Chronic Middle Ear Inflammation Research Articles

Hearing Impairment in Cases of Chronic Middle Ear Inflammation with Cholesterin Granuloma

Hearing Impairment in Cases of Chronic Middle Ear Inflammation with Cholesterin Granuloma

Toll-Like Receptor 2-Dependent NF-κB Activation Is Involved in Nontypeable Haemophilus influenzae -Induced Monocyte Chemotactic Protein 1 Up-Regulation in the Spiral Ligament Fibrocytes of the Inner Ear

Inner ear dysfunction secondary to chronic otitis media (OM), including high-frequency sensorineural hearing loss or vertigo, is not uncommon. Although chronic middle ear inflammation is believed to cause inner ear dysfunction by entry of OM pathogen components or cytokines from the middle ear into the inner ear, the underlying mechanisms are not well understood. Previously, we demonstrated that the spiral ligament fibrocyte (SLF) cell line up-regulates monocyte chemotactic protein 1 (MCP-1) expression after treatment with nontypeable Haemophilus influenzae (NTHI), one of the most common OM pathogens. We hypothesized that the SLF-derived MCP-1 plays a role in inner ear inflammation secondary to OM that is responsible for hearing loss and dizziness. The purpose of this study was to investigate the signaling pathway involved in NTHI-induced MCP-1 up-regulation in SLFs. Here we show for the first time that NTHI induces MCP-1 up-regulation in the SLFs via Toll-like receptor 2 (TLR2)-dependent activation of NF-kappaB. TLR2(-/-)- and MyD88(-/-)-derived SLFs revealed involvement of TLR2 and MyD88 in NTHI-induced MCP-1 up-regulation. Studies using chemical inhibitors and dominant-negative constructs demonstrated that it is mediated by the IkappaKbeta-dependent IkappaBalpha phosphorylation and NTHI-induced NF-kappaB nuclear translocation. Furthermore, we demonstrated that the binding of NF-kappaB to the enhancer region of MCP-1 is involved in this up-regulation. In addition, we have identified a potential NF-kappaB motif that is responsive and specific to certain NTHI molecules or ligands. Further studies are necessary to reveal specific ligands of NTHI that activate host receptors. These results may provide us with new therapeutic strategies for prevention of inner ear dysfunction secondary to chronic middle ear inflammation.

Influence of Chronic Middle Ear Diseases on Gustatory Function

We aimed to quantitatively determine whether middle ear inflammation associated with unilateral chronic otitis media (COM), cholesteatoma, or otosclerosis affects gustatory function. Prospective study. University Hospital, Department of Otolaryngology. Forty-two patients had unilateral COM (22 men, 20 women; mean age, 54.2 yr), 57 had unilateral cholesteatoma (35 men, 22 women; mean age, 42.1 yr), and 19 had unilateral otosclerosis (10 men, 9 women; mean age, 49.3 yr). Patients underwent taste testing using electrogustometry (EGM) and sensation thresholds were compared in the affected and unaffected ears among groups and between affected and unaffected ears in each group. Patients with COM and cholesteatoma exhibited an increase in taste threshold in the affected ears compared to the unaffected ears (p < 0.05), whereas otosclerosis patients did not. The extent of the increase of the sensation thresholds in the affected ears was very similar between patients with COM and those with cholesteatoma (p = 0.548). Our EGM study showed that cholesteatoma and chronic middle ear inflammation affected gustatory function to a similar degree.

How to reliably evaluate middle ear diseases? Comparison of different methods of post-processing based on multislice computed tomography examination

Conclusions. Multislice computed tomography (MSCT) virtual endoscopy was useful in evaluating mainly post-traumatic and postoperative cases. In other pathological conditions axial images and MPR reformations were most useful. Objectives. Evaluation of cross-sectional images, multiplanar 2-D reformations, 3-D reconstructions and virtual endoscopy (VE) in assessment of the middle ear in inflammatory diseases, trauma, otosclerosis and tumours. Comparison of each method and correlation with surgical findings. Materials and methods. Investigations were carried out in 80 patients with middle ear pathology. In each case MSCT of the petrous bone was performed. In addition to cross-sectional native scans, frontal and sagittal images were achieved using MPR reconstructions. 3-D volume rendering (VR) and VE images were also generated. The value of native scans information, 2-D, 3-D reconstructions and VE of the tympanic cavity structures was assessed in comparison to intraoperative findings. Results. MPR reconstructions were most useful in the assessment of skull base trauma, skull base tumours and in cases of chronic middle ear inflammation. Highly vascularized tumours, disruption of ossicular chain and stapes prosthesis were best evaluated on 3-D reconstructions. Axial images proved to be the best for otosclerosis interpretation.

