Clinical Considerations in Diagnosis of the Pathomechanical Temporomandibular Joint

Dennis P. Steigerwald, D.C.
Wesley Shankland, II, D.D.S., M.S., Ph.D.

Temporomandibular disorders (TMD) are a subclassification of musculoskeletal disorders (62, 63). Symptoms of TMD are associated with dysfunction of the craniomandibular region. Tumors, vascular disorders, primary neurologic disorders and odontogenic pains are not included under the heading of TMD. Rheumatologic disorders which affect the temporomandibular joints include rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and psoriatic arthritis (62). Local TMD symptoms include jaw pain, painful clicking in the temporomandibular joints and limited capacity for mandibular function such as chewing and mouth opening. Limitations in mandibular function are usually pain-mediated, however mechanical limitations which the patient perceives as dysfunctional are also considered local TMD symptoms. Other symptoms reported to be produced by this region include, but are not limited to, neck pain, headache, upper trapezius pain/stiffness, upper extremity pain/paresthesia, ear pain, subjective hearing loss, dizziness and tinnitus (14, 33, 40, 62, 105, 106). It should be noted that a wide variety of rather obscure symptoms have been attributed to TMD with little scientific work supporting a direct relationship between tissues of the craniomandibular region and these symptoms. Chronic pain has been associated with TMD, although a clear etiologic relationship between psychological profile and TMD has not been established (48). Research in the form of anesthetic injection studies and retrospective surgical analyses have developed some statistically supported statements that dysfunctional craniomandibular tissues can produce symptoms at some distance from themselves including certain symptoms which appear quite general in nature. It has been demonstrated for example that headache, neck pain, upper shoulder muscle pain, dizziness and tinnitus can be direct manifestations of the pathophysiology/pathomechanics of the temporomandibular joints specifically (105). These findings may be explained by the impact of the trigemino-cervical system on other cranial nuclei (e.g. cranial XI), the cervical dorsal horn, the thalamus and higher order brain centers. The extreme caudal extent of the spinal tract of the trigeminal nerve is still under investigation (1).

TMD SYMPTOMS AND SYMPTOM CHARACTERISTICS

  1. The most common symptoms of a temporomandibular disorder are:
    1. Ear symptoms.
    2. Headache.
    3. Neck and upper shoulder muscle pain.
    4. Jaw pain.
    5. Temporomandibular joint noise (clicking, grating) with mandibular movement.
      (This is only a symptom if it is painful or associated with dysfunction)
    6. Limited mouth opening and/or disturbances in capacity for mandibular movement.
    7. Dizziness.
    8. Pain and paresthesia in the upper extremities.
    9. Difficulty swallowing.

  2. Ear symptoms associated with temporomandibular disorders include:
    1. Fullness in the ears.
    2. Tinnitus.
    3. Ear pain.
    4. Subjective hearing loss.
    5. The sensation of itching in the ears.

  3. The most common headache presentations associated with a temporomandibular disorder are frontotemporal and suboccipital (109). It is not uncommon for a patient to express the experience that the headache comes up from the neck to the skull when the driving force behind the headache is in fact the inflammation in the temporomandibular joints (105). If inflammation and/or derangement of the temporomandibular joints is producing the headache, patients usually experience these headaches at least two to three times per week if they are not receiving treatment or are not placed on a home care program (109). Less frequent experience of untreated headaches is more likely to be a functional myofascial disorder or a headache which is unrelated to the temporomandibular joints specifically.

  4. When inflamed temporomandibular joints produce neck and upper shoulder pain, this pain is predominantly in the lateral cervical, upper trapezius and/or suboccipital regions. This is not referred pain as the involved muscles will be hypertonic and tender to palpation. It is very unusual for inflamed temporomandibular joints to produce only posterior central cervical pain.

Research into the pathomechanics and pathophysiology of TMD has been extensive (8, 25, 39, 52, 85, 87, 100) and parallels investigation of the dysfunctional and symptomatic intervertebral joint motion segment closely. In both bodies of research the biochemistry, architectural relationships, kinematics and neurology of joints, muscles, tendons, discs and ligaments have been investigated. All of these tissues have been implicated in various clinical disorders. Recent interest in both fields has focused on the impact of musculoskeletal pathology on the central nervous system and the complexities of symptoms generated therein. Despite this rather large body of research, clinical approaches to TMD still tend to be rather general and often are based on unfounded or even disproved hypotheses. The primary pathomechanics, pathophysiology and neuropathology of the region are in fact often ignored in the clinical setting.

