Cao Ye, Li Kai, Fu Kai-yuan, Xie Qiu-fei
Department of Prosthodontics, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Beijing Da Xue Xue Bao Yi Xue Ban. 2010 Feb 18;42(1):50-5.
To investigate the peripheral mechanism by studying the histological changes of masseter muscles using HE stains and substance P (SP) and protein gene product 9.5 (PGP9.5) immunohistochemical stains.
Fifteen male Sprague-Dawley were randomly assigned into occlusal interference group (n=12) and control group (n=3). In occlusal interference group, 0.4 mm thick crowns were bonded to the rats' first molar of the maxillary. In the control group, rats were anesthetized and mouths were forced open for about 5 min but restorations were not applied. 1, 5, 10, and 21 d after 0.4 mm occlusal alteration treatment, mechanical pain thresholds of bilateral masseter muscles were quantitatively measured by modified electronic anesthesiometer in control group and occlusal interference group. The rats were euthanized by transcardiac perfusion after deep anesthetization at different time points. The paraffin sections of masseter muscles were made and processed for HE, SP, and PGP9.5 immunohistochemical staining.
Decreased head withdrawal threshold to mechanical pressure was detected in masseter muscles on both sides following occlusal interference. Histological stains of masseter muscles presented intact following occlusal interference, and no inflammatory cells were observed in both sides. Intensely stained PGP9.5 was observed at 1 d in occlusal interference groups and maintained until the end of the experiment. SP expression was the most obviously increased at 5 d in both sides and gradually decreased to the level of control.
Experimental occlusal interference-induced masticatory muscle pain is associated with peripheral sensitization of nociceptive neurons rather than muscle damage and inflammation.
通过苏木精-伊红（HE）染色以及P物质（SP）和蛋白基因产物9.5（PGP9.5）免疫组织化学染色研究咬肌的组织学变化，以探讨其外周机制。
将15只雄性Sprague-Dawley大鼠随机分为咬合干扰组（n = 12）和对照组（n = 3）。在咬合干扰组中，将0.4毫米厚的牙冠粘结到大鼠上颌的第一磨牙上。在对照组中，将大鼠麻醉并强行张口约5分钟，但不进行修复处理。在进行0.4毫米咬合改变处理后的1、5、10和21天，使用改良电子麻醉仪定量测量对照组和咬合干扰组双侧咬肌的机械性疼痛阈值。在不同时间点深度麻醉后，通过心脏灌注使大鼠安乐死。制作咬肌的石蜡切片并进行HE、SP和PGP9.5免疫组织化学染色。
咬合干扰后双侧咬肌对机械压力的缩头阈值降低。咬合干扰后咬肌的组织学染色显示完整，两侧均未观察到炎性细胞。在咬合干扰组中，1天时观察到PGP9.5染色强烈，并持续到实验结束。两侧SP表达在5天时增加最为明显，随后逐渐降至对照组水平。
实验性咬合干扰诱导的咀嚼肌疼痛与伤害性神经元的外周敏化有关，而非肌肉损伤和炎症。
