Temporomandibular dysfunction or TMD for short, is a condition that may lead to excruciating pain in the jaw joint area. Further more, related symptoms such as such as TMJ clicking, painful jaw muscles, facial neuralgia (trigeminal neuralgia), tinnitus, headaches, migraines are a few worth mentioning (D’Urso et al., 2016; Attanasio et al., 2015; Romero-Reyes & Uyanik, 2014; Franco et al., 2010).

It has been estimated that up to 33% of the population is affected with some kind of TMJ disorder, and between 3-7% are in so much pain that they require treatment. Sadly, there’s no real consensus with regards to the cause nor treatment protocols for temporomandibular dysfunction. In this article, however, I will detail what I consider to be the true cause and cure for TMD, a protocol that I use myself in my clinic on all TMD patients, with overwhelming results.

Approximately 33% of the population has at least one TMD symptom and 3.6% to 7% of the population has TMD with sufficient severity to cause them to seek treatment. – Edward & North, 2009 Patients with chronic TMD frequently report symptoms of depression, poor sleep quality, and low energy. Furthermore, chronic TMD has been found to interfere with normal social activity and interpersonal relationships and to negatively affect the ability to maintain employment. – Morris et al., 1997 Evidence for the effect of electrophysical modalities and surgery is insufficient, and occlusal adjustment seems to have no effect. One limitation of most of the reviewed systematic reviews was that the considerable variation in methodology between the primary studies made definitive conclusions impossible. – List & Axelsson, 2010

The true cause of TMD

Fig. 1

The true cause of temporomandibular dysfunction, is habitual retraction of the mandible, jamming the glenoid fossa (joint socket). Underdevelopment of the maxilla bone (upper jaw), improper tongue posture, mouth breathing habits and similar will establish an excessively posterior tooth occlusion, and thus encourage posterior translation of the mandible, ultimately jamming it into the joint socket, causing deterioration over time.

This video does illustrate the cause of TMD well. It does not, however, mention the causes of horizontal underdevelopment of the maxilla; improper tongue posture. Pacifiers, thumb sucking and chewing overly soft foods in our youth, inhibits horizontal growth of the maxilla, leading to a more posteriorly established dental occlusion. The mandible (lower jaw) keeps growing into its full potential, even when the maxilla did not. The result of this is a mandible that is proportionally longer than the maxilla, which often lead to TMJ compression and TMD if postural occlusion is to be maintained. The more underdeveloped the maxilla is, the more compressed the TMJ joint socket will become, as the differential of length ratio between the two parts increase.

From a postural perspective, a whole different approach seems logical and almost too simple. When they bite together, the joint [when dysfunctional] is not centric, so is not balanced; it’s over-closed, with the head of the jaw joint set in the top back of the joint often squeezing the disk out of the way, possibly causing great damage. – Dr. Mike Mew When the maxilla and mandible do not achieve their genetic potential in length, width, or vertical position, the effects are seen in mal-relationships and dysfunctions in the patient’s tissues, bones, muscles, and nerves. The temporomandibular joint (TMJ) relationship may then become compromised when this occurs, as it compensates for the discrepancies in normal growth and development. Normal spacing between the roof of the glenoid fossa of the temporal bone and the condyle of the mandible should be approximately three mm to support the disk between them. The retrodiskal tissues originate from the distal portion of the glenoid fossa and are inserted into the posterior portion of the disk. This tissue contains a matrix of blood vessels and nerves, particularly fibers of the auriculotemporal nerve, cranial nerve V, an afferent branch of the trigeminal nerve. If this space is insufficient or reduced or restricted and the condylar head grows posterosuperiorly or is iatrogenically repositioned posteriorly or posterosuperiorly, the condyle will pinch this tissue and usually the result will be pain. – Sims & Stack, 2007 Adults with clicking joints had a saggitally shorter maxilla and mandibular diagnonal, whereas adults with crepitating joints had, in addition, a shorter anterior and posterior cranial base and pharynx. This sagittal “shortness” could already be demonstrated for many of the reported dimensions at the corresponding cephalograms taken about the age of 12.5 years, and did not appear to have changed much over time. It is concluded that the reported TMD signs in adults were associated with a sagittal shorter midface. – Dibbets & Weele, 1996

Fig. 2

It is very important to understand that the TMJ is not a hinge joint. Most dentists, and even so called “TMD specialists” believe that the mandibular condyle should rest in the posterior position of the joint socket. This is absolutely wrong. The TMJ is an elliptical joint, allowing movement in all directions, from center. It is absolutely critical to understand that a centrated TMJ is equivalent to slight protraction of the mandible, and not maximal retraction; it should rest a minimum 2-4 millimeters more anterior than complete retraction, preferably more.

Fig. 3

When the mandibular condyle rests too far back in the glenoid fossa (socket), this may lead to an array of issues, as mentioned earlier. We will speak more about the causes of this, but one important reason is that the pterygoid muscles will inhibit (become inactive). The pterygoid muscles are have very important functions, as they pull the mandible forward (anteriorly). Anterior translation of the mandible = unjammed / decompressed TMJ, right? Yes, indeed.

The lateral pterygoid controls protraction (forward translation) of the mandible during opening of the mouth. Ipsilaterally, it also rotates the jaw toward the other side (longitudinal axis). It has two heads; a superior and inferior portion. The medial pterygoid on the other hand, controls protraction during closing of the mouth. It also shifts the mandible contralaterally. Because these muscles protract the jaw, they become inhibited when the jaw is habitually retracted in posture.

Fig. 4 – Professor and TMJ-surgeon, Dr. John Mew

The studies below show that there are no official beneficial diagnostic or treatment protocols with regards to TMD. It is therefore not very surprising that the researchers also do not find any significant difference between psychological treatment and physical treatment, when they didn’t know the cause in the first place.

