Histopathological Observations of Presbycusis

1976 ◽  
Vol 85 (2) ◽  
pp. 169-184 ◽  
Author(s):  
Fumiro Suga ◽  
John R. Lindsay

Temporal bone histopathology of 17 aged patients who had spontaneous and gradually progressive bilateral sensorineural hearing losses associated with aging was studied. Six cases in the present material showed the gradually sloping audiometric curve; nine cases, abrupt high tone hearing loss; and two cases, the flat audiometric curve. The most prominent histopathological change in the inner ear was a decrease in the population of the spiral ganglion cells. However, diffuse senile atrophy was also often seen in the organ of Corti and the stria vascularis. A positive correlation between the degree of arteriosclerosis and the degree of sensorineural degeneration in the cochlea was not obtained in the present cases. Also, the correlation was not found to be consistent between the type of the audiometric curve and the localization of lesions in the sensory, the neural or the vascular elements in the cochlea. Our observations show that a certain type of audiometric curve does not necessarily indicate a lesion in a specific cochlear element.

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 399 ◽  
Author(s):  
Jhang Ho Pak ◽  
Junyeong Yi ◽  
Sujin Ryu ◽  
In Ki Kim ◽  
Jung-Woong Kim ◽  
...  

Free radicals formed in the inner ear in response to high-intensity noise, are regarded as detrimental factors for noise-induced hearing loss (NIHL). We reported previously that intraperitoneal injection of cobalt chloride attenuated the loss of sensory hair cells and NIHL in mice. The present study was designed to understand the preconditioning effect of CoCl2 on oxidative stress-mediated cytotoxicity. Treatment of auditory cells with CoCl2 promoted cell proliferation, with increases in the expressions of two redox-active transcription factors (hypoxia-inducible factor 1α, HIF-1α, nuclear factor erythroid 2-related factor 2; Nrf-2) and an antioxidant enzyme (peroxiredoxin 6, Prdx6). Hydrogen peroxide treatment resulted in the induction of cell death and reduction of these protein expressions, reversed by pretreatment with CoCl2. Knockdown of HIF-1α or Nrf-2 attenuated the preconditioning effect of CoCl2. Luciferase reporter analysis with a Prdx6 promoter revealed transactivation of Prdx6 expression by HIF-1α and Nrf-2. The intense immunoreactivities of HIF-1α, Nrf-2, and Prdx6 in the organ of Corti (OC), spiral ganglion cells (SGC), and stria vascularis (SV) of the cochlea in CoCl2-injected mice suggested CoCl2-induced activation of HIF-1α, Nrf-2, and Prdx6 in vivo. Therefore, we revealed that the protective effect of CoCl2 is achieved through distinctive signaling mechanisms involving HIF-1α, Nrf-2, and Prdx6.


Author(s):  
Xiaomin Tang ◽  
Yuxuan Sun ◽  
Chenyu Xu ◽  
Xiaotao Guo ◽  
Jiaqiang Sun ◽  
...  

Caffeine is being increasingly used in daily life, such as in drinks, cosmetics, and medicine. Caffeine is known as a mild stimulant of the central nervous system, which is also closely related to neurologic disease. However, it is unknown whether caffeine causes hearing loss, and there is great interest in determining the effect of caffeine in cochlear hair cells. First, we explored the difference in auditory brainstem response (ABR), organ of Corti, stria vascularis, and spiral ganglion neurons between the control and caffeine-treated groups of C57BL/6 mice. RNA sequencing was conducted to profile mRNA expression differences in the cochlea of control and caffeine-treated mice. A CCK-8 assay was used to evaluate the approximate concentration of caffeine. Flow cytometry, TUNEL assay, immunocytochemistry, qRT-PCR, and Western blotting were performed to detect the effects of SGK1 in HEI-OC1 cells and basilar membranes. In vivo research showed that 120 mg/ kg caffeine injection caused hearing loss by damaging the organ of Corti, stria vascularis, and spiral ganglion neurons. RNA-seq results suggested that SGK1 might play a vital role in ototoxicity. To confirm our observations in vitro, we used the HEI-OC1 cell line, a cochlear hair cell-like cell line, to investigate the role of caffeine in hearing loss. The results of flow cytometry, TUNEL assay, immunocytochemistry, qRT-PCR, and Western blotting showed that caffeine caused autophagy and apoptosis via SGK1 pathway. We verified the interaction between SGK1 and HIF-1α by co-IP. To confirm the role of SGK1 and HIF-1α, GSK650394 was used as an inhibitor of SGK1 and CoCl2 was used as an inducer of HIF-1α. Western blot analysis suggested that GSK650394 and CoCl2 relieved the caffeine-induced apoptosis and autophagy. Together, these results indicated that caffeine induces autophagy and apoptosis in auditory hair cells via the SGK1/HIF-1α pathway, suggesting that caffeine may cause hearing loss. Additionally, our findings provided new insights into ototoxic drugs, demonstrating that SGK1 and its downstream pathways may be potential therapeutic targets for hearing research at the molecular level.


