Tratamiento de regeneración endodóntica en pulpa vital y necrótica, utilizando fibrina rica en plaquetas y Biodentine: reporte de caso

Endodontic regeneration is an inductive and reparative biological treatment indicated to replace cell damage at the level of the dentinopulp complex. The objective of this study is to report a case of Endodontic Regenerative Therapy, in young permanent first molars, in a 10-year-old patient, using platelet-rich fibrin and Biodentine, applying two different protocols for combined diagnoses of irreversible pulpitis and pulp necrosis. The patient attended consultation due to extensive carious lesions. Clinical and imaging evaluations (X-rays and Cone Beam) were performed. The protocol in the necrotic canal consisted of disinfection with a bi-antibiotic paste and placement of a second-generation autologous scaffold matrix, made of biodegradable platelet-rich fibrin which is also , biocompatible and therefore without risk of immune rejection. The protocol in the canals with irreversible pulpitis consisted in a complete pulpotomy and placement of Biodentine calcium silicate cement, a material considered as first choice for pulp-conserving treatments, with properties similar to dentin. Eight weeks after the end of the treatment, a clinical control was conducted revealing an asymptomatic chart and negative palpation without the presence of fistula or abscess. This result indicated regeneration of the pulp tissues and success of the applied protocols. Controls will be carried out at 6, 12 and 18 months. Conclusion: The application of endodontic regenerative treatments, as performed in this reported case, is a favorable and innovative option to preserve, restore or replace the dental pulp. In comparison with conventional treatments, this procedure allows to return pulp functionality, complete development of the root, thickening of the dentinal walls and closure of the apical foramen of young permanent teeth affected by pulp pathologies. It is important that regenerative therapies are publicized and applied by dental professionalsLa regeneración endodóntica es un tratamiento inductivo y reparativo con bases biológicas, indicado para reemplazar los daños celulares a nivel del complejo dentinopulpar. El objetivo de este estudio es reportar un caso de Terapia Regenerativa Endodóntica, en primeros molares permanentes jóvenes, en un paciente de 10 años, a través del uso de fibrina rica en plaquetas y Biodentine, se aplicaron dos protocolos diferentes por diagnósticos combinados de pulpitis irreversible y necrosis pulpar. El paciente acude a consulta por presentar lesiones cariosas extensas; se realizaron evaluaciones clínicas e imagenológicas (radiografías y Cone Beam), el protocolo en el conducto necrótico consistió en la desinfección con pasta biantibiótica y la colocación de una matriz de andamiaje autóloga de segunda generación, elaborada de fibrina rica en plaquetas que es biodegradable, biocompatible y no existe riesgo de rechazo inmunológico. El protocolo en los conductos con pulpitis irreversibles consistió en pulpotomía total y colocación de cemento de silicato de calcio Biodentine, el cual se considera el material de primera elección para los tratamientos conservadores de la pulpa, con propiedades similares a la dentina. A 8 semanas de finalizado el tratamiento se realizó control clínico y el paciente mostró un cuadro asintomático, palpación negativa sin presencia de fístula o absceso lo que podría indicar regeneración de los tejidos pulpares y éxito de los protocolos aplicados. Los siguientes controles se realizán a los 6, 12 y 18 meses. Conclusión: la aplicación de los tratamientos regenerativos endodónticos como se realizó en el caso reportado, es una opción favorable e innovadora para preservar, restaurar o sustituir la pulpa dental, que en comparación con los tratamientos convencionales nos permiten devolver la funcionalidad pulpar, finalizar el desarrollo radicular, engrosamiento de las paredes dentinales y cierre del foramen apical de dientes permanentes jóvenes que han sido afectados por patologías pulpares. Es importante que las terapias regenerativas sean divulgadas y aplicadas por los profesionale

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg =-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

Novel genetic loci associated with hippocampal volume

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer’s disease (rg=−0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness

A saturated map of common genetic variants associated with human height

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes(1). Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel(2)) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

A saturated map of common genetic variants associated with human height.

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40–50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes1. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel2) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10–20% (14–24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries

Rare and low-frequency coding variants alter human adult height

Pathophysiology, epidemiology and therapy of agein

A saturated map of common genetic variants associated with human height

Common single-nucleotide polymorphisms (SNPs) are predicted to collectively explain 40-50% of phenotypic variation in human height, but identifying the specific variants and associated regions requires huge sample sizes1. Here, using data from a genome-wide association study of 5.4 million individuals of diverse ancestries, we show that 12,111 independent SNPs that are significantly associated with height account for nearly all of the common SNP-based heritability. These SNPs are clustered within 7,209 non-overlapping genomic segments with a mean size of around 90 kb, covering about 21% of the genome. The density of independent associations varies across the genome and the regions of increased density are enriched for biologically relevant genes. In out-of-sample estimation and prediction, the 12,111 SNPs (or all SNPs in the HapMap 3 panel2) account for 40% (45%) of phenotypic variance in populations of European ancestry but only around 10-20% (14-24%) in populations of other ancestries. Effect sizes, associated regions and gene prioritization are similar across ancestries, indicating that reduced prediction accuracy is likely to be explained by linkage disequilibrium and differences in allele frequency within associated regions. Finally, we show that the relevant biological pathways are detectable with smaller sample sizes than are needed to implicate causal genes and variants. Overall, this study provides a comprehensive map of specific genomic regions that contain the vast majority of common height-associated variants. Although this map is saturated for populations of European ancestry, further research is needed to achieve equivalent saturation in other ancestries.Public Health and primary carePrevention, Population and Disease management (PrePoD