This review aims at presenting a current view on the most frequent factors involved in the mechanisms causing temporomandibular disorders (TMD). The etiology of TMD is multidimensional: biomechanical, neuromuscular, bio-psychosocial and biological factors may contribute to the disorder. Occlusal overloading and parafunctions (bruxism) are frequently involved as biomechanical factors; increased levels of estrogen hormones are considered biological factors affecting the temporo–mandibular-joint. Among bio-psychosocial factors, stress, anxiety or depression, were frequently encountered. The etiopathogenesis of this condition is poorly understood, therefore TMDs are difficult to diagnose and manage. – Chisnoiu et al., 2015 No evidence was found to distinguish the clinical effectiveness between «usual treatment» and psychosocial interventions for myofascial TMD pain. – Roldán-Barraza et al., 2014

There are some studies showing significant improvement by utilizing some methods, although lacking consensus. It is however important to note that they are talking about symptom relief, and that they are not aware of the cause of TMD, in similar fashion to the above-mentioned studies. At the very least, postural correctives are portrayed as something positive – which they absolutely are, when done correctly.

This systematic review concluded that “active and passive oral exercises and exercises to improve posture are effective interventions to reduce symptoms associated with TMD. – McNeely et al., 2006 This systematic review analyzed studies examining the effectiveness of various physical therapy interventions for temporomandibular disorder. Active exercises and manual mobilizations may be effective. programs involving relaxation techniques and biofeedback, electromyography training, and proprioceptive re-education (bevegelseskorrigering) may be more effective than placebo treatment or occlusal splints. A combinations of active exercises, manual therapy, postural correction, and relaxation techniques may be effective. – Medlicott et al., 2006

Why forward head posture encourages TMD

There is a high correlation between foward head posture (FHP) and temporomandibular dysfunction. The reason is because the mandible is attached to the sternum through the hyoid musculature. The further forward the head translates, the higher the tension of posterior mandibular pull through the hyoid structures will become. The added posterior retractive forces on the mandible will exacerbate the existing dysfunction, which is caused by underdevelopment of the maxilla, leading to a double compression force to the temporomandibular joint. This especially applies for mouth breathers and people with open-mouth postures, as the hyoidal posterior mandibular pull will not have great effect if occlusion is intact.

Special emphasis has been put on the influence of forward head posture on the craniofacial growth as it can determine a morphoskeletal and neuromuscular pattern leading to a dysfunctional condition. A correlation is established between Class II Occlusion, forward head posture, and craniomandibular dysfunction. The concept of craniocervical postural position is defined, as well as its close relation to the mandibular postural position. – Gonzales & Manns, 1996

It is possible to treat TMD without dealing with the craniocervical position, but it makes it harder to maintain proper mandibular resting position due to the retractive forces imposed by the infra- and suprahyoid stretching that occur when the head is forward. Let us have a closer look at common postural myths, and how to really correct FHP.

Fig. 5

To correct forward head posture, one must also address general postural sway. If the point of gravity is too far back, as with the utmost common swayback posture, the head and shoulders will naturally come forward in order to maintain equilibrium. No amount of cervical corrective procedures will ever be able to correct this! The point of gravity must be altered in order to be able to change and promote proper craniocervical resting position.

I must emphasize that no amount of exercising can ever fix postural anomalies. It’s a complete myth. The only way to permanently alter posture, is by altering habits. In other words, you need to get into proper position, and get used to staying there. Sure, exercises can help with making this process easier, but habits (posture) and exercises must both encourage proper function. The simplest way is by making sure of the following:

The chest must be in line with, or anterior to the hip. The shoulders should never be posterior to the hip. The shoulder smust be raised slightly (half an inch), to avoid clavicular depression, if they are indeed depressed.

Swayback posture and clavicular depression both contribute to forward head posture. By maintaining proper thoracopelvic and clavicular alignment, this will lay the foundation for proper craniocervical posture, making it easier to maintain good structural habits. In practice, all you need to do is get your hip slightly backward, chest slightly forward, and shoulders slightly upward. Then stay there. You’ll get used to it within 4-8 weeks. For more information on thoracopelvic correctives, look into my lower back article.

Fig. 6

The TMJ’s relation to body posture

I’ve written a long article about the TMJ and its relation to body posture in my atlas-article (link – coming soon). The point is, though, that imbalanced occlusion and open-jaw postures will encourage both forward head posture due to loss of tensegrity of the hyoid musculature that pull the head into flexion when the mouth is closed, and encourages rotation of the atlas, most likely due to the occlusive state’s effect on the sphenoid bone that the optic nerves (CN2), as well as CN3, CN4 and CN6 pass through. The relation between occlusion and sphenoidal alignment, is formed by the temporalis and pterygoid muscles that attach to it.

It is however important to note, that even if you have a very crooked occlusion, you are not doomed to live with horrible posture. Our consciousness and habits may override the body’s automatic postural “baseline”, meaning that we can get out of forward head posture or pelvic imbalances by simply being aware of it and avoid letting it happen. You will most likely need to be taught how to do that, but it’s definitely possible and is something I teach my clients daily in clinic.

