Obstructive sleep apnea: a follow-up program in its relation to temporomandibular joint disorder, sleep bruxism and orofacial pain

Obstructive sleep apnea (OSA), affecting 9%—49% of the general population [1], is characterized by intermittent complete or partial collapse and obstruction of the upper airway during sleep, often accompanied by snoring, sleep structure disorders, nocturnal hypoxemia, daytime sleepiness and even apnea or hypopnea [2], which is associated with diverse comorbidities including hypertension, myocardial ischemia, stroke, arrhythmias, cognitive impairment, attention deficit and depression. Severe OSA even has an increased risk of all-cause mortality if left untreated in time [3, 4]. It has received more and more attention from respiratory medicine, otolaryngology, stomatology and other disciplines for its high morbidity and potentially fatal dangers [5]. A combination of factors accounts for the etiology and mechanism of OSA, including obesity, locally abnormal anatomy, impaired reflex mechanism of airway, unstable central respiratory regulation, and disordered neuromuscular function. Overnight full-channel PSG has been regarded as the gold standard for confirming and diagnosing OSA, allowing the quantitative recording of rhythmic masticatory muscular activity (RMMA), respiratory events, oxygen reduction events and other sleep parameters. Nasal CPAP is highly efficacious in keeping airway patency in OSA, as are oral appliances such as snore guard that hold the mandible in the forward position. Orthodontic and orthognathic treatment for OSA is also pretty vital, as the upper airway morphology is affected by craniofacial skeletal pattern [6]. For instance, an open bite accompanied by clockwise mandibular rotation influence the airway volume [7]; some congenital syndromes, eg. clefts, also have deformations within the upper airways and the nose itself [8, 9]. Under the circumstances, orthognathic surgery, mandibular advancement (MAD), rapid maxillary expansion (RME), et al. can significantly affect the upper airway morphology.

In addition to OSA, the disease sleep bruxism, orofacial pain and temporomandibular disorders (TMD) are also common in stomatological department [10, 11]. TMD is a collective term for a group of diseases referring pain conditions and functional jaw disabilities occurring, involving masticatory muscles, peripheral nervous system, and TMJs. Orofacial pain is the pain related with the hard and soft tissues of the head, face, and oral cavity [12], also including dental and TMD pain with significant influence on individual daily life, such as eating, drinking, and speaking [13]. Bruxism is a repetitive masticatory muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible [14]. It is not a movement disorder or a sleep disorder in otherwise healthy individuals, but it can be a risk factor for certain clinical conditions or be a concomitant symptom of certain disease [15]. The pathogenesis of them has not been fully clarified and various therapies can be used for symptom relief.

Clinically, patients are usually diagnosed with two or more with above diseases, but clinicians sometimes take stopgap measures for them, such as one single elastic dental pad, physiotherapy, surgery, acupuncture, etc. In other word, such patients often fail to obtain standardized, comprehensive and complete treatment due to the single department they visited. There are problems in the outpatient clinic such as unclear treatment procedures and lack of standardized treatment system, which can only be solved through interdisciplinary diagnosis and sequence therapies.

Interestingly, these diseases in fact interact with one another and reinforce one another. According to a recent investigation, chronic TMD patients had markedly impaired sleep quality than healthy controls [16]. The prevalence of TMD signs and symptoms is significantly higher in untreated OSA patients when compared to controls [17]. A long-term cohort study also reported that OSA was a risk factor for the occurrence of first onset TMD [18]. Back in 2009, Smith et al [19] had emphasized the need to refer TMD patients complaining of sleep disturbance for polysomnographic evaluation; Additionally, it has been noted that patients with OSA are more likely to experience sleep bruxism [20, 21], and that the relationship between OSA and sleep bruxism depended on the degree of severity of OSA [22, 23]. The possible mechanism is that muscles contract and relax in a regular manner to keep the upper airway open. In the long run, euphoria-induced muscular traction will result in occlusal alterations and sleep bruxism [24], and this excessive bite force caused by bruxism may cause muscle fatigue, orofacial pain, and abnormal pressure on TMJ. Of course, there still are studies with different results. One polysomnographic research reported that the intensity of bruxism is associated to muscle activity, but not to pain related to TMD [25]. Wieckiewicz et al. also indicated that the distribution of TMD among sleep bruxers and non-bruxers is similar [26]. When talking about the relationship between OSA and orofacial pain, OSA has been associated with a higher risk of chronic pain [27], particularly with musculoskeletal pain disorders [28‐30]. The patients with chronic orofacial pain proved to suffer from decreased sleep duration, increased stress and tiredness [31].

