Psychological aspects, the existence of subjectively perceived sleep problems, or objective sleep indices examined by portable PSG could affect TMD symptom severity in different ways in acute and chronic TMD. In our study, PI was significantly higher in patients with chronic TMD than in those with acute TMD. Interestingly, patients with chronic TMD were psychologically more vulnerable than those with acute TMD. The eight psychological subscales of SCL-90R, except for PAR, including SOM, O-C, I-S, DEP, ANX, HOS, PHOB, and PSY, had significantly higher values in chronic TMD than in acute TMD. Furthermore, OSA was observed in many patients with TMD (n = 32, 62.7%). In the multiple regression analysis, the 'TMD group' was not a significant predictor of OSA. PI was the strongest predictor of OSA (OR = 17.550), followed by psychological stress (OR = 12.226), self-reported sleep problems (OR = 10.222), and DEP (OR = 1.443). In acute TMD, the decrease in the lowest SpO2 value and an increase in CAI were correlated with an increase in the PI score. In chronic TMD, an increase in REI was correlated with an increase in DI.
The severity of temporomandibular myofascial pain, measured by PI, was significantly higher in the chronic TMD group than in the acute TMD group. Conversely, DI, which quantifies TMJ pain and dysfunction, did not differ between the acute and chronic TMD groups. As TMD pain becomes chronic, the effect of pain of myogenous origin rather than arthrogenous origin may increase. TMD pain of myofascial origin is difficult to diagnose and treat and is considered a chronic pain disorder 21. The overall prevalence of myofascial TMD pain is up to 45.3%, and TMD itself is also commonly considered a chronic pain condition 22. General treatment of temporomandibular myofascial pain in our clinical environment combines pharmacological therapy, stabilisation splint therapy, cognitive therapy, and meditation, which produces relief of symptoms. However, no consensus protocol for the treatment of temporomandibular myofascial pain has been established. In our previous study, myofascial pain was associated with poor sleep quality in patients with chronic TMD 8. More approaches to sleep and biopsychosocial aspects are needed to manage TMD pain of myogenous origin.
The pathophysiological mechanism of TMD has shifted from a mechanistic-based theory to a biopsychosocial model, particularly in patients with chronic TMD 23,24. In the present study, the distribution of TMD contributing factors, such as bruxism and history of macrotrauma, did not differ significantly between acute and chronic TMD. According to the International Classification of Sleep Disorders, the classification criteria for sleep bruxism include the objective signs and symptoms observed by clinicians 25. However, this study was conducted based on self-reported bruxism and its interpretation was limited. Unsolved psychological problems such as anxiety and depression can cause an increase in muscle tension that can lead to tooth clenching or bruxism, which in turn can lead to the onset and persistence of TMD 9. In addition, macrotrauma, such as whiplash injury, may be associated with the chronicity of TMD pain because a series of peripheral and central sensitisation and psychological damage from macrotrauma occur 26,27. In this study, a macrotrauma history did not increase the risk of OSA and did not significantly affect the symptom severity of TMD.
OSA is a common sleep disorder that leads to hypoxemia and sleep fragmentation. Interrupted breathing attributed to OSA leads to a reduced level of oxygen in the blood, which can trigger inflammation 28. OSA has been associated with many medical conditions, such as cardiovascular diseases, juvenile idiopathic arthritis, and neuromuscular disorders 29,30. OSA patients with chronic pain also have higher pain levels, higher disability levels, and lower quality of life 31. OSA more than tripled the incidence of chronic TMD in a previous OPPERA study 32. Sleep disturbances due to hypoxia and sleep fragmentation reliably predict new occurrences and exacerbations of chronic pain 33. In this study, the prevalence of OSA in patients with TMD was 62.7%, and it occurred more frequently in patients with chronic TMD (68.0%) than in those with acute TMD (57.7%). Regarding the occurrence of OSA in patients with TMD, abnormal movement of the lower jaw can increase the myofascial pain intensity and tightness of the surrounding muscles 34. Only in chronic TMD was the increase in REI correlated with an increase in DI. Poor sleep quality is very common in patients with TMD and has been observed in up to 90% of patients 35. OSA is a common comorbidity in the general population with chronic pain, with an overall prevalence of approximately 37%, and is reported to be approximately 29% in patients with TMD 36. Poor sleep quality was strongly associated with chronic TMD pain 8. However, the relationship between OSA and TMD chronicity was unclear in this study.
Furthermore, the PI score was the strongest predictor of OSA (OR = 17.550) in patients with TMD, followed by psychological stress (OR = 12.226), self-reported sleep problems (OR = 10.222), and DEP (OR = 1.443). Myofascial pain in TMD is associated with a mild increase in sleep fragmentation 37. In acute TMD, the decrease in the lowest SpO2 value and an increase in CAI were correlated with an increase in the PI score. Repeated intermittent hypoxia or ischaemia ultimately leads to muscle damage 38. Decreased sleep quality, pain, and psychological vulnerability interact inseparably with each other. Compared with healthy controls, patients with OSA had more perceived psychological stress, and stress was closely related to anxiety and depressive symptoms 39. Furthermore, psychological stress contributes to the formation of trigger points for pain-causing muscle tension and myofascial pain 40. Although somewhat complicated, clinicians should always consider the effects of nocturnal hypoxemia and fragmented sleep during OSA on pain intensity in patients with TMD inpatient screening. Furthermore, based on the biopsychosocial model, factors such as psychological stress, depression, and myofascial pain should be considered in patients with chronic pain. More studies are needed to determine how each of the various factors affects acute and chronic TMD and how they have complex correlations.
This study had several limitations. Although the portable SPG device has a simpler configuration than the general PSG, patients still feel uncomfortable even when they fall asleep with the device installed on their body in a comfortable environment at home. This discomfort caused a decrease in the total sleep time and monitoring time. Additionally, since this study was conducted on patients who agreed to perform portable PSG among those who visited during the study period, bias may have occurred in selecting patients with TMD.