Fig. 7

A clear pattern of associations between crowding and craniocervical posture was found. – Solow et al., 1998 According to the literature reviewed, we believe that there are real correlations between posture and the SS (stomatognathic system). In this way, an increase in postural swaying may indicate a general malaise caused by problems in the SS. – Cuccia et al., 2009 The individual’s postural position can suffer biomechanical alterations due to stomatognathic alterations, causing clinically visible changes in dysfunctional individuals and affecting the performance of the involved structures. – Strini et al., 2009 Significant correlations could be obtained with respect to the facial axis and the lordotic angle, the facial axis and the pelvic inclination, the inner gonial angle and the lordotic angle, the inner gonial angle and the pelvic inclination, the mandibular plane angle and the lordotic angle, the mandibular plane angle and the pelvic inclination, as well as the facial depth and the pelvic inclination. – Lippold et al., 2006 Five animals received no alteration on their bite. Bite was increased on 10 animals and molar teeth were extracted on 10 other animals. Frontal and lateral radiographs were taken on days 0, 7, 14 and 21. Distances from landmarks to a true vertical line were measured on both radiographs. Results: Repeated measures analysis showed statistically significant differences between the amount of the curvature at the cervical and thoracic spines on frontal and lateral radiographs over time Ramirez-Yanez et al 2014 The data that is available points to the existence of a correlation between posture and occlusion and also asserts the prevalence of associations between cranio-facial anomalies and idiopathic scoliosis in adolescents. – Amat et al., 2009 The data confirmed a beneficial effect of balancing the occlusion with an acrylic wafer on the following paired postural muscles: sternocleidomostoid, erector spinae, and soleus. – bergamini et al., 2008 Based on these findings, it was concluded that changing mandibular position affected body posture. Conversely, changing body posture affected mandibular position. – Sakaguchi et al., 2007

Identification of dysfunction

Identifying TMD itself is not difficult. Reduced horizontal maxillary growth is indicated by an unproportionally bigger and more protruding nose than the cheeks, and reduction of the naso-maxillary line. This is, however, something that dentists and people with special orofacial interests may pay more attention to. It’s really not that important, in order to deal with TMD itself. Check out dentists Mike and John Mew’s youtube channel for more information on this.

Fig. 8

First off we have the symptoms, also mentioned earlier: jaw pain, myofascial pain in the chewing muscles such as temporalis, masseter and pterygoids, headaches, tinnitus, trigeminal neuralgia, etc. There may of course also be more symptoms, but they are not as common as the ones mentioned.

The ultimate TMD assessment technique, is measuring the distance between resting mandibular position and maximal retraction. Its resting position is usually maximally retracted already, crushing the TMJ socket for each day that passes. Additionally, the jaw will most of the time be unable to protract when opened, causing further posterior shearing forces into the joint socket and TMJ articulate disc.

Here’s what you do:

Close your jaw with full occlusion (molar contact). Relax the jaw without moving it. Try to retract (pull back) the mandible.

If it moves minimally, or not at all, that means the mandibular resting position is causing the condyle to jam into the TMJ, often leading to pain, disc injuries, arthritis and so on over time. In other words, the occlusive state is causing chronic joint deterioration and must be altered, either by posturally moving the jaw forward, or expanding the maxilla horizontally. As a myoskeletal therapists, the first mentioned is my approach. A dentist who really knows how to deal with TMD, will probably choose the latter. There are also some splint therapies, such as Starecta, that supports mandibular protraction.

Fig. 9

The next step is to assess its movement. It is important to teach a dysfunctional jaw how to move properly, especially with regards to protraction, as this movement is often (always) inhibited. To identify improper opening and closing of the jaw, watch yourself in the mirror (or your patient) and look for mandibular retraction as the mouth opens. This is an unnatural way for the mandible to articulate within the joint socket, and will often lead to laxity of the TMJ capsular ligaments over time, causing anterior displacement of the mandibular condyle. If present, it will reveal itself as a bulge appearing anterior to the jaw joint, as illustrated in the picture below when the mouth opens to a certain degree. The bulge is the mandibular condyle subluxing anteriorly.

Once again, the mandible should protract (come forward) when the mouth opens, and not reflexively retract. The latter is what I almost always identify in people with temporomandibular dysfunction. You can also watch for left or right deviation as the mouth opens. The direction it deviates to indicates higher TMJ compression on that side, although many experience TMD bilaterally.

Fig. 10 – Red arrow=subluxing condyle, black arrow=mandibular retraction

Sadly, many therapists teach their patients to force greater mandibular depression (mouth opening) as an exercise, if mouth opening is restricted. This is highly detrimental and must not be done! The cause of reduced mandibular depression is improper TMJ articulation (lack of protraction) and not a simple “tight muscle”-problem. Patients who are exposed to these quacky protocols will end up getting worse and not better, as the TMJ is crushed due to lack of mandibular protraction! The TMJ restrictions are infact the body’s way to try to hinder further damage and excessive compression to the joint socket.

On the other hand, this is how optimal TMJ kinematics should look like, in the picture below. The mouth opens by encouraging downward and forward translation of the mandible, by utilizing the hyoid and pterygoid muscles. Also note the lack of bulging of the mandibular condyle, which does not displace when the TMJ is healthy and used normally.

Fig. 11

Here’s a video walkthrough of proper and improper TMJ mechanics.

Common sideeffects of TMD

Habitual excessive retraction of the mandible will often cause many secondary effects. I will address the most common ones here below.

Articular disc displacement

A common sideeffect of TMD, is articular disc displacement. The articular disc is a structure that lies between the mandibular condyle and temporal bone (joint socket). Its function is to glide forward and backward in symmetry with the condyle’s movement, covering the condyle from grinding bone into bone. When the TMJ is compressed by an excessively posterior position of the mandibular condyle, the ligament (the retrodiscal tissue) that’s holding the disc may gradually degenerate, eventually causing the disc to slip forward in front of the condyle.

There are two main types of displacement: with, and without reduction (WOR). “With reduction” means that the mandibular condyle is able to pop back onto the disc, causing the infamous “pop” as the jaw opens. If the disc is severely displaced, it may be unable to slide back into position between the temporal bone and mandibular condyle as the mouth opens, and this scenario is referred to as “without reduction”, which sometimes cause the joint to lock up or greatly restrict in mobility.

