Nocturnal masseter muscle activity is related to symptoms and somatization in temporomandibular disorders

https://doi.org/10.1016/j.jpsychores.2012.07.008Get rights and content

Abstract

Objective

Temporomandibular disorders (TMD) have often been related to sleep bruxism and elevated nocturnal masseter muscle activity (NMMA). However, previous studies have revealed controversial results, and the role of somatization, depression and anxiety has not been studied in this context. The aim of this study was to investigate the association between NMMA and pain intensity, TMD related symptoms, somatoform symptoms, depression, and anxiety in chronic TMD.

Methods

Thirty-six subjects with chronic painful TMD, 34 subjects with pain free bruxism, and 36 healthy controls recorded their nocturnal masseter muscle activity during three consecutive nights with portable devices. In addition, participants completed pain diaries and questionnaires. Diagnoses were established using the research diagnostic criteria for TMD.

Results

Subjects with chronic TMD reported a reduced general health state (p < .001), higher levels of somatoform symptoms (p < .001), depression (p < .05), and anxiety (p < .001) compared to control subjects with or without sleep bruxism. The amount of NMMA did not differ significantly between the groups. In subjects with TMD, pain intensity was not related to NMMA. However, higher NMMA was related to higher intensity of jaw related symptoms such as headache or tinnitus, and higher somatization in general.

Conclusion

Chronic TMD is associated with elevated levels of psychopathology. These findings suggest a common link between NMMA, somatization, and symptom intensity in chronic TMD.

Introduction

Temporomandibular disorders (TMD) are a heterogenic group of conditions characterized by pain or dysfunction in the masticatory muscles and the temporomandibular joint [1]. Patients with TMD most frequently present with muscle pain or discomfort, limited mandibular motion, and temporomandibular joint sounds, but also report associated symptoms such as pain in head, neck, back and teeth, tinnitus or dizziness.

Bruxism is considered to be an important factor in the onset and perpetuation of TMD pain. However, findings depend on the type of bruxism studied and the methods used. Sleep bruxism (i.e., parafunctional clenching and grinding activities during sleep) and awake bruxism (i.e., oral parafunctions such as tooth contacting or lip sucking) seem to be two different phenomena [2], [3]. There is strong evidence that bruxism is related to TMD. Studies using ecological momentary assessment report higher frequencies of tooth contact in subjects with TMD compared to healthy controls [4]. Experimental research suggests that long lasting low level clenching might provoke muscle soreness and pain [1].

With respect to sleep bruxism, findings strongly differ between self-reported or clinically diagnosed bruxism on the one hand and instrumentally detected bruxism on the other. Studies support a positive association between self-reported or clinically assessed sleep bruxism and TMD symptoms in population-based surveys as well as in clinical samples [2], [3]. Sleep bruxism in childhood and adolescence emerges as a risk factor for TMD symptoms 20 years later [5]. Sleep bruxism itself has been associated with higher levels of anxiety, sleep arousals, and urinary catecholamines [6]. However, when sleep bruxism is assessed through polysomnography or electromyography, results are more controversial, with two studies reporting lower levels of sleep bruxism in the presence of myofascial pain [7], [8], one reporting higher levels of sleep bruxism [9], and four studies reporting no relationship [10], [11], [12], [13] (for an overview see [3]). On the other hand, two electromyography studies suggest that sleep bruxism is related to jaw dysfunction, joint sounds and tooth wear [14], [15].

Besides bruxism, psychological factors such as somatization and depression play an important role in the etiology of TMD [16]. Subjects with TMD often suffer from somatic complaints, and some authors have argued that chronic TMD can be understood as just another manifestation of somatoform pain disorder, with few factors specific to TMD [17]. Somatization is a risk factor for the onset and chronic manifestation of TMD pain [18]. A recent trial confirmed that somatization moderates treatment outcome [19]. Similarly, many subjects with TMD show high rates of affective and anxiety disorders as well as elevated levels of depressive and anxiety symptoms [20], [21]. Depression and anxiety are risk factors for the development of chronic TMD and contribute to its progression [22], [23].

To our knowledge, associations between sleep bruxism and psychological variables such as somatization, depression, and anxiety have not been investigated. Many subjects with TMD report other stress-related syndromes such as irritable bowel syndrome, premenstrual syndrome, chronic fatigue or fibromyalgia [24], [25], [26]. Nocturnal masseter muscle activity is positively related to elevated urinary catecholamine levels in subjects with TMD [27]. There is evidence that distress and dysfunctional coping strategies are related to sleep bruxism [28] and TMD [29]. Higher levels of distress and psychophysiological arousal might be reflected in higher nocturnal masseter muscle activity. Thus, exploring these associations may be important for a better understanding of underlying etiological mechanisms in TMD.

The present study had two aims. First, we aimed to examine differences in psychopathology (number of psychiatric disorders, somatization, depression, and anxiety) and nocturnal masseter muscle activity (NMMA) between subjects with chronic TMD, subjects with pain free bruxism, and healthy controls. We hypothesized that subjects with chronic TMD show higher levels of psychopathology compared to subjects with pain free bruxism; in turn, subjects with pain free bruxism are expected to have higher levels of psychopathology compared to healthy controls. We assumed that subjects with pain free bruxism show higher levels of NMMA compared with healthy controls, but refrained from formulating a directional hypothesis concerning the level of NMMA in TMD, because former studies have been rather inconclusive on this matter. Second, our aim was to investigate whether nocturnal masseter muscle activity was related to (a) pain intensity and TMD related symptoms, and (b) to psychopathology (somatization, depression, anxiety, and stress level).

Section snippets

Subjects

Initially, 117 subjects (age range of 18 to 40 years) were recruited for this study. Nine subjects (9.4%) had to be excluded due to incomplete EMG data, mainly due to loosened electrodes or failure to charge batteries. The final sample consisted of 106 subjects: 36 patients with chronic TMD (mean ± SD age = 27.4 ± 6.8 years), 34 subjects with pain free bruxism (mean ± SD age = 25.7 ± 4.5 years), and 36 healthy controls (mean ± SD age = 24.3 ± 5.8 years).

Subjects with TMD were consecutive patients from the Department

Demographic and psychological variables

Table 1 shows the demographic characteristics for the three groups. Subjects with chronic painful TMD reported a characteristic pain intensity of 5.5 (SD ± 2.1), and a mean pain duration of 31.2 months (SD ± 36.8). 29 subjects (81%) reported sleep bruxism. On average, they had consulted health care professionals on 6.8 (SD ± 6.8) occasions during the past 6 months and had received 3.6 (SD ± 2.9) different treatments for TMD. Subjects with chronic painful TMD did not differ from pain free subjects with

Discussion

The purpose of the present study was to explore associations between NMMA and psychopathology. Moreover, we aimed to compare levels of somatization, depression, anxiety, and nocturnal masseter muscle activity in patients with chronic TMD to subjects with pain free bruxism, and healthy controls. Our results show that patients with chronic painful TMD had more psychopathology compared to healthy control subjects with or without bruxism. Subjects with TMD showed higher levels of somatic

Conclusion

This study provides first evidence that nocturnal masseter muscle activity might be related to somatization and TMD related symptoms in chronic TMD. As one possible explanation for common features, the clinical overlap between chronic TMD pain and other somatic complaints may reflect a shared underlying pathophysiologic basis involving dysregulation of the hypothalamic-pituitary-adrenal stress hormone axis [54]. In other words, autonomic dysregulation might result in both elevated levels of

Competing interest statement

The authors have no competing interests to report.

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