2005 ◽  
Vol 114 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Steven P. Tinling ◽  
Vishad Nabili ◽  
Hilary A. Brodie

Labyrinthitis ossificans (LO) is the pathological deposition of new bone within the lumen of the cochlea and labyrinth. This process occurs most commonly as a result of infection or inflammation affecting the otic capsule. Trauma and vascular compromise can also lead to neo-ossification within the otic capsule. The mechanism that regulates this process remains unestablished. This study details the end-stage histopathology in high-resolution plastic thin sections. Twenty Mongolian gerbils were infected by intrathecal injection of Streptococcus pneumoniae type 3 followed by subcutaneous penicillin G procaine (8 days) and were painlessly sacrificed 3 months later. The cochleas were serially divided and sectioned for light and electron microscopy. Sixteen of 20 animals (27 of 40 cochleas) demonstrated LO. Cochlear damage was most extensive in the vestibule and basal turn and decreased toward the apex, which often appeared normal. The histopathologic findings consisted of 1) new bone, calcospherites, osteoid, and fibrosis without dense connective tissue or osteoblasts extending from the endosteal wall into the lumen of the vestibule and scala tympani; 2) areas of dense connective tissue and osteoid enclosed by epithelial cells conjoined with the organ of Corti, stria vascularis, spiral ligament, and vestibular (Reissner's) membrane; and 3) partial to complete loss of the organ of Corti, spiral ligament cell bodies, stria vascularis, and spiral ganglion cells. Osteoblastic activity was not demonstrated in end-stage ossification in LO in the gerbil model. Neoossification appears to occur by calcospherite deposition along collagen-like fibrils within osteoid. The destruction of the organ of Corti, spiral ganglion cells, stria vascularis, and cells of Reissner's membrane and the spiral ligament occurs even in the absence of ossification of the cochlear duct.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba

Age-related hearing loss (ARHL), the progressive loss of hearing associated with aging, is the most common sensory disorder in the elderly population. The pathology of ARHL includes the hair cells of the organ of Corti, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Mitochondria play a crucial role in the induction of intrinsic apoptosis in cochlear cells. ARHL can be prevented in laboratory animals by certain interventions, such as caloric restriction and supplementation with antioxidants. In this review, we will focus on previous research concerning the role of the oxidative stress and mitochondrial dysfunction in the pathology of ARHL in both animal models and humans and introduce concepts that have recently emerged regarding the mechanisms of the development of ARHL.


2008 ◽  
Vol 122 (11) ◽  
pp. 1151-1155 ◽  
Author(s):  
R Ramírez-Camacho ◽  
J R García-Berrocal ◽  
A Trinidad ◽  
J M Verdaguer ◽  
J Nevado

AbstractIntroduction:The ototoxic effects of cisplatin include loss of outer hair cells, degeneration of the stria vascularis and a decrease in the number of spiral ganglion cells. Scanning microscopy has shown balloon-like protrusions (blebs) of the plasma membrane of inner hair cells following cisplatin administration. The present study was undertaken to identify the possible role of inner and outer hair cell blebs in the pathogenesis of cisplatin-induced ototoxicity.Materials and methods:Twenty-five guinea pigs were injected with cisplatin and their hearing tested at different time-points, before sacrifice and examination with scanning electron microscopy.Results and analysis:Seven animals showed blebs in the inner hair cells at different stages. Hearing thresholds were lower in animals showing blebs.Discussion:Cisplatin seems to be able to induce changes in inner hair cells as well as in other structures in the organ of Corti. Blebbing observed in animals following cisplatin administration could play a specific role in the regulation of intracellular pressure.