Should we worry about disc displacements? Well, first of all it has been shown that patients with displacement WOR usually (~70%) resolve on their own, within a certain period of time. Surgery, rehab (of course, rehab without consensus), medication and psychological treatment were all found to be equally effective (or should I say ineffective) for treating TMD and disc displacement, indicating that the actual displacement is an unlikely cause of the pain by itself. Reports also note that the retrodiscal tissue may harden and create a ‘pseudodisc’ function. Additionally, scientists have conducted experiments where they purposely injured the retrodiscal tissue in goats, finding it to be reformed a month later. Why? In my view, because the goat doesn’t have the predisposing factor of TMD; TMJ compression due to continuous retraction of the mandible, and of course because the retrodiscal tissue has a decent vascular supply. Sure, the tissues were weaker (scar tissue), but this doesn’t really matter. The point is that the disc heals if there’s no continuous irritation to the joint, and the same applies, of course, to humans. Once the continuous injuring effect cease, the disc can heal.

If there has occurred retrodiscal tissue perforation, meaning that the tissue is completely torn, then this requires surgery.

Fig. 12

Clinical evidence and previous experimental animal work suggest that mandibular condylar cartilage shows the capacity for repair, after trauma or degeneration, that can reconstitute a functional articular surface; a facility not shared by other synovial joints. This study aims to test the regenerative capability of condylar cartilage in the repair of standardised full-thickness articular defects, and thereby to test the hypothesis that the healed wounds comprise tissues identical in form and composition to those of similar, but uninjured areas. The results showed reconstitution of all tissue elements of condylar cartilage within 6 months of injury. – Robinson, 1993 MRI of a 30-year-old woman 1 year after discectomy showed a residual disc-like tissue. The observation was initially confusing, but a close comparison of pre- and post-operative images suggested that the inferior wall of the anterior joint capsule had migrated superiorly after the removal of the disc and mimicked a residual disc on the follow-up MR images. – Petersson et al., 2005 The result of this prospective cohort study indicated that approximately 40% of patients with symptomatic disc displacement without reduction will be free of symptoms within 2.5 years, one-third will improve, whereas one-quarter will continue to be symptomatic. This knowledge should be valuable for the treatment planning and evaluation of prognosis of patients with non-reducing symptomatic disc displacement. – Kurita et al., 1998 This result demonstrates that therapeutic exercise brings earlier recovery of jaw function compared with splints. – Haketa et al., 2010 These results suggest that ADDwor subjects will improve with only minimal treatment intervention, and no significant difference was evident for the treatments tested and the control condition. – Minakuchi et al., 2001 MR images depicted anterior disc position in 32% of the asymptomatic joints (8/24 males, 5/18 females). Anterior disc position in asymptomatic subjects may be a predisposing factor to TMJ dysfunction or simply an anatomic variant whose prevalence must be considered when evaluating TMJ dysfunction. – Kircos et al., 1987 For individuals with temporomandibular joint (TMJ) disc displacement without reduction with limited mouth opening (closed lock), interventions vary from minimal treatment to surgery. In a single-blind trial, 106 individuals with TMJ closed lock were randomized among medical management, rehabilitation, arthroscopic surgery with post-operative rehabilitation, or arthroplasty with post-operative rehabilitation. Using an intention-to-treat analysis, we observed no between-group difference at any follow-up for CMI (p > or = 0.33) or SSI (p > or = 0.08). Both outcomes showed within-group improvement (p < 0.0001) for all groups. – Schiffman et al., 2007 Retrodiscal tissue of female goats received trauma or sham trauma. Following a healing period of 30 days, the tissues were pulled to failure on an extensometer. Thirty days after surgical section of retrodiscal tissues, the tissue had reformed, but the composition and biomechanics were substantially changed. Healed tissue manifested less than half the strength of normal tissue. – Cooper et al., 1999 The purpose of this study was to evaluate histologically the healing potential of surgical incisions placed in various areas of the TMJ disc and retrodiscal tissue. Eight weeks after surgery, it was found that incisions completely within retrodiscal tissue had healed and had a normal appearance. Incisions at the junction of the disc and retrodiscal tissue also had healed, but at a slower rate and with more random orientation of the collagen fibers. Defects within the disc had not healed, however, and degenerative changes had developed in the hard and soft tissues. – Wallace et al., 2010

Headaches

The most common cause of TMD-related headaches are caused by the temporalis muscle, in my experience. Continuous retraction of the mandible will cause great imbalances between the muscles of mastication, often leaving the very strong masseter (a muscle that protracts the jaw) underused, overburdening the temporalis muscle (that pulls the mandible back / retraction). In addition to further the compressive forces in the TMJ, it will often cause trigger points in the temporalis muscles that cause headaches.

Although it may be beneficial to treat these trigger points, either by massage or needling, it will not really address the cause of the dysfunction; improper mandibular resting position and articulation. Proper resting position and mandibular movement must occur for the temporalis overuse to cease and the trigger points to disappear for good.

Fig. 13

The results indicate in the studied sample of cervicogenic headache patients, 44.1% had TMD. The group that received additional temporomandibular manual therapy techniques showed significantly decreased headache intensities and increased neck function after the treatment period. Based on these observations, we strongly believe that treatment of the temporomandibular region has beneficial effects for patients with cervicogenic headaches, even in the long-term. – Von Piekartz et al., 2011

Trigeminal neuralgia

The trigeminal nerve is the fifth and biggest cranial nerve, innervating a great load of structures. It has both somatic and autonomic innervations. The trigeminal ganglion spreads out and becomes three main parts called the ophthalamic (V1), maxillary (V2) og mandibular (V3) branches. It is mainly responsible for sensory feedback in the face, and motor functions with regards to mastication.

Symptoms of affection may vary greatly. Facial numbness, excruciating headaches, lightning type pain into the face and head, tinnitus, involuntary tear secretion, salivary gland pain, hyperacusis, hearing loss, palatal numbness, and more, are potential symptoms that I’ve seen in my office. Some of this occurs due to the trigeminal nerve’s relations to the pterygopalatine and submandibular ganglions that spreads into the salivary & lacrimal glands, palate, and due to its control over the tensor tympani and tensor veil palatini muscles which controls sound modulation in the ear.

