Utilidad de la Fosfatasa Alcalina salival como marcador bioquímico de la Enfermedad Periodontal

El objetivo de este trabajo de investigación fue la de establecer el rol de Fosfatasa Alcalina (FAL) presente en la saliva como marcador bioquímico de Enfermedad Periodontal (EP). El presente proyecto fue enmarcado dentro de los diseños de estudios observacionales de corte transversal

Concentración de mucina salival en pacientes con enfermedad periodontal

El objetivo de este trabajo fue estudiar la relación entre la concentración de mucina salival y la enfermedad periodontal. La muestra se dividió en tres grupos de 20 individuos cada uno: Grupo 1 sin enfermedad periodontal; Grupo 2 con gingivitis; y Grupo 3 con periodontitis. En todas las muestras salivales se confirmó la presencia de mucina, el Grupo 1 presentó un valor promedio de 1,27 mg/ml. En el Grupo 2 se registró un promedio de 1,93 mg/ml. En el Grupo 3 se observó un promedio de 3,01 mg/ml. El Análisis de la Variancia y posterior prueba de F (F = 25,01, p < 0,0001) confirman diferencias significativas en los contenidos de mucina entre grupos. El aumento de la concentración de mucina salival en pacientes periodontales podría representar un marcador químico de utilidad como coadyuvante en el diagnóstico clínico de esta enfermedad

Diabetes y enfermedad periodontal, una relación de doble vía

La asociación entre diabetes mellitus y la enfermedad periodontal ha sido motivo de estudio durante mucho tiempo. Son varias las hipótesis que se barajan a la hora de explicar dicha relación. El propósito de este artículo, es revisar los estudios publicados en la literatura periodontal hasta la fecha sobre la relación entre enfermedad periodontal y diabetes mellitus.

Presencia de Prostaglandina E2 del fluido crevicular en relación con el estado clínico-radiográfico del periodonto

Introducción y objetivos: La prostaglandina E2 (PGE2), está presente en el fluido crevicular gingival (FCG) y es evidenciada en la enfermedad periodontal (EP). Sin embargo, no existen informes suficientes para correlacionar las concentraciones de PGE2 del FCG en la salud y la EP con indicadores clínicos y radiográficos, edad y género. Por lo tanto, el presente estudio tiene como objetivo estimar los niveles de PGE2 en el FCG de sujetos sin enfermedad periodontal y con enfermedad periodontal. Materiales y Métodos: Se seleccionaron 99 sujetos, 33 sin EP (G1) y 66 con EP, 33 con gingivitis (G2) y 33 con periodontitis (G3), que fueron sometidos a un diagnóstico clínico-radiográfico, registrándose muestras de FGC, siendo almacenadas, centrifugadas y refrigeradas para su conservación. Posteriormente se midió la concentración de prostaglandina E2 crevicular mediante el ensayo por inmunoabsorción ligado a enzimas (ELISA), determinándose la concentración de cada sujeto. Resultados: PGE2 se detectó en todas las muestras. El G1 presentó una concentración de 28,82±2,88 pg/mL, el G2 44,91±4,37 pg/mL y el G3 148,67±74,74 pg/mL (p0.0001). Los niveles de PGE2 se correlacionaron significativamente con la hemorragia al sondaje, profundidad de sondaje, pérdida de inserción y pérdida ósea (p 0,05). Los niveles de PGE2 fueron modificados por la edad, pero no por el género. Conclusión: Es bien sabido que las células inflamatorias activadas producen mediadores inflamatorios que estimulan la producción de PGE2. Los hallazgos de este estudio demuestran un aumento de la concentración de PGE2 del FCG de acuerdo a la presencia de mayor severidad de la EP. PGE2 puede ser considerada como un biomarcador en la progresión de la EP. Sin embargo, se necesitan estudios controlados longitudinales para confirmar esta posibilidad.Background and Objectives: Prostaglandin E2 (PGE2) is present in gingival crevicular fluid the (GCF) and is evidenced in periodontal disease (PD). However, there are no enough reports to correlate the PGE2 concentrations in GCF in periodontal health and disease with clinical and radiographic indicators, age and gender. Hence, the present study is aimed to estimate the levels of PGE2 in GCF of subjects without periodontal disease (SEP) and periodontal disease (CEP). Materials and Methods: 99 subjects were selected, 33 without PD (G1) and 66 with PD, 33 with gingivitis (G2) and 33 with periodontitis (G3), which were submitted to a clinical and radiographic diagnosis, registering samples FGC, being stored, centrifuged and refrigerated for preservation. Subsequently the concentration of crevicular PGE2 was measured by using the enzyme linked immunosorbent assay (ELISA), determining the concentration of each subject. Results: PGE2 was detected in all the samples. The G1 presented a concentration of 28.82 ± 2.88 pg / mL, G2 44.91 ± 4.37 pg / mL and G3 148.67 ± 74.74 pg / mL (p 0.0001). PGE2 levels were significantly correlated with bleeding on probing, probing depth, attachment loss and bone loss (p 0.05). PGE2 levels were modified by age, but not gender. Conclusion: It is well known that activated inflammatory cells produce inflammatory mediators that stimulate the production of PGE2. The findings of this study demonstrate an increased concentration of PGE2 in FCG according to the presence of greater severity of PD. PGE2 may be considered as a biomarker in PD progression. However, controlled, longitudinal studies are needed to confirm this possibility

