Temporomandibular Joint Disorder is Not a Dental Problem

Temporomandibular joint disorder (TMD) has classically been considered a disease of dental origin despite a lack of supporting evidence.¹

Medical practitioners encountering temporomandibular joint disorder most often include those in primary and urgent care settings. Patients present with complaints of headache, facial and jaw pain, and occasionally tinnitus.² Medical treatment has focused on conservative self-care although high-quality data is limited.³  

Mouthguards for TMJ Pain?

The most common intervention after conservative care, such as moist heart and a soft diet, includes referral to a general dentist or another odontologist for fabrication of an occlusal splint.^2,4,5 The supposed mechanism behind this approach is the creation of mechanical disadvantage and/or masking a triggering malocclusion.^6,7 Unfortunately, many primary care providers do not realize that data on the efficacy of this treatment is controversial at best and contradictory at worst.^2,4,8

One recent meta-analysis on the topic of occlusal splint use in patients with temporomandibular joint disorder, for example, was based on very low to moderate quality evidence.³ Another recent systematic review showed absolutely no benefit to occlusal splints in the treatment of TMD pain.³ 

If dental splints are not effective in the long-term treatment of bruxism and TMD-related pain, is it possible that the etiology lies outside of the oropharynx? 

Grinding Teeth and Poor Sleep

Kato, et. al. suggest that nocturnal bruxism, a potential driver of temporomandibular joint disorder, is preceded by characteristic neurological and cardiovascular events such as an increase in heart rate and cortical EEG activity.^9,10 Bruxism appears to be the result of micro-arousals during slow-wave sleep.^9,10 Not every patient who grinds or clenches their teeth, develops temporomandibular joint disorder, however. 

As new evidence emerges showing central vs peripheral regulation of bruxism, there is interest in moving away from less effective, expensive, and poorly tolerated dental appliances and moving toward a treatment that modifies the underlying etiology.^8,9,11–16 Some experts now consider temporomandibular joint disorder to be on a spectrum of fibromyalgia-like disorders. The unifying mechanism is disordered pain processing and central sensitization now referred to as nociplastic pain.

As bruxism and temporomandibular joint disorder are accepted as a parasomnia, or perhaps a manifestation of fibromyalgia (FM) vs dental malocclusion, the goal of treatment should be aimed at decreasing microarousals, improving slow-wave sleep, and optimizing pain processing and maladaptive behaviors. Centrally-acting medications such as tiagabine, gabapentin, amitriptyline, clonidine, and clonazepam, among others, have all shown promise in either decreasing micro-arousals and improving slow-wave sleep or modulating pain processing in the CNS thus reducing bruxing behavior and TMD-related pain and dysfunction.^8,9,12,15

Nocturnal biofeedback has also been explored as a method to intercept efferent signaling before a bruxing episode is triggered.^13,16,17

With many questions still unanswered, this paper aims to answer the following: What should be the focus of TMD-related research going forward, and is it time to rethink our current treatment strategy?

Methodology

This qualitative exploratory research was conducted through PubMed searching for keywords including temporomandibular disorder, bruxism, occlusal splint, and malocclusion. Cited works include those published since the year 1970. Preference was given to the latest published works as well as systematic reviews and meta-analyses. Descriptive analysis is utilized to summarize emerging characteristics, patterns, and correlations between temporomandibular joint disorder, its neuromuscular origin, and its similarity to other chronic pain states such as fibromyalgia.   

