Clinical Considerations in Diagnosis of the Pathomechanical Temporomandibular Joint
P. Steigerwald, D.C.
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:
2. Ear symptoms associated with temporomandibular disorders include:
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.
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 joints are no exception. The following structural characteristics contribute to the integrity and biomechanics of this joint system.
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).
The temporomandibular joint is classified as a compound joint. A compound joint, by definition, requires the presence of at least three bones or surfaces (e.g. the capitulurn and trochlea of the humerus articulating with the radius and ulna forming the elbow). However, the articular disc interposed between the condyle and mandibular fossa functions like a non-ossified third bone, thus forming a compound joint. The articular disc of a temporomandibular joint articulates superiorly with the articulating surface of the temporal bone and inferiorly with the capitulum of the mandibular condyle. The disc is continuous on its lateral and medial surfaces with the joint capsule, posteriorly with the retrodiscal tissue, and anteriorly with the joint capsule and a small portion of the superior head (approximately 2.4-6%) of the lateral pterygoid muscle (5).
The disc is a true disc. That is, a temporomandibular joint disc will divide the joint into two separate compartments. This is in contrast to a meniscus (e.g. the knee) which does not divide the joint, but extends freely into the joint compartment and attaches to the capsule only by one edge (3). The space between the disc and the temporal bone is called the superior joint space or compartment and is anatomically discrete from the smaller, inferior joint space between the disc and the condyle. Violation of this relationship occurs when the disc or retrