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The shape of the epithelial monolayer can be depicted as a curved tissue in three-dimensional (3D) space, where individual cells are tightly adhered to one another. The 3D morphogenesis of these tissues is governed by cell dynamics, and a variety of mathematical modeling and simulation studies have been conducted to investigate this process. One promising approach is the cell-center model, which can account for the discreteness of cells. The cell nucleus, which is considered to correspond to the cell center, can be observed experimentally. However, there has been a shortage of cell-center models specifically tailored for simulating 3D monolayer tissue deformation. In this study, we developed a mathematical model based on the cell-center model to simulate 3D monolayer tissue deformation. Our model was confirmed by simulating the in-plane deformation, out-of-plane deformation, and invagination due to apical constriction.

Introducción: Son numerosos los factores que pueden influenciar el éxito o fracaso del tratamiento de conductos, entre ellos, es imprescindible un buen conocimiento anatómico y manejo de las técnicas de instrumentación, irrigación y obturación. El calibrado apical es una técnica que permite determinar el diámetro de la constricción apical durante la instrumentación Esta revisión pretende esclarecer qué limite se debe establecer para realizar la instrumentación y el calibrado, evaluar la precisión de las técnicas de localización de ápices, determinar el diámetro adecuado para el calibrado apical mediante las innovadoras técnicas de agrandamiento en dientes con patologías periapicales y el manejo clínico de dientes cona anomalías que afectan a la constricción. Metodología: se realizaron diferentes búsquedas según los parámetros que se querían analizar. Se obtuvieron un total de 242, 20 de los cuales se ajustaron a los criterios de inclusión y exclusión. También se realizó una búsqueda manual en revistas de gran factor de impacto, obteniendo 7 estudios. Resultados y conclusiones: en esta revisión bibliográfica, se han expuesto estudios experimentales in vivo e in vitro. Estos estudios establecen la constricción apical como límite de la instrumentación. La combinación del localizador de ápices y las radiografías aportan mayor precisión en la determinación de la longitud de trabajo. Preflaring y limas sin ahusamiento proporcionan mayor precisión en el calibrado del diámetro de la constricción. Estudios recientes muestran casos de periodontitis apicales, donde el alargamiento apical junto con la limpieza mecánica, proporciona buenos resultados reduciendo los tratamientos a una sola visita. En reportes de casos recientes, se ha visto como en anomalías que afectan a la constricción apical como dientes taurodónticos o dens invaginatus, el uso de CBCT, microscopía, irrigación ultrasónica a concentraciones bajas y sistema de obturación termoplástica favorecen el éxito de estos, Introduction: There are many factors that can influence on the success or failure of root canal treatment, among them, a good anatomical knowledge and a management of instrumentation, irrigation and obturation techniques. Apical gauging is a technique use to determine the diameter of apical constriction during instrumentation. This review aims to clarify what limit should be established to perform the instrumentation, to evaluate the precision of apex locators techniques, determine the appropriate diameter to apical gauge using innovative enlargement methods in teeth with periapical pathologies and the clinical management of teeth with anomalies that affect the apical constriction. Methodology: Different searches were carried out according to the parameters to be analyses on Pubmed. A total of 242 were obtained, 20 of which were adjusted to the inclusion and exclusion criteria. A manual search was also carried out in journals with a high impact factors obtaining 7 studies. Results and conclusions: In this literature review, experimental in vivo and in vitro studies have been reported. These studies establish the apical constriction as the limit of the instrumentation. The combination technique of the apex locator and radiography provide greater precision in determining the working length. Preflaring and non-taper files provide better results in the apical gauging of apical constriction`s diameter. Recent studies show cases of apical periodontitis, where apical enlargement with mechanical cleaning provides good results reducing treatment to a single visit. In recent case reports, it has been seen the use of CBCT, microscopy, ultrasonic irrigation at low concentrations and thermoplastic obturation system to the complex treatments of teeth with anomalies.