Fig. 14

There are two main entrapment points for the trigeminal nerve. One is behind the mandibular ramus; the auriculotemporal part of the V3 mandibular branch (this is also called “Costen’s syndrome”). Excessive retraction of the mandible may compress this nerve between the mandibular ramus and temporal bone. This can be confirmed either by purposely retracting the jaw during opening and closing of the mouth, or by pushing into the nerve manually with your fingers. If this reproduces the symptoms in question, it is indeed affected, meaning it’s being compressed due to a continuously retracted position of the mandible. Information on how to deal with this is the main topic of this article, and will be addressed shortly, in the ‘Correctives’ section.

Secondly, the buccal nerve may be entrapped between the superior and inferior heads of the lateral pterygoid muscle. The buccal nerve is yet another part of the V3 mandibular branch, and may lead to the same symptoms as already mentioned, as nerve compression almost always spread to nearby structures (i.e sciatic compression within the piriformis spreading to the calf). Confirmation of this nerve’s affection may be performed by forcibly protracting the jaw against a resistance (don’t cheat by clenching your hyoid muscles). If the pain is reproduced, the buccal nerve is probably entrapped.

To solve buccal nerve entrapment, you need to strengthen the lateral pterygoid. You may massage it to get some relief, but it will always return, as the real cause (weakness, and habitual retraction of the mandible) hasn’t been dealt with. Symptoms may worsen initially, but that’s a normal part of rehabbing the muscle and is a positive sign that you’re doing it correctly. Don’t go harder than necessary, strengthen it gradually and the symptoms will resolve eventually, usually within a month or two.

Fig. 15

MANDIBULAR joint neuralgia (Costen’s syndrome), first reported by Costen in 1934,1 is accepted by otorhinolaryngologists and members of the dental profession as a definite clinical entity. It should be considered in every differential diagnosis of recurring facial pain. – Beyes & Teich, 1952 According to the author’s hypothesis, the lack of posterior support of the alveolar ridge led to mandibular vertical height loss which caused a slipping backward of the condyles over the articular disc thus resulting in TMJ discal damage, erosion of the glenoid fossa bone, compression of the Eustachian tubes and tympanic plates and consequent impingement of the auriculotemporal nerve (ATN), which runs on the postero-medial aspect of the TMJ capsule, and chorda tympani nerve4 . – Paparo et al., 2008 Normal spacing between the roof of the glenoid fossa of the temporal bone and the condyle of the mandible should be approximately three mm to support the disk between them. The retrodiskal tissues originate from the distal portion of the glenoid fossa and are inserted into the posterior portion of the disk. This tissue contains a matrix of blood vessels and nerves, particularly fibers of the auriculotemporal nerve, cranial nerve V, an afferent branch of the trigeminal nerve. If this space is insufficient or reduced or restricted and the condylar head grows posterosuperiorly or is iatrogenically repositioned posteriorly or posterosuperiorly, the condyle will pinch this tissue and usually the result will be pain. – Sims & Stack, 2007 Our clinical work suggests that the auriculotemporal (AT) nerve, a branch of the mandibular nerve, the largest of the three divisions of the trigeminal nerve, plays a critical role in TMD sequelae. The AT nerve provides the somatosensory fibers that supply the joint, the middle ear, and the temporal region. By projecting fibers toward the otic ganglion, the AT nerve establishes an important bridge to the sympathetic system. As it courses posteriorly to the condylar head of the TMJ, compression, injury or irritation of the AT nerve can lead to significant neurologic and neuro-muscular disorders, including Tourette’s syndrome,Torticolli, gait or balance disorders and Parkinson’s disease. Subsequent irritation and compression of the AT nerve can occur, with associated parasthesia, pain and discomfort. Symptoms can be local and specific (e.g., TMD), as well as varied and systemic (e.g., neurologic, dystonic and neuro-muscular disorders, including tremors, muscle spasms leading to impaired and awkward positional control of the head, hands, other extremities, speech impairment, incontinence, impaired sleep, associated depressive symptomatology). – Demerjian et al., 2011 Anatomical relationships between the auriculotemporal nerve and the muscles of mastication, temporomandibular joint, and surrounding vessels in the area of the infratemporal fossa create favourable conditions for entrapment syndromes. Entrapment of the auriculotemporal nerve plays a role in the pathogenesis of temporomandibular joint pain syndromes, headaches, as well as pain symptoms or paraesthesias within the external acoustic meatus and auricle. Komarnitki et al., 2012 The syndrome of symptoms (Table 1) as first described by Costen, an American otolaryngologist, was discussed. Costen attributed the symptoms to temporomandibular joint dysfunction consequent upon mandibular overclosure with distal condylar displacement. He assumed that the displaced condyle might lead to any of the following: Compression of the eustachian tube, erosion of the glenoid fossa or tympanic plate, pressure on the chorda tympani, or pressure on the main trunk of the auriculotemporal nerve. – Clarke, 1962 When a primary otologic cause is discarded in the diagnostic workup for tinnitus, vertigo, hypoacusis, hyperacusis, ear pain, or sensation of occluded ear, TMD may be the cause of these symptoms. Among patients with this dysfunction, the prevalence of ear pain, tinnitus, and dizziness varies between 33 and 76%.25 – de Moraes Marchiori et al., 2014 This study was undertaken in a retirement town, and the mean age of these TMD study patients was a mature 49.1 years. The data likely underrepresent the occurrence of TMD in younger adults. In the Figure, the statistical mode in the study group was 40 to 49 years; it was 60 to 69 years in the control group. The older control group would be expected to have an increased prevalence of recruitment hyperacusis, tinnitus, hearing changes, disequilibrium, and dysesthesias because these conditions increase with age. – Cox, 2008 Symptoms consistent with TTTS can include: a sharp stabbing pain in the ear; a dull earache; tinnitus, often with a clicking [11,12], rhythmic or buzzing quality; a sensation of aural pressure or blockage [8,9] tympanic flutter [13] pain/numbness/burning around the ear, along the cheek and the side of the neck; [7,8], mild vertigo and nausea [8,9]; a sensation of “muffled” or distorted hearing [14] and headache. Central pain sensitization can develop from chronic trigeminal neuralgic TTTS-induced pain. Tensor tympani spasm has been implicated in a range of conditions including Meniere’s disease, for which sectioning of the tensor tympani muscle has been a suggested treatment [15,16] and the secondary otologic symptoms, such as tinnitus, ear pain and other symptoms in and around the ear, which can develop in myofascial pain syndrome [16,17] temporomandibular disorder (TMD) and TMJ dysfunction [8,9,18,19]. – Westcott et al., 2016, Hyperacusis-induced Pain: Understanding and Management of Tonic Tensor Tympani Syndrome (TTTS) Symptoms

