The Biopsychosocial Model for Diagnosis and Treatment of TMDs: A Review.

What is the biopsychosocial model of diagnosis and treatment of TMDs?

George L Engel proposed the biopsychosocial model of diagnosis and treatment to incorporate the biological, psychological and social behavioral dimensions of illness in 1977.¹ According to Jones et al it was intended to incorporate the biological, psychological and social factors of health into one combined approach.² The creation of a biopsychosocial approach requires respecting all three aspects.³ However, according to Sadler & Hulgus, a key factor that cannot be evaded is that many patient-reported symptoms are undifferentiable between these three types potential etiologies, especially when faced with syndromes and idiopathic conditions where there is no consensus with respect to etiology. Consequently, it is accepted in psychotherapy in general that physical (biological) etiologies must be eliminated before psychological or social causes can be taken seriously.⁴ Thus, before any patient can be diagnosed as a somatic symptom disorder (SSD) or a social anxiety disorder (SAD),⁵ the presence of all possible physical etiologies must have been ruled out. The same consideration should be applied to the attribution of psychosocial factors as being an etiological factor with respect to TMDs.

Social Anxiety Disorder

“The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria for SAD include eight components including fear of social situations, continuous triggering of anxiety by social situations, exaggerated fear that is out of proportion to the seriousness of the threat posed by social situations, avoidance of social situations due to intense fear, impaired social or occupational functions, the persistence of fear for six months, the fear not being attributed to any substance abuse, symptoms that cannot be explained by another mental illness, and avoidance that is not related to a medical condition.”⁶

Considering the complexity of the SAD diagnosis and the different aspects of Panic Disorder (PD),⁷ Generalized Anxiety Disorder (GAD),⁸ Social Anxiety Disorder,⁹ Obsessive-Compulsive Disorder (OSD),¹⁰ and Post-Traumatic Stress Disorder (PTSD),¹¹ their diagnoses and treatments should require substantial expertise in psychotherapy. DSM-5 has recently added a new criterion for a diagnosis of PTSD requiring the presence of persistent symptoms for over a month.¹¹ Thus, if one suspects any SAD condition, it is necessary to wait one month to confirm it before any treatment should be planned.

Many subjective symptoms that are reported in anxiety disorders overlap with those observed in temporomandibular disorders (TMDs); however, their underlying etiologies often cannot be definitively distinguished through diagnostic measures alone and may only be clarified following symptom resolution with either physical or psychological intervention.

1. Paresthesia

2. A feeling of being choked or smothered

3. Abrupt onset of physical symptoms

4. Restlessness

5. Being easily fatigued

6. Inability to concentrate

7. Irritability

8. Muscle tension

9. Sleep disturbances

10. Dizziness

The fact that dentists, even most TMDs specialists, lack the expertise and training necessary to diagnose or treat SAD conditions, makes a referral more appropriate than any effort to diagnose with GAD-7 or treat with cognitive behavioral therapy (CBT)¹² and/or by prescribing medications like SSRIs, serotonin-norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs), GABA-ergic drugs, benzodiazepines (BZDs), beta-blockers, and other anxiolytics.¹³ Accurate diagnosis of Generalized Anxiety Disorder requires careful differentiation from other anxiety-related conditions, including GAD, PD, OSD, and PTSD. Few dentists possess the training to make such distinctions, and doing so may be perceived as extending beyond the traditional scope of dental practice into the domain of medicine.

Somatic Symptom Disorders

Somatic Symptom Disorders are difficult to diagnose unless somatic symptoms do not respond rather quickly to common physical treatments routinely applied to TMDs such as computerized occlusal adjustments, mandibular repositioning, splints, orthodontic and prosthodontic corrections and some surgical procedures.^14–16 One possible explanation for the observed responsiveness of many somatic symptoms to physically applied biological treatments is the relative rarity of true SSDs. According to Sam Dworkin, the father of the RDC/TMD,¹⁷ “True somatization disorder is very rare (< 1%) and requires a DSM-III-R diagnosis including at least 13 different physical symptoms which cannot be explained by, or are in gross excess of physical findings, and have caused patients to seek health care or alter their lifestyles.”¹⁸ Note the requirement regarding symptoms being far in excess of physical findings. And that the routine use of Axis II of the RDC/DC/TMD for psychosocial diagnoses inevitably results in a high rate of false positive diagnoses of Somatic Symptom Disorders when applied without first eliminating any physical causes of patients’ chronic pains. The routine use of PHQ-9 and GAD-7 for the initial diagnosis of TMDs can produce false positive SSD diagnoses whenever a physical etiology is present. The exclusive use of subjective patient-reported surveys is likely to generate false positive SSD diagnoses, especially when the common biological etiologies associated with TMDs are ignored. It is well known that subjective emotional symptoms (depression, anxiety, etc.) are very prevalent among patients with chronic pain due to physical conditions.¹⁹ Jiang R et al reviewed a large database (14,000 +) of pain patients and found a positive relationship between increasing pain and increasing depression regardless of the area of the body.¹⁹ Independently, it has been shown that successful reduction of the physical pain has dramatically reduced or eliminated depression in TMD patients.¹⁴ A separate study revealed the dramatic reduction in somatic symptoms when chronic pain patients were treated physically.^15,16