Cell delamination is a conserved morphogenetic process important for the generation of cell diversity and maintenance of tissue homeostasis. Here, we used Drosophila embryonic neuroblasts as a model to study the apical constriction process during cell delamination. We observe dynamic myosin signals both around the cell adherens junctions and underneath the cell apical surface in the neuroectoderm. On the cell apical cortex, the nonjunctional myosin forms flows and pulses, which are termed medial myosin pulses. Quantitative differences in medial myosin pulse intensity and frequency are crucial to distinguish delaminating neuroblasts from their neighbors. Inhibition of medial myosin pulses blocks delamination. The fate of a neuroblast is set apart from that of its neighbors by Notch signaling-mediated lateral inhibition. When we inhibit Notch signaling activity in the embryo, we observe that small clusters of cells undergo apical constriction and display an abnormal apical myosin pattern. Together, these results demonstrate that a contractile actomyosin network across the apical cell surface is organized to drive apical constriction in delaminating neuroblasts. © 2017.

Epithelial invagination is a fundamental module of morphogenesis that iteratively occurs to generate the architecture of many parts of a developing organism. By changing the physical properties such as the shape and/or position of a population of cells, invagination drives processes ranging from reconfiguring the entire body axis during gastrulation, to forming the primordia of the eyes, ears and multiple ducts and glands, during organogenesis. The epithelial bending required for invagination is achieved through a variety of mechanisms involving systems of cells. Here we provide an overview of the different mechanisms, some of which can work in combination, and outline the circumstances in which they apply.This article is part of the themed issue 'Systems morphodynamics: understanding the development of tissue hardware'.

Cell delamination is a conserved morphogenetic process important for the generation of cell diversity and maintenance of tissue homeostasis. Here, we used Drosophila embryonic neuroblasts as a model to study the apical constriction process during cell delamination. We observe dynamic myosin signals both around the cell adherens junctions and underneath the cell apical surface in the neuroectoderm. On the cell apical cortex, the nonjunctional myosin forms flows and pulses, which are termed medial myosin pulses. Quantitative differences in medial myosin pulse intensity and frequency are crucial to distinguish delaminating neuroblasts from their neighbors. Inhibition of medial myosin pulses blocks delamination. The fate of a neuroblast is set apart from that of its neighbors by Notch signaling-mediated lateral inhibition. When we inhibit Notch signaling activity in the embryo, we observe that small clusters of cells undergo apical constriction and display an abnormal apical myosin pattern. Together, these results demonstrate that a contractile actomyosin network across the apical cell surface is organized to drive apical constriction in delaminating neuroblasts. © 2017.

The Müllerian duct (MD) and Wolffian duct (WD) are embryonic tubular tissues giving rise to female and male reproductive tracts, respectively. In amniote embryos, both MD and WD emerge in both sexes, but subsequently degenerate in the males and females, respectively. Here, by using MD-specific gene manipulations in chicken embryos, we identify the molecular and cellular mechanisms that link early MD specification to tubular invagination. Early (pre-)specification of MD precursors in the coelomic epithelium requires BMP signaling and its downstream target Pax2 in a WD-independent process. Subsequently, the BMP/Pax2 axis induces Lim1 expression, a hallmark of MD specification, for which FGF/ERK and WD-derived signals are also required. Finally, the sequential actions of the BMP/Pax2 and FGF/Lim1 axes culminate in epithelial invagination to form a tubular structure driven by an apical constriction, where apical accumulation of phospho-myosin light chain is positively regulated by FGF/ERK signaling. Our study delineates mechanisms governing the early formation of the MD, and also serves as a model of how an epithelial cell sheet is transformed to a tubular structure, a process seen in a variety of developmental contexts.

