNA samples extracted from human saliva and blood. In this report, we tested a real-time PCR assay developed to detect copies of genomic DNA from Streptococcus mutans in 1,424 DNA samples from humans. Our results suggest that we can determine the presence of genomic DNA copies of Streptococcus mutans in both DNA samples from caries-free and caries-affected individuals. However, we were not able to detect the presence of genomic DNA copies of Streptococcus mutans in any DNA samples extracted from peripheral blood, which suggests the assay may not be sensitive enough for this goal. Values of the threshold cycle of the real-time PCR reaction correlate with higher levels of caries experience in children, but this correlation could not be detected for adults

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

EARLY CHILDHOOD CARIES

For years, rampant caries in the primary dentition of infants and young children has been described by several terma including nursing bottle caries. nursing caries. rampant caries baby bottle caries. baby bottle tooth decay. milk bottle syndrome. AAPD indicators that; breastfeeding or other nursing practices alone could not cause the condition and therdote, the term "Early Childhood Caries" has become widely accepted by AAPD. Dental caries occurs in the primary dentition. there is a very good likelihood that xcaries will continue to be a problem in the mixed and early permanent dentitios. Early Childhood Caries is also an important predictor of subsequent caries experience. This subject has been reseached in different aspects to date. But it is thought to be this subject is important and has been discussed currently. In this article, the information about the characteristic propperties, etiology, bacterial relation and the treatment of the Early Chilhood Caries is given

ELLIS-VAN CREVELD SYNDROME: CASE REPORT

Ellis-van Creveld syndrome, or chondroectodermal dysplasia, is an autosomal recessive disorder with characteristic clinical manifectations, The syndrome seems as a result of the mutattion at the 61 th band of the of the long arm of 4th chromosome. Its incidence in the general popultion is 7/1.000.000. Chondroectodermal Dysplasia is a disease complex consisting of bilateral manual polidactyly, chondrodysplasia of long bones resulting in acrornelic dwaefism, hydrotic actodermal dysplasia affecting principally the nails. teeth and hair and congential heart malformations. The presence of a great varity of oral microdontic teeth, and congenitally missing teeth requires multidisciplimanary dental treatment. with consideration for the high incidence of cardiac defects in these patients. In this article, a case of a 9 year old child with chondroectodermal dyplasia is presented. After the physical, radyologic. intra-oral and extra-oral investigations; bilateral manul polydactyly, acromelic dwarfism, distrofic nails, abnormally shaped and microdontic teeth, congenitally missing teeh is identifed. As the intra-oral treatments are done for the patient, it is considered that she needs a longer follow up

Periodontal Healing After Traumatic Injury

After traumatic dental injuries, wound healing process is observed in periodonsium, pulp tissue and soft tissues. This process can occur with tissue reparation - the provision of progression by another tissue having different anatomy and function-or tissue regeneration - the provision of progression by a tissue having same anatomy and function-.Response of soft tissues and mineralized tissues against operational or traumatic injuries is identified as a very sensitive process and changes made in the treatment procedure is reported to have effect on healing ratio and quality. Therefore cellular and humoral elements taking place in the wound healing of the subjected tissue should be well understood to identify proper treatment procedures

INCIDENCE OF BAD ORAL HABITS AMONG 8-12 YEAR OLD CHILDREN

The aim of this study was to evaluate the prevalence of bad oral habits among 8-12 year-old children and to compare the results according to age and oral health. 107 children aged 8-12 years were examined for df, dfs, DMFT, DMFS, dental plaque and gingival bleeding indices, improper oral hygenie habits and bad oral habits (mouth breathing, finger sucking, nail biting, tongue thrust, bruxizm, pacifier sucking, pushing of the tongue using a finger/object, lip biting, cheek/pencil biting, self injuries behaviour, toothpick usage). 59 children were in high caries risk group (55.1%), 19 children were in low caries risk group (17.8%). The mean average of plaque index of low caries risk group was statistically lower than the mean average plaque index of high and moderate caries risk groups (p = 0.031, p = 0.022). Statistically significant differences were found between self injuries behaviour and age (p = 0.042). The most frequent habit was cheek/pencil biting, which was present in 38 subjects (35.5%). Mouth breathing, nail biting and tongue thrust were observed in 20 (18.7%), 17 (15.9%), 12 (11.2%) subjects. Significant differences were found between pushing of the tongue and plaque index, toothpick usage and bleeding index (p = 0.013, p = 0.01). Early diagnosis of the bad oral habits by dentists and appliying the adequete therapy in cooperation with other disciplines may help the child to get out of oral habits and may prevent the development of severe anomalies