High Helicobacter pylori Bacterial Load and Low Cytokine Expression Levels Are Associated with Nodular Gastropathy.

BACKGROUND AND AIMS: Nodular gastropathy (NG) is an inflammatory condition of the gastric mucosa characterized by the endoscopic detection of multiple millimeter protrusions. A strong association between NG and Helicobacter pylori and a possible role of NG as a risk factor for undifferentiated gastric cancer have been described. The aim of this study was to characterize the pathogenic and inflammatory profile of patients with NG. METHODS: Adult patients referred for upper gastrointestinal endoscopy were prospectively enrolled in this study. H. pylori infection status was determined by rapid urease test. Biopsies were stained with hematoxylin-eosin. Sydney and OLGA scores were used to assess gastritis characteristics and gastric cancer risk. PCR analysis was performed to determine bacterial load and virulence factors CagA (and its EPIYA motifs) and VacA alleles. Finally, gastric mucosa cytokine gene expression (IL-8, IL-1ß, and TNF-α) was determined by real-time RT-PCR. RESULTS: Forty-eight patients, mean age of 36 years, were recruited. All NG patients were infected by H. pylori. OLGA score was similar in both groups (NG patients and non-NG patients). NG patients had higher bacterial load in the gastric corpus (p = 0.01) and significantly less pro-inflammatory cytokine levels than non-NG infected patients (p = 0.01). CONCLUSIONS: In our study, NG is not associated with preneoplastic lesions. An increase in bacterial load without a concomitant increase in mucosal inflammatory cytokine responses in H. pylori-infected subjects with NG may represent a general dampening of immune responses or an additional mechanism of H. pylori active immune evasion.

Proteomic Analysis of Epithelial to Mesenchymal Transition (EMT) Reveals Cross-talk between SNAIL and HDAC1 Proteins in Breast Cancer Cells.

Epithelial to mesenchymal transition (EMT)(1) occurs naturally during embryogenesis, tissue repair, cancer progression, and metastasis. EMT induces cellular and microenvironmental changes resulting in loss of epithelial and acquisition of mesenchymal phenotypes, which promotes cellular invasive and migratory capabilities. EMT can be triggered by extracellular factors, including TGF-ß, HGF, and EGF. Overexpression of transcription factors, such as SNAIL, SLUG, ZEB1/2, and TWIST1, also induces EMT and is correlated to cancer aggressiveness. Here, the breast adenocarcinoma cell line MCF7 was transduced with SNAIL to identify specific mechanisms controlled by this transcription factor during EMT. Overexpression of SNAIL led to EMT, which was thoroughly validated by molecular, morphological, and functional experiments. Subcellular proteome enrichment followed by GEL-LC-MS/MS was performed to provide extensive protein fractionation and in-depth proteomic analysis. Quantitative analysis relied on a SILAC strategy, using the invasive breast cancer cell line MDA-MB-231 as a reference for quantitation. Subsets of proteins enriched in each subcellular compartment led to a complementary list of 4289 proteins identified with high confidence. A subset of differentially expressed proteins was validated by Western blot, including regulation in specific cellular compartments, potentially caused by protein translocation. Protein network analysis highlighted complexes involved in cell cycle control and epigenetic regulation. Flow cytometry analysis indicated that SNAIL overexpression led to cell cycle arrest in G0/G1 phases. Furthermore, down-regulation of HDAC1 was observed, supporting the involvement of epigenetic processes in SNAIL-induced EMT. When HDAC1 activity was inhibited, MCF7 not only apparently initiated EMT but also up-regulated SNAIL, indicating the cross-talk between these two proteins. Both HDAC1 inhibition and SNAIL overexpression activated the AKT pathway. These molecular mechanisms appear to be essential to EMT and therefore for cancer metastasis. Specific control of such epigenetic processes might then represent effective approaches for clinical management of metastatic cancer.

Helicobacter pylori-Clarithromycin Resistance in Symptomatic Pediatric Patients in a High Prevalence Country.