Epithelial invagination is a morphological process in which flat cell sheets transform into three-dimensional structures through bending of the tissue. It is accompanied by apical constriction, in which the apical cell surface is reduced in relation to the basal cell surface. Although much is known about the intra-cellular molecular machinery driving apical constriction and epithelial invagination, information of how extra-cellular signals affect these processes remains insufficient. In this study we have established several in vivo assays of placodal invagination to explore whether the external signal BMP regulates processes connected to epithelial invagination. By inhibiting BMP activity in prospective cranial placodes, we provide evidence that BMP signals are required for RhoA and F-actin rearrangements, apical constriction, cell elongation and epithelial invagination. The failure of placode invagination after BMP inhibition appears to be a direct consequence of disrupted apical accumulation of RhoA and F-actin, rather than changes in cell death or proliferation. In addition, our results show that epithelial invagination and acquisition of placode-specific identities are two distinct and separable developmental processes. In summary, our results provide evidence that BMP signals promote epithelial invagination by acting upstream of the intracellular molecular machinery that drives apical constriction and cell elongation.

Epithelial invagination is a morphological process in which flat cell sheets transform into three-dimensional structures through bending of the tissue. It is accompanied by apical constriction, in which the apical cell surface is reduced in relation to the basal cell surface. Although much is known about the intra-cellular molecular machinery driving apical constriction and epithelial invagination, information of how extra-cellular signals affect these processes remains insufficient. In this study we have established several in vivo assays of placodal invagination to explore whether the external signal BMP regulates processes connected to epithelial invagination. By inhibiting BMP activity in prospective cranial placodes, we provide evidence that BMP signals are required for RhoA and F-actin rearrangements, apical constriction, cell elongation and epithelial invagination. The failure of placode invagination after BMP inhibition appears to be a direct consequence of disrupted apical accumulation of RhoA and F-actin, rather than changes in cell death or proliferation. In addition, our results show that epithelial invagination and acquisition of placode-specific identities are two distinct and separable developmental processes. In summary, our results provide evidence that BMP signals promote epithelial invagination by acting upstream of the intracellular molecular machinery that drives apical constriction and cell elongation.

Epithelial invagination is a morphological process in which flat cell sheets transform into three-dimensional structures through bending of the tissue. It is accompanied by apical constriction, in which the apical cell surface is reduced in relation to the basal cell surface. Although much is known about the intra-cellular molecular machinery driving apical constriction and epithelial invagination, information of how extra-cellular signals affect these processes remains insufficient. In this study we have established several in vivo assays of placodal invagination to explore whether the external signal BMP regulates processes connected to epithelial invagination. By inhibiting BMP activity in prospective cranial placodes, we provide evidence that BMP signals are required for RhoA and F-actin rearrangements, apical constriction, cell elongation and epithelial invagination. The failure of placode invagination after BMP inhibition appears to be a direct consequence of disrupted apical accumulation of RhoA and F-actin, rather than changes in cell death or proliferation. In addition, our results show that epithelial invagination and acquisition of placode-specific identities are two distinct and separable developmental processes. In summary, our results provide evidence that BMP signals promote epithelial invagination by acting upstream of the intracellular molecular machinery that drives apical constriction and cell elongation.

Now days is more the trust we can have to the Apex-locator in endodontics. Now we can expect more accuracy results working length measure, not only of the apical constriction but the total length of the roots. Endodontics can’t left behind the use of the Apex-locator, because of its useful work, not only on the determination of the works length, also in the diagnostic of perforations or fractures. Even do, this article displays a reliable and simple guide in the use of apex locator during enodontic treatment., En la actualidad es cada vez más la aceptación y confiabilidad que tienen los localizadores apicales en las consultas endodónticas, ya que cada vez logran mediciones más exactas de la longitud de trabajo al localizar no solamente la constricción apical sino que también determina la salida del foramen apical y, por ende se puede predecir más certeramente el resultado de la terapia endodóntica; todo esto gracias a un largo período de desarrollo y perfeccionamiento de estos aparatos desde mediados del siglo pasado, así como también suficientes estudios que avalan resultados positivos y confiables. La endodoncia moderna no puede ni debe dejar de lado el uso los localizadores de ápice ya que como hemos mencionado es una herramienta fundamental no solo en la determinación de la longitud de trabajo sino también en el diagnóstico de perforaciones y fracturas. Sin embargo, así como tiene sus ventajas también tiene sus desventajas, las cuales hay que tener presentes al momento de utilizar estos aparatos, sin olvidar tampoco seguir al pie de la letra las indicaciones del fabricante y mantenerse actualizado respecto a los usos, indicaciones y contradicciones que arrojen estudios recientes.

