The high incidence of the mtDNA4977 deletion in the temporal bones of presbyacusis patients suggests a correlation between the mtDNA4977 deletion and presbyacusis. Hypoxia of the cochlea may cause the mtDNA4977 deletion and other mtDNA mutants and furthermore may cause a reduction in mitochondrial oxidative phosphorylation and decreased function of the acoustic neural system. The symptoms of presbyacusis may occur when the function of the acoustic neural system is impaired as a result of abnormal mtDNA metabolism reaching a particular threshold.

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The purpose of this study was to observe the protective effects of basic fibroblast growth factor (bFGF) on the cells of the inner ear using in vivo experiments. The studies were carried out using guinea pigs in which bFGF or artificial perilymph was perfused into the cochlea. The compound action potential (CAP) was measured before and after exposure to a sound simulating an explosion. The difference in CAP was significant between the bFGF-perfused group and the control group (p < 0.01, t = 3.896) and between the bFGF-perfused group and the artificial perilymph-perfused group (p < 0.05, t = 2.520). The cochleae were removed and hair cell loss estimated from surface preparations. Acoustic trauma caused loss of outer hair cells in the first and second turns of the cochlea in the bFGF-perfused group and the artificial perilymph-perfused group and partial loss of inner hair cells in the control group. Treatment with bFGF reduced the loss of inner hair cells compared to that of control animals. Our results demonstrate that treatment with bFGF protects the hair cells from acoustic trauma and may facilitate the recovery of hearing.

Giant cell reparative granuloma (GCRG) is an uncommon non-neoplastic lesion that typically occurs in the mandible and maxilla: however, its involvement with the temporal bone is rare. It is usually misdiagnosed as a giant cell tumor. Although regarded as a benign process, GCRG may be locally aggressive. In this paper, we describe two cases of GCRG of the temporal bone and review the pertinent literature published in English. The clinical course, histological evaluation, diagnosis, differential diagnosis, treatment and prognosis of GCRG of the temporal bone were investigated.

The embryonic development of the human ethmoid labyrinth was studied in 24 fetal heads aged between 8 and 40 weeks of gestation under light microscopy. The uncinate process was identifiable at 8 weeks of gestation on the laterosuperior portion of the inferior turbinate; however, at this stage of development, the ethmoid bulla was not apparent. The ethmoid bulla developed on the lateral wall of the middle meatus by 12 weeks of gestation. By 14 weeks, the primordial ethmoid infundibulum and primordial maxillary sinus were seen developing between the uncinate process and the ethmoid bulla. It was obvious that the anterior and middle ethmoid cells developed from the ethmoid bulla. By 22 weeks of gestation, the first cell of the anterior ethmoid group was evident in the anterior-inferior portion of the ethmoid bulla. By 23 weeks of gestation, the first cell of the middle ethmoid group was visible in the superior portion of the ethmoid bulla. Pneumatization of the middle turbinate occurred as part of normal development of the ethmoid labyrinth. By 32 weeks of gestation, the ostium for the development of the middle turbinate cell was seen in the superior-interior portion of the middle turbinate. These observations provide new insight into the development of the ethmoid labyrinth and have important implications for the understanding of normal anatomy and developmental variants of the ethmoid labyrinth.