Ohsaki K, Shibata A, Yamashita S, Oe M, Wang K Q, Cui P C, Ye Q
Division of Clinical Otology, University Hospital, School of Medicine, University of Tokushima, Japan.
Cell Mol Biol (Noisy-le-grand). 1995 Dec;41(8):1155-67.
In investigations of the process of bone destruction caused by chronic otitis media complicated with cholesteatoma, we proposed previously a hypothesis to explain its mechanism. In the present study, we substitute a synthetic auditory ossicle (Apaceram) for the bone to simplify the model system of experiments for our hypothesis. Its process was studied on a model simulation in vitro, in vivo and clinically at molecular level, using laser-Raman spectrometry. An increase of conductivity in both the saline solution and double-distilled water immersed Apaceram indicated demineralization depending on time lapse. The process of demineralization was revealed by the Raman spectral profiles as shown by narrowing a half-peak breadth (p < 0.01) of v1 signal (PO4(3-), 960 cm-1) and the disappearance of the shoulder at circa 950 cm-1 on the Apaceram surface implanted for 6 months. On the other hand, the process of remineralization was revealed in vivo by the spectral profiles: 1) a broader half-peak breadth (p < 0.01) of v1 signal on the Apaceram surface implanted for 10 months than that implanted for 6 months; 2) a weak reappearance of the shoulder at ca. 950 cm-1 on the Apaceram surface after 10 months; 3) four signals (v1 through v4) of PO4(3-) on the HOAP observed for inside the Apaceram shaft and 4) a weak v1 signal on both the granular fluorescent substance in the clinical case and the high density area of subcutaneous tissue after contact with the Apaceram in rats for 3 months. Judging from these investigations, it is proposed that the mechanism of bone destruction associated with cholesteatoma is a form of de- and remineralization.
在对慢性中耳炎合并胆脂瘤所致骨破坏过程的研究中，我们之前提出了一个假说来解释其机制。在本研究中，我们用人工听小骨（Apaceram）替代骨骼，以简化针对我们假说的实验模型系统。使用激光拉曼光谱法，在体外、体内和临床模型模拟中，从分子水平对其过程进行了研究。浸泡在盐溶液和双蒸水中的Apaceram的电导率增加表明脱矿作用随时间推移而发生。拉曼光谱图显示了脱矿过程，如植入6个月的Apaceram表面v1信号（PO4(3-)，960 cm-1）的半峰宽变窄（p < 0.01）以及约950 cm-1处的肩峰消失。另一方面，体内光谱图揭示了再矿化过程：1）植入10个月的Apaceram表面v1信号的半峰宽比植入6个月的更宽（p < 0.01）；2）10个月后Apaceram表面约950 cm-1处的肩峰微弱再现；3）在Apaceram杆内部观察到HOAP上PO4(3-)的四个信号（v1至v4）；4）临床病例中的颗粒状荧光物质以及大鼠与Apaceram接触3个月后的皮下组织高密度区域均出现微弱的v1信号。根据这些研究，提出与胆脂瘤相关的骨破坏机制是一种脱矿和再矿化的形式。