1982 ◽  
Vol 91 (3) ◽  
pp. 250-255 ◽  
Author(s):  
Yasuya Nomura ◽  
Shigeo Mori ◽  
Mineko Tsuchida ◽  
Teruhisa Sakurai

We present a histopathological study of a 44-year-old female with essential cryoglobulinemia. She had suffered from purpura and ulcer in winter, bilateral tinnitus and progressive hearing loss. An audiogram taken a week before her death showed bilateral total deafness. In the cochlea of the left temporal bone, the organ of Corti was either missing or present as a mound. The stria vascularis was atrophic throughout the cochlea. The tectorial membrane showed drooping and encapsulation. Reissner membrane was in the normal position. Eosinophilic precipitate was noted in the scala media at the site where Reissner membrane bulged. The spiral ganglion cells were well preserved. In the lower basal turn, there was fibrosis and ossification intermingled in the scala tympani. Ossification was most marked near the basal end. The semicircular canals and vestibule were almost totally ossified and fused with surrounding bone. There was a small, cyst-like structure in the vestibule containing eosinophilic fluid. Our findings indicate that the deafness was the result of circulatory disturbance due to cryoglobulinemia. To our knowledge, this is the first cryoglobulinemia case in which temporal bone findings are reported.


1976 ◽  
Vol 85 (2) ◽  
pp. 268-275 ◽  
Author(s):  
Naomi Fitch ◽  
John R. Lindsay ◽  
Herbert Srolovitz

Histological study of the temporal bones of an infant with the preauricular pit, cervical fistula, hearing loss syndrome revealed abnormalities in the middle ear, the vestibular system, and the cochlea. There is a gross bilateral abnormality in the form and relationship of the middle ear spaces, the middle cranial fossa and the inner ear. The horizontal canal lacks ampulla and crista; the posterior canal terminates a short distance from the ampulla. The cochlear cavity is approximately four fifths of normal size. The modiolus of the cochlea shows minor abnormalities. Spiral ganglion cells and peripheral nerve fibers are present in all coils, but are below normal in population in the basal and apical coils. The stria vascularis is slightly deformed and partly atrophic in the upper apical coil. An occasional concretion is present in the base of the stria vascularis in the middle and apical coils.


2021 ◽  
Vol 12 (1) ◽  
pp. 2
Author(s):  
Annamaria Tisi ◽  
Jochebed Rovers ◽  
Henk A. Vink ◽  
Dyan Ramekers ◽  
Rita Maccarone ◽  
...  

We investigated whether treatment with brain-derived neurotrophic factor (BDNF), which is known to protect spiral ganglion cells (SGCs), could also protect hair cells (HCs) and supporting cells (SCs) in the organ of Corti of a guinea pig model of sensorineural hearing loss. Hearing loss was induced by administration of kanamycin/furosemide and two BDNF treatments were performed: (1) by gelatin sponge (BDNF-GS) with acute cochlear implantation (CI), and (2) through a mini-osmotic pump (BDNF-OP) with chronic CI. Outer HCs (OHCs), inner HCs (IHCs), Border, Phalangeal, Pillar, Deiters’, and Hensen’s cells were counted. The BDNF-GS cochleas had significantly fewer OHCs compared to the untreated ones, while the IHC and SC numbers did not differ between treated and untreated cochleas. The BDNF-OP group showed similar cell numbers to the untreated group. SGC packing density was not correlated with the total number of SCs for either BDNF group. Our data suggest that: (1) BDNF does not prevent cell death in the organ of Corti, and that the protection of SGCs could result from a direct targeting by BDNF; (2) BDNF might induce a different function/activity of the remaining cells in the organ of Corti (independently from cell number).


2015 ◽  
Vol 20 (4) ◽  
pp. 267-272 ◽  
Author(s):  
Joseph B. Nadol Jr ◽  
Jan D. Marshall ◽  
Roderick T. Bronson

Alström's syndrome is an autosomal recessive syndromic genetic disorder caused by mutations in the ALMS1 gene. Sensorineural hearing loss occurs in greater than 85% of patients. Histopathology of the inner ear abnormalities in the human has not previously been fully described. Histopathology of the inner ear in Alström's syndrome is presented in 2 genetically confirmed cases. The predominant histopathologic correlates of the sensorineural loss were degeneration of the organ of Corti, both inner and outer hair cells, degeneration of spiral ganglion cells, and atrophy of the stria vascularis and spiral ligament.


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