Dystonia & Tourette’s

Dr. Antomy Sims, DDS (et al., 2007) has written extensively about the connections between the underlying connections between the jaw, trigeminal dysfunction and its impact on other cranial nerves. He believes, and has proven with several patients, that removing the compression imposed on the auriculotemporal nerve caused by a too posteriorly positioned mandibular condyle will cure dystonia and tourette’s.

He believes that chronic noxious (damage) input to the auriculotemporal nerve caused by TMJ compression will cause signalling dysfunction between the trigeminal ganglia, subnucleus caudalis and the other cranial nerves, and that this is what caused involuntary movement of the neck, eyes, coughing, utterances, and so on. By decompressing the trigeminal nerve, he has seen that these symptoms vanish completely.

Constant stimulation of the auriculotemporal nerve (CN V) may then result in the stimulation of CN’s V, VII, IX, X, via crossover interneurons (ephapses) and other neural elements in the reticular formation. All of these nerves are intimately involved with movement disorders. In summary, we find that chronic noxious input via the auriculotemporal nerve causes reflex reactions with CN’s V, VII, IX, and X via the crossover pathways at various segmental levels within the spinal cord. All patients showed a total discontinuance of their movement disorders immediately. All patients stated that their breathing was improved and better. All patients stated they did not have the urge to tic or make their involuntary movements. An upper appliance was made for the seven-year-old patient and again, the movement disorder ceased. – Sims & Stack, 2007

If the connection proposed by Dr. Sims et al is true, I believe these same results can be achieved without any dental appliance at all, but by simply altering the postural resting position of the mandible, as well as rehabilitating the lateral pterygoid muscles. Now, I have not had any dystonic or tourette’s patient in my clinic so far, but I think this was interesting enough to mention in this article.

Ménière’s disease

Several studies suggest a connection between temporomandibular disorder and ménière’s disease, which is not surprising, considering the close relationship between the trigeminal nerve and TMD. The trigeminal nerve is involved controlling the eustachian tube, and dysfunction of the latter has been strongly associated with ménière’s disease. Problems with the cervical spine may contribute to dysfunction of the eustachian tube, which I have written about in detail in my atlas joint article.

Irritation of the trigeminal nerve, most likely caused by impingement of its auriculotemporal branch due to TMD, can thus affect the eustachian tube’s function to such a degree that attacks of vertigo occur. So, by decompressing the trigeminal nerve, the noxious input will cease, and the jaw’s impairing effect on the eustachian tube will be resolved.

Fig. x

Unquestionably, the upper cervical spine, the temporomandibular joints, the eustachian tube, and the autonomic nervous system can contribute to the global symptom complex of Ménière’s disease. The eustachian tube is suspected to be the critical link. It has quite a remarkable representation of sensory neurons. This system could be activated through an axon reflex of the mandibular branch of the trigeminal nerve that innervates the temporomandibular joints and upper cervical facet joints. The autonomic nervous system, particularly the sympathetic portion of the autonomic nervous system, can be activated by a neck and temporomandibular joint disorder, and this combination can have the effect of neurogenic inflammation in the eustachian tube, with the consequence of reduced middle-ear ventilation.- Franz & Anderson, 2007 TMD patients often have associated complaints. Many of these patients complained of masticatory fatigue (40%), stiffness (20%), swelling (12%), and weakness (18%) in spite of no observable cranial nerve deficit. Otologic symptoms are also commonly reported among TMD patients. Many of these patients reported tinnitus (42%), ear pain (42%), dizziness (23%) and diminished hearing (18%). – Wright & Bifano, 1997 Symptoms of temporomandibular pain- dysfunction disorder include joint crepitus, joint locking, tinnitus, aural congestion, vertigo, hyper- or hypoacusis, blurred vision, hoarseness and orofacial dysaesthesia – Chan et al., 1994 The findings show that cholinergic nerve transmission, most likely from the parasympathetic division of the autonomic nervous system, can influence Eustachian tube function. We hypothesize that this effect is due to changes in surface tension in the Eustachian tube as a result of changes in secretion. – Franz & Anderson, 2002 Patients suffering from Ménière’s disease are particularly sensitive to negative pressure in the middle ear. For example, attacks of vertigo can be triggered by a descent in an aircraft when ventilation of the middle ear can become critical. – Franz & Van Der Laan, 2005

Bruxism

Bruxism, being teeth grinding in the night, is a response to mandibular instability. Lack of vertical height of the teeth, improper tongue posture (especially a completely lowered tongue), as well as TMJ stability will cause the nervous system to try to find stability in occlusion, by clenching the teeth together. This, of course, will just reduce the vertical dental height further over time as they are wearing out, and thus exacerbate the bruxism.