Catastrophizing is a cognitive distortion within a person who is imagining the worst possible outcome of a poor or undefined condition or situation. With respect to patients with TMDs, when catastrophizing occurs, the patients usually have TMDs signs and/or symptoms (painful or arthrological) but without a valid diagnosis or any effective treatment,²⁰ and often they have experienced being passed from one practitioner to others. Kinesiophobia is the fear of moving, in this case the jaw, afraid that something bad will happen. Both painful symptoms and non-painful articular symptoms tend to produce significantly greater kinesiophobia.²⁰ It is understandable that TMJ clicking, popping or grating sounds could make patients cautious with their jaw movements.

Central Sensitization

Central sensitization suggests that the CNS is the source of pain signals not the periphery and was originally hypothesized by those trying to explain phantom limb pain. The Neuromatrix Model of Pain proposed by Melzack,²¹ was an attempt to explain phantom limb pain and extend the Gate Control theory.²² However, the successful use of TENS device to block pain signals in the periphery and dynamic reverberation have opposed a central origin of many specific pains.²³ More recently central pain modulating systems have been shown to either inhibit or enhance nociceptive inputs from the periphery.²⁴ This suggests an interactive relationship rather than an etiologic one. “Incorporating vestibular pathways into pain models may, therefore, improve our understanding of chronicity and open novel therapeutic avenues for neuromodulation.”²⁵ PET, fMRI, and MEG have uncovered cortical processing of human pain within the thalamus, the primary somatosensory cortex, and secondary somatosensory cortex (both in the lateral brain) and in the anterior cingulated cortex and prefrontal cortical area (in the medial brain).²⁶ It has been hypothesized that each of these areas processes different aspects of pain.²⁶

The OPPERA study

The multi-year OPPERA study followed more than 4,000 subjects initially without signs or symptoms of TMDs for several years to detect the onset of TMDs and whether any somatic symptoms could predict its incipient onset.²⁷ Their strongest associations with chronic TMDs were seen for pressure pain in the trapezius and temporalis muscles, unlikely to be somatically induced. Demographically their findings appeared opposed to the most recent National Health Interview Survey.²⁸ The objective of the study was early detection based upon somatic symptoms, under the assumption that early detection might enhance treatment outcomes. However, no effort to treat any of the thousands of subjects was reported.

How does all this relate to TMDs?

The history of claims that temporomandibular disorders are somatic symptom disorders began at least 56 years ago. In fact, Laskin and Greene claimed that TMJ syndrome was caused by stress already in 1969, which they renamed the then current TMJ Syndrome as Myofascial Pain Dysfunction Syndrome (MPDS).²⁹ In the early 1970s Laskin was awarded a $10,000,000 10-year grant from NIDR to fund research to find support for their MPDS theory. Although they published one study that claimed a placebo non-occluding splint was 60 % effective at treating MPDS, and as effective as their occluding splint, that result has never been replicated by anyone since.³⁰ Their grant was never renewed.

The psychosocial portion of the biopsychosocial theory has been based upon the frequent findings that many TMDs patients are depressed and/or suffer from other somatic symptoms when reporting chronic orofacial pain.^31–33 Patient frustration associated with not receiving a concise diagnosis and/or the all-too-common experience of sequential treatment failures can certainly take an emotional toll on TMDs patients. However, if stress, depression and anxiety were the primary causes of orofacial pain and dysfunction, one should expect that psychotherapy would be able to provide logical and effective treatments. While cognitive behavioral therapy (CBT) has been promoted as an alternative or co-treatment for TMDs, it has only been shown to temporarily improve coping skills for patients with continuing chronic pain even when combined with some basic physical treatments.^34,35 A review of CBT as a treatment for TMDs found that “…the methodological qualities of included studies on CBT on TMD are generally low, and its reporting quality which is checked by CONSORT is also unsatisfactory.”³⁶ In another Systematic Review of randomized clinical trials that used psychological therapies for TMDs, the conclusions indicated that “…overall, we found insufficient evidence on which to base a reliable judgement about the efficacy of psychological therapies for painful TMD.”³⁷ When only 50 % of a CBT treatment group indicated they “had clinically meaningful improvement in pain intensity” versus 29 % of an “education/attention control group” it appeared to be an improvement but not a definitive solution.³⁸

