RESUMEN
Ectopic teeth are rarely found in the maxillary sinus. When they are, they represent an anomaly of odontogenic development that is generally associated with odontogenic cysts, trauma, or idiopathic etiology. Although affected patients are often asymptomatic, documented morbidities include sinus disease that is often refractory to treatment. The diagnosis is usually made by plain-film radiography. Computed tomography is indicated when an ectopic tooth is associated with an antral mass and prior to surgery. Treatment of symptomatic patients and those with an antral mass is surgical, with either a Caldwell-Luc operation or an endoscopic procedure. We describe what we believe is the first reported case of a third molar in the roof of the maxillary sinus associated with a mucocele, and we review the literature.
Asunto(s)
Coristoma/complicaciones , Seno Maxilar , Tercer Molar , Mucocele/etiología , Enfermedades de los Senos Paranasales/complicaciones , Adulto , Coristoma/diagnóstico por imagen , Coristoma/cirugía , Humanos , Masculino , Tercer Molar/diagnóstico por imagen , Tercer Molar/cirugía , Mucocele/diagnóstico por imagen , Mucocele/patología , Enfermedades de los Senos Paranasales/diagnóstico por imagen , Enfermedades de los Senos Paranasales/cirugía , Tomografía Computarizada por Rayos XRESUMEN
HYPOTHESIS: Mitomycin C is ototoxic when applied topically to the structures of the middle ear. BACKGROUND: Mitomycin C is a topically applied medication widely used in a variety of surgical procedures to prevent excessive scar tissue formation. Its safety for use during otologic procedures has not been fully evaluated. METHODS: A laboratory study was undertaken using the Mongolian gerbil as an animal model. Both acute and chronic effects on cochlear function of mitomycin C were assessed with measurements of compound action potential (CAP) thresholds of the auditory nerve, CAP input/output functions, distortion product otoacoustic emissions, and endocochlear potentials. Morphologic changes were assessed with light microscopy using hematoxylin-eosin staining as well as transmission electron microscopy. RESULTS: Five-minute applications of mitomycin C (0.5 mg/ml) to the entire surface of the middle ear adversely affected CAP thresholds, input/output functions, distortion product otoacoustic emissions, and the endocochlear potential. Ninety-minute exposures of mitomycin C solely to the round window produced similar changes. Histologic evaluation of animals 1 week after treatment showed damage to cochlear hair cells, the stria vascularis, and spiral ganglion neurons when compared with controls. CONCLUSION: Mitomycin C can produce substantial sensorineural hearing loss when applied topically to the gerbil middle ear for even brief periods. Consequently, its safety for topical use in the human middle ear is highly questionable.
Asunto(s)
Antibióticos Antineoplásicos/toxicidad , Cóclea/efectos de los fármacos , Oído Medio/efectos de los fármacos , Mitomicina/toxicidad , Potenciales de Acción/efectos de los fármacos , Administración Tópica , Animales , Audiometría de Respuesta Evocada , Umbral Auditivo/efectos de los fármacos , Cóclea/fisiología , Cóclea/ultraestructura , Femenino , Gerbillinae , Masculino , Microscopía Electrónica de Transmisión , Factores de TiempoRESUMEN
OBJECTIVE: To gain insight into molecular and cellular mechanisms regulating cochlear potassium (K+) recycling, including the possible effects of mutations in the gene, which encodes the gap junction protein connexin 26. Intercellular K+ flux was manipulated in vivo by infusion of the gap junction uncoupler proadifen (SKF-525A) into perilymph. Functional and structural alterations induced by gap junction blockade were assessed by electrophysiological and morphologic analysis. STUDY DESIGN: Laboratory study using an animal model. METHODS: Physiological effects of acute and chronic uncoupling of gap junctions in the Mongolian gerbil inner ear were evaluated by measurement of compound action potential (CAP) thresholds and input-output (I/O) functions, distortion product otoacoustic emissions (DPOAE), and the endocochlear potential (EP). Morphologic changes were assessed by electron microscopy. RESULTS: Acute exposures to proadifen resulted in large decreases in EP values, DPOAE magnitudes, and CAP I/O maximum amplitudes and an increase in high-frequency CAP thresholds. These physiological changes were accompanied by vacuolization of type II and type V fibrocytes in the lateral wall of the cochlea. Chronic treatments revealed some recovery in EP values and CAP thresholds, which showed a relatively flat 15- to 20-dB elevation across frequencies. CONCLUSIONS: Gap junctions play a significant role in normal cochlear function. In particular they appear to be essential for maintaining the EP, an activity that could be related to their participation in K+ recycling. Thus, hearing losses associated with mutations in the gene that alter the expression or function of connexin 26 may result from a diminished capacity to recycle K+ from perilymph back to the stria vascularis and a consequent decline in the EP.