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      Etiología del colesteatoma ótico Translated title: Etiology of otic cholesteatoma

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          Abstract

          El colesteatoma es una estructura quística caracterizada por la presencia de epitelio escamoso productor de queratina, que sustituye o recubre la mucosa normal en la hendidura del oído medio y ápex petroso, y puede ser causa de hipoacusia irreversible, destrucción ósea y graves complicaciones por su crecimiento expansivo. Clásicamente se describen los colesteatomas en congénitos y adquiridos. La etiología de su formación es multifactorial y continúa siendo poco claro y controversial. Se reportan diferentes teorías que han tratado de explicar el colesteatoma congénito, la transición de un bolsillo de retracción hasta la aparición del colesteatoma adquirido primario, y otras en la génesis del colesteatoma adquirido secundario. Se describe la presencia de algunas citoquinas dentro del colesteatoma que inducen la hiperproliferación e invasión incoordinada de los queratinocitos de la piel del conducto auditivo externo y la pars fláccida, más agresiva en el colesteatoma adquirido pediátrico, y que desempeñan un papel fundamental en la proliferación y en la apoptosis del queratinocito. En cultivo in vitro de una muestra de tejido colesteatomatoso, se ha identificado recientemente que el TNF-a estimula la producción de la IL-8. Se considera de interés ofrecer esta revisión sobre la etiología del colesteatoma, que aún se mantiene en el campo de la investigación y continúa siendo un reto para los otocirujanos por su alta incidencia de recidivas y posibles complicaciones.

          Translated abstract

          Cholesteatoma is a cystic structure characterized by presence of squamous epithelium producing keratin substituting or recovering the normal mucosa in the groove of middle ear and petrous apex and may to be caused by irreversible hypoacusia, bone destruction and severe complications due to its expansive growth. Typically the cholesteatomas are described as congenital and acquired. The etiology of its formation is multifactor and still remains a subject not very clear and controversial. Different theories are reported to explain the congenital cholesteatoma, the transition of a retraction pocket until the appearance of primary acquired cholesteatoma and other on the genesis of the secondary acquired cholesteatoma. Presence of some cytokines in cholesteatoma is described inducing to hyperproliferation and not coordinated of keratinocytes of the external auditory meatus and the pars flaccida more aggressive in the pediatric acquired cholesteatoma playing a fundamental role in the proliferation and in apoptosis of keratinocyte. In a sample of choleastomatous tissue in vitro culture has been recently identified that the a-TNF stimulates the production of IL-8. It is interesting to offer present review on the etiology of cholesteatoma that still is under research and a challenge for otologists due to its high relapses incidence and potential complications.

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          Most cited references59

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          Monoclonal antibodies against recombinant parts of the Ki-67 antigen (MIB 1 and MIB 3) detect proliferating cells in microwave-processed formalin-fixed paraffin sections.

          The monoclonal antibody Ki-67 reacts with a human nuclear cell proliferation-associated antigen that is expressed in all active parts of the cell cycle. Recently we have raised monoclonal antibodies, MIB 1-3, against recombinant parts of the Ki-67 antigen. These antibodies are true Ki-67 equivalents, as demonstrated by immunostaining of fresh specimens, biochemistry, and molecular biological techniques. Formalin-fixed, paraffin-embedded sections routinely processed for immunohistochemistry failed to stain for Ki-67 and MIB 2. Antibodies MIB 1 and MIB 3 labelled mitotic figures, while non-mitotic proliferating cells were negative under these conditions. However, when dewaxed microwave oven-processed paraffin sections of formalin-fixed tissues were used, MIB 1 and MIB 3 gave strong nuclear staining of those cells presumed to proliferate under a variety of normal and neoplastic conditions. Moreover, routine decalcification or depigmentation techniques did not alter the immunoreactivity of MIB 1 and MIB 3 with microwave-processed paraffin sections. This method is highly reproducible, easy to perform at low cost, and no additional technical skill is needed because after microwave treatment just routine immunohistochemical methods are used. Since we have successfully applied this new method to sections obtained from paraffin blocks stored for a long time (in one case more than 60 years), the assessment of cell kinetics through the detection of Ki-67 antigen is now possible on archival material collected in histopathology departments all over the world.
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            Eya4-deficient mice are a model for heritable otitis media.

            Otitis media is an extremely common pediatric inflammation of the middle ear that often causes pain and diminishes hearing. Vulnerability to otitis media is due to eustachian tube dysfunction as well as other poorly understood factors, including genetic susceptibility. As EYA4 mutations cause sensorineural hearing loss in humans, we produced and characterized Eya4-deficient (Eya4(-/-)) mice, which had severe hearing deficits. In addition, all Eya4(-/-) mice developed otitis media with effusion. Anatomic studies revealed abnormal middle ear cavity and eustachian tube dysmorphology; thus, Eya4 regulation is critical for the development and function of these structures. We suggest that some human otitis media susceptibility reflects underlying genetic predisposition in genes like EYA4 that regulate middle ear and eustachian tube anatomy.
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              Incidence, etiology and pathogenesis of cholesteatoma in children.

              M Tos (1988)
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                ped
                Revista Cubana de Pediatría
                Rev Cubana Pediatr
                Editorial Ciencias Médicas (Ciudad de la Habana )
                1561-3119
                December 2011
                : 83
                : 4
                : 393-404
                Affiliations
                [1 ] Hospital Pediátrico Docente Universitario William Soler Cuba
                [2 ] Instituto de Hematología e Inmunología Cuba
                [3 ] Centro de Neurociencias de Cuba Cuba
                [4 ] Facultad de Ciencias Médicas Enrique Cabrera Cuba
                Article
                S0034-75312011000400007
                a0504a4f-a41b-4256-be69-675eb91c172f

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Cuba

                Self URI (journal page): http://scielo.sld.cu/scielo.php?script=sci_serial&pid=0034-7531&lng=en
                Categories
                PEDIATRICS

                Pediatrics
                congenital otic cholesteatoma,acquired cholesteatoma,pathogenesis,cytokines,colesteatoma ótico congénito,colesteatoma adquirido,etiopatogenia,citoquinas

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