The primary areas of TMD investigation include: the nature of TMD, etiologies of TMD, prevalence of TMD and the effects of treatment on TMD. There are, of course, many other issues being investigated concerning TMD, e.g. predictability, prevention and risk factors. This parallels research on the symptomatic intervertebral joint motion segment and other disorders of articular origin.

FUNCTIONAL ANATOMY

The temporomandibular joint or craniomandibular articulation is a ginglymoid-arthrodial joint. Each joint is an articulation between the articular tubercle eminence of the squamous portion of the temporal bone (the mandibular fossa or glenoid fossa) and the mandibular condyle. A fibrous disc, which acts as a third bone, is interposed between the condyle and the fossa formed by the temporal bone. These paired joints and the mandible, a single bone that crosses the skeletal midline, function together since neither joint is capable of independent movement. That is, one temporomandibular joint cannot possibly move without producing movement in the opposite joint.

The human mandible is the first bone of the body to demonstrate an ossification center. At approximately six weeks in utero, developing from the mandibular process of the first branchial arch, the mandible is seen as a thin plate of bone in close association to the lateral side of the anterior region of Meckel's cartilage on both sides of the developing face (24). Although Meckel's cartilage does not contribute much to mandibular development, it does to the incus, malleus, sphenomandibular and malleo-mandibular ligaments. All major portions of the mandible (the body, ramus, coronoid and condylar processes), develop by intramembranous ossification. Only the articular surface of the condyle and the tip of the coronoid process develop by endochondral ossification. The articular eminence of the temporal bone is composed of compact bone overlying trabecular bone with marrow spaces. Both the articular eminence and the articulating surface of the condyle are covered with fibrocartilage, not hyaline cartilage, as in most other articulations of the body.

The temporomandibular joint is richly innervated by three different branches of the third division of the trigeminal nerve (10). The auriculotemporal nerve, providing innervation to the posterior, lateral and some medial portions of the joint, contributes approximately 75% of the total sensory supply to the joint. Anterior and medial innervation of the temporomandibular joints is provided by the masseteric nerve, giving about 15% of the total innervation. The posterior deep temporal nerve, supplying about 10% of the this innervation, furnishes sensory innervation to a small area in the anterolateral portion of the joint.

Blood flow to the temporomandibular joints is also abundant and from many sources. The principle blood supply comes from the superficial temporal artery and branches of the maxillary artery, both of which are the terminal branches of the external carotid artery. Venous drainage is provided by companion veins, all of which contribute to the retromandibular vein, and by the facial vein, which contributes to the anterior jugular vein.

ANATOMICAL CHARACTERISTICS OF THE TEMPOROMANDIBULAR JOINTS

The temporomandibular joints are synovial joints and share many characteristics common to all synovial articulations (2). The temporomandibular joints exhibit several anatomical features which are somewhat unique and delineate them from other synovial joints, however. All synovial joints are weight or load bearing and the temporomandibular jomts are no exception. The following structural characteristics contribute to the integrity and biomechanics of this joint system.

ENCAPSULATION

To meet the demands of the metabolism of the non-vascular articular surfaces of any synovial joint, synovial fluid must be present at all times. Total enclosure or encapsulation of such a joint allows for the containment of this fluid. Each temporomandibular joint is confined within a fibrous capsule which is attached superiorly to the articular eminence of the temporal bone, posteriorly to the squamotympanic fissure and between these attachments to the edges of the mandibular fossa, and inferiorly to the neck of the mandibular condyle (37). The joint capsule is highly vascularized, well innervated and lined with synovium. The synovium lines all aspects of the joint that are not subject to load bearing. The capillaries in the capsular walls engage in free metabolic exchange with the synovial fluid within the joint. In addition, the synovial fluid provides lubrication and phagocytic activity. The fluid is a dialysate of plasma and lymph, consisting of a mucopolysaccharide complex (80) chiefly, hyaluronic acid. The capsule is innervated by both free nerve endings and specialized receptors (54, 69). Specialized receptors include Rufftni endings and Vater-Pacini corpuscles. Free nerve endings (small, type III and IV) are the dominant receptor type in the temporomandibular joints (108). Nerve endings are not found on the load bearing surfaces of the temporomandibular joint nor are they found in the articular disc except for mechanoreceptors at the extremes of its periphery (69). Free nerve endings in the temporomandibular joint serve as both mechanoreceptors and nociceptors (108). All receptors have their cell bodies in the trigeminal ganglion and relay information to the nuclei of the trigerninal nerve (10, 22, 28), the thalamus (74, 75) and higher brain centers (28).

NEXT (page 2 of 7)