INTRODUCTION: Failure to eradicate Helicobacter pylori despite antibiotic treatment is generally attributed to increasing clarithromycin resistance conferred by point mutations in the 23S-rRNA gene or metronidazole resistance attributed to rdxA gene (HP0954) deletion in patients. Scarce data for pediatric population are available from developing countries. OBJECTIVES: The aim of the present study was to determine the presence of A2142G/C and A2143G mutations in the 23S-rRNA gene and/or rdxA gene (HP0954) deletion in a group of symptomatic H pylori-infected children recruited from an area with high infection rate and risk of gastric cancer. PATIENTS AND METHODS: We recruited 118 patients referred for upper endoscopy for gastrointestinal symptoms. The presence of H pylori was determined by urease test and histological staining. The rdxA gene (HP0954) deletion, and 2142G/C and A2143G mutations were determined by polymerase chain reaction-restriction fragment length polymorphism. A subgroup of infected patients received a 14-day regimen of omeprazole, amoxicillin, and clarithromycin. The effectiveness of this regime was determined by stool antigen determination 8 weeks after treatment. RESULTS: About 21% of the analyzed infected patients showed mutation in the 23S-rRNA gene, with the A2143G transition as the more frequent mutation, and 2% of the patients showed rdxA gene (HP0954) deletion. After treatment, 25% of the patients continued to harbor the bacteria; of these, 67% carried the A2143G mutation. CONCLUSIONS: H pylori-infected pediatric patients from Chile show high prevalence of the mutation responsible for clarithromycin resistance. The failure to eradicate H pylori can be attributed to the presence of the A2143G mutation.

Proteomics analysis reveals the role of ubiquitin specific protease (USP47) in Epithelial to Mesenchymal Transition (EMT) induced by TGFß2 in breast cells.

Epithelial to Mesenchymal Transition (EMT) is a normal cellular process that is also triggered during cancer progression and metastasis. EMT induces cellular and microenviromental changes, resulting in loss of epithelial features and acquisition of mesenchymal phenotypes. The growth factor TGFß and the transcription factor SNAIL1 (SNAIL) have been described as inducers of EMT. Here, we carried out an EMT model with non-tumorigenic cell line MCF-10A induced with the TGFß2 specific isoform of TGF protein family. The model was validated by molecular, morphological and functional experiments and showed correlation with the up-regulation of SNAIL. In order to identify additional regulators of EMT in this non-tumorigenic model, we explored quantitative proteomics, which revealed the Ubiquitin carboxyl-terminal hydrolase 47 (USP47) as one of the top up-regulated proteins. USP47 has a known role in cell growth and genome integrity, but not previously correlated to EMT. After validating USP47 alterations using MRM and antibody-based assays, we demonstrated that the chemical inhibition of USP47 with the inhibitor P5091 reduced expression of EMT markers and reverted morphological changes in MCF-10A cells undergoing EMT. These results support the involvement of USP47 in our EMT model as well as potential applications of deubiquitinases as therapeutic targets for cancer progression management. BIOLOGICAL SIGNIFICANCE: Metastasis is responsible for most cancer-associated mortality. Additionally, metastasis requires special attention, as the cellular transformations make treatment at this stage very difficult or occasionally impossible. Early steps in cancer metastasis involve the ability to detach from the solid tumor mass and invade the surrounding stromal tissues through cohesive migration, or a mesenchymal or amoeboid invasion. One of the first steps for metastatic cascade is denominated epithelial to mesenchymal transition (EMT), which can be triggered by different factors. Here, our efforts were directed to better understand this process and identify new pathways that contributes for acquisition of EMT, mainly focused on post translational modifications related to ubiquitin proteasome system. Our model of EMT induction by TGFß2 mimics early stage of metastatic cancer in epithelial breast cells and a proteomic study carried out for such model demonstrates that the deubiquitinase enzyme USP47 acts in SNAIL stabilization, one of the most important transcription factors for EMT phenotype acquisition and consequent metastasis. In addition, the inhibiton of USP47 with P5091, reverted the EMT phenotype. Together the knowledge of such processes of cancer progression and regulation can help in designing new strategies for combined therapies for control of cancer in early stages.

Early Childhood Caries in Peru.

Early Childhood Caries (ECC) is a global oral health problem, and Peru may be one of the countries with high prevalence of untreated ECC in South America. In this study, we constructed an epidemiologic profile of ECC in Peru through a comprehensive review of published data. The prevalence of ECC, risk factors for it, its impact on child development, and public oral health interventions on ECC have been included. The study revealed extremely high rates of ECC in Peru and significant oral-health disparities. Risk factors for ECC were poverty, high sugar consumption, and low oral health literacy. However, the number of studies is limited and their quality questionable. Oral health has not received high public-health priority in Peru. However, in recent years, new regulations and evidence-based documents (the first Clinical Practice Guideline for the Prevention, Diagnosis, and Management of Caries in Children; the Guideline for Children's healthy Growth and Development; the Law on Healthy Diet; and the Manual on Food Advertising) give hope for the future of infants' oral health in the nation.

