Takahiro Okura

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 month 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.

Pneumatization of the Tympanic Bulla after Blockage of the Ventilation Route through the Eustachian Tube in the Pig

To examine whether gas exchange occurs in the middle ear air cell system independent of the eustachian tube (ET), we occluded the middle ear clefts of piglets, whose tympanic bullae closely resemble the human mastoid air cell system, and investigated subsequent changes in the air cell system. We anticipated that pneumatization and development of the air cell system would continue if gas were exchanged through the mucosa lining the air cell system. If, on the other hand, mastoid air cells depend on the ET, mastoid development would be impaired or arrested. In noninflamed ears, pneumatization was maintained, and development of the air cell system continued after the middle ear cleft had been occluded with an acrylate adhesive and the bullar air cell system was thus excluded from any communication with the ET. These results indicate that the normal middle ear air cell system has the capacity to perform gas exchange independently of the ET, with gas exchange appearing to occur through the submucosal capillary network.

Acquired airway obstruction caused by hypertrophic mucosa of the arytenoids and aryepiglottic folds

Congenital laryngomalacia is the most common condition that causes stridor in the neonate, infant, and child. It is characterized by laryngeal collapse, including: (1) inward collapse of the aryepiglottic fold and enlarged cuneiform cartilage; (2) a long tubular epiglottis, or the so-called “omega-shaped” epiglottis, which becomes curled in on itself; (3) anterior medial collapse of the arytenoid cartilages; and (4) posterior inspiratory displacement of the epiglottis against the posterior pharyngeal wall or vocal cord. These symptoms usually appear within the first 2 weeks of 1ife.l In 1988, Peron et al2 reported 7 cases of redundant aryepiglottic fold in elderly patients as a new cause of stridor. Since then, several reports have investigated acquired laryngeal collapse caused by epiglottis prolapse and edematously swollen mucosa of the arytenoid and aryepiglottic fold in elderly patients.3-6 Most of these patients had sustained severe central nervous system injury, a head and neck tumor, and/or undergone head-andneck surgery. Two elderly patients without such history, but complaining of stridor and inspiratory dyspnea as a result of hypertrophic mucosa of the arytenoids and aryepiglottic folds, were studied.

Tympanic bulla pneumatization following experimental mastoidectomy in a porcine animal model

The effect of mastoidectomy on mastoid pneumatization was investigated in an animal model. Experimental mastoidectomy was performed on the air cell system of the tympanic bullae in 10 four-week-old piglets. The developmental process of this structure is very similar to that of the human mastoid air cell system. Two piglets each were decapitated at 1 and 2 weeks, and 1, 3 and 5 months after the operation, and hematoxylin and eosin sections of the bullae were examined histopathologically. The development of the tympanic bulla itself was not affected by the operation. However, inside the bulla, a great amount of bone tissue had proliferated peripheral to the surgical cavity without new formation of normal pneumatized cells. When mastoidectomy was performed in the course of the pneumatization, subsequent pneumatization did not occur in this animal model. This result suggests that mastoidectomy in childhood may arrest the new formation of mastoid air cells in humans.