Gómez F M, Areso M P, Giralt M T, Sainz B, García-Vallejo P
Department of Stomatology, Faculty of Medicine and Odontology, University of the Basque Country, Leioa, Vizcaya, Spain.
J Dent Res. 1998 Jun;77(6):1454-64. doi: 10.1177/00220345980770061001.
Observational methods and the recording of nonspecific jaw movements or masticatory muscle activity have been used to evaluate oral parafunctional movements in animal models of bruxism. In this study, we have used a new approach in which the non-functional masticatory activity in the rat was assessed by the measurement of incisal attrition, with the aim of investigating the role of diverse factors involved in the etiology of bruxism. We quantified the attrition rate weekly by making superficial notches in the lower incisors and measuring the distances to the incisor edges. Repeated stimulation of the dopaminergic system with apomorphine led to an enhancement of the non-functional masticatory activity (p < 0.0001). The severity of the apomorphine-induced oral behavior was positively correlated (r(s) = 0.69, p < 0.01) with an increase in the incisal attrition rate (20.9%, p < 0.0001). Apomorphine-induced non-functional masticatory activity was strongly enhanced by the placement of an acrylic cap on both lower incisors (306%, p < 0.0001), but not by the cutting of a lower incisor. Repeated cocaine administration also increased the attrition rate (22.5%, p < 0.0001). However, neither chronic blockade of dopaminergic receptors with haloperidol, nor its withdrawal, modified attrition. In addition, since emotional disturbances are considered to be causal factors of bruxism, we tested whether experimental stress might accelerate tooth wear. Exposure to two different chronic stress regimes did not induce significant changes in incisal attrition. Moreover, exposure to chronic stress after the withdrawal of chronic haloperidol treatment did not alter attrition either. These results partially support the role of the central dopaminergic system in bruxism and suggest that stress, in general, may not be a relevant factor in tooth wear.
观察方法以及非特异性下颌运动或咀嚼肌活动的记录已被用于评估磨牙症动物模型中的口腔副功能运动。在本研究中,我们采用了一种新方法,即通过测量切牙磨损来评估大鼠的非功能性咀嚼活动,目的是研究磨牙症病因中各种因素的作用。我们每周通过在下切牙上制作浅切口并测量到切牙边缘的距离来量化磨损率。用阿扑吗啡反复刺激多巴胺能系统导致非功能性咀嚼活动增强(p < 0.0001)。阿扑吗啡诱导的口腔行为严重程度与切牙磨损率的增加呈正相关(r(s) = 0.69,p < 0.01)(增加20.9%,p < 0.0001)。在下切牙上放置丙烯酸帽可强烈增强阿扑吗啡诱导的非功能性咀嚼活动(306%,p < 0.0001),但切断一颗下切牙则不会。反复给予可卡因也会增加磨损率(22.5%,p < 0.0001)。然而,用氟哌啶醇慢性阻断多巴胺能受体及其撤药均未改变磨损情况。此外,由于情绪障碍被认为是磨牙症的病因,我们测试了实验性应激是否会加速牙齿磨损。暴露于两种不同的慢性应激方案均未导致切牙磨损出现显著变化。此外,在慢性氟哌啶醇治疗撤药后暴露于慢性应激也未改变磨损情况。这些结果部分支持了中枢多巴胺能系统在磨牙症中的作用,并表明一般而言,应激可能不是牙齿磨损的相关因素。