Department of Basic and Oral Biology, School of Dentistry of Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.
Department of Morphology, Presidente Prudente Medical School, Universidade do Oeste Paulista, Presidente Prudente, SP, Brazil.
Sci Rep. 2020 May 29;10(1):8787. doi: 10.1038/s41598-020-65524-w.
Psychological stress and occlusal alteration are important etiologic factors for temporomandibular/masticatory muscular disorders. In particular, the exact physiologic mechanism underlying the relation by occlusal alteration and temporomandibular disorders remains unclear. Our purpose was to test the hypothesis that benzodiazepine therapy is able to prevent metabolic and vascular changes in the medial pterygoid muscle of rats under chronic stress after 14 days of unilateral exodontia. Adult Wistar rats were submitted to unpredictable chronic mild stress (10 days) and/or unilateral exodontia and their plasma and medial pterygoid muscles were removed for analysis. A pre-treatment with diazepam was used to verify its effect on stress. The parameters evaluated included anxiety behavior, plasma levels of corticosterone, metabolic activity by succinate dehydrogenase, capillary density by laminin staining and ultrastructural findings by transmission electron microscopy. Occlusal instability induced anxiety-like behavior on elevated plus-maze test and diazepam administration blocked the appearance of this behavior. Unilateral exodontia promoted in the contralateral muscle an increase of oxidative fibers and capillaries and modification of sarcoplasmic reticulum. Chronic stress caused increased glycolytic metabolism, reduced capillary density and morphological changes in mitochondria on both sides. Association of both factors induced a glycolytic pattern in muscle and hemodynamic changes. Pharmacological manipulation with diazepam inhibited the changes in the medial pterygoid muscle after stress. Our results reveal a preventive benzodiazepine treatment for stress and occlusal instability conditions affecting masticatory muscle disorders. In addition, provide insights into the mechanisms by which chronic stress and exodontia might be involved in the pathophysiology of masticatory muscular dysfunctions.
心理压力和咬合改变是颞下颌/咀嚼肌功能紊乱的重要病因。特别是，咬合改变与颞下颌紊乱之间的关系的确切生理机制仍不清楚。我们的目的是验证以下假说：即在单侧拔牙后 14 天的慢性应激下，苯二氮䓬类药物治疗能够预防大鼠翼内肌的代谢和血管变化。成年 Wistar 大鼠接受不可预测的慢性轻度应激（10 天）和/或单侧拔牙，并取出其血浆和翼内肌进行分析。使用地西泮进行预处理以验证其对压力的影响。评估的参数包括焦虑行为、皮质酮的血浆水平、琥珀酸脱氢酶的代谢活性、层粘连蛋白染色的毛细血管密度以及透射电子显微镜的超微结构发现。咬合不稳定在高架十字迷宫测试中引起类似焦虑的行为，而地西泮的给药阻止了这种行为的出现。单侧拔牙导致对侧肌肉中氧化纤维和毛细血管增加，肌浆网改变。慢性应激导致两侧糖酵解代谢增加、毛细血管密度降低和线粒体形态改变。这两个因素的结合导致肌肉的糖酵解模式和血液动力学变化。地西泮的药理学处理抑制了应激后翼内肌的变化。我们的研究结果揭示了一种预防性苯二氮䓬类药物治疗方法，可用于治疗影响咀嚼肌功能紊乱的应激和咬合不稳定情况。此外，还为慢性应激和拔牙如何参与咀嚼肌功能障碍的病理生理学提供了新的见解。
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