There are some dentists that repair the teeth’s dental height, or make night splints for the teeth. Usually though, establishing TMJ stability through strengthening the pterygoids, getting the tongue up to the roof of the mouth and changing the resting position of the mandible in daily posture will be sufficient measures. If this does not cure the bruxism, a splint or other relevant dental procedure may be necessary.

Tinnitus

As already mentioned, the trigeminal nerve innervates the muscles that control sound modulation in the ear, namely the tensor tympani and tensor veli palatini muscles. Compression of this nerve’s branches will often spread to the ear, which is why there is a high correlation between TMD and tinnitus complaints. Tinnitus may also occur because of buccal nerve compression, in which case it is not necessarily a TMD problem but a lateral pterygoid problem.

Additionally, the pterygoid muscles have fascial connections to the inner ear. Both pulsatile tinnitus and ordinary tinnitus may be treated by strengthening the pterygoid muscles and optimizing mandibular articulation and resting position.

Tinnitus may also be caused by sympathetic plexus irritation. Review my thoracic outlet syndrome and atlas articles for further information.

Fig. 16

Many patients with temporomandibular disorder and coexisting tinnitus find that therapy improves or resolves their tinnitus in conjunction with their TMD symptoms. – Wright & Bifano, 1997 It was observed that tinnitus was significantly associated with age, bruxism, otalgia, loss of posterior teeth, pain in masticatory muscles, TMJ pain, and existence of TMJ sounds (p<0.05). – Beriat at al., 2011 A few cases of tinnitus have been relieved temporarily by novocain block of the auriculotemporal nerve. – Garnett Passe, Sympathectomy in Relation to Meniere’s Disease, Nerve Deafness and Tinnitus We surveyed 1032 patients: 338 had TMD and 694 served as two age-matched control groups. Tinnitus and vertigo symptoms were significantly more prevalent in the TMD group than in either of the control groups. – Chole & Parker, 1992 TMD patients with coexisting tinnitus report 46 to 96 percent have tinnitus improvement or resolution from TMD therapy (Table 1).9-15 A survey taken two years after TMD therapy suggests the tinnitus improvement is sustained over time – Wright & Bifano, 1997 Several findings indicating a relatively strong relationship between CMD, tinnitus and subjective hearing loss were noted. This relationship seemed to be independent of objectively assessed degree of hearing loss, occupational noise exposure, general morbidity, medication or socioeconomic status. The prevalence of frequent headaches and fatigue or tenderness in jaw muscles was higher in tinnitus patients than would be expected if these conditions were unrelated. About one third of the individuals affected by tinnitus reported influence on tinnitus by jaw movements or pressure on the temporomandibular joint (TMJ). – Rubinstein, 1993 The study concludes with a recommendation for TMJ referral for those tinnitus patients with unknown etiology who demonstrate any three or more of the TMJ indicators. – Vernon et al., 1992

Correctives

As the Mews mentioned, the solution may be perceived as too simple to be true. Although I don’t follow the exact same protocol that they use as dentists, their principles definitely led me to the solution of this issue as a structural corrective that can be maintained with proper myofascial and postural work.

I’ve touched on it already; maintain proper mandibular resting position by protracting the jaw slightly. You may disregard your occlusion, it is ok that the teeth are not touching, because your dysfunctional occlusion is what’s causing your TMD in the first place. Dentists probably won’t agree with me, but I have a close to 100% success rate treating TMD this way, and strongly believe that this outweighs any benefit that a dysfunctional occlusion may yield (if any). By optimizing tongue posture, and chewing harder foods, the maxilla may develop in a parallel manner and thus lead to a win win situation.

Here is the protocol:

From maximal mandibular retraction, protract the jaw (2)-4 millimeters, and stay there. Read that twice if you need to, because it’s the foundation of this article and the most important principle of curing TMD. This single postural act will open up the TMJ, completely removing the chronic shear forces between the mandibular condyle and the joint’s disc and socket. You may end up with a slight underbite (rare), but this is still better than eating through a straw and living with chronic facial pain. Most people won’t end up with an underbite though; it’ll just feel a little weird not to maintain occlusion in posture. Once again, the molars can no longer occlude in this position, which is normal and not a problem. The key is to unjam the TMJ by getting the mandible forward.

The lips should be sealed, and you should breathe through the nose. This will keep the front teeth in check, hindering them from protruding. In fact, it’ll keep them in line. Of course, you must maintain your normal occlusion when eating, to crush the food with your molars. That’s fine, it won’t cause any injury as long as the TMJ is centrated at all other times. The body can cope with this minor joint shearing, as long as it ceases at the remainding hours of the day.

Pain levels will usually reduce quite quickly after optimizing joint resting position, unless there is severe bruxism at play. In such case, as mentioned, a night splint may be necessary.

Fig. 17

Additionally, it’s important to optimize mandibular movement by teaching it to protract properly during opening, and gradually (not maximally) retracting during closing. It’s difficult to learn both a new mandibular resting position and way of opening, but definitely doable with some practice and motivation.

Honestly, proper opening and closing of the mouth is something anyone can benefit from, TMD or not, as the pterygoids which promote proper mandibular kinematics also attach to the sphenoid bone. I’ve written more extensively about this in my atlas article, but my theory is that it controls posture due to its relations to the optic chiasm and nerve tracts. This is probably why so many studies show correlation between occlusion and posture; due to its relation and altered pull on this very special cranial bone.

Teeth clenching during stress, mouth breathing, etc, must also cease. Jaw clenching often reduce or cease on its own when proper resting position is assumed, as it’s not possible to protract the mandible and clench the molars simultaneously. Mouth breathing however, may be more difficult to stop with if the airways have been restricted as shown in the initial video in this article. If this is your or your patient’s problem, I recommend looking into the “Buteyko breathing method”, which addresses this issue.