The contribution and perspectives of proteomics to uncover ovarian cancer tumor markers.

Despite all the advances in understanding the mechanisms involved in ovarian cancer (OC) development, many aspects still need to be unraveled and understood. Tumor markers (TMs) are of special interest in this disease. Some aspects of clinical management of OC might be improved by the use of validated TMs, such as differentiating subtypes, defining the most appropriate treatment, monitoring the course of the disease, or predicting clinical outcome. The Food and Drug Administration (FDA) has approved a few TMs for OC: CA125 (cancer antigen 125; monitoring), HE4 (Human epididymis protein; monitoring), ROMA (Risk Of Malignancy Algorithm; HE4+CA125; prediction of malignancy) and OVA1 (Vermillion's first-generation Multivariate Index Assay [MIA]; prediction of malignancy). Proteomics can help advance the research in the field of TMs for OC. A variety of biological materials are being used in proteomic analysis, among them tumor tissues, interstitial fluids, tumor fluids, ascites, plasma, and ovarian cancer cell lines. However, the discovery and validation of new TMs for OC is still very challenging. The enormous heterogeneity of histological types of samples and the individual variability of patients (lifestyle, comorbidities, drug use, and family history) are difficult to overcome in research protocols. In this work, we sought to gather relevant information regarding TMs, OC, biological samples for proteomic analysis, as well as markers and algorithms approved by the FDA for use in clinical routine.

Helicobacter pylori pediatric infection changes FcεRI expression in dendritic cells and Treg profile in vivo and in vitro.

H. pylori infection shows an inverse relationship with allergies. Dendritic cells regulate mucosal immune responses including the induction of T regulatory cells which are fundamental in Helicobacter pylori-induced dampening of allergies. In this respect expression of high-affinity IgE receptor (FcεRI) has been associated with a regulatory dendritic cell profile. Therefore we aimed to evaluate possible mechanisms by which H. pylori infection might modify atopy in pediatric patients. Here we show that H. pylori-infected children exhibited both increased expression of FcεRI on peripheral myeloid and plasmacytoid dendritic cells and higher levels of Foxp3 and Latency Associated Peptide on T regulatory cells. Moreover, exposure to H. pylori drove increased FcεRI expression and IL-10 secretion by both pediatric H. pylori-exposed monocyte derived dendritic cells and T cells. Finally, we show a positive correlation between expression of FcεRI in circulating myeloid DCs and total Treg cells, suggesting that in children, H. pylori infection may have a modulating role in atopy, mediated by both altered surface expression of FcεRI on children's DC and an increased T regulatory cell profile.

Proteomic analysis of ovarian cancer cells during epithelial-mesenchymal transition (EMT) induced by epidermal growth factor (EGF) reveals mechanisms of cell cycle control.

Epithelial to mesenchymal transition (EMT) is a well-orchestrated process that culminates with loss of epithelial phenotype and gain of a mesenchymal and migratory phenotype. EMT enhances cancer cell invasiveness and drug resistance, favoring metastasis. Dysregulation of transcription factors, signaling pathways, miRNAs and growth factors including EGF, TGF-beta and HGF can trigger EMT. In ovarian cancer, overexpression of the EGFR family is associated with more aggressive clinical behavior. Here, the ovarian adenocarcinoma cell line Caov-3 was induced to EMT with EGF in order to identify specific mechanisms controlled by this process. Caov-3 cells induced to EMT were thoroughly validated and a combination of subcellular proteome enrichment, GEL-LC-MS/MS and SILAC strategy allowed consistent proteome identification and quantitation. Protein network analysis of differentially expressed proteins highlighted regulation of metabolism and cell cycle. Activation of relevant signaling pathways, such as PI3K/Akt/mTOR and Ras/Erk MAPK, in response to EGF-induced EMT was validated. Also, EMT did not affected the proliferation rate of Caov-3 cells, but led to cell cycle arrest in G1 phase regulated by increased levels of p21Waf1/Cip1, independently of p53. Furthermore, a decrease in G1 and G2 checkpoint proteins was observed, supporting the involvement of EGF-induced EMT in cell cycle control. BIOLOGICAL SIGNIFICANCE: Cancer is a complex multistep process characterized by accumulation of several hallmarks including epithelial to mesenchymal transition (EMT), which promotes cellular and microenvironmental changes resulting in invasion and migration to distant sites, favoring metastasis. EMT can be triggered by different extracellular stimuli, including growth factors such as EGF. In ovarian cancer, the most lethal gynecological cancer, overexpression of the EGFR family is associated with more aggressive clinical behavior, increasing mortality rate caused by metastasis. Our proteomic data, together with specific validation of specific cellular mechanisms demonstrated that EGF-induced EMT in Caov-3 cells leads to important alterations in metabolic process (protein synthesis) and cell cycle control, supporting the implication of EGF/EMT in cancer metastasis, cancer stem cell generation and, therefore, poor prognosis for the disease.