What is the likelihood of a given TMD being a somatic symptom disorder (somatization)

From the early 90s the efforts to incorporate psychological and social factors into the diagnosis and treatment of TMDs have been pervasive. Sam Dworkin, credited with the creation of the Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD), has plainly indicated that less than 1 % of TMDs are likely to be real Somatic Symptom Disorders (SSDs).¹⁷ If physical treatment is not pursued and only management of pain is deemed necessary, cognitive behavioral therapy has only been claimed to potentially reduce catastrophizing and kinesiophobia in patients that remain in chronic pain by improving coping skills.³⁹ The improvement of coping skills is a reasonable objective in cases of terminal diseases, but since TMDs are not often considered terminal, it is not a very suitable objective.

Are control cases required for all research?

A control group can be useful, and it is the standard option of the pharmaceutical industry for detecting the marginal effects of new drugs, but it is not needed in every case, especially when the outcome of treatment is at issue. The treatment of Lyme disease with an antibiotic does not need a control case: 1) a patient is diagnosed with acute Lyme disease, 2) the patient is prescribed an antibiotic for 10 days, 3) the Lyme disease is irradicated. A control group is only necessary if a placebo effect is likely to cure the patient or an attempt is made to compare one treatment to another. Consider a group of patients diagnosed with occlusal-muscle disorder of the head & neck (a TMD), found to have multiple painful symptoms and depression. After treatment with Disclusion Time Reduction (DTR), one week, one month and 3 months later, the patients are totally symptom-free and emotionally normalized.¹⁴ There is zero scientific support in the literature for such a placebo effect. The statistical paired comparison can reveal even subtle yet significant changes between pre-treatment and post treatment status without any control group.⁴⁰

Are TMDs multifactorial?

The category of TMDs is obviously multifactorial. Some cases of TMDs are also multifactorial with TMJ involvement, structural and occlusal factors all prevalent.⁴¹ While the category of TMDs is absolutely multifactorial, many individual TMDs patients have only one primary etiology, which precipitates and/or perpetuates secondary physical signs and somatic symptoms.¹⁴ To avoid using a trial-and-error approach an accurate diagnosis is required to determine the actual etiology of the case so an efficacious treatment plan can developed. Note: Although PubMed lists 75 published articles touting a “usual” treatment approach to TMDs, (as if one-size-fits-all), no efficacious universal TMDs treatment plan has ever been validated. Effective treatments must be focused on correcting specific abnormal conditions. Even oral appliances have many different designs from simple to complex that are optimized for specific corrective actions.

Some of the oral appliances used to treat TMDs

1. Sleep Apnea Appliances (SAA).⁴²

2. Rigid Arch Bar Appliances (RABA).⁴³

3. Functional Appliance for Juvenile Idiopathic Arthritis (FAJIV).⁴⁴

4. Mandibular Advancement Device to reduce bruxism (MAD).⁴⁵

5. Maxillary Occlusal Splint to reduce bruxism (MOS).⁴⁵

6. Disk Repositioning Appliance (DRA).⁴⁶

7. Michigan Stabilization Splint for distoverted maxillary 3^rd molars (MSS).⁴⁷

8. Double Repositioning Splint for muscle relaxation (DRS).⁴⁸

9. Anterior Positioning Splint for disk recapture (ARS).^40,49

10. Nociceptive Trigeminal Inhibition appliance (NTI).⁵⁰

Occlusion

Why is the claim of poor study design always only applied to studies showing occlusal treatment success? It appears to be a rationalization for the poor comparison with the psychosocial studies (CBT, etc.) that have only helped patients to cope a little better with their chronic pains. In stark contrast, depression and somatic symptoms have been shown to be fully relieved by physically successful TMDs treatments.^14–16 In stark contrast, CBT has not succeeded in fully correcting even mild TMDs.^34,35 At best, it can improve coping, but when combined with physical treatments it is unclear which treatment has had the more positive effect.^36,37 The common depression and other somatic symptoms that TMDs patients exhibit are routinely secondary to the physically painful conditions, not etiological of the painful conditions. The presence of occlusal interferences to real masticatory function has been revealed as the primary etiology of muscularly symptomatic TMDs, when no other structural factors (E.g., TMJ internal derangements, etc.) are present.^51–55 Their removal using the highly efficacious immediate complete anterior guidance development procedure creates canine protected occlusion, eliminating group function occlusion.⁵⁶

If occlusion truly has no relationship to TMDs as a few do say, splints and DTR must be considered as the world’s two most effective placebo treatments ever for TMDs.^57,58 Adjusting occlusion by removing interfering contacts to masticatory function^14,54 or temporarily removing occlusion entirely with an oral appliance are both focused solely on the occlusion.¹⁵ Although occlusion is not the only culprit that is responsible for producing TMDs, there can be no other conclusion but that a relationship does exist between human occlusion and a majority of TMDs.