Strengthening the pterygoids

Strengthening the lateral and medial pterygoids will often be necessary to promote proper joint kinematics (jaw movement), resting position, and also to free the buccal nerve from potential entrapment. An indication of weakness can be buccal nerve pain, tinnitus, or difficulty maintaining the new mandibular resting position.

A small number of sufferers may struggle to protract the jaw without clenching the suprahyoid musculature. This is a strong dysfunction, and indicates extreme weakness of the pterygoids. In such case, very light protractions without any resistance must take place, while simultaneously palpating the suprahyoid musculature and ensuring that it is not activating during protraction. To resolve TMD, it is CRITICAL to learn how to protract the jaw without tensing the supra hyoid muscles. Read this several times, if needed! It is vital.

Here are the exercises. Again, make sure that you’re not clenching the suprahyoid, which is a common cheat when the pterygoids are forced to work harder than their capacity allows.

The lateral pterygoid can be strengthened by opening the jaw forward and downward while resisting with your palm. Make sure to also control the eccentric phase (reversal).

The medial pterygoid can be strengthened by closing the jaw forward, form an open base position. Once again, use your palm as resistance and make sure to control the eccentric phase.

Epiglottic function after mandibular correction

The epiglottis is a flap made out of elastic cartilage, a valve that diverts air to the windpipe (trachea) and food contents into the stomach pipe (esophagus). Normal resting position of the epiglottis is a relatively closed resting position.

If the epiglottis not sufficiently closed during inspiration, it will not be able to deflect pathogen from the stream of air properly, and all of these will pass into the trachea and lungs, something that may lead to chronic respiratory infections, clogged nose and so on. Similar symptoms may also occur if the epiglottis opens up excessively during expiration, as the contents from the esophagus may follow the air flow through the nose, causing buildup of fungi and bacteria and thus clogging up the nose. Likewise, if the epiglottis is not sufficiently closed when we talk, the stomach pipe will be open, and gasses and odours from it will be let out as we speak, which may cause chronic bad breath.

Fig. 18

For the epiglottis to rest in proper closure, the hyoid bone must not have dropped down or come forward in posture, i.e general resting position. The hyoid should be situated in level with the mid-C3 vertebrae, and it should not be pulled excessively to one side (this often causes clicking hyoid syndrome, as it rubs into the thyroid cartilage). If the hyoid has dropped, the chin will appear to be ‘double’, i.e appear to be adipose tissue, even if the person is slim. This is not adipose tissue, however, it is a dropped hyoid bone. And when the hyoid drops, the epiglottis will come down and forward as well, i.e open up.

Fig. 19 – Dropped hyoid (levelled with C4), false appearance of double chin. Note the poor cervical posture

Sometimes, the epiglottis is resting in proper position when breathing, but opens up too much when speaking, leading to bad breath, but not excessive pathogen inflow and respiratory infections. Proper resting position of the epiglottis is encouraged by proper swallowing techniques as well as proper tongue posture. However, the epiglottis should still stay relatively closed when the tongue is articulating (i.e speaking), so it’s not solely dependant on the tongue’s position.

Because the mandible and the epiglottis are connected through the tongue and hyoid bone, protracting the mandible in posture (to resolve TMD) may sometimes also cause dysfunction of the epiglottic valve, because it will somewhat pull the hyoid bone forward, and nervous system isn’t used to or able to close the epiglottis normally in the new mandibular position. This is simply a matter of training it to do so, by learning to control it. The epiglottis closes when we initiate swallowing. Palpate your hyoid bone while swallowing and you’ll feel it move up and posteriorly.

Fig. 20

Instead of allowing the valve to be completely open when breathing and talking, which would also be indicated by downward and forward drop of the hyoid bone, it’s important to train it to remain in proper position. Proper position is just open enough to maintain steady and full airflow. Initiate swallowing and try to breathe; it won’t work as the epiglottis is blocking the trachea. Now reverse the swallowing by a few millimeters; breathing should be possible but restricted. Reverse it some more; breathing should now be fully possible without restrictions, but the hyoid has still not dropped down or forward.

Learn to breathe, and talk without allowing the epiglottis to drop down and forward.

Cervical instability

Clenching of the hyoid muscles may also be a compensatory strategy which is secondary to cervical instability. Poor cervical postures, muscle weakness or injury (especially of the longus capitis & colli muscles), etc., may cause the patient to clench his throat (hyoidal muscles) as they have similar functions as that of the deep neck flexors. Clenching them will somewhat increase cervical stability. However, it will also pull the hyoid bone caudally (down) as well as the mandible back, and is thus an important factor to evaluate in neck and jaw patients. If the patient is clenching their throat in order to stabilize their necks, it is important to re-incorporate the impaired muscles’ function (often the deep neck flexors) and simultaneously work on ceasing his or her throat clenching. Read my atlas article for more information on this topic.

Summary

Temporomandibular dysfunction or TMD occurs when the mandibular condyle (head) is continuously resting or being pushed too far back into the joint socket. Over time, this may injure the articulate disc and cause its displacement, lead to joint degeneration, trigeminal neuralgia, postural anomalies and so on.

The main cause of the posterior position of the mandibular condyle, is an underdeveloped maxilla bone (upper jaw). This causes occlusion to establish too far back, ultimately jamming up the joint due to length differentials between the mandible and maxilla bones (as the mandible keeps growing to its full potential, no matter if the maxilla’s growth is inhibited). Proper tongue posture, nasal breathing and lip sealing may encourage the once inhibited maxillary horizontal growth process to reinitiate, even in adulthood.

Swayback posture leads to forward head posture, which causes the mandible to pull backward due to its sternal attachment through the hyoid musculature. Thoracopelvic and craniocervical posture is therefore a relatively important aspect in the treatment of TMD.

Maxillary underdevelopment or not, TMD may be relieved by these simple points, in the utmost majority of cases: