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人工耳蜗植入后的免疫反应。

Immune Response After Cochlear Implantation.

作者信息

Simoni Edi, Gentilin Erica, Candito Mariarita, Borile Giulia, Romanato Filippo, Chicca Milvia, Nordio Sara, Aspidistria Marta, Martini Alessandro, Cazzador Diego, Astolfi Laura

机构信息

Bioacoustics Research Laboratory, Department of Neurosciences, University of Padua, Padua, Italy.

Otorhinolaryngology Unit, Department of Neurosciences, University of Padua, Padua, Italy.

出版信息

Front Neurol. 2020 May 14;11:341. doi: 10.3389/fneur.2020.00341. eCollection 2020.

DOI:10.3389/fneur.2020.00341
PMID:32477241
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7240074/
Abstract

A cochlear implant (CI) is an electronic device that enables hearing recovery in patients with severe to profound hearing loss. Although CIs are a successful treatment for profound hearing impairment, their effectivity may be improved by reducing damages associated with insertion of electrodes in the cochlea, thus preserving residual hearing ability. Inner ear trauma leads to inflammatory reactions altering cochlear homeostasis and reducing post-operative audiological performances and electroacoustic stimulation. Strategies to preserve residual hearing ability led to the development of medicated devices to minimize CI-induced cochlear injury. Dexamethasone-eluting electrodes recently showed positive outcomes. In previous studies by our research group, intratympanic release of dexamethasone for 14 days was able to preserve residual hearing from CI insertion trauma in a Guinea pig model. Long-term effects of dexamethasone-eluting electrodes were therefore evaluated in the same animal model. Seven Guinea pigs were bilaterally implanted with medicated rods and four were implanted with non-eluting ones. Hearing threshold audiograms were acquired prior to implantation and up to 60 days by recording compound action potentials. For each sample, we examined the amount of bone and fibrous connective tissue grown within the scala tympani in the basal turn of the cochlea, the cochleostomy healing, the neuronal density, and the correlation between electrophysiological parameters and histological results. Detection of tumor necrosis factor alpha, interleukin-6, and foreign body giant cells showed that long-term electrode implantation was not associated with an ongoing inflammation. Growth of bone and fibrous connective tissue around rods induced by CI was reduced in the scala tympani by dexamethasone release. For cochleostomy sealing, dexamethasone-treated animals showed less bone tissue growth than negative. Dexamethasone did not affect cell density in the spiral ganglion. Overall, these results support the use of dexamethasone as anti-inflammatory additive for eluting electrodes able to protect the cochlea from CI insertion trauma.

摘要

人工耳蜗(CI)是一种电子设备,可使重度至极重度听力损失患者恢复听力。尽管人工耳蜗是治疗重度听力障碍的成功方法,但通过减少与电极植入耳蜗相关的损伤,从而保留残余听力能力,可提高其有效性。内耳创伤会导致炎症反应,改变耳蜗内环境稳态,并降低术后听力表现和电声刺激效果。保留残余听力能力的策略促使了药物装置的研发,以尽量减少人工耳蜗引起的耳蜗损伤。最近,地塞米松洗脱电极显示出了积极的效果。在我们研究小组之前的研究中,在豚鼠模型中,鼓膜内释放地塞米松14天能够保护残余听力免受人工耳蜗植入创伤的影响。因此,我们在同一动物模型中评估了地塞米松洗脱电极的长期效果。七只豚鼠双侧植入药物棒,四只植入非洗脱棒。在植入前直至60天,通过记录复合动作电位获取听力阈值听力图。对于每个样本,我们检查了耳蜗基底转鼓阶内生长的骨组织和纤维结缔组织的数量、蜗窗愈合情况、神经元密度,以及电生理参数与组织学结果之间的相关性。肿瘤坏死因子α、白细胞介素-6和异物巨细胞的检测表明,长期电极植入与持续炎症无关。地塞米松释放减少了鼓阶内由人工耳蜗引起的棒周围骨组织和纤维结缔组织的生长。对于蜗窗封闭,地塞米松治疗的动物比未治疗的动物骨组织生长更少。地塞米松不影响螺旋神经节中的细胞密度。总体而言,这些结果支持将地塞米松用作洗脱电极的抗炎添加剂,能够保护耳蜗免受人工耳蜗植入创伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/926aac372516/fneur-11-00341-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/c602cf7a519f/fneur-11-00341-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/28c384dfc43f/fneur-11-00341-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/b557b686b05c/fneur-11-00341-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/dfe6ab349cd7/fneur-11-00341-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/9528ec949b3b/fneur-11-00341-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/926aac372516/fneur-11-00341-g0010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/c602cf7a519f/fneur-11-00341-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/e50f73763937/fneur-11-00341-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/8a8801c80e42/fneur-11-00341-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/432c5546064d/fneur-11-00341-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/2ab0d525bf00/fneur-11-00341-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/28c384dfc43f/fneur-11-00341-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/b557b686b05c/fneur-11-00341-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/dfe6ab349cd7/fneur-11-00341-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/9528ec949b3b/fneur-11-00341-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23af/7240074/926aac372516/fneur-11-00341-g0010.jpg

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