This is the first study to comprehensively investigate and measure sleep quality with PSQI in chronic TMD patients who were diagnosed based on RDC/TMD and DC/TMD Axis I. Our findings in the present study imply that chronic state TMD patients had poorer sleep than healthy controls, and the magnitude of impaired sleep was associated with increased age, female sex, certain subtypes of TMD diagnosis, including myofascial pain and headache attributed to TMD, and the number of TMD diagnoses in a person. Regarding summary scores and cut-off values of each questionnaire, the presence of EDS was a significant predictor for the poor sleep quality in cTMD patients, whereas the high risk for OSA was not a major predictor.
The cause of chronic TMD is varied, and its localization, and clinical characteristics are vaguer than with acute pain. Chronic TMD is typically associated with joint dysfunctions such as disc displacement with or without reduction [22], and psychological distress [23]. It is difficult to infer a causal relation between sleep and chronic pain; patients with chronic pain commonly suffer from poor sleep quality [32]. Approximately 45.5% of patients with chronic pain suffer from sleep disorders, and older age was significantly associated with pain experience [7]. In this study, 56.9% of the cTMD group met the proposed cut-off of 5 of PSQI for poor sleep, compared to 22.2% of the control group that had impaired sleep. The proportion of TMD patients with poor sleep (56.9%) in our study is higher than the rate reported among adults with TMD (43.3%) in other studies [33,34] but lower than those in other studies involving older TMD patients (69.6-90.0%) [16,35].
The etiology of chronic TMD fundamentally related to peripheral and central factors together. Peripheral factors of TMD include inflammatory processes, including synovitis and myositis, infection, or irritation. Peripheral factors are the main cause of acute pain, but as the pain becomes chronic, the importance of the central factor increases [36]. Central factors include sleep deterioration, impairment of psychological health, and dysfunction of central pain inhibitory system [37,38]. Furthermore, central sensitization is a key characteristic of chronic pain presented as hypersensitivity, particularly tactile allodynia, hyperalgesia, and enhanced temporal summation [39,40], which commonly presents in chronic TMD patients. As in other idiopathic pain disorders such as fibromyalgia and irritable bowel syndrome, TMD patients frequently present with overlapping signs and symptoms of sleep disorders [41].
Sleep quality of cTMD patients was more impaired by increased age. In the present study, the increase of age (OR = 2.551, 95% CI = 1.662–3.917) was the most powerful predictor for poor sleep, and female sex (OR = 1.885, 95% CI = 1.193–2.978) was followed. In young adults, consolidated sleep at night and wakefulness during the day emerges from a balance between the brainstem, hypothalamus, and midbrain[42]. In older adults, this operation is not effective, and decreased sleep duration, increased sleep latency, impaired sleep quality, shallow sleep, and changes in sleep structure can lead to sustained or deepening pain [43]. In addition, sleep patterns and structures are known to change across the lifespan, with up to 50% of older adults report difficulties initiating and/or maintaining sleep [44]. Chronic sleep disturbances are considered as indications of poor health, vice versa, older adults commonly suffer from pain syndromes, arthritis, hormonal changes, neurodegeneration, psychological distress, cancer, renal and urologic diseases, and medical comorbidities all of which can contribute to sleep disorders [45]. Thus, older adults with cTMD are less likely to get enough rest and recovery through sleep than younger ones.
Female sex was also a major contributor to poor sleep quality in cTMD patients. There is limited recent evidence of interactions among sex, TMD chronicity, and sleep. However, it has been found that females shows higher clinical and experimental pain sensitivity, and worse sleep impairments than males [2]. Few probable causes for poor sleep quality in the female sex may be explained based on sex differences concerning mechanisms of pain of the craniofacial system [46]. Furthermore, contribution of female sex may reflect changes of systems beyond the physical axis of the orofacial area and in line with the biopsychosocial model, blending centrally mediated factors. Especially in postmenopausal female, an increase in sleep problems may be associated with the presence of noticeable hormonal changes, age-associated changes in sleep and psychosocial distress [2]. In clinical research, females reported TMD symptoms, headache, and had muscle tenderness and joint sounds more often than males [47]. It will be crucial to determine whether the effect of sleep on chronic TMD pain, and vice versa, is moderated by key demographic variables, such as age or sex.
