Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Temporomandibular Joint Dysfunction
December 14, 1991
J. Cary Moorhead, M.D.

Temporomandibular Joint Dysfunction (TMJ) affects between 4 and 28 percent of the population. There is a distinct female predominance of approximately 4 to 1. It usually affects people in their 20s to 50s but may involve any age group. Finally, there is an increased incidence of the disease in patients with other emotional disorders.

The essential parts of the temporomandibular joint are the condyle, the glenoid fossa, the articular eminence and the disk. The disk consists of an articular surface called the meniscus as well as the fibroelastic anterior and posterior ligaments. The posterior ligament inserts around the squamotympanic fissure. The anterior ligamentous attachment is classically described as inserting directly onto the lateral pterygoid muscle, although this is controversial. The lateral aspects of the disk insert onto the side of the condyle. Finally, a capsule encompasses the entire joint. The disk divides the joint space into the superior and inferior compartments. The inferior compartment functions as a hinge joint and is responsible for the first 15 to 20 mm of movement of the mandible. The superior articulation functions as a sliding joint, and is responsible for movement beyond 20 mm.

TMJ disorders are commonly divided into Myofascial Pain Dysfunction or MPD which is primarily a muscular phenomenon and Intrinsic Joint Derangement or IJD, which is a more organic disruption of the joint.

The most commonly implicated causes of TMJ disease include stress, bruxism or teeth clenching, malocclusion, and acute trauma. The relative contribution of each of these factors is controversial, however.

Laskin, in 1969, described the progression of MPD in terms of emotional stress leading to bruxism which eventually leads to muscle fatigue and spasm. It is this spasm in the muscles which is felt to be responsible for the majority of pain experienced by patients with TMJ

disorders. If the disease is allowed to continue, spasm may progress to myositis and fibrosis, eventually leading to intrinsic joint derangement (IJD) and even osteoarthritis.

The classical teaching on the development of IJD states that spasm of the external pterygoid contributes to anterior displacement of the disk, disarticulating it from the head of the mandible. As the condyle glides forward during jaw opening, the disk is reduced back into its correct position with an audible "click." Repeated pressure leads to stretching of the posterior attachment, so that eventually the disk is no longer reducible and remains anterior to the condyle impeding jaw movement. The retrodiskal tissue may become thinned, and eventually perforate.

This theory has some problems, however. Recent anatomic studies by Yung failed to show any significant insertion of the lateral pterygoid onto the disk. Instead, the fibers were found to insert onto the head of the condyle. If this is so, the idea of muscular spasm leading to disk disarticulation does not work. Also, direct visualization of joint movement during arthroscopy does not appear to show disk disarticulation but merely disk hesitancy.

New theories suggest that joint dysfunction may be initiated by inadequate lubrication of the joint. This may be secondary to excess load being placed on the joint, by disturbances in the articular surfaces, or by a combination of these. Inadequate lubrication leads to friction, which causes the meniscus to hesitate and then snap free. In this scheme, the sudden release of the disk from its "stuck" position is responsible for the click.

The cardinal signs and symptoms of TMJ dysfunction consist of pain, tenderness, joint noise and limitation of movement. Pain occurs in almost all patients. It is usually unilateral, and may be localized or ill-defined and may be referred to any area of the masticatory system. It is often worse during mealtimes or upon awakening secondary to nighttime bruxism. Tenderness is also found in the vast majority of patients. "Trigger points" represent hyperirritable foci within the muscles. Palpation of these points can result in a painful sensation at that point, or in referred pain at a remote site. Disk noise is reported in between 15 to 80% of patients. The usual noise heard is a click with jaw opening and closing. Classically, the later a click is heard in opening of the jaw, the more severe the disease is felt to be. However, the validity of this claim is uncertain. Crepitus is a late finding. Limitation of movement presents in approximately 25% of patients. It can be painful or painless, and can occur in both vertical and lateral movement. This may be due to adhesive bands within the joint, muscle spasm, or possibly impedance by the disk.

Arthrography and MRI are the current radiographic methods of choice in evaluating IJD. The advantages of arthrography are its ability to show disk position and ability to demonstrate meniscal perforations. MRI provides excellent soft tissue resolution, is noninvasive, and can show multiple projections. Its main disadvantage is its inability to demonstrate meniscal perforations.

Arthroscopy offers direct visualization of pathology as well as the opportunity for therapeutic intervention.

Explaining the disease process to the patient is probably the single most important aspect of therapy, since the disease has a strong psychological component. The initial treatment modalities consist of home therapy, including application of moist heat over the jaw, maintaining a soft diet, use of NSAID's or muscle relaxants, and encouragement to avoid bruxing or teeth clenching. These simple methods will result in total or near total resolution of symptoms in approximately 70 percent of patients.