Profiling Cell Lines Nuclear Sub-proteome.

Proteins are very dynamic within the cell and their localization and trafficking between subcellular compartments are critical for their correct function. Indeed, the abnormal localization of a protein might lead to the pathogenesis of several diseases. The association of cell fractionation methods and mass spectrometry based proteomic methods allow both the localization and quantification of proteins in different sub-compartments. Here we present a detailed protocol for enrichment, identification, and quantitation of the nuclear proteome in cell lines combining nuclear subproteome enrichment by differential centrifugation and high-throughput proteomics.

A proteomic signature of ovarian cancer tumor fluid identified by highthroughput and verified by targeted proteomics.

UNLABELLED: Tumor fluid samples have emerged as a rich source for the identification of ovarian cancer in the context of proteomics studies. To uncover differences among benign and malignant ovarian samples, we performed a quantitative proteomic study consisting of albumin immunodepletion, isotope labeling with acrylamide and in-depth proteomic profiling by LC-MS/MS in a pool of 10 samples of each histological type. 1135 proteins were identified, corresponding to 505 gene products. 223 proteins presented associated quantification and the comparative analysis of histological types revealed 75 differentially abundant proteins. Based on this, we developed a panel for targeted proteomic analysis using the multiple reaction monitoring (MRM) method for validation of 51 proteins in individual samples of high-grade serous ovarian tumor fluids (malignant) and benign serous cystadenoma tumor fluids. This analysis showed concordant results in terms of average amounts of proteins, and APOE, SERPINF2, SERPING1, ADAM17, CD44 and OVGP1 were statistically significant between benign and malignant group. The results observed in the MRM for APOE were confirmed by western blotting, where APOE was more abundant in malignant samples. This molecular signature can contribute to improve tumor stratification and shall be investigated in combination with current biomarkers in larger cohorts to improve ovarian cancer diagnosis. BIOLOGICAL SIGNIFICANCE: Despite advances in cancer research, ovarian cancer has a high mortality and remains a major challenge due to a number of particularities of the disease, especially late diagnosis caused by vague clinical symptoms, the cellular and molecular heterogeneity of tumors, and the lack of effective treatment. Thus, efforts are directed to better understand this neoplasia, its origin, development and, particularly the identification and validation of biomarkers for early detection of the disease in asymptomatic stage. In the present work, we confirmed by MRM method in individual ovarian tumor fluid samples the regulation of 27 proteins out of 33 identified in a highthroughput study. We speculate that the presence and/or differential abundance observed in tumor fluid is a cooperation primarily of high rates of secretion of such tumor proteins to extra tumor environment that will at the end accumulate in plasma, and also the accumulation of acute-phase proteins throughout the entire body. On top of that, consideration of physiological influences in the interpretation of expression observed, including age, menopause status, route-of-elimination kinetics and metabolism of the tumor marker, coexisting disease, hormonal imbalances, life-style influences (smoking, alcoholism, obesity), among others, are mandatory to enable the selection of good protein tumor marker candidates for extensive validation.

Clinical management of regional odontodysplasia.

Regional odontodysplasia (ROD) is a rare, localized developmental anomaly of the dental tissues with distinctive clinical, radiographic, and histologic findings. The purpose of this study was to describe the characteristics and clinical management of 2 patients diagnosed with ROD at the Pediatric Dentistry Service at the Hospital Sant Joan de Déu, Barcelona, Spain. In both cases, temporary and permanent dentition were involved. It was concluded that therapeutic decisions during childhood must be based on the degree of involvement and each case's functional and aesthetic needs. Autotransplantation may be a good partial treatment option during the period of mixed dentition in some cases. Definitive treatment will include prosthetic rehabilitation with implants once the patient reaches adulthood.