Temporomandibular Joints

Internal derangement of the temporomandibular joint disc is a common finding (up to 70 %) associated with TMDs.⁵⁹ The common TMJ treatment options include 1) pain medications, 2) extracellular matrix injections,⁶⁰ 3) anterior repositioning appliance, 4) arthrocentesis, 5) discectomy with fat graft,⁶¹ and 6) open surgery including total joint replacement in the worst cases.⁶²

No one can predict the adaptive capacity of a patient with a TMJ internal derangement with a displaced disc, a common occurrence. In the acute stage there are two options; 1) attempt to recapture the normal disc position or 2) promote as much as possible successful adaptation.⁴⁹ When an appliance is used to recapture a displaced disc, the appliance is also altering the occlusion as the mandible is advanced 0.6 mm to 3 mm.^63–66 When a decompression appliance is created to reduce pressures in the TMJs it is also altering the occlusion.^67,68

It is also possible to assess the level of adaptation that has already occurred in a chronic case. Good adaptation means no treatment is indicated and poor adaptation in chronic cases with distorted non-reducing discs means no recapture is possible.⁶⁸

A focus on effective treatment can elucidate etiology

Instead of obsessing only about what are the best diagnostic methods for TMDs, it is well past time to focus on the efficacy of specific treatment regimens. To evaluate TMDs patients’ outcomes, their qualities of life before treatment can be compared to that after maximum medical improvement, regardless of the treatment method. The most successful treatments obviate the etiology that is present, whether physical or psychosomatic. The diagnosis of somatic symptoms, even when accurate, does little to relieve the physical pains and suffering that are very common among TMDs patients. The resolution of TMDs with successful treatments cannot come from literature reviews, meta-analyses and opinions, it requires expert practitioners able to diagnose and treat TMDs successfully.

Summary

An exclusive reliance on psychosocial frameworks for TMDs management overlooks the need for objective biomechanical assessment, including occlusal functional interferences and the determination of whether the maximum intercuspal position (MIP) lies inside or outside of a patient’s physiological boundary of adaptation. While some have claimed that anxiety represents a risk for TMDs, their “positive association” does not support anxiety as a TMDs etiology.⁶⁹ The reverse is far more likely. For those who have rejected the whole possibility of occlusion ever being an etiology of TMDs, the physical measuring tools necessary to evaluate occlusion have either been dismissed or more often ignored.⁷⁰ Masticatory system measurement tools (jaw tracking, EMG, JVA and T-Scan) are widely used every day by successful TMDs treatment providers. For the occluso-muscle disorder segment of TMDs, the disclusion time reduction (DTR) protocol has proven very successful in dramatically reducing or eliminating symptoms, including somatic symptoms, when occlusal functional interferences have been detected and eliminated from TMDs.^51–54

While some TMJs do successfully adapt to internal derangement, most do not. Therefore, it is necessary to be able to differentiate those that do from those that do not and treat or not treat appropriately.

Splints and numerous oral appliances have been the most used TMDs treatments since the 1950s (Sears pivot splint)⁷⁰ to reduce painful symptoms in bruxers and non-bruxers. They can do more than protect the teeth if designed to be specific to the patient’s needs. TMDs treatment providers have had no “need to justify their use of appliances,” the known efficacy associated with splints, which is better than medications, and/or psychotherapy has already been in place for decades. “Contraction of elevator muscles without tooth contact” can only occur at a very minimal level (a few microvolts) such as during posturing or while speaking. The small motor units involved in posturing are separate and distinct from the large motor units activated during mastication. The most important function of the masticatory system is measurably efficacious mastication. As a group, psychotherapists have no idea how that happens, but it does not include “a large number of behaviors independent of occlusion.”⁷¹ Mastication is very difficult and the quality of it is very poor without any occlusion.

Asking the patient to self-diagnose their own TMD is ludicrous. The DC/TMD has not been “validated” as a diagnostic system. Axis I without imaging fails in sensitivity and/or specificity for all physical TMDs conditions except detecting the presence of sore muscles without revealing any reason for the soreness. Using Axis II at the initial examination without first eliminating any possible physical etiologies is guaranteed to routinely produce false positive diagnoses of Somatic Symptom Disorders. If psychological or social factors were most important in the etiologies of TMDs psychotherapists and social counselors should be the most successful providers of TMDs treatments. Since without doubt, the vast majority of successes in TMDs treatment fall within the biology of orofacial pain, the psychological and social aspects must be secondary by default and inordinately less consequential.

Funding Statement

No funding was received in support of this commentary.

Disclosures

The authors reported no conflicts of interest.