Photodynamic effect of argon and diode laser on cholesteatoma cell cultures after intravital staining with absorption enhancers

Chronic epitympanic otitis media, or chronic suppurative osteitis, is a destructive form of chronic middle-ear inflammation. The therapy of choice is complete surgical removal of the squamous epithelium from the middle ear. It is often impossible to inspect all areas of the middle ear with the posterior canal wall intact. Not all recesses can be reliably monitored with the microscope, particularly in the area of the antrum and hypotympanum. Residual squamous epithelium here causes frequent recurrences following cholesteatoma surgery. This study examines the effect of argon and diode lasers on cholesteatoma tissue. The aim is to develop a laser treatment selectively directed against cholesteatoma cells that can be performed after cholesteatoma surgery to eliminate any residual squamous epithelium. Intraoperatively harvested monolayer-cultured cholesteatoma cells stained in vivo with various absorption enhancers served as the in vitro examination model. Argon (499 nm) and diode lasers (810 nm) were applied since their irradiation has an appropriate tissue penetration depth and is absorbed by various chromophores such as neutral red (475-500 nm), fluorescein (488 nm), and indocyanine green (790-810). Intracellular staining of cultured cells increased the optical density at the wavelength corresponding to the dye. Neutral red damaged 50-60% of cultured cells merely by intracellular accumulation at high concentrations. An additive cell destruction of about 30% was achieved by also applying argon laser irradiation. Fluorescein diacetate caused no appreciable stain-induced damage to cultured cholesteatoma cells. Argon laser irradiation destroyed up to 60% of the cultures. Indocyanine green resulted in only minor damage to cultured cells. The diode laser destroyed up to 60% of the irradiated cells. Selective staining of cholesteatoma cells was not achieved with any of the dyes examined. Thus, other stained tissue could be damaged. Staining and subsequent laser irradiation destroys up to 60% of cultured cholesteatoma cells. Unstained irradiated cells are not affected. Indocyanine green and fluorescein are nontoxic and may thus be used as absorption enhancers. The diode and argon lasers appear to be basically suitable. Cell staining is not selective, i.e., other tissues would also be stained and damaged. To avoid such unwanted damage, it would be desirable to couple the chromophore to a specific antibody that binds only to cholesteatoma cells.

Investigations on the clinical significance of cochlear implantation in the modiolus

Problem: The purpose of this study was to disclose the possibilities for implantation of an electrode in the modiolus for stimulation of auditory nerve in cases of severe hearing loss. Methods: Our methods consisted of the dissection of human temporal bones, and histological investigation of modiolar structure before and after the insertion of an electrode. Results: Ten dissections of human temporal bones were carried out. A plastic copy of an electrode was implanted in the modiolus. Histological investigations were made in order to clarify the anatomic variations of modiolus and the eventual destructive changes that may occur during the implantation. Conclusion: It was found that the best surgical approach to the modiolus is through middle cranial fossa. The cupula of the cochlea is located medially and anteriorly to ganglion geniculi. The greater petrosal nerve serves as a landmark. The nerve is elevated, the bone is drilled from its sulcus to the cupula cochleae, which is found at about 2 mm depth. After entering the cupula, the top of the modiolus is visualized. A canal should be made by a special probe, which should be introduced without any pressure along canalis longitudinalis modioli, due to the very soft modiolar tissue. Invasion of the electrode into the first 2 mm of internal auditory canal does not harm the hearing nerve fibers, which are still not fused to form the auditory nerve. Histological studies did not show injury of modiolar structures. Significance: We believe that the implantation of an electrode in the modiolus could be an alternative to standard cochlear implantation and may even be preferable in cases with chronic middle ear inflammation and cochlear ossification. Support: None reported.