List of keywords: temporomandibular disorder, bruxism, occlusal splint, malocclusion, facial pain, chronic headache, myofascial pain

Literature Review

Alqutaibi and Aboalrejal explained in 2015 how oral splints were theorized to treat temporomandibular joint disorder pain.⁷ They also point out the flaws in that theory. The authors stated that oral splints are considered as deprogrammers or jaw repositioners intended to create an ideal contact between the maxillary and mandibular teeth which is believed to alleviate pain. The authors point out that this theory makes several unfounded assumptions: 1) TMD pain is principally related to malocclusion; 2) oral splits alter multiple occlusal relations; 3) oral splints can lead to permanent modifications to the patient’s bite.⁷ Besides potential alterations of the teeth, previously reported by Conti in 2012, oral splints have also been found to worsen sleep apnea.^18,19

The idea of dental malocclusion as a primary driver behind TMD pain was addressed by Scrivani, et.al. in 2008 where the authors found little evidence to support that hypothesis.²⁰ The authors suggest that obvious deficiencies, such as missing teeth, should be addressed to improve masticatory function but that occlusal interference as the etiology of TMD pain was not supported by evidence.

The Argument for Mouthguards in Temporomandibular Joint Disorder

In 2020 Al-Moraissi, et. al. conducted the first meta-analysis evaluating oral splint therapy with 48 RCTs comparing various oral splint types with or without counseling to an untreated control.³ The duration of follow-up was <12 months. Patients were identified as having either muscular,  arthrogenous or mixed pain. The primary outcome was pain intensity; secondary outcomes were masticatory muscle tenderness. The authors found that occlusal splints were likely to be more effective in TMD treatment than the untreated control.³

However, the evidence of Al-Moraissi, et. al ranged from moderate to very low-quality due to lack of blinding, attrition bias, lack of allocation concealment, and imprecision due to small sample size and crossing the null hypothesis (suggesting the low likelihood of reproducibility and statistically insignificant differences between treatment arms).^3,21 

No Evidence for Mouthguards in TMJ Treatment

In 2020, Fouda analyzed 22 studies in a systematic review that came to the opposite conclusion as Al-Moraissi, et. al.²¹ The primary outcome was pain intensity while the secondary outcome was maximal mouth opening. In short-term follow-ups (<3 months) of oral splint therapy, there was no significant impact on pain reduction. Behavioral therapy was associated with the most significant pain reduction in long-term follow-ups (>3 months, <1 year). Any small effect of splint therapy was lost in long-term follow-up. The author concludes that myofascial pain cannot be managed with oral splint therapy when compared with placebo or no treatment.²¹ Seeming short-term improvements were thought to be due to the placebo effect or the natural resolution of the condition.  Oral splints may inhibit dental damage related to bruxism, however.

Fouda was not the first to demonstrate the ineffectiveness of oral splints for TMD pain. Macedo, et. al. published a systematic review in 2007 that concluded there was insufficient evidence that oral splints reduced nocturnal bruxism, one possible source of TMD pain.²² The authors did find, however, that oral splints could help protect the teeth from wear. Harada confirmed that objective EMG changes, which measure bruxing behavior, were transient and not sustained in oral splint users which speaks to their inadequacy as a core treatment modality.²³

Why Evidence Matters

Reviewing several of the studies that Al-Moraissi, et.al included in their meta-analysis is enlightening. Dao and colleagues reported in 1994 that the beneficial effects of three different oral splint types were likely related to the placebo effect, spontaneous remission or the natural course of the condition, a conclusion also reached by Ismail in 2007.^5,25

Several papers included in Al-Moraissi’s optimistic analysis concluded that oral splint therapy was no more effective than physical therapy or self-care with Truelove suggesting that most patients should be treated with self-care measures and not oral appliances.²⁶

Mental Health and TMJ Pain

According to Turk, depression plays a significant role in TMD; depression is correlated with chronic pain in general.¹⁷ Ebrahim, et. al. found in a 2012 systematic review that although there might be a benefit in pain reduction compared to placebo, oral splints had no positive impact on quality of life or depression in patients with TMD.²⁴ Affective symptoms are common in fibromyalgia and other chronic pain states.

Somatization is an outward expression of depression and anxiety. Ohlmann, et. al. suggest that somatization is a stronger predictor of a TMD diagnosis than sleep bruxism. They state, “Subjects with painful TMD often exhibit an emotional personality with high to moderate levels of somatization and/or depression, suggesting that factors other than sleep bruxism might contribute to TMD pain.”