In order to carry out the interdisciplinary evaluation and comprehensive treatment for these diseases, understanding the association between OSA and TMD, bruxism, orofacial pain is very important, which would help provide references with new treatment options, would also help prevent and treat possible complications of OSA. However, limited study focused on the four diseases simultaneously, and such associations need further investigation and scientific evidence. The aim of this study is to explore whether OSA will affect sleep bruxism, orofacial pain and TMJ morphology, to explore if considerable OSA therapies have benefit in alleviating bruxism, orofacial pain and TMD symptoms, providing references for clinical practitioners. The null hypothesis is that no association would be found between OSA and TMD, bruxism, orofacial pain.

The intra-observer reliability of the measurements of all descriptions using SPSS software was from fair to good to excellent, with ICC’s ranging from 0.673 to 0.916.

With the transformation of the traditional medical model to the bio-psycho-social medical model, the goal of oral disease treatment is to restore the morphology and function of the oromaxillofacial region to the best on the basis of multidisciplinary cooperation. Clinicians ought to provide patients with a suitable bite, to help them regain favorable chewing, swallowing, pronunciation and respiratory functions, while maintaining the continuous stability of the efficacy. OSA, TMD, bruxism, and orofacial pain are multidisciplinary and sometimes they may appear concomitantly without standardized, comprehensive and complete treatment. In order to explore comprehensive treatment for these diseases, understanding the association between OSA and TMD, bruxism, orofacial pain can help a lot, which would help provide references with new treatment options, or even prevent and treat possible complications of OSA.

The pathogenesis of sleep bruxism has not been fully clarified, which is related to emotional stress, anxiety disorders, OSA, consumption of certain groups of drugs, tobacco, alcohol, or coffee, and so on [38]. Long-term severe tooth grinding without treatment can lead to complications such as tooth sensitivity, periodontitis, dental fracture, and pulpitis. Sleep bruxism has been considered as a sign of a disorder in some healthy people, be regarded as a motor behavior with multifactorial etiology that can be a risk factor for a state of sub-health or certain diseases such as tooth wear, TMD, headaches, fatigue or pain in the masticatory muscles, and poor quality of sleep [39‐41]. Recently, the association between OSA and sleep bruxism has drawn much attention, that is to say, OSA is considered as a new risk factor for sleep bruxism [42]. Currently, the treatment of sleep bruxism is limited to elastic dental pads to avoid extensive, continuous tooth wear at night. The result of this study indicated that considerable treatment of mild and moderate OSA may be beneficial in reducing sleep bruxism, as the wear score didn’t increase any more after OSA treatment. In the future, maybe clinicians can give other unconventionally potential treatment methods a try, especially when OSA and sleep bruxism associated together, such as biofeedback. Gender and BMI of our study groups were significantly different, but it is now generally accepted that there notably no differences between female and male, and just prevalence decreases with increasing age [43]. The association between BMI and bruxism is also negligible. So, we can conclude the difference may have no influence on the results.

One of the hypotheses connecting sleep bruxism and OSA is that bruxism at night plays a protective role against OSA by protruding the jaw and restoring upper airway patency [44, 45]. The mandibular depressors such as genioglossus will occur rhythmic movements, and the subsequent RMMA resulting in mandibular protrusion and opening of the airways [46]. On the other hand, oromaxillary muscles in the state of euphoria traction may lead to occlusal changes and become one of the causative factors of bruxism [20]. So, bruxism may be a secondary manifestation with OSA, that is to say OSA is a risk factor for sleep bruxism. However, Sjöholm [47] reported this mechanism was not adequate to prevent the airway from collapsing in too severe OSA, as individuals with severe OSA have significantly less deep sleep. That is inconsistent with the results of our study, and we suspected the race factor might explain the discrepancy, which need to be justified by the divergent pattern of sleep structure in patients with different degrees of severity of OSA.

