Tratamiento quirúrgico-ortodóncico del canino superior incluido en posición vestibular

En el maxilar superior, el canino es el diente que se encuentra incluido con mayor frecuencia, después de los terceros molares. Se observa aproximadamente en un 2% de los pacientes que acuden a una consulta para tratamiento ortodóncico. Su ubicación es normalmente palatina, con una relación 2-3: I respecto a la localización vestibular o media. Para colocar este diente en una posición correcta dentro de la arcada debe realizarse en muchas ocasiones un tratamiento combinado ortodóncico­quirúrgico. Cuando el canino tiene una localización palatina, la técnica quirúrgica de elección suele ser una fenestración para hacer tracción extramucosa; pero cuando se ubica en posición vestibular, existen diversas opciones que dependen principalmente de la altura y de la cantidad de encía adherida que rodea al diente. Hemos realizado una revisión bibliográfica de los diversos abordajes quirúrgicos posibles ante un canino incluido por vestibular, sus indicaciones, ventajas e inconvenientes, y la ilustraremos con diversos casos tratados en nuestro servicio

Documento de consenso sobre el tratamiento antimicrobiano de las infecciones bacterianas odontogénicas

Las infecciones de la cavidad bucal son un problema de salud pública frecuente y motivo constante de prescripción antibiótica; el 10% de los antibióticos se emplean para tratar este problema. Sin embargo, hasta la fecha son pocos los estudios realizados para determinar su incidencia. Asímismo, su relación con ciertas enfermedades sistémicas (cardiacas, endocrinas, etc...) confiere a estas patologías una importancia vital. A pesar de la reconocida frecuencia e importancia de las infecciones odontogénicas, llama la atención la actual dispersión de criterio en varios aspectos referentes a su clasificación, terminología y recomendaciones terapéuticas. El objetivo principal de este documento, realizado con el consenso de especialistas en microbiología y odontología, es establecer unas recomendaciones útiles para todos los profesionales implicados en el manejo clínico de estas patologías. Recibe especial atención el aumento de la prevalencia de resistencias bacterianas observado durante los últimos años y, en concreto, la proliferación de cepas productoras de betalactamasas. Otro factor causal importante de la aparición de resistencias es la falta de cumplimiento terapéutico, en especial en lo que respecta a la dosis y a la duración del tratamiento. Así pues, estas patologías constituyen un problema complejo cuyo abordaje requiere la instauración de antimicrobianos de amplio espectro, con adecuados parámetros farmacocinéticos, con buena tolerancia y una posología cómoda que permita que el paciente reciba la dosis adecuada durante el tiempo necesario. Amoxicilina/ácido clavulánico a dosis altas (2000mg/ 125mg) ha demostrado buenos resultados y capacidad para superar resistencias. Otros agentes como metronidazol y clindamicina, seguidos de claritromicina y azitromicina han demostrado también ser activos frente a la mayoría de los microorganismos responsables de las infecciones odontogénicas.The infection of the oral cavity is a common public health problem and constant cause for antibiotic prescription, with 10% of antibiotics used to treat this problem. However, few studies have so far aimed to determine its incidence. Added to this, its relationship with certain sytemic diseases (cardiac, endocrine, etc') confers this pathology vital importance. In spite of the frequency and importance of odontogenic infection, the current dispersion in criteria regarding key aspects in classification, terminology and therapeutic recommendations is noticeable. The main objective of this document, compiled as a consensus statement by specialists in microbiology and odontology, is to establish useful recommendations for all of those involved in the clinical management of this pathology. Special attention has been placed on the rise in bacterial resistance observed over the last years, specifically the proliferation of betalactamase producing strains. Another important factor causing the resistance to appear is lack of therapeutic compliance, specially what regards dosage and treatment duration. Therefore, this pathology constitutes a complex problem which requires the instauration of broad spectrum antimicrobials, well tolerated and a convenient posology so that patients receive the adequate dose over the necessary period. High doses of amoxicillin/clavulanate (2000 mg / 125 mg) have showed good results and power to overcome resistance. Other agents such as metronidazole and clindamycin, followed by de claritromycin and azithromycin have also proved to be active against most of microorganisms responsible for odontogenic infection