鼓膜チューブ留置後の乳突蜂巣発育

Although it is generally believed that the development of the mastoid pneumatization is suppressed by chronic middle ear inflammation, it is not yet known whether the suppressed mastoid air cells can develop again after the treatment of otitis media with effusion (OME) in children. In this study, of 20 children (31 ears) with OME who had had poor pneumatization, the extent of mastoid pneumatization was compared on X-ray images (Schuller's view) obtained between the period before, and 10 to 24 months after, ventilation tube insertion. In 19 of 27 ears, the size of the mastoid air cells had increased. In the ears of children under 6 years old, the degree of increase was significantly greater than in children over 7 of age. It is possible that mastoid pneumatization in children with OME can start developing again if their ventilation tube was inserted before 6 years of age.

Residual Mesenchyme in Temporal Bones of Children

The role of mesenchyme in the temporal bone is still poorly understood. A microscopic study of residual mesenchyme was undertaken in temporal bones of children from birth to 5 years of age. Residual mesenchyme was found to be located in the mastoid antrum and epitympanum more often than in the mesotympanum. The amount of mesenchymal tissue remaining in the temporal bones decreased with increasing age. Persistence of mesenchyme in the temporal bone was related to congenital morphologic ear anomalies and syndromes. There was also an association evident with pulmonary disease, but not with congenital heart defects. Persistent mesenchyme was also found to be significantly associated with chronic middle ear inflammation, and in cases of unilateral otitis media the ear with otitis media had more residual mesenchyme than the non-otitis media ear.

The relationship between the degree of chronic middle ear inflammation and tympanic bulla pneumatization in the pig as animal model.

The relationship between the degree of chronic middle ear inflammation and pneumatization was investigated in the pig as an animal model, since its tympanic bulla closely resembles the human mastoid air cell system. Ten piglets (sire: Landrace-Hampshire crossbreed; dam: Duroc) were used for this experiment. Four ears of two animals served as the normal control group and 16 ears of eight animals were the experimental group. In this latter group, otitis media was induced by injecting glycerin into the middle ear clefts 1 months after birth, and the degree of inflammation was varied by administering or withholding antibiotics (cefamandole and dibekacin) and adjusting the dosage regimen. The animals were sacrificed 6 months after birth and examined for the relationship between the degree of chronic middle ear inflammation present and tympanic bulla pneumatization. Various degrees of inflammation were successfully induced by injecting the antibiotics: the more severe the inflammation found, the greater was the inhibition of pneumatization. Findings demonstrated that the degree of inhibition of pneumatization produced was directly proportional to the severity of chronic middle ear inflammation.

COMPLICATIONS OF NITROUS OXIDE ANESTHESIA FOR EAR SURGERY

SUMMARY Middle ear pressure measured in surgical patients has been as high as 450 mm H2O after only 15 to 20 minutes of nitrous oxide inhalation. This increase in pressure bulges the eardrum outward and complicates otologic procedures such as replacement of the tympanic membrane or closing of a perforation. Increased middle ear pressure can also contribute to postoperative pain, delirium, nausea, and vomiting. Furthermore, discontinuation of nitrous oxide brings a decrease in middle ear pressure that can displace a tympanic graft. For all these reasons, many authors suggest avoiding nitrous oxide anesthesia for surgical procedures on the middle ear: tympanoplasty, stapedectomy, ossicular repositioning, and mastoidectomy. Finally, the possible lingering presence of nitrous oxide within the middle ear makes it wise to avoid nitrous oxide for all surgical patients who have middle ear disease and abnormalities of the eustachian tube. Because of the possibility of tympanic membrane rupture during or after nitrous oxide anesthesia, specific information concerning previous otologic surgery should be obtained prior to anesthesia. Patients especially vulnerable are those with acute or chronic middle ear infections or inflammation or scarring of the nasopharynx. Techniques that promote rapid recovery from anesthesia and the early return of pharyngeal reflexes facilitate venting of middle ear gas through the eustachian tube. The clinician can prevent the diffusion problem encountered with nitrous oxide by using a mixture of oxygen and air as the vaporizing vehicle for a more potent halogenated agent. If the anesthetist wants to use nitrous oxide, however, the lowest concentration feasible (50% or less) should be combined with a more potent agent for the shortest period possible and then discontinued as soon as the level of anesthesia is adequate.

