Sølvsten Sørensen M, Nielsen L P, Bretlau P, Jørgensen M B
Department of Otolaryngology, Rigshospitalet, University of Copenhagen, Denmark.
Acta Otolaryngol. 1988 Mar-Apr;105(3-4):242-7. doi: 10.3109/00016488809097004.
A recent theory, suggesting that otosclerosis results from autoreactivity to type II collagen present in the fetal cartilaginous remnants of the human bony labyrinth, is based on two observations. Otosclerotic patients have increased concentrations of circulating antibody to type II collagen, and immunization of rodents with cartilage collagen induces 'otosclerosis-like' lesions. Independent researchers have been unable to confirm the first promising results. No significant abnormalities could be found in immunized animals. We report the result of type II collagen antibody recordings in a well described group of otosclerotic patients and controls, and the histological findings in temporal bones of MRL/1-mice with spontaneous type II collagen autoreactivity. Our results cannot support the view of autoreactivity to type II collagen as an etiopathogenetic factor in otosclerosis.
最近有一种理论认为，耳硬化症是由于对人类骨迷路胎儿软骨残余中存在的II型胶原产生自身反应性所致，该理论基于两项观察结果。耳硬化症患者循环中针对II型胶原的抗体浓度升高，用软骨胶原免疫啮齿动物会诱发“耳硬化症样”病变。独立研究人员未能证实最初令人鼓舞的结果。在免疫动物中未发现明显异常。我们报告了一组详细描述的耳硬化症患者和对照组中II型胶原抗体记录的结果，以及具有自发性II型胶原自身反应性的MRL/1小鼠颞骨的组织学发现。我们的结果不支持将对II型胶原的自身反应性视为耳硬化症发病机制中的一个病因因素的观点。