Lysosome-mediated processing of chromatin in senescence

Cellular senescence is a stable proliferation arrest, a potent tumor suppressor mechanism, and a likely contributor to tissue aging. Cellular senescence involves extensive cellular remodeling, including of chromatin structure. Autophagy and lysosomes are important for recycling of cellular constituents and cell remodeling. Here we show that an autophagy/lysosomal pathway processes chromatin in senescent cells. In senescent cells, lamin A/C–negative, but strongly γ-H2AX–positive and H3K27me3-positive, cytoplasmic chromatin fragments (CCFs) budded off nuclei, and this was associated with lamin B1 down-regulation and the loss of nuclear envelope integrity. In the cytoplasm, CCFs were targeted by the autophagy machinery. Senescent cells exhibited markers of lysosomal-mediated proteolytic processing of histones and were progressively depleted of total histone content in a lysosome-dependent manner. In vivo, depletion of histones correlated with nevus maturation, an established histopathologic parameter associated with proliferation arrest and clinical benignancy. We conclude that senescent cells process their chromatin via an autophagy/lysosomal pathway and that this might contribute to stability of senescence and tumor suppression

Documento de consenso sobre el tratamiento antimicrobiano de las infecciones bacterianas odontogénicas

Las infecciones de la cavidad bucal son un problema de salud pública frecuente y motivo constante de prescripción antibiótica; el 10% de los antibióticos se emplean para tratar este problema. Sin embargo, hasta la fecha son pocos los estudios realizados para determinar su incidencia. Asímismo, su relación con ciertas enfermedades sistémicas (cardiacas, endocrinas, etc...) confiere a estas patologías una importancia vital. A pesar de la reconocida frecuencia e importancia de las infecciones odontogénicas, llama la atención la actual dispersión de criterio en varios aspectos referentes a su clasificación, terminología y recomendaciones terapéuticas. El objetivo principal de este documento, realizado con el consenso de especialistas en microbiología y odontología, es establecer unas recomendaciones útiles para todos los profesionales implicados en el manejo clínico de estas patologías. Recibe especial atención el aumento de la prevalencia de resistencias bacterianas observado durante los últimos años y, en concreto, la proliferación de cepas productoras de betalactamasas. Otro factor causal importante de la aparición de resistencias es la falta de cumplimiento terapéutico, en especial en lo que respecta a la dosis y a la duración del tratamiento. Así pues, estas patologías constituyen un problema complejo cuyo abordaje requiere la instauración de antimicrobianos de amplio espectro, con adecuados parámetros farmacocinéticos, con buena tolerancia y una posología cómoda que permita que el paciente reciba la dosis adecuada durante el tiempo necesario. Amoxicilina/ácido clavulánico a dosis altas (2000mg/ 125mg) ha demostrado buenos resultados y capacidad para superar resistencias. Otros agentes como metronidazol y clindamicina, seguidos de claritromicina y azitromicina han demostrado también ser activos frente a la mayoría de los microorganismos responsables de las infecciones odontogé[email protected]

Down-Regulation of Telomerase Activity and Activation of Caspase-3 Are Responsible for Tanshinone I-Induced Apoptosis in Monocyte Leukemia Cells in Vitro

Tanshinone I (Tan-I) is a diterpene quinone extracted from the traditional herbal medicine Salvia miltiorrhiza Bunge. Recently, Tan-I has been reported to have anti-tumor effects. In this study, we investigated the growth inhibition and apoptosis inducing effects of Tan-I on three kinds of monocytic leukemia cells (U937, THP-1 and SHI 1). Cell viability was measured by MTT assay. Cell apoptosis was assessed by flow cytometry (FCM) and AnnexinV/PI staining. Reverse transcriptase polymerase chain reaction (RT-PCR) and PCR–enzyme-linked immunosorbent assay (ELISA) were used to detect human telomerase reverse transcriptase (hTERT) expression and telomerase activity before and after apoptosis. The activity of caspase-3 was determined by Caspase colorimetric assay kit and Western blot analysis. Expression of the anti-apoptotic gene Survivin was assayed by Western blot and Real-time RT-PCR using the ABI PRISM 7500 Sequence Detection System. The results revealed that Tan-I could inhibit the growth of these three kinds of leukemia cells and cause apoptosis in a time- and dose-dependent manner. After treatment by Tan-I for 48 h, Western blotting showed cleavage of the caspase-3 zymogen protein with the appearance of its 17-kD subunit, and a 89-kD cleavage product of poly (ADP-ribose) polymerase (PARP), a known substrate of caspase-3, was also found clearly. The expression of hTERT mRNA as well as activity of telomerase were decreased concurrently in a dose-dependent manner. Moreover, Real-time RT-PCR and Western blot revealed a significant down-regulation of Survivin. We therefore conclude that the induction of apoptosis by Tan-I in monocytic leukemia U937 THP-1 and SHI 1 cells is highly correlated with activation of caspase-3 and decreasing of hTERT mRNA expression and telomerase activity as well as down-regulation of Survivin expression. To our knowledge, this is the first report about the effects of Tan-I on monocytic leukemia cells