EDS was a significant predictor for poor sleep in chronic TMD patients. In our study, EDS was more prevalent in chronic TMD patients than in healthy controls (19.7% vs. 12.8%, p < 0.05), and its OR value for poor sleep quality was 1.069. Our EDS prevalence was higher than the prevalence among the general population (12–16%) [48], and lower than 28.57% of TMD patients, the rate previously reported [49]. The discrepancy may have occurred due to differences in age distribution, race, and method of study. In older adults, they are prone to have daytime napping and EDS and the presence of comorbid conditions such as chronic pain, sleep disorders, and frequent nighttime urination breaks [50]. Diminished melatonin secretion and a reduced circadian modulation of rapid-eye-movement sleep and less pronounced day-night differences in the lower alpha activity occurs in the older group [51]. Furthermore, females are more likely than males to have more trouble sleeping at night and experience EDS [52]. Thus, EDS in cTMD may have different underlying mechanisms of a homeostatic drive for sleep and pain control systems according to age and sex. Hence, it is necessary to consider age-and sex-related differences in cTMD patients to obtain accurate results translation.
Headache attributed to TMD was associated with an increase of PSQI global scores, and a significant predictor for poor sleep. As headaches are a common symptom of accompanying TMD [53], few research has been done on the nature of headache attributed to cTMD. Headache can promote sleep disturbances, and sleep disturbances can also precede or trigger a headache attack [54]. Moreover, sleep deterioration has been associated with an increased risk for headaches, and in individuals with chronic headaches, shorter sleep duration has been associated with more severe pain [55]. Of course, the underlying pathophysiology contributing to the close association and complex relationship among headache attributed to TMD, headache disorders, and sleep disorders are not fully explained. There may be complex bidirectional relationships, and can be explained by peripheral and central sensitization, malfunctions of neuroendocrine, immune, and vascular system, and even gene polymorphism.
Myofascial pain was also associated with poor sleep quality in cTMD patients. Similar to our study, the substantial influence of myofascial pain on poor sleep quality in patients with TMD was documented [56]. Other researchers also observed a higher impact in patients with myogenous complaints than those with disc disorders [57,58]. While joint pain is characterized by a well-defined inflammatory process, chronic muscle pain presents with enigmatic pathophysiologic mechanisms, of which central sensitization is the common factor unifying these conditions [59]. In addition, females have more pain and widespread pain in more body areas than males, which may be related to their worse quality of sleep [60]. Therefore, depending on the subgroup of TMD, the mechanisms by which TMD signs and symptoms occur are different, and further investigation is needed on the effects on sleep quality.
Finally, the quality of sleep was lower in cTMD patients with multiple diagnoses than in patients with a single diagnosis. According to Gil-Martínez et al., patients with mixed pain, having arthrogenous and myogenous origin simultaneously, showed greater craniomandibular and neck disability than patients diagnosed with chronic joint pain or muscle pain only [61]. Patients with headache and TMDs reported significantly higher levels of pain and disability compared to patients with only TMDs [53]. These findings can be interpreted as increasing the number of TMD subgroup diagnoses can increase the severity of TMD symptoms. Overall, chronic TMD symptoms and multiple diagnoses may have a bidirectional cross-correlation, which can impair sleep quality. Chronic TMD, especially myofascial pain, headaches attributed to TMD, and sleep disturbance factors, may share the mechanism of occurrence and exacerbation.
Limitations of this study include the case-control study design, which cannot address a causal direction of effects and suggests only associations/correlations between the variables. A study design with repeated polysomnography (PSGs) may be more powerful in detecting phase‐related differences. Instead of using PSG, we used self-assessment measures of sleep due to feasibility and convenience, especially because of our large sample size. PSG is an objective measure of biophysiologic sleep parameters, so we are planning further studies to expand our findings with PSG. In addition, to get a deeper understanding of the relation between cTMD and poor sleep quality, we need to investigate their biopsychosocial aspects; however, this study did not evaluate psychological distress in patients with cTMD. Further studies on the psychological aspects of cTMD patients are ongoing.