Spiral ligament pathology in quiet-aged gerbils

被引:85
作者
Spicer, SS
Schulte, BA
机构
[1] Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA
[2] Med Univ S Carolina, Dept Otolaryngol Head & Neck Surg, Charleston, SC 29425 USA
关键词
cochlea; lateral wall; fibrocytes; ultrastructure; aging; presbyacusis;
D O I
10.1016/S0378-5955(02)00581-6
中图分类号
R36 [病理学]; R76 [耳鼻咽喉科学];
学科分类号
100104 ; 100213 ;
摘要
The ultrastructure of the spiral ligament was compared in aged and young gerbils to assess the involvement of connective tissues in the lateral wall and particularly the fibrocytes in development of presbyacusis. Pathologic features in fibrocytes of senescent gerbils spanned a wide range reflecting different stages of lateral wall involution. All of the type II, IV and V fibrocytes selectively developed cytosolic vacuoles in an early degenerative phase showing minimal strial involvement. Clear spaces indicative of interstitial edema separated the vacuolated cell bodies and their plasmalemmal processes. As a presumed intermediate phase, profiles of amorphous substance apparently derived from apoptosis/necrosis of type II fibrocytes infiltrated the type II fibrocyte area among nearly normal appearing cells. In cochlear turns with advanced strial degeneration, type II fibrocytes disappeared from the spiral prominence area leaving only type I-like fibrocytes occasionally accompanied by a collagen infiltrate. Type V fibrocytes disappeared similarly from the suprastrial area. The extent of atrophy in type II fibrocytes corresponded in general with that in the neighboring stria vascularis. Age-dependent atrophy in the lateral wall largely spared type I fibrocytes except that they often enclosed discrete amorphous foci lacking organelles. The involution thus affected principally the Na,K-ATPase-positive fibrocytes functioning in active uptake rather than passive conductance of K+. The vacuolization and degeneration exclusive to ATPase-rich fibrocytes and the associated intercellular edema are interpreted as secondary responses, possibly as a result of impaired diffusion of K+ through downstream marginal cells. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:172 / 185
页数:14
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