A p53-Dependent Response Limits Epidermal Stem Cell Functionality and Organismal Size in Mice with Short Telomeres

Telomere maintenance is essential to ensure proper size and function of organs with a high turnover. In particular, a dwarf phenotype as well as phenotypes associated to premature loss of tissue regeneration, including the skin (hair loss, hair graying, decreased wound healing), are found in mice deficient for telomerase, the enzyme responsible for maintaining telomere length. Coincidental with the appearance of these phenotypes, p53 is found activated in several tissues from these mice, where is thought to trigger cellular senescence and/or apoptotic responses. Here, we show that p53 abrogation rescues both the small size phenotype and restitutes the functionality of epidermal stem cells (ESC) of telomerase-deficient mice with dysfunctional telomeres. In particular, p53 ablation restores hair growth, skin renewal and wound healing responses upon mitogenic induction, as well as rescues ESCmobilization defects in vivo and defective ESC clonogenic activity in vitro. This recovery of ESC functions is accompanied by a downregulation of senescence markers and an increased proliferation in the skin and kidney of telomerase-deficient mice with critically short telomeres without changes in apoptosis rates. Together, these findings indicate the existence of a p53-dependent senescence response acting on stem/progenitor cells with dysfunctional telomeres that is actively limiting their contribution to tissue regeneration, thereby impinging on tissue fitness

Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability

Background: Histone modification H4K20me3 and its methyltransferase SUV420H2 have been implicated in suppression of tumorigenesis. The underlying mechanism is unclear, although H4K20me3 abundance increases during cellular senescence, a stable proliferation arrest and tumor suppressor process, triggered by diverse molecular cues, including activated oncogenes. Here, we investigate the function of H4K20me3 in senescence and tumor suppression. Results: Using immunofluorescence and ChIP-seq we determine the distribution of H4K20me3 in proliferating and senescent human cells. Altered H4K20me3 in senescence is coupled to H4K16ac and DNA methylation changes in senescence. In senescent cells, H4K20me3 is especially enriched at DNA sequences contained within specialized domains of senescence-associated heterochromatin foci (SAHF), as well as specific families of non-genic and genic repeats. Altered H4K20me3 does not correlate strongly with changes in gene expression between proliferating and senescent cells; however, in senescent cells, but not proliferating cells, H4K20me3 enrichment at gene bodies correlates inversely with gene expression, reflecting de novo accumulation of H4K20me3 at repressed genes in senescent cells, including at genes also repressed in proliferating cells. Although elevated SUV420H2 upregulates H4K20me3, this does not accelerate senescence of primary human cells. However, elevated SUV420H2/H4K20me3 reinforces oncogene-induced senescence-associated proliferation arrest and slows tumorigenesis in vivo. Conclusions: These results corroborate a role for chromatin in underpinning the senescence phenotype but do not support a major role for H4K20me3 in initiation of senescence. Rather, we speculate that H4K20me3 plays a role in heterochromatinization and stabilization of the epigenome and genome of pre-malignant, oncogene-expressing senescent cells, thereby suppressing epigenetic and genetic instability and contributing to long-term senescence-mediated tumor suppression

Conserved genes and pathways in primary human fibroblast strains undergoing replicative and radiation induced senescence

Additional file 3: Figure S3. Regulation of genes of Arrhythmogenic right ventricular cardiomyopathy pathway during senescence induction in HFF strains Genes of the “Arrhythmogenic right ventricular cardiomyopathy” pathway which are significantly up- (green) and down- (red) regulated (log2 fold change >1) during irradiation induced senescence (120 h after 20 Gy irradiation) in HFF strains. Orange color signifies genes which are commonly up-regulated during both, irradiation induced and replicative senescence

7th Drug hypersensitivity meeting: part two

No abstract availabl