Pathophysiology ofStreptococcus PneumoniaeOtitis Media: Kinetics of the Middle Ear Biochemical and Cytologic Host Responses

Streptococcus pneumoniae is an important bacterial pathogen in the pathophysiology of otitis media. To elucidate the inflammatory responses that occur during pneumococcal otitis media, the kinetics of the biochemical and cytologic middle ear responses to heat-killed encapsulated and nonencapsulated pneumococci were studied in the chinchilla model. Inoculation of the middle ear cavity with at least 10(6) S pneumoniae cells induced an early, brief vascular response with leakage of small (albumin) followed by larger (alpha 2-macroglobulin) proteins, followed by sustained influx of acute inflammatory cells and lysozyme. The threshold for a sustained lysozyme response was 1,000 times lower for nonencapsulated than for encapsulated pneumococci. These results indicate that nonviable S pneumoniae organisms with an intact envelope initiate the middle ear inflammatory response. Therefore, interventions that enhance the clearance of pneumococcal cells from the middle ear may reduce the inflammatory response and prevent chronic middle ear inflammation.

A controlled trial comparing three treatments for chronic otitis media with effusion

A randomized, controlled clinical trial was conducted in 76 children to evaluate the efficacy of trimethoprim-sulfamethoxazole for 4 weeks, prednisone for 2 weeks and aluminum ibuprofen suspension for 2 weeks in resolving chronic otitis media with effusion which had persisted for more than 8 weeks. After 2 weeks of treatment resolution rates of chronic otitis media with effusion in the prednisone and trimethoprim-sulfamethoxazole groups were significantly greater than those in the control (no treatment) and ibuprofen groups. After 4 weeks the differences in resolution rates between the control, trimethoprim-sulfamethoxazole and prednisone groups became smaller. After 12 months of follow-up, differences in hearing sensitivity among study groups were not statistically significant, although 83% of patients had a 15-dB or greater hearing loss. Therefore short term antimicrobial and antiinflammatory treatment did not appear to have a long lasting effect on chronic middle ear inflammation.

HRCT diagnosis in the evaluation of chronic middle ear inflammation

HRCT diagnosis in the evaluation of chronic middle ear inflammation

Relation between the Onset of Chronic Middle Ear Inflammation and the Development of the Middle Ear Air Cell System

The relation between the onset of chronic middle ear inflammation and the degree of pneumatization was investigated in porcine tympanic bullae, which closely resemble the human mastoid air cell system. Pneumatization was inhibited in all inflamed ears, and the later the induction of otitis media, the lesser the degree of inhibition of pneumatization. It was concluded that chronic middle ear inflammation inhibits the development of the middle ear air cell system, and the time of onset plays an important role in the degree of pneumatization.

乳突蜂巣-中耳慢性炎症状態と乳突蜂巣発育-

The effect of chronic middle ear inflammation on the pneumatization of the tympanic bulla was investigated in pigs. The pig tympanic bulla has an air cell system that is divided by trabeculae, and closely resembles the human mastoid air cell system. The tympanic bulla and its air cell system in normal ears were well developed because of the bone formation and the bone resorption inside the cortex. On the other hand, the tympanic bulla affected by chronic otitis media in young pigs exhibited reduced pneumatization arising from impaired bone resorption, and the later otitis media developed, the more the air cell system was preserved. It was concluded that the occurrence of chronic middle ear inflammation in the early stages of life causes inhibition of pneumatization by hindering the development of the air cell system, and the degree of the inhibition was related to the time of the onset of the disease.

The effect of chronic middle ear inflammation on the pneumatization of the tympanic bulla in pigs.

The effect of chronic middle ear inflammation on the pneumatization of the tympanic bulla was investigated in piglets. The pig tympanic bulla has an air cell system which is divided by trabeculae and closely resembles the human mastoid air cell system. The tympanic bulla and its air cell system in normal ears were well developed because of the bone formation and the bone resorption inside the cortex, whereas the tympanic bulla affected by chronic otitis media in the early stages of life exhibited retardation of pneumatization arising from the disturbed bone resorption by inflammatory stimulus. It was concluded that affliction with chronic middle ear inflammation in the early stages of life causes inhibition of pneumatization by hindering the development of the air cell system.