Oral manifestations in Ellis-van Creveld syndrome: report of five cases.

Ellis-van Creveld syndrome, or chondroectodermal dysplasia, is an autosomal recessive disorder with characteristic clinical manifestations. Its incidence in the general population is low. The oral manifestations of Ellis-van Creveld are found in soft tissues and teeth, but the dental literature on the subject is scarce. In the last 20 years, 5 cases of Ellis-van Creveld syndrome have been followed at the Pediatric Dentistry Service of the Hospital Sant Joan de Déu, Barcelona. The present study describes the constant and variable oral findings in these patients, which play an important role in the diagnosis criteria for the syndrome. The presence of a great variety of oral manifestations such as fusion of the upper lip to the gingival margin, presence of multiple frenula, abnormally shaped and microdontic teeth, and congenitally missing teeth requires multidisciplinary dental treatment, with consideration for the high incidence of cardiac defects in these patients.

Failure of eruption of first and second permanent molars.

Failure of eruption of permanent molars is an uncommon condition with a range of possible causative factors. This retrospective study of 35 pediatric subjects assesses the influence of these factors in the prognosis. The study aims to broaden our understanding of an abnormality, which has a considerable clinical impact, and proposes a treatment protocol for the management of these patients.

The secretome analysis by high-throughput proteomics and multiple reaction monitoring (MRM).

The secretome is a sub-proteome of great interest in several fields of biomedical sciences, especially as a source of diagnostics and therapeutic targets. Proteomics has been contributing significantly to elucidate the secretome of a great diversity of cells, tissues, and organisms, turning profiles of thousands of proteins a usual practice. After elucidation of long protein lists, targeted proteomics also plays important roles in accurate quantification and validation of such secreted proteins. Here we present detailed protocols to explore and quantify the secretome of cancer cells, even though this protocol can be employed to any kind of biological material.

Reflexiones sobre la caries de la infancia temprana severa / Reflections on early childhood caries

Introducción: el incremento de las visitas de infantes en nuestras respectivas consultas (menores de tres años) con caries de la infancia temprana severa (CIT-S) en estos últimos años es el origen del presente artíuculo de análisis. Objetivo: describir las características de la (CIT-S) plantear hipótesis sobre su presentación clínica; así como agrupar y resumir los factores de riesgo de este particular grupo etéreo. Conclusiones: mientras mejor comprendamos todos los factores de riesgo que participan en esta enfermedad tan multifactorial y prevalente en la infancia, mejores pautas podremos ofrecer a los padres de nuestros pacientes, basadas en el riesgo individual del infante

Introduction: increased visits in our private practice of infants (under 3 years) with severe early childhood caries (CIT-S) in the recent years is the source of this analysis article. Aim: describe the characteristics of the early childhood caries, hypothesize about its clinical presentation; as well as group and summarize the risk factors of this particular age group. Conclusions: the better we understand all the risk factors involved in this disease as multifactorial and prevalent in childhood, best guidelines we offer parents of our patients, based on the individual risk of the infant.

Hipomineralización incisivo-molar: de la teoría a la práctica / Hypomineralization incisor-molar: from theory to practice

La hipomineralización incisivo-molar (HIM) es una alteración cualitativa del esmalte de origen sistémico y con etiología aún desconocida. Se trata de un síndrome con repercusiones a nivel funcional, estético y terapéutico que varían de acuerdo a la severidad del defecto. El objetivo de este trabajo es describir la etiología, epidemiología, características clínicas, consideraciones especiales y tratamiento de esta alteración que parece ir en aumento alrededor del mundo. La HIM preocupa especialmente a los odontopediatras debido a la dificultad de tratamiento de los casos más severos, representado un reto tanto por el manejo de conducta de estos pacientes como por la dificultad para mantener un buen pronóstico de los molares afectados a largo plazo.

Molar Incisor Hypomineralization (MIH) is an enamel qualitative defect of systemic origin and unknown aethiology. It is a syndromic disturbance with funtional, aesthetic and therapeutic implications varying on the severity of the condition. The aim of this paper is to describe the aethiology, epidemiology, clinical features and special considerations of MIH syndrome which is increasing considerably worldwide. MIH particularly concerns pediatric dentists due to the challenging behaviour management of these patients as well as the difficulty of mantaining a good prognosis of the affected molars in the long term.

