Resorption of auditory ossicles and hearing loss in mice lacking osteoprotegerin
Resorption of auditory ossicles and hearing loss in mice lacking osteoprotegerin
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DOI：
10.1016/j.bone.2006.01.155
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发表时间：
2006-08-01
期刊：
影响因子：
4.1
通讯作者：
Matsuo, Koichi
中科院分区：
文献类型：
--
作者：
Kanzaki, Sho;Ito, Masako;Matsuo, Koichi
骨头在中耳传导声音。这三个小骨--锤骨、砧骨和镫骨--形成一个链条，将振动从鼓膜传递到内耳的卵圆窗。关于这些听小骨的骨重建事件以及骨质疏松对听力损失的潜在影响知之甚少。在缺乏骨保护素的Opg（-/-）小鼠中，骨吸收增强，骨保护素是破骨细胞生成细胞因子RANKL的可溶性诱饵受体。我们询问Opg（-/-）小鼠的听小骨是否被吸收，以及这些小鼠是否患有听觉功能受损。Opg（-/-）小鼠的三个听小骨均变薄，尤其是在锤骨手骨和砧骨体。最值得注意的是，与野生型小鼠的情况不同，Opg（-/-）小鼠的镫骨和耳囊之间的连接是固定的，镫骨足板更薄更宽。放射学分析显示，在Opg（-/-）和对照同窝小鼠中，踝皮质厚度与胫骨骨密度呈正相关。此外，在Opg（-/-）小鼠中从6至15周龄开始检测到进行性听力损失。这些数据表明，骨保护素在听力中起着至关重要的作用，通过保护听小骨和耳囊骨吸收。(c)2006年爱思唯尔公司All rights reserved.
Bones conduct sound in the middle ear. The three ossicles-the malles, incus, and stapes-form a chain that transmits vibrations from the tympanic membrane to the oval window of the inner ear. Little is known about bone remodeling events in these ossicles and about potential effects of osteoporosis on hearing loss. Osteoclastic bone resorption is enhanced in Opg(-/-) mice lacking osteoprotegerin, which is a soluble decoy receptor for the osteoclastogenic cytokine RANKL. We asked whether auditory ossicles are resorbed in Opg(-/-) mice, and whether these mice suffer from impaired auditory function. All three ossicles in Opg(-/-) mice showed thinning, especially at the malleal manubrium and incus body. Most notably, unlike in the case in wild-type mice, the junction between the stapes and the otic capsule was fixed in Opg(-/-) mice, and the stapedial footplate was thinner and broader. Radiological analyses revealed that malleal cortical thickness was positively correlated with tibial bone mineral density in Opg(-/-) and control littermate mice. Furthermore, progressive hearing loss was detected in Opg(-/-) mice starting at 6 to 15 weeks of age. These data suggest that osteoprotegerin plays a crucial role in hearing by protecting the auditory ossicles and otic capsule from osteoclastic bone resorption. (c) 2006 Elsevier Inc. All rights reserved.