Epithelial invagination is a morphological process in which flat cell sheets transform into three-dimensional structures through bending of the tissue. It is accompanied by apical constriction, in which the apical cell surface is reduced in relation to the basal cell surface. Although much is known about the intra-cellular molecular machinery driving apical constriction and epithelial invagination, information of how extra-cellular signals affect these processes remains insufficient. In this study we have established several in vivo assays of placodal invagination to explore whether the external signal BMP regulates processes connected to epithelial invagination. By inhibiting BMP activity in prospective cranial placodes, we provide evidence that BMP signals are required for RhoA and F-actin rearrangements, apical constriction, cell elongation and epithelial invagination. The failure of placode invagination after BMP inhibition appears to be a direct consequence of disrupted apical accumulation of RhoA and F-actin, rather than changes in cell death or proliferation. In addition, our results show that epithelial invagination and acquisition of placode-specific identities are two distinct and separable developmental processes. In summary, our results provide evidence that BMP signals promote epithelial invagination by acting upstream of the intracellular molecular machinery that drives apical constriction and cell elongation.

Epithelial invagination is a morphological process in which flat cell sheets transform into three-dimensional structures through bending of the tissue. It is accompanied by apical constriction, in which the apical cell surface is reduced in relation to the basal cell surface. Although much is known about the intra-cellular molecular machinery driving apical constriction and epithelial invagination, information of how extra-cellular signals affect these processes remains insufficient. In this study we have established several in vivo assays of placodal invagination to explore whether the external signal BMP regulates processes connected to epithelial invagination. By inhibiting BMP activity in prospective cranial placodes, we provide evidence that BMP signals are required for RhoA and F-actin rearrangements, apical constriction, cell elongation and epithelial invagination. The failure of placode invagination after BMP inhibition appears to be a direct consequence of disrupted apical accumulation of RhoA and F-actin, rather than changes in cell death or proliferation. In addition, our results show that epithelial invagination and acquisition of placode-specific identities are two distinct and separable developmental processes. In summary, our results provide evidence that BMP signals promote epithelial invagination by acting upstream of the intracellular molecular machinery that drives apical constriction and cell elongation.

Objectives: The aim of this study is to assess the morphology, the prevalence and the topography of the apical constriction (AC) through a tridimensional analysis and compare the results with the available data reported in the literature. Materials and methods: 15 teeth were selected. The teeth were intact and atraumatically extracted, without signs of radicular resorption or previous root canal treatments. Each tooth was scanned with the micro-computed tomography at a resolution of 9 mm. Through computer reconstruction the roots were made transparent, in order to reveal the endodontic anatomy; two calibrated examiners assessed the prevalence and the morphology of the AC on two different projections for each tooth. The AC was classified as present (single, multiple, tapered) or absent (flaring, parallel, apical delta). Inter-rater agreement was computed applying Cohen's kappa. The distance between the AC and the apical foramen was determined by means of a digital ruler. Results and conclusion: 52.6% of the observed ACs was ambiguous (present on one projection but not on the other one). Only 21.0% of the canals showed a tridimensional AC (present on both projections). Inter-rater agreement was very good (k = 0.839). The morphology, from greater to least, was flaring (25%), single (21.1%), parallel (21.1%), tapered (19.7%), apical delta (10.5%) and multiple (2.6%). Inter-rater agreement was again very good (kappa = 0.869). Root canal anatomy as described in the literature is more conceptual than real. The presence of AC appears to be an exception rather than a canon. © 2014 Società Italiana di Endodonzia. Production and hosting by Elsevier B.V. All rights reserved

