Temporal mandibular joint syndrome

Author(s): Rosanna Sabini, DO

Originally published:07/17/2013

Last updated:03/27/2017

1. DISEASE/DISORDER:

Definition

The American Academy of Orofacial Pain (AAOP) divides temporomandibular disorder (TMD) into two broad syndromes: (1) muscle-related or myogenous TMD secondary to myofacial pain and dysfunction, and (2) joint-related or arthrogenous TMD secondary to true articular disease. Both can be present at the same time, making diagnosis and treatment challenging.

Etiology

TMD can be caused by:

  • Myofascial pain dysfunction (temporalis, masseter, lateral and medial pterygoid)
  • Internal derangement of the joint space (trauma, muscle hyperactivity, condylar restriction, anterior crowding of teeth, disc perforation or displacement)
  • Degenerative joint disorders (rheumatoid arthritis, psoriasis, pseudogout, ankylosing spondylitis and lupus erythematosus)
  • Fractures
  • Infections
  • Tumors
  • Psycho-physiologic factors (stress, tension, depression and habitual clenching, grinding of the teeth and fingernail biting)
  • Mal-alignment of the jaws or internal components of the joint space.

Epidemiology including risk factors and primary prevention

Prevalence of TMD varies, with 3-10% for males and 9-18% for women. In women, TMD is second to headache as a cause of facial pain and occurs primarily in females in their reproductive years, between 20-40 years of age. Overall white adults were more likely to report TMD-type pain than Hispanic and Black adults. The increased risk in women is thought to be due to female sex hormones, which have been shown to increase susceptibility for chronic musculoskeletal facial pain. Women over the age of 40 years had a 30% increased risk of TMD with estrogen replacement and 20% risk when oral contraceptives are used. Rates of TMD decrease in both men and woman after the age of 45 years.

Patho-anatomy/physiology

The temporal mandibular joint (TMJ) is a synovial articulation between the condyle of the mandible and the squamous portion of the temporal bone. Innervation is supplied by the branches of the mandibular nerve (auriculotemporal and posterior temporal nerves). The pathophysiology of TMD is thought to occur at the molecular level with release of inflammatory mediators (tumor necrosis factor, interleukin-1, prostaglandin E2, leukotriene B4, matrix metalloproteinases and serotonin- 5-hydroxytryptamine). In response to their release there is vasodilatation, extravasation, activation of nociceptors and release of neuropeptides, which cause histamine and serotonin release from afferent nerve endings and hyperalgesia in TMJ.1 As a result, the pathoanatomical changes in the joint include proliferative changes in the synovia and primary degeneration of the cartilage and surrounding tissues with destruction of the bone structures.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

The stages of disease are commonly classified according to Wilkes, using clinical and radiological data:3

Early stage

  • Clinical: No significant mechanical symptoms other than opening reciprocal clicking; no pain or limitation of motion.
  • Radiologic: Slight forward displacement, good anatomic contour of the disc, negative tomograms, no bone structure changes.
  • Pathoanatomy: Excellent anatomic form, slight anterior displacement, passive in-coordination demonstrable.

Early intermediate stage

  • Clinical: One or more episodes of pain; beginning of mechanical problems consisting of mid-to-late opening loud clicking; transient catching and locking
  • Radiologic: Slight forward displacement; beginning disc deformity, slight thickening of posterior edge; negative tomograms, no bone structure changes.
  • Pathoanatomy: Anterior disc displacement; early disc deformity; good central articulating area.

Intermediate stage

  • Clinical: Multiple episodes of pain; major mechanical symptoms consisting of locking (intermittent or fully closed); restriction of motion, function difficulties.
  • Radiologic: Anterior disc displacement with significant deformity or prolapse of disc (increased thickening of posterior edge), negative tomograms, no bone structure changes.
  • Pathoanatomy: Marked anatomic disc deformity with anterior displacement; no hard tissue changes.

Late intermediate stage

  • Clinical: Slight increase in severity over intermediate stage.
  • Radiologic: Increase in severity over intermediate stage; positive tomograms showing early-to-moderate degenerative changes – flattening of eminence, deformation of condylar head, erosions, sclerosis.
  • Pathoanatomy: Increase in severity over intermediate stage; hard tissue degenerative remodeling of both bearing surfaces (osteophytes), multiple adhesions in anterior and posterior recesses; no perforation of disk or attachments.

Late stage

  • Clinical: Characterized by crepitus; variable and episodic pain; chronic restriction of motion and difficulty with function.
  • Radiologic: Disc or attachment perforation, filling defects, gross anatomic deformity of disc and hard tissues, positive tomograms with essentially degenerative arthritic changes.
  • Pathoanatomy: Degenerative changes of disc and hard tissues; perforation of posterior attachment; multiple adhesions, osteophytes, flattening of condyle and eminence, subcortical cyst formation.

Specific secondary or associated conditions and complications

The natural history of TMD is variable, but the majority of patients have chronic pain or intermittent flare-ups of symptoms. Pain can resolve in one-third of patients, while two-thirds of patients have ongoing pain or a relapsing course.4

2. ESSENTIALS OF ASSESSMENT

History

Careful history taking should include all forms of TMD, as it is often difficult to separate physical, behavioral, habitual, traumatic and psycho-physiologic factors. Symptoms can include:

  • Diffuse jaw pain
  • Unilateral pain in muscles of mastication, radiating to temples, side of face or ear
  • Clicking at joint
  • Limited mouth opening with/without lateral deviation of jaw
  • Tinnitus or other ear symptoms
  • Nocturnal clenching or bruxism
  • Spasticity of muscles of mastication with prolonged chewing
  • Recent change in bite
  • Psychological stress (resulting in nocturnal teeth grinding)
  • Facial trauma
  • Long-term/heavy computer use
  • Dental work
  • Headaches

Physical examination

Physical exam may reveal asymmetry with smallness of facies on the ipsiliateral side. The joint should be palpated with the mouth open and closed to elicit tenderness. Restricted active opening of the jaw can be apparent with joint clicking heard. Passive motion may also be restricted when pulling the jaw forward (fingertips are placed behind the tragi). The masseter, temporalis, lateral pterygoid, digastric, sternomastoid and neck may be painful to palpation when compared to the uninvolved side. Percussion tenderness may be noted for several teeth and tooth wear may be present with clenching and bruxism.

Functional assessment

The TMJ is important for functional activities such as chewing, speaking, yawning, kissing, and facial expressions. Careful history should include an assessment on how TMD is impacting quality of life.

Laboratory studies

Laboratory testing is generally not required for myofascial pain dysfunction and is limited to testing for the presence of systemic arthritic diseases (e.g. rheumatoid arthritis, lupus, etc.), including sedimentation rate, rheumatoid factor, and antinuclear antibody.3

Imaging

Radiological changes of the TMJ are evaluated by orthopantomography (OPTG), computed tomography (CT) and/or magnetic resonance imaging (MRI). OPTG provides limited information but is easily available and can demonstrate structural bone changes of the TMJ. A CT provides detailed three-dimensional imaging of small bony and articular changes in the TMJ such as erosion, sclerosis, subchondral pseudocyst, space flattening and osteophytes.3 An MRI is the study of choice because it detects internal derangements of the TMJ and soft tissue abnormalities.

Supplemental assessment tools

Ultrasonography is a noninvasive and inexpensive diagnostic procedure that can also be used. It can detect, with reasonable accuracy, disc displacement and joint effusions. However, limitations include the scarce accessibility of the medial part of the TMJ structures and having trained operators.5

Early predictions of outcomes

Presence of a high degree of jaw function interference, such as clicking or locking is associated with a poor prognosis. Brief self-directed physical therapy, use of occlusal splints and NSAIDs are also correlated with poorer outcomes.6

Environmental

Behavioral and psychological factors can play a role in TMD, specifically myofascial pain dysfunction and internal derangement. Depression, anxiety and decreased ability to cope with work and family responsibilities must be addressed.