The effect of chronic middle ear inflammation on the development of the mastoid air cell system--an experimental study

The effect of chronic middle ear inflammation on the development of mastoid air cell system was investigated in piglings, whose tympanic bullae closely resemble the human mastoid air cell system. Experimental chronic otitis media was produced by the injection of glycerin into the middle ear cleft of piglings aged from 5 days to 5 weeks after birth. The piglings were subsequently decapitated and the temporal bones removed at 50 days, 2 months, 4 months and 6 months after birth, to examine and compare the degree of pneumatization of the tympanic bullae histologically, against that of non-treated control group. In the non-treated control group free of inflammations, the tympanic bullae were developed as a result of the bone formation by the osteoblasts, and the air cell system was developed widely inside of the cortex due to the bone resorption by osteoclasts. On the other hand, in the tympanic bullae of treated animals, non-specific chronic middle ear inflammation was noted and, although the bone formation by osteoblasts progressed as in normal tympanic bullae, very few osteoclasts were observed. This suggested reduced bone resorption by osteoclasts due to the inflammatory stimulus. Moreover, it was found that later the time of removal of the temporal bone, the larger the proportion of the bone mass occupying the tympanic bullae, and only slight remnants of the air cell system was detectable near the middle ear cleft in glycerin treated 6 months old piglings. The tympanic bullae and the air cell system of normal piglings were well developed due to the bone formation and the bone resorption inside the cortex, whereas the tympanic bullae of piglings afflicted with chronic otitis media in the early stages of life exhibited retardation of pneumatization arizing from the disturbance of bone resorption by inflammatory stimulus, resulting in thickened residual bone mass with development. Therefore, the development of air cell system was inhibited severely in spite of the normal growth of tympanic bulla itself. In conclusion, it was thought that affliction with chronic middle ear inflammation in the early stages of life induces the inhibition of pneumatization by hindering the developmental process of the air cell system.

Chronic Middle Ear Inflammation and the Development of Mastoid Air Cell System

Chronic Middle Ear Inflammation and the Development of Mastoid Air Cell System

Bacterial and Polymorphonuclear Leukocyte Contribution to Middle Ear Inflammation in Chronic Otitis Media with Effusion

Bacteria can be cultured from approximately one third of chronic middle ear effusions, yet the contribution of these bacteria to the pathogenesis of chronic otitis media with effusion (OME) is not clear due to the absence of signs and symptoms of acute infection in most children with this disease. To explore the role of bacteria in chronic OME, lysozyme, lactoferrin, serum complement factors C3 and C5a, and polymorphonuclear leukocyte (PMNL) chemotaxin content was measured in 21 chronic middle ear effusion samples. Concentrations of lysozyme, lactoferrin, and chemotaxin were significantly higher in culture-positive than in sterile effusions. Lysozyme appeared to be contributed by both PMNL and non-PMNL sources in the middle ear space. These non-PMNL sources, presumably middle ear epithelial cells, accounted for 50% to 80% of the lysozyme variation in middle ear effusion. Although C3 and C5a were present in effusion, chemotaxin content correlated poorly with the C3 and C5a content, suggesting that chemotaxins were derived from bacterial peptides rather than from complement activation products. These results suggest that bacteria contribute to chronic middle ear inflammation with effusion. The eradication of bacteria from chronic middle ear effusion might disrupt the host responses which maintain chronic OME.

Clinical Survey of Peripheral Vestibular Disorders (1980-1982)

Eight hundred and seventy-seven patients were diagnosed to have peripheral vestibular diseases among 3, 602 patients who had visited the Neurootological Clinic of the Kitasato University Hospital from 1980 to 1982. The percentage of peripheral vestibular diseases was as follows: sensorineural deafness, 20.8%; vertigo and dizziness in chronic middle ear inflammation, 19.3%; Meniere's disease, 16.4%; sudden deafness, 14.9%; postional vertigo of benign paroxysmal type, 11.1%; and vestibular neuritis, 3.4%.Several clues for the diagnosis of peripheral vestibular diseases and the importance of neurological examination were discussed.