Objectives: The aim of this study is to assess the morphology, the prevalence and the topography of the apical constriction (AC) through a tridimensional analysis and compare the results with the available data reported in the literature. Materials and methods: 15 teeth were selected. The teeth were intact and atraumatically extracted, without signs of radicular resorption or previous root canal treatments. Each tooth was scanned with the micro-computed tomography at a resolution of 9 mm. Through computer reconstruction the roots were made transparent, in order to reveal the endodontic anatomy; two calibrated examiners assessed the prevalence and the morphology of the AC on two different projections for each tooth. The AC was classified as present (single, multiple, tapered) or absent (flaring, parallel, apical delta). Inter-rater agreement was computed applying Cohen's kappa. The distance between the AC and the apical foramen was determined by means of a digital ruler. Results and conclusion: 52.6% of the observed ACs was ambiguous (present on one projection but not on the other one). Only 21.0% of the canals showed a tridimensional AC (present on both projections). Inter-rater agreement was very good (k = 0.839). The morphology, from greater to least, was flaring (25%), single (21.1%), parallel (21.1%), tapered (19.7%), apical delta (10.5%) and multiple (2.6%). Inter-rater agreement was again very good (kappa = 0.869). Root canal anatomy as described in the literature is more conceptual than real. The presence of AC appears to be an exception rather than a canon. © 2014 Società Italiana di Endodonzia. Production and hosting by Elsevier B.V. All rights reserved

Aim To compare the reproducibility of three electronic apex locators (EALs), Dentaport ZX, RomiApex A-15 and Raypex 5, under clinical conditions. Methodology Forty-eight root canals of incisors, canines and premolars with or without radiographically confirmed periapical lesions required root canal treatment in 42 patients. In each root canal, all three EALs were used to determine the working length (WL) that was defined as the zero reading and indicated by 'Apex', '0.0' or 'red square' markings on the EAL display. A new K-file of the same size was used for each measurement. The file length was fixed with a rubber stop and measured to an accuracy of 0.01 mm. Measurements were undertaken by two calibrated operators. Differences in zero readings between the three EALs in the same root canal were statistically analysed using paired t-tests with the Bonferroni correction, Bland-Altman plot and Linn's concordance correlation coefficients at alpha = 0.05. Results Mean and standard deviation values measured by the three EALs showed no statistically significant differences. Identical readings by all three EALs were found in 10.4% of root canals. Forty-three per cent of readings differed by less than +/- 0.5 mm and 31.3% exceeded a difference of +/- 1 mm. Conclusions The clinical reproducibility of Dentaport ZX, RomiApex A-15 and Raypex 5 was confirmed with the majority of readings within the +/- 1.0 mm range. However, the small number of identical zero readings suggests that EALs are not reliable as the sole means of WL determination under clinical conditions.

Many epithelial tissues undergo extensive remodelling during morphogenesis. How their epithelial features, such as apicobasal polarity or adhesion, are maintained and remodelled and how adhesion and polarity proteins contribute to morphogenesis are two important questions in development. Here, we approach these issues by investigating the role of the apical determinant protein Crumbs (Crb) during the morphogenesis of the embryonic Drosophila tracheal system. Crb accumulates differentially throughout tracheal development and is required for different tracheal events. The earliest requirement for Crb is for tracheal invagination, which is preceded by an enhanced accumulation of Crb in the invagination domain. There, Crb, acting in parallel with the epidermal growth factor receptor (Egfr) pathway, is required for tracheal cell apical constriction and for organising an actomyosin complex, which we propose is mediated by Crb recruitment of moesin (Moe). The ability of a Crb isoform unable to rescue polarity in crb mutants to otherwise rescue their invagination phenotype, and the converse inability of a FERM-binding domain mutant Crb to rescue faulty invagination, support our hypothesis that it is the absence of Crb-dependent Moe enrichment, and not the polarity defect, that mainly underlies the crb invagination phenotype. This hypothesis is supported by the phenotype of lethal giant larvae (lgl); crb double mutants. These results unveil a link between Crb and the organisation of the actin cytoskeleton during morphogenesis.