Professional Issues

TMD is commonly seen by both medical and dental professionals who must work collaboratively in the diagnosis and management.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

Considering the multitude of variable etiological factors, at present, no definitive treatment guidelines exist for TMD. However, goals of treatment include reducing or eliminating pain and restoring normal jaw function. Fortunately, most patients respond to simple, noninvasive treatment regimes.

At different disease stages

New onset/Acute

  • Heat – A heating pad, hot towel or water bottle to side of face may alleviate muscle spasms.
  • Oral Rest – Downgrade diet to mechanically soft for 2 weeks, avoid yawning and laughing with mouth open. Restrict repetitive jaw motions (chewing gum, biting fingernails).
  • Medications –
    • NSAIDS (Ibuprofen, Naproxen, Indomethacin) for 2 weeks are commonly prescribed.
    • Antidepressants are often indicated given the strong association between TMD and psychological factors. Tricyclic antidepressants are most widely used and bedtime dosing can often relieve symptoms in 1 to 2 weeks.7 The effect of other antidepressants has not been well studied.7
    • Benzodiazepines are also used and can assist with sleep.7 Use should be limited to 2 weeks due to risk of dependency.
    • Narcotic use should be avoided.
  • Oral Splinting – An array of interocclusal appliances exist to provide full-arch occlusal stabilization and have been proven to be most effective, up to 70-90% of patients.7 The splints improve the function of the TMJ and the masticatory motor system to reduce abnormal muscle function and protect teeth from attrition and abnormal occlusal loading. As a result, masticatory muscle pain is reduced.
  • Behavioral modification – Because of the psychological component in this disorder, decreasing stress is important. Relaxation techniques, conditioning and biofeedback all have been advantageous.7
  • Rehabilitation Therapy – Exercise programs are designed to improve muscular coordination, relax tense muscles, and increase range of motion and strength. The most useful techniques for re-education and rehabilitation of the masticatory muscles were found to be manual therapy, muscle stretching and strengthening exercises.8 Use of splints in combination with therapy has been found to significantly reduce pain than just therapy or splints alone.9 Electrophysical modalities, such as shortwave diathermy, ultrasound, laser and TENS are used to reduce inflammation, promote muscular relaxation and increase blood flow by altering capillary permeability.10
  • Acupuncture – Although the mechanism is unclear, acupuncture may relieve pain by stimulating the production of endorphins, serotonin and acetylcholine within the central nervous system, or by acting as a noxious stimulus.11
  • Although limited in studies and consensus, other options to consider are dry needling and injections. Possible injection medication include steroids, autologous blood, botulinum toxin and sodium hyaluronate injections

Subacute

  • Similar treatment options as the new onset/acute stage are utilized.

Chronic/stable

  • Surgical Intervention – If there is internal derangement, ankylosis and/or failed conservative treatment of the TMD, arthroscopy and/or arthrocentesis may decrease pain and clicking and increase ROM.12 Joint replacement is also an option, but rarely performed secondary to high risk and poor outcomes.
  • Total temporomandibular joint (TMJ) reconstruction or implants can also be considered.
  • Other – A small body of evidence exists for the use of Neuro-reflexotherapy for reducing pain.13

Pre-terminal or end of life care

N/A

Coordination of care

Due to the multifactorial pathogenesis in TMD, therapeutic treatment must be multidisciplinary. As an example, cognitive behavioral therapy, physical therapy, pharmacological therapy and intraoral splints could be a potential approach to first line management.8 Communication among all the treatment members can provide individualized treatment plans for improved success.

Patient & family education

Since stress can cause and/or and worsen TMD, educating patients on stress-reducing techniques could decrease jaw clenching or teeth grinding. Such techniques include deep breathing, progressive muscle relaxation, guided imagery, meditation and/or yoga. Patients should be encouraged to practice daily to relieve symptoms as part of the overall treatment plan. With myogenous etiology of TMJ disorder, symptoms are generally self-limiting, and patients should be reassured that no disease exists. Patients may also require education on the benign nature of muscle spasms.7

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

ROM of the TMJ throughout the course of treatment is the most objective indicator of treatment outcomes. Other outcomes can include alleviation of symptoms, but these are subjective. In addition, it is important to understand that proper diagnosis involves exclusion of other potential disease processes such as headaches, migraines, dental infections, otitis media, sinusitis, temporal arteritis or trigeminal neuralgia.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Current studies of TMD are focused on understanding the nature of the pain, the population affected, factors which lead to chronicity of the condition and various stressors that induce the symptoms. In addition, correlation of OA with orofacial pain, the efficacy of using a multidisciplinary treatment approach and tissue replacement of damaged cartilage are also being studied.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Overall, the evidence-based knowledge in the treatment of TMJ is limited, partly based on the fact that the majority of cases are self-limiting. No long-term clinical trials studying efficacy and safety of surgical investigations are currently being conducted.

REFERENCES

  1. Bonica’s Management of Pain. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.
  2. LeResche L, Saunders K, Von Korff MR, Barlow W, Dworkin SF. Use of exogenous hormones and risk of temporomandibular disorder pain. Pain.1997;69(1-2):153-160.
  3. Leibur E, Jagur O, Voog-Oras Ü. Temporomandibular joint arthroscopy. In: Dragoo JL, ed. Modern Arthroscopy. 1st ed. Rijeka, Croatia InTech; 2011.
  4. Buescher JJ. Temporomandibular joint disorders. American Family Physician. 2007;76(10):1477-1482.
  5. Melis M, Secci S, Ceneviz C. Use of ultrasonography for the diagnosis of temporomandibular joint disorders: a review. American Journal of Dentistry. 2007;20(2):73-78.
  6. Clark GT, Baba K, McCreary CP. Predicting the outcome of a physical medicine treatment for temporomandibular disorder patients. Journal of Orofacial Pain. 2009;23(3):221-229.
  7. Warfield CA, Bajwa ZH. Principles and Practice of Pain Medicine. 2nd ed. New York, NY: McGraw-Hill; 2004.
  8. Madani AS, Mirmortazavi A. Comparison of three treatment options for painful temporomandibular joint clicking. Journal of Oral Science. 2011;53(3):349-354.
  9. Fricton JR. Management of masticatory myofascial pain. Seminars in Orthodontics. 1995;1(4):229-243.
  10. Weiner DK, Ernst E. Complementary and alternative approaches to the treatment of persistent musculoskeletal pain. Clinical Journal of Pain.2004;20(4):244-255.
  11. Gray RJ, Quayle AA, Hall CA, Schofield MA. Physiotherapy in the treatment of temporomandibular joint disorders: a comparative study of four treatment methods. British Dental Journal.1994;176(7):257-261.
  12. Neeli AS, Umarani M, Kotrashetti SM, Baliga S. Arthrocentesis for the treatment of internal derangement of the temporomandibular joint. Journal of Oral and Maxillofacial Surgery. 2010;9(4):350-354.
  13. Berguer A, Kovacs F, Abraira V, et al. Neuro-reflexotherapy for the management of myofascial temporomandibular joint pain: a double-blind, placebo-controlled, randomized clinical trial. Journal of Oral and Maxillofacial Surgery. 2008;66(8):1664-1677.

Original Version of the Topic

Rosanna Sabini, DO, Dayna McCarthy, DO, Navdeep Jassal, MD. Temporal mandibular joint syndrome. 07/17/2013

Author Disclosure

Rosanna Sabini, DO
Nothing to Disclose

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