ABSTRACT
Background: Oral cancer is the 15th most common cause of cancer death in the world. In Chile, 1% of all cancer deaths are related to oral and pharyngeal cancer. Aim: To determine mortality rates for oral cancer in Chile and its regions between 2002-2012. Material and Methods: Deaths and their causes between the years 2002-2012 were obtained from the Chilean National Statistics Institute. Crude and adjusted rates by age and sex were calculated for the country and its regions. The denominator was Chilean population on June 30, 2012 and the WHO standard population. Results: In the period studied, 1,611 individuals with a mean age of 67.6 years (63% men) died because of oral cancer. The most common location of the tumor was the tongue in 27% of cases and the parotid gland in 16%. The adjusted mortality rate in Chile was 0.85 / 100,000 inhabitants (1.13 and 0.58 in men and women, respectively). The regions with the highest rates were Antofagasta (1.51), Aysén (1.22) and Magallanes (1.17). Deaths among men occurred at younger ages than women. Conclusions: Mortality rates due to oral cancer in Chile are lower than abroad. The highest rates observed in some regions may be influenced by environmental factors such as arsenic contamination in Antofagasta and the lack of specialists and specialized care centers in Aysén and Magallanes.
Subject(s)
Humans , Infant, Newborn , Infant , Child, Preschool , Child , Adolescent , Adult , Middle Aged , Aged , Young Adult , Mouth Neoplasms/mortality , Chile/epidemiology , Sex Distribution , Age Distribution , Geographic MappingABSTRACT
Objective: to evaluate the extent of interstitial fibrosis in samples of normal oral mucosa (NOM), oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC). Materials and method: descriptive study. eighteen samples of NOM, 15 samples of OED, and 13 samples of OSCC were analyzed; all stained with Masson's trichrome stain. the areas of greatest fibrosis underlying the normal, dysplastic, and malignant neoplastic oral epithelium were identified in order to determine the extent of interstitial fibrosis. interstitial fibrosis was classified according to its proportion in the total image, being 0 (without fibrosis), +1 (1-25 percent), 2+ (26-50 percent), 3+ (51-75 percent) and +4 (76-100 percent). variables were analyzed using the Kruskal-Wallis test and Dunn's Pairwise post-hoc test. Results: the samples of NOM and OED did not present interstitial fibrosis (type 0) in the majority of the cases respectively. OSCC samples were characterized by an extension of type 2+ interstitial fibrosis in 45 percent of all cases of OSCC. the extent of interstitial fibrosis was different between NOM and OSCC (p<0.001), and between OED and OSCC (p<0.001). Conclusion: the extent of interstitial fibrosis is directly proportional to the malignization of the analyzed samples, being an adequate marker for OSCC.
Subject(s)
Humans , Child , Adolescent , Adult , Middle Aged , Aged , Aged, 80 and over , Oral Submucous Fibrosis/diagnosis , Carcinoma, Squamous Cell/diagnosis , Carcinoma, Squamous Cell/pathology , Mouth Mucosa/pathology , Mouth Mucosa/diagnostic imaging , Fibrosis , Epidemiology, Descriptive , Age and Sex DistributionABSTRACT
RESUMEN: El grupo de neoplasias malignas de tejido blando de la región de cabeza y cuello en pacientes pediátricos está representado por carcinomas, sarcomas, melanomas y tumores de diferenciación incierta. La neoplasia más prevalente en la población pediátrica es el Rabdomiosarcoma, seguido por el carcinoma de células escamosas. Los rangos de presentación son muy amplios, siendo los grupos entre 2-6 años y 15-19 años los que presentan mayor incidencia. Se ha planteado que la etiología de estas neoplasias es incierta. El tratamiento de estas neoplasias es comúnmente de enfoque multimodal, combinando un procedimiento quirúrgico con quimioterapia y radioterapia. El pronóstico y sobrevida del paciente dependerán principalmente del momento en que se realice el diagnóstico de la lesión. Un diagnóstico y tratamiento temprano favorecen las posibilidades de sobrevida y el pronóstico del paciente. Este estudio corresponde a la 3ra parte de "Cáncer bucomaxilofacial en niños". Se hará referencia a los distintos tumores malignos del tejido blando en la población pediátrica en el territorio de cabeza y cuello, abarcando sus generalidades, etiología, epidemiología, tratamiento y pronóstico.
ABSTRACT: Head and neck malignant tumors in pediatric patients comprise carcinoma, sarcoma, melanoma and tumours of uncertain differentiation. Within the pediatric population, the most prevalent neoplasm is rhabdomyosarcoma, followed by squamous cell carcinoma. There is a wide range in the presentation, and it varies significantly with age groups of 2-6 and 15-19 year-olds who present the higher incidence rates. For this reason, it has been suggested that the etiology of head and neck neoplasms remains unclear. Treating these pathologies usually involves a multimodal approach that combines surgery, radiation and chemotherapy. Prognosis and survival rates depend mainly of the stage at the time of diagnosis. Early diagnosis and treatment can improve prognosis and survival rates. In this 3rd part of "Maxillofacial Cancer in Pediatric Patients", we studied a variety of malignant tumors in head and neck soft tissue from a paediatric sample. Specifically, we aim to analyze their etiology, epidemiology, treatment and prognosis.
Subject(s)
Humans , Child , Adolescent , Facial Neoplasms/epidemiology , Mouth Neoplasms/etiology , Mouth Neoplasms/epidemiology , Carcinoma/epidemiology , Maxillary Neoplasms/epidemiology , Prognosis , Sarcoma/epidemiology , Maxillary Neoplasms/etiology , Incidence , Lymphoma/epidemiology , Mouth Mucosa/pathology , Neoplasms/classificationABSTRACT
El Fibroma Odontogénico Periférico fue definido por la OMS en el año 2005 como una neoplasia benigna rara constituida por tejido fibroso maduro y una cantidad variable de epitelio odontogénico inactivo. Dada su presentación clínica, localización y baja prevalencia suele ser mal diagnosticado como una lesión reaccional. Se presenta un caso clínico de fibroma odontogénico periférico tratado mediante remoción quirúrgica y se realiza una revisión de la bibliografía respecto a la patología con el propósito de esclarecer algunos aspectos de esta lesión, además de incluirla dentro de los posibles diagnósticos diferenciales de lesiones reaccionales gingivales. El objetivo del siguiente artículo es presentar un caso clínico de FOP tratado mediante remoción quirúrgica y aportar en el diagnóstico diferencial de las lesiones reaccionales gingivales.
Peripheral odontogenic fibroma was described by the World Health Organization (WHO) in 2005, as a rare benign tumor containing mature fibrous connective tissue with a varying amount of inactive odontogenic epithelium. Though its clinical presentation, localization and low prevalence, it tends to be misdiagnosed as a reactive lesion. We present a case report of a Peripheral Odontogenic Fibroma treated by surgical resection and a narrative review of the literature with the purpose of clarifying different aspects of this lesion besides considering it as a possible differential diagnosis of reactive gingival lesions. The purpose of this article is to present a case report of peripheral odontogenic fibroma treated by surgical resection. Also to contribute to the differential diagnosis of gingival reactive lesions.
Subject(s)
Humans , Female , Middle Aged , Gingival Neoplasms/surgery , Gingival Neoplasms/diagnosis , Odontogenic Tumors/surgery , Odontogenic Tumors/diagnosis , Tooth Resorption/etiology , Gingival Neoplasms/pathology , Odontogenic Tumors/pathology , Diagnosis, Differential , FibromaABSTRACT
Abstract: epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein, with an intracellular domain and tyrosine kinase function (TK) involved in cell proliferation. Dysfunctions in EGFR signaling pathways have been associated with oral malignant tumors such as oral squamous cell carcinoma (OSCC). Dysfunctions of EGFR may result from: increased EGF ligand; EGFR overexpression and copy number gain of the EGFR gene (EGFR CNG); EGFR mutations; failure in the downregulation of EGFR; and EGFR crosstalk. Of these alterations, overexpression of EGFR is by far the most studied dysfunction in OSCC. Clinicians should identify possible alterations of EGFR in the oral mucosa of patients, as EGFR can act as a biomarker for the diagnosis and prognosis of OSCC. Currently, there are several methods and techniques for detecting EGFR. Immunohistochemistry (IHC), fluorescence in situ hybridization (FISH) and polymerase chain reaction (PCR), are used to identify overexpression of EGFR, EGFR CNG and EGFR mutations, respectively. Detection of EGFR as a biomarker is key to identify any oral malignant transformation. Consequently, it becomes imperative to implement a non-invasive and inexpensive method of early diagnosis for OSCC in clinical practice.
Resumen: el receptor del factor de crecimiento epidérmico (EGFR) es una glicoproteína transmembrana, con un dominio intracelular y función tirosina quinasa (TK) que participa en la proliferación celular. Las fallas en las vías de señalización del EGFR se han asociado con la formación de tumores malignos orales como el carcinoma oral de células escamosas (COCE). El incorrecto funcionamiento del EGFR puede producirse por: aumento del ligando EGF; sobreexpresion del EGFR y ganancia en el número de copias del gen EGFR (GNC EGFR); mutaciones del EGFR; falla en la regulación negativa del EGFR; y diafonía del EGFR. De las alteraciones mencionadas, la sobreexpresion de EGFR es por lejos la disfunción más estudiada en COCE. Para el clínico es importante poder identificar las posibles alteraciones del EGFR en la mucosa oral del paciente, esto debido a que el EGFR puede actuar como un biomarcador de diagnóstico y pronóstico para COCE. En la actualidad existen diversos métodos para detectar el EGFR. La inmunohistoquímica (IHC), la hibridación fluorescente in situ (FISH) y la reacción en cadena de la polimerasa (PCR), son técnicas utilizadas para identificar la sobreexpresion del EGFR, GNC EGFR y mutaciones del EGFR, respectivamente. La necesidad de detección de estas alteraciones se debe a la transcendencia del EGFR como biomarcador de transformación maligna. Lo anterior, hace necesario implementar un método de diagnóstico precoz para COCE que sea no invasivo y de bajo costo para la práctica clínica.
