Etiopathogenesis of Acquired Cholesteatoma: Prominent Theories and Recent Advances in Biomolecular Research

被引:112
作者
Kuo, Chin-Lung [1 ,2 ,3 ,4 ,5 ]
机构
[1] Taipei Vet Gen Hosp, Dept Otolaryngol Head & Neck Surg, Taipei, Taiwan
[2] Natl Yang Ming Univ, Sch Med, Dept Otolaryngol, Taipei 112, Taiwan
[3] Natl Yang Ming Univ, Inst Brain Sci, Taipei 112, Taiwan
[4] Natl Def Med Ctr, Dept Otolaryngol, Taipei, Taiwan
[5] Taoyuan Armed Forces Gen Hosp, Dept Otolaryngol, Taoyuan, Taiwan
关键词
Connexin; 26; cytokines; etiology; microRNA; pathogenesis; MIDDLE-EAR CHOLESTEATOMA; EPIDERMAL-GROWTH-FACTOR; BONE DESTRUCTION; FACTOR-ALPHA; POSTTRANSCRIPTIONAL REGULATION; EPITHELIAL PROLIFERATION; FACTOR RECEPTOR; EXPRESSION; PATHOGENESIS; P53;
D O I
10.1002/lary.24890
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
ObjectiveTo review recent biomolecular advances in etiopathogenesis of acquired cholesteatoma. Data SourcesMEDLINE via OVID (to March 2014) and PubMed (to March 2014). Review MethodsAll articles referring to etiopathogenesis of acquired cholesteatoma were identified in the above databases, from which 89 articles were included in this review. ResultsThe mechanisms underlying the etiopathogenesis of acquired cholesteatoma remain a subject of competing hypotheses. Four theories dominate the debate, including theories of invagination, immigration, squamous metaplasia, and basal cell hyperplasia. However, no single theory has been able to explain the clinical characteristics of all cholesteatoma types: uncoordinated hyperproliferation, invasion, migration, altered differentiation, aggressiveness, and recidivism. Modern technologies have prompted a number of researchers to seek explanations at the molecular level. First, cholesteatomas could be considered an example of uncontrolled cell growth, capable of altering the balance toward cellular hyperproliferation and enhancing the capacity for invasion and osteolysis. Second, the dysregulation of cell growth control involves internal genomic or epigenetic alterations and external stimuli, which induce excessive host immune response to inflammatory and infectious processes. This comprises several complex and dynamic pathophysiologic changes that involve extracellular and intracellular signal transduction cascades. ConclusionsThis article summarizes the existing theories and provides conceptual insights into the etiopathogenesis of acquired cholesteatoma, with the aim of stimulating continued efforts to develop a nonsurgical means of treating the disorder. Laryngoscope, 125:234-240, 2015
引用
收藏
页码:234 / 240
页数:7
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