Chronic widespread pain with psychologic factors, increasing age, and female gender are risk factors for chronic orofacial pain [48, 49]. Orofacial pain is in connection with high morbidity, negative social effects, and high medical expense if not accurately diagnosed and managed. People coming to the clinic often complain about headache, neck pain, vertigo, tinnitus, phonophobia, photophobia, strange taste, or bruxism [50]. Sometimes there is no good treatment other than massage and physical therapy. Our results showed that no treatment of moderate and severe OSA may aggravate myofascial pain and arthralgia. The significant reduction of VAS value six months after reasonable OSA therapies also indicated OSA treatment sometimes can relieve orofacial pain although no statistical significance was observed in the mild group. In addition, Spearman correlation analysis displayed that AHI value was positively correlated with VAS value. We assume that the following reasons may account for such phenomenon.

A famous hypotheses connecting sleep pain and OSA is that sleep deprivation and recurring nocturnal hypoxemia in OSA individuals during sleep would enhance pain sensitivity, promote inflammation, and increase spontaneous pain [51‐53], would lead to myalgia, tenderness, and chronic fatigue. Choy [54] reported that sleep deprivation and fragmented sleep impairs descending pain-inhibition pathways that are crucial for controlling and dealing with pain. Besides long-term tooth grinding may cause fatigue, tenderness, and tension pain in the masticatory muscles.

Main symptoms of TMD are pain, joint friction, irregular or limited mandibular function. The current mainstream non-surgical therapies of TMD include hard occlusal splint therapy, counselling, exercises, massage, manual therapy, and so on. Psychosocial factors, immunity, occupational strain, TMJ overload and its anatomical factors are recognized as important risk factors of TMD among adults [55]. Furthermore, certain previous studies also have elaborated the relationships between OSA and TMD [16, 17, 56‐58]. Alessandri et al. reported that the prevalence of TMD signs and symptoms is significantly high in untreated OSA patients [11], which is consistent with our study. Our results indicated that no treatment of moderate and severe OSA may lead to a decrease in the condylar volume and superficial area. After OSA treatment, the decrease of condylar volume and superficial area in moderate and severe group stopped along with a decreased R value. In addition, Spearman correlation analysis displayed that AHI value was negatively correlated condylar volume and superficial area. It can be considered to provide new references for TMD therapies based on this association. In other word, OSA treatment may be effective in reducing the morphological changes of TMJ.

Gender plays a controversial role in the occurrence and development of TMD. Although it is now generally accepted that TMD and orofacial pain are more common in female, several researches were inconsistent with such consensus. Razi et al. reported there was no significant relationship between condyle morphology and gender [59]. Görürgöz et al. thought being male was associated with radiographically detectable degenerative findings in the mandibular condyle [60]. In our study, gender has statistical differences in the three study groups. Contrary to that consensus, severe group had a more absorbed condyle and higher VAS, but the group also contains more male. From this, we hypothesized the gender difference didn't affect our results.

We analyze that bruxism may be related in TMD occurrence and development. It is possible that in people with OSA, apnea and hypopnea resulted from the airway collapses and obstructs will produce an abnormal muscle environment and varying degrees of neuromuscular dysfunction. TMJ is subjected to abnormal stress and pulling force that is different from that of normal people under such neuromuscular dysfunction. By this time the fragile condyle, condylar neck, and joint disc may shift, finally leading to TMJ injury. Diatchenko [61] indicated that people with OSA have an increased stimulation of the sympathetic nervous system, that underlies an incremental risk of developing first-onset TMD [62].

There are certain limitations of this follow-up analysis. Not every subject has been recorded with RMMAs during PSG examination, and no other bruxism instrumental method was performed. Only self-reported assessment was used in the study is a limitation; Gender and BMI have statistic differences in the three groups. Although we believe the impact of this point is small enough, whether the results dependent on gender and BMI will be investigated in our next study. However, despite causality couldn’t be inferred from observational data alone, the findings from this research could imply that OSA contributes to the onset of sleep bruxism and orofacial pain to some extent, which could still provide important clinical references.

Moderate to severe OSA is a risk factor for orofacial pain, sleep bruxism and condylar absorption, which affect condylar volume and superficial area. Appropriate OSA therapies may be effective ways to relieve orofacial pain, reduce tooth grinding at night, and prevent condylar absorption in the long run.