Subject(s)
Humans , Mouth Neoplasms/diagnosis , Mouth Neoplasms/metabolism , ErbB Receptors , BiomarkersABSTRACT
The transforming growth factor beta (TGF-beta) is a cytokine that plays crucial roles in the regulation of angiogenesis, immune response, proliferation, migration and apoptosis of cells. In addition, it can inhibit cell progression and stimulate apoptosis in early stages of cancer. TGF-beta is a multifunctional homodimeric protein secreted by various cell lines, which have three different isoforms: TGF-beta1, TGF-beta2 and TGF-beta3. In normal conditions, TGF-beta1 activates some tumor suppressor cell signaling pathways that inhibit proliferation and are involved in cell migration, differentiation and apoptosis. However, in more advanced stages of cancer, when TGF-beta1 is altered, it acts as a promoter of tumorigenesis and may cause: 1) increased TGF-beta1, 2) overexpression of TGF-beta1 receptors (TbetaR), 3) TbetaR mutations, and 4) downregulation of TGF-beta receptor. In oral squamous cell carcinoma, the path is altered especially at the level of transmembrane receptors, with the TbetaR-II and TbetaR-III subtypes being the most affected. However, there is little information on the prognostic role it plays in the various types of cancers. It is important to study the signaling pathways of TGF-beta in order to develop techniques that may help detect their alterations and restore their normal operation. The objective of this review is to describe the alterations of TGF-beta in oral squamous cell carcinoma.
El factor de crecimiento transformante beta (TGF-beta) es una citocina que cumple funciones fundamentales en la regulación de la angiogénesis, respuesta inmune, proliferación, migración y apoptosis celular. Además, puede inhibir la progresión celular y estimular la apoptosis en etapas tempranas del cáncer. El TGF-beta es una proteína homodimérica multifuncional secretada por diversas líneas celulares, que presentan 3 isoformas: TGF-beta1, TGF-beta2 y TGF-beta3. En condiciones normales TGF-beta1 activa a algunas vías de señalización celular supresoras de tumores que inhiben la proliferación, y participan en la migración, diferenciación y apoptosis. Sin embargo, cuando esta se ve alterada, en etapas más avanzadas del cáncer actúa como promotor de la tumorogénesis, pudiendo producir: 1) aumento del TGF-beta1, 2) sobre expresión de los receptores del TGF-beta1 (TbetaR), 3) mutaciones de TbetaR, y 4) falla en la regulación negativa de TbetaR. En el carcinoma oral de células escamosas, la vía se ve alterada especialmente a nivel de sus receptores transmembranales, siendo los subtipos TbetaR-II y TbetaR-III los más afectados. Sin embargo, es escasa la información sobre el rol pronóstico que juega en los diversos tipos de cánceres. Es importante estudiar las vías de señalización de TGF-beta para desarrollar técnicas que detecten sus alteraciones y restauren el funcionamiento del sistema. El objetivo de esta revisión es describir las alteraciones de TGF-beta en carcinoma oral de células escamosas.
Subject(s)
Humans , Carcinoma, Squamous Cell/metabolism , Mouth Neoplasms/metabolism , Transforming Growth Factor beta1/metabolism , /metabolismABSTRACT
El carcinoma oral de células escamosas (COCE) es el tipo de cáncer más frecuente en la cavidad oral, y constituye el 95% de la totalidad de neoplasias malignas a escala bucal. La etiología de COCE es multifactorial y su patogenia se ha asociado, entre otros, a los cambios que acontecen en su microambiente. La inflamación que invade el microambiente de COCE se ha relacionado con la invasión, progresión, carácter fuerte y pronóstico de COCE. Es por tal motivo, que la periodontitis, inflamación del tejido periodontal, de alta prevalencia en la población adulta, se ha relacionado con COCE. Al respecto, estudios clínicos advirtieron que la periodontitis representa un riesgo para desarrollar COCE y estudios in vitro, puntualizaron que la periodontitis favorece la tumorogenicidad y lo combativo de COCE. El objetivo de la siguiente revisión narrativa es describir los efectos de la periodontitis en el comportamiento del carcinoma oral de células escamosas.
Oral squamous cell carcinoma (OSCC) is the most common type of cancer in the mouth, accounting for 95% of all malignancies in the oral cavity. The etiology of OSCC is multifactorial and its pathogenesis has been associated, among others, with the changes that occur in its microenvironment. The inflammation that invades the OSCC microenvironment has been related to the invasion, progression, aggressiveness and prognosis of OSCC. It is for this reason that periodontitis, inflammation of the periodontal tissue, of high prevalence in the adult population, has been related to OSCC. In this regard, clinical studies reported that periodontitis presents a risk for developing OSCC and in vitro studies, reported that periodontitis favors the tumorogenicity and aggressiveness of OSCC. The aim of this review is to describe the effects of periodontitis on oral squamous cell carcinoma.