Periimplantitis: fisiopatología y diagnóstico mediante pruebas bioquímicas

El objetivo de este trabajo fue realizar una revisión de la bibliografía internacional sobre la enfermedad periimplantaria, destacando los aspectos fisiopatológicos y su diagnóstico. Los procesos periimplantarios son infecciones por biofilms bacterianos de implantes osteointegrados, que pueden resultar en la pérdida implantaria y la disminución de los niveles óseos que resulta en una grave complicación en nuestra clínica pues dificulta aún más el tratamiento de los pacientes edéntulos. El conocimiento de la fisiopatología y biología molecular es clave en la detección de patología periimplantaria, permitiendo de esta manera una acción terapéutica precoz para evitar la pérdida de implantes dentales y la pérdida ósea asociada

Lipopolysaccharide Inhibits the Channel Activity of the P2X7 Receptor

The purinergic P2X7 receptor (P2X7R) plays an important role during the immune response, participating in several events such as cytokine release, apoptosis, and necrosis. The bacterial endotoxin lipopolysaccharide (LPS) is one of the strongest stimuli of the immune response, and it has been shown that P2X7R activation can modulate LPS-induced responses. Moreover, a C-terminal binding site for LPS has been proposed. In order to evaluate if LPS can directly modulate the activity of the P2X7R, we tested several signaling pathways associated with P2X7R activation in HEK293 cells that do not express the TLR-4 receptor. We found that LPS alone was unable to induce any P2X7R-related activity, suggesting that the P2X7R is not directly activated by the endotoxin. On the other hand, preapplication of LPS inhibited ATP-induced currents, intracellular calcium increase, and ethidium bromide uptake and had no effect on ERK activation in HEK293 cells. In splenocytes-derived T-regulatory cells, in which ATP-induced apoptosis is driven by the P2X7R, LPS inhibited ATP-induced apoptosis. Altogether, these results demonstrate that LPS modulates the activity of the P2X7R and suggest that this effect could be of physiological relevance

Oxidative Damage in Lymphocytes of Copper Smelter Workers Correlated to Higher Levels of Excreted Arsenic

Arsenic has been associated with multiple harmful effects at the cellular level. Indirectly these defects could be related to impairment of the integrity of the immune system, in particular in lymphoid population. To characterize the effect of Arsenic on redox status on this population, copper smelter workers and arsenic unexposed donors were recruited for this study. We analyzed urine samples and lymphocyte enriched fractions from donors to determinate arsenic levels and lymphocyte proliferation. Moreover, we studied the presence of oxidative markers MDA, vitamin E and SOD activity in donor plasma. Here we demonstrated that in human beings exposed to high arsenic concentrations, lymphocyte MDA and arsenic urinary levels showed a positive correlation with SOD activity, and a negative correlation with vitamin E serum levels. Strikingly, lymphocytes from the arsenic exposed population respond to a polyclonal stimulator, phytohemaglutinin, with higher rates of thymidine incorporation than lymphocytes of a control population. As well, similar in vitro responses to arsenic were observed using a T cell line. Our results suggest that chronic human exposure to arsenic induces oxidative damage in lymphocytes and could be considered more relevant than evaluation of T cell surveillance

Extracellular Tuning of Mitochondrial Respiration Leads to Aortic Aneurysm

Marfan syndrome (MFS) is an autosomal dominant disorder of the connective tissue caused by mutations in the FBN1 (fibrillin-1) gene encoding a large glycoprotein in the extracellular matrix called fibrillin-1. The major complication of this connective disorder is the risk to develop thoracic aortic aneurysm. To date, no effective pharmacologic therapies have been identified for the management of thoracic aortic disease and the only options capable of preventing aneurysm rupture are endovascular repair or open surgery. Here, we have studied the role of mitochondrial dysfunction in the progression of thoracic aortic aneurysm and mitochondrial boosting strategies as a potential treatment to managing aortic aneurysms.Fondo de Investigacion Sanitaria del Instituto de Salud Carlos III (PI16/188, PI19/855), the European Regional D evelopment Fund, and the European Commission through H2020-EU.1.1, European Research Council grant ERC-2016-StG 715322-EndoMitTalk, and Gobierno de Espana SAF2016-80305P. This work was partially supported by Comunidad de Madrid (S2017/BMD 3867 RENIM-CM) and cofinanced by the European Structural and Investment Fund. M.M. is supported by the Miguel Servet Program (CP 19/014, Fundacion de Investigacion del Hospital 12 de Octubr

Fully automatic landmarking of 2D photographs identifies novel genetic loci influencing facial features

We report a genome-wide association study for facial features in > 6,000 Latin Americans. We placed 106 landmarks on 2D frontal photographs using the cloud service platform Face++. After Procrustes superposition, genome-wide association testing was performed for 301 inter-landmark distances. We detected nominally significant association (P-value < 5×10− 8) for 42 genome regions. Of these, 9 regions have been previously reported in GWAS of facial features. In follow-up analyses, we replicated 26 of the 33 novel regions (in East Asians or Europeans). The replicated regions include 1q32.3, 3q21.1, 8p11.21, 10p11.1, and 22q12.1, all comprising strong candidate genes involved in craniofacial development. Furthermore, the 1q32.3 region shows evidence of introgression from archaic humans. These results provide novel biological insights into facial variation and establish that automatic landmarking of standard 2D photographs is a simple and informative approach for the genetic analysis of facial variation, suitable for the rapid analysis of large population samples.- Introduction - Results And Discussion -- Study sample and phenotyping -- Trait/covariate correlation and heritability -- Overview of GWAS results and integration with the literature -- Follow-up of genomic regions newly associated with facial features: Replication in two human cohorts -- Follow-up of genomic regions newly associated with facial features: effects in the mouse -- Genome annotations at associated loci - Conclusion - Methods -- Study subjects -- Genotype data -- Phenotyping -- Statistical genetic analysis -- Interaction of EDAR with other genes -- Expression analysis for significant SNPs -- Detection of archaic introgression near ATF3 and association with facial features -- Annotation of SNPs in FUMA -- Shape GWAS in outbred mic