The middle ear of guinea pig has long been used for experimental studies. However, in spite of numerous otologic studies on guinea pig's middle ear, there are few investigations on measuring the size of each part of the middle ear. Therefore, in this study, a computer-aided 3-D reconstruction method was applied to the middle ear of a guinea pig, and the ossicles, tympanic membrane, ligaments and bulla were reconstructed three-dimensionally in detail. Then, the length, angle, volume and area of each part of the middle ear were obtained from these reconstructed images. Finally, the mechanism of the sound pressure enhancement in the middle ear was examined.

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The expression of P-glycoprotein (P-gp), a membrane-bound drug efflux pump for many anti-cancer drugs in multidrug-resistant cells, in endothelial cells of capillary blood vessels of the cochlea in mice was investigated.
The cochlea of the FVB mouse was decalcified in 10% EDTA solution (pH7.4) for 4 days. After embedding in OCT compounds (Miles, USA), the cochlea was cut on a cryostat into 12μm sections. Sections were fixed in cold acetone, then incubated with mouse anti-P-gp monoclonal antibody C219 (Centocor, USA) overnight at 4°. A peroxidase-conjugated goat anti-mouse IgG (Dako, Denmark) was applied for 1h at room temperature. As negative control, the sections were similarly immunostained except that the primary antibody was replaced with PBS. Sections from the brain were used as positive control.
P-gp was found only in the capillary endothelial cells of cochlear tissue. Tissues or cells other than capillary blood vessels were not stained. In the cochlea, positive-staining was observed in the stria vascularis, spiral ligament, spiral limbus, basilar membrane, spiral ganglion, and cochlear nerve in the modiolus, but not in the bony capsule. Immunoreactivity in the cochlea was similar to that in the brain.
The present investigation suggests that P-gp expression in the capillary endothelial cells of the cochlea might play an important role in the blood-inner ear barrier.

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Bilateral endolymphatic hydrops after unilateral endolymphatic sac (ES) immune injury were investigated using a graphic analyzer over a 3-week period. Fifty-one Hartley guinea pigs were used in this study. Twenty-eight animals were induced immune injury after keyhole limpet hemocyanin (KLH) secondary challenge into the right ES (KLH group). Fourteen animals underwent sham operation using PBS instead of KLH (PBS group) and 9 animals were used as non-surgical control (control group).
Control and PBS groups showed neither the histological changes nor the significant differences between the bilateral endolymphatic space area. In KLH group, endolymphatic hydrops and a massive cell infiltration within the ES in the right inner ear were observed on days 1-7. The inflammation and the hydrops were gradually decreased on days 14-21. On the other hand, the remarkable change of the contralateral left endolymphatic space compared with the right ear space were observed without cell infiltration on days 14-21. The above results suggested that unilateral immune injury in the ES could induce the change of the endolymphatic space in the contralateral inner ear.

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Several point mutations of mitochondrial DNA have recently been identified as a cause of hearing loss. In Japan, there are considerable number of patients with A-to-G mutations at nucleotide position 3243 and at 1555. We investigated the prevalence of these mutations in patients with hearing loss using polymerase chain reaction method (PCR). We identified 3243 point mutation in 2 of 72 patients (2.8%) and 1555 point mutation in one of 57 patients (1.8%). The clinical neuro-otologic findings in patients with point mutations were consistent with those previously reported. The number of patients examined was composed of 9% of a total in our outpatient clinic. Therefore, we estimated 0.4% of patients in our clinic have a point mutation at nucleotide position 3243 or 1555.

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Distribution of mast cells in the subepithelial layer of cholesteatoma matrix and adhesive eardrum were studied to elucidate the role of mast cells in chronic otitis media. The sections were stained with alcian blue for 16 hours following pretreatment with 0.7N hydrochloric acid solution. The number of mast cells per mm2 ranged from 0 to 60.9, with the mean ± standard error being 20.5±3.6 cells/mm² in all cases (n=17), 28.0±4.8cells/mm² in the cholesteatoma matrices (n=9) and 12.1±3.8cells/mm² in-the adherent eardrums (n=8). The difference in mast cell counts between the cholesteatoma matrices and the adherent eardrums was significant (p<0.05). The number of mast cells tended to be high in specimens that were closely associated with granulation tissue. Obstruction of the mastoid cavity due to cholesteatoma may enhance mast cell degranulation due to hypoxic conditions when the ventilation route is blocked. Mast cells seem to be involved in the pathogenesis or development of cholesteatoma.

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Hearing results of forty two ears received tympanoplasty without ossicular reconstruction (so called type 0 tympanoplasty) between 1994 and 1997 were evaluated.
Hearing results of forty two ears received tympanoplasty without ossicular reconstruction (so called type 0 tympanoplasty) between 1994 and 1997 were evaluated.
The results were as follows: 1) unexpectedly nearly 59.5% of the cases after type 0 tympanoplasty were classified as success in terms of hearing in spite of the fact that the ossicular chain was not reconstructed. 2) there was statistical difference in success rate between the cases underwent surgery by open methods (72.7%) and those underwent surgery by closed methods (54.8%). 3) in cases those airbone gap was within 20dB, it was suggested that the mobility of the stapes and the extent of the inflammation surrounding the stapes seemed to be important factors to influence the postoperative hearing after type 0 tympanoplasty.

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In tympanoplasty, we always used cortical bone chips for reconstruction of the posterior bony external ear canal and for obliteration of the radical mastoid cavity. But if enough bone chips were not obtained, we used hydroxyapatite (Apaceram ^®) plate for posterior ear canal reconstruction and hydroxyapatite (Apaceram^®) granules for mastoid obliteration.
Hydroxyapatite plate and/or hydroxyapatite granules were used in 33 ears, between 1989 and 1996 with an average follow-up period of 44 months. These cases were 3.4% of 965 ears undergone tympanoplasty with posterior ear canal reconstruction and mastoid obliteration at the same period. We have no serious complication in these 33 ears.
It was concluded that tympanoplasty using hydroxyapatite with scrupulous care is safe and useful.

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In a 11-year-old male patient with left hearing loss, otoscopic examination revealed the intact tympanic membrane, and the left ossicular anomaly was suspected by preoperative examinations. During surgery, the long process of the incus and the superstructure of the stapes were not recognized and two different types of congenital cholesteatomas (an open type and a closed type) were found in the middle ear cavity.
Coexistance of open and closed type cholesteatomas in the middle ear was very rare. We discussed the origin of the open type congenital cholesteatoma and embryological problems.

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