Dentinogénesis imperfecta: a propósito de un caso / Dentinogenesis imperfecta: report of a case

La dentinogénesis imperfecta (DI) es una anomalía hereditaria que afecta la dentina de una o ambas denticiones. Como la DI tipo I se relaciona con osteogénesis imperfecta, ante un niño con DI, el odontopediatra siempre debe estar alerta y descartar esta posibilidad. Las características orales en niños con DI incluyen fracturas del esmalte, atrición dental severa, sensibilidad, molares con coronas bulbosas que dificultan las restauraciones tradicionales y en algunos casos exposiciones pulpares e infecciones periapicales. El manejo terapéutico incluye la instauración de medidas preventivas precoces y un tratamiento restaurador para evitar las atriciones y la pérdida de dimensión vertical. Asimismo, las implicaciones estéticas pueden tener una importante repercusión en el desarrollo psicosocial de los niños con DI. El objetivo de este artículo es hacer una revisión bibliográfica actualizada sobre la DI y presentar un caso clínico en un paciente de 5½ años.

Dentinogenesis imperfecta (DI) is a hereditary disorder characterized by abnormal dentine structure affecting either the primary or both the primary and secondary dentitions. Dentinogenesis imperfecta type I is inherited with osteogenesis imperfecta (OI), for this reason pediatric dentistry must always be alert and to discard this possibility in a child with DI. The oral characteristics in children with DI include breaks of the enamel due to the underlying dentinal defect of mineralization, severe dental attrition, sensibility, molars with bulbous crowns with marked cervical constriction that make the traditional restorations difficult and in some cases pulp exposures and periapical infections. The therapeutic treatment includes the establishment of early preventive measures and a treatment to avoid the attritions and the loss of vertical dimension. Also, the aesthetic implications can have an important effect in the psychosocial development of the children with DI. The aim of this article is to do a bibliographical updated review on DI and to present a clinical case in a patient of 5½ years old.

Pautas para la salud bucal en los primeros años de vida / Guidelines for oral health during early childhood

La caries es una enfermedad infecciosa crónica de marcada prevalencia en niños de diferentes países del mundo. Sin embargo, es una enfermedad potencialmente prevenible si se controlan los factores de riesgo que la ocasionan. Estos factores etiológicos pueden ser influenciados por los padres y los profesionales que asisten alniño y su entorno, siempre y cuando se tengan los conocimientos adecuados sobre las pautas de salud bucal. Por ello creemos que es indispensable la elaboración de una guía integral para uniformar los criterios y orientaciones enlo que se refiere a la salud bucal en la primera infancia, con el fin de proveer una información única a los padres de nuestros pacientes y no generar conflictos de información. Objetivo: Esta guía de salud bucal para los primeros años de vida es una propuesta para esclarecer y definir algunos puntos en común desde el punto de vista de la salud bucal. De esta forma, los padres tendrán más seguridad sobre el cuidado bucodental de sus hijos si poseen la misma información de todos los profesionales. Se plantean temas como la lactancia materna, el uso del biberón y del chupón, la transmisión bacteriana precoz, los alimentos con potencial cariogénico, la higiene bucal, el uso de flúor y la primera visita al odontopediatra. Conclusión: Como odontopediatras, sabemos que la instauración de una educación precozes una estrategia clave para evitar una necesidad futura y que toda la información de salud oral debe ser uniforme y estar consensuada por los diferentes profesionales que trabajan con el niño. Estas pautas de salud oral, basadas en la evidencia actual, son una propuesta para estandarizar criterios, los cuales se basan en la salud y no en la enfermedad.

Dental caries is a prevalent and chronic infectious disease in children across the world. However, it can be potentially prevented if the risk factors are controlled. Parents and health care professionals that assist the child can influence the different etiological factors implied in the caries process, provided that correct knowledge about oral health is available. Therefore, it seems imperative to elaborate a healthcare guide to standardize recommendations and guidance concerning oral health in early childhood,so that parents receive standardized information concerning their childrenÆs oral health. Objective: This oral health guideline for the first years of life aims to clarify and define some commonissues concerning oral health. In this way, parents will feel more secure if they hear the same information from all health care professionals. Issues such as breastfeeding, bacterial transmission, use of pacifiers and baby bottles, diet, oral hygiene, use of fluoride and the firstdental visit are discussed. Conclusion: As pediatric dentists, we know that the establishment of an early education isa key strategy to avoid a future need. All oral health education should be standardized and agreed upon by all professionals working with children. This oral health guideline, based oncurrent evidence, is a proposal to standardize criteria, which is based on health rather than disease.