If the patient fails to improve, the next step is usually a flat plate occlusal splint, which adds vertical height to the bite, stretching the muscles and relieving the muscular spasm. Approximately 80% of patients who were refractory to home therapy claim to have significant relief of pain with splint therapy.

If more conservative methods fail, the next step in therapy is often arthroscopy. The most common procedures performed through the arthroscope are lysis of adhesions, removal of debris and simple irrigation of the joint space. Many patients who have been vigorously lavaged experience complete relief of pain and return of jaw range of motion, possibly due to a pneumatic lysis of adhesions between the lateral disk margins and the joint capsule.

If all other treatment options fail, patients may require open joint surgery, including disk tie back procedures, reduction of the articular eminence, removal of the disk, and placement of disk, condylar or glenoid fossa prostheses.

Case Presentation

A 24-year-old female presented to Ben Taub General Hospital with a complaint of bilateral ear and preauricular pain, worse on the right than the left. This was exacerbated by eating and was associated with a "popping" sensation when she opened her mouth. A thorough examination failed to reveal any ear or other head and neck pathology but loudly audible bilateral clicks were heard with jaw movement. The patient was started on nonsteroidal anti-inflammatory agents and referred to Oral Surgery with a diagnosis of TMJ syndrome. She was started on a program of jaw rest and fitted with a maxillary fitting flat occlusal splint. The patient underwent regular follow-up in the Oral Surgery Clinic and reported virtually complete relief of her pain and cessation of joint clicking.

Bibliography

Benson BJ, Keith DA: Patient response to surgical and nonsurgical treatment of internal derangement of the temporomandibular joint. J Oral Maxillofac Surg 43:770-777, 1985.

Bronstein SL, Tomasetti BJ, Ryan DE: Internal derangements of the temporomandibular joint: correlation of arthrography with surgical findings. J Oral Surg 39:572-584, 1981.

Costen JB: A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otol Rhinol Laryngol 43:115, 19-34.

Franklin DJ, Smith RJH, Catlin FI, Helfrick JF, Foster JH: Temporomandibular joint dysfunction in infancy. Int J Pediatr Otorhinolaryngol 12:99-104, 1986.

Goss AN, Bosanquet AG: Temporomandibular joint arthroscopy. J Oral Maxillofac Surg 44:614-617, 1986.

Greenberg SA, Jacobs JS, Bessette RW: Temporomandibular joint dysfunction: evaluation and treatment. Clin Plast Surg 16:707-724, 1989.

Hodges JM: Managing temporomandibular joint syndrome. Laryngoscope 100:60-66, 1990.

Konzelman JL: TMJ:Is it a syndrome or symptom? Dent Manage 28:40-46, 1988.

Laskin DM: Etiology of the paindysfunction syndrome. J Am Dent Assoc 79:147-153, 1969.

Laskin DM, Block S: Diagnosis and treatment of myofacial paindysfunction (MPD) syndrome. J Prosthet Dent 56:75-84, 1986.

McCain JP: Arthroscopy of the human temporomandibular joint. J Oral Maxillofac Surg 46:648-655, 1988.

Nitzan DW, Dolwick MF, Martinez GA: Temporomandibular joint arthrocentesis: A simplified treatment for severe, limited mouth opening. J Oral Maxillofac Surg 49:1163-1167, 1991.

Randolph CS, Greene CS, Moretti R, Forbes D, Perry HT: Conservative management of temporomandibular disorders: A posttreatment comparison between patients from a university clinic and from private practice. Am J Orthod Dentofac Orthop 98:77-82, 1990.

Rao VM, Farole A, Karasick D: Temporomandibular joint dysfunction: Correlation of MR imaging, arthrography, and arthroscopy. Radiology 174:663-667, 1990.

Schwartz LL: Pain associated with the temporomandibular joint. J Am Dent Assoc 51:394-397, 1955.

Soldberg WK: Temporomandibular disorders: masticatory myalgia and its management. Br Den J 160:351-356, 1986.

Stegenga B, De Bont LGM, Boering G, Van Willigen JD: Tissue responses to degenerative changes in the temporomandibular joint: A review. J Oral Maxillofac Surg 49:1079-1088, 1991.

Stockstill JW: The placebo effect in the management of chronic myofascial pain: A review. J Am Coll Dent 56:14-18, 1989.

Suvinen T, Reade P: Prognostic features of value in the management of temporomandibular joint paindysfunction syndrome by occlusal splint therapy. J Prosthet Dent 61:55-61, 1989.

Talaat AM, ElDibany MM, ElGarf A: Physical therapy in the management of myofacial pain dysfunction syndrome. Ann Otol Rhinol Laryngol 95:225-228, 1986.

Wright WJ, Jr.: Temporomandibular disorders: Occurrence of specific diagnoses and response to conservative management. J Craniomandibular Pract 4:150-155, 1986.

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