Medications to Treat Bruxism and TMJ Disorder

Cyclobenzaprine had been found to have a positive effect on TMD-related pain and gabapentin was found to be equivalent to splint therapy at two months.^12,14,27 Madani, et. al. found that gabapentin was also effective for nocturnal bruxism, though as previously stated, not all bruxers develop TMD.¹⁴ Gabapentin was also associated with improved sleep quality, another familiar complaint in FM patients.¹⁴

Other medications found to reduce either nocturnal bruxism or TMD pain include clonidine, clonazepam, and tiagabine.^8,9,12,15 Huynh, et. al. concluded that clonidine decreased sympathetic tone just prior to bruxing episodes and is theorized to prevent motor activation by the autonomic nervous system.¹⁵ Kast found that tiagabine had completely stopped teeth grinding as well as morning jaw and tooth pain in several individuals.⁹ Rizzatti-Barbosa, et. al. added that amitriptyline, another agent used for chronic pain of many types, proved to be effective for chronic pain in TMD patients.¹¹ Tricyclic antidepressants, such as amitriptyline, as well as their more favorably tolerated successors, the serotonin-norepinephrine reuptake inhibitors (SNRIs), are cardinal treatments in fibromyalgia. The SNRI duloxetine has FDA indications for diabetic neuropathy and chronic musculoskeletal pain.

Many of these agents are older with significant side effects. Dry mouth, constipation, weight gain, and somnolence are not uncommon. But the therapeutic effect of centrally acting medications speaks to the neurological and psychiatric underpinnings of TMD. This coincides with Turk’s observations that chronic TMD pain is often accompanied by comorbid depression.¹⁷ Aggarwhal, et. al. summarized that CBT and other psychosocial interventions should always be part of TMD care.¹³ Exercise and cognitive therapies are first-line interventions in the management of FM pain.

Discussion

Given the lack of evidence for dental malocclusion as the origin of TMD pain and the contradictory evidence of oral splints as an effective treatment option, it stands to reason that clinicians should investigate alternative treatment options. TMD may very well be on a spectrum of fibromyalgia-like disorders with its chronic pain and neuropsychiatric features. 

Once conservative, self-care measures have been exhausted, clinicians should carefully consider their next steps. Oral splint therapy has not been conclusively shown to provide meaningful, long-lasting relief of TMD pain.^{2,21,23,24,26} In addition to reconsidering de facto prescriptions for oral splint therapy, clinicians should avoid procedures that permanently alter the bite.² 

Clinicians dealing with TMD pain should recognize nocturnal hyperarousal and alterations in slow-wave sleep as potential causes of bruxism and TMD-related dysfunction. Patients should be screened for depression, unrefreshing sleep, fatigue, and cognitive slowing. A diagnosis of fibromyalgia may be more explanatory. 

The decision to refer patients with TMD pain to a dental professional should be carefully weighed in light of the evidence. Oral splints are rarely covered by insurance and can cost well over a thousand dollars. Procedures that permanently alter occlusal relationships are not recommended. 

Conclusion

The strength of this analysis is that it used a patient-centered approach rather than focusing on statistical significance. Special attention was given to results that would meaningfully and enduringly affect even a single patient’s quality of life.  

The weakness of this commentary includes a practical inability to critically dissect all available research on the subject of TMD pain and oral splint use. Studies using oral appliances are difficult to blind and are inherently subject to bias. The author’s own experience and bias toward medical vs dental interventions are also relevant. 

Future research should aim to better understand the neuromuscular origin of TMD pain and associated neuropsychiatric symptoms. Biofeedback is a poorly researched and underutilized intervention that could complement other cognitive and behavioral therapies which are essential in the treatment of TMD and other chronic pain states. Future research should also identify pharmacotherapeutic agents for the management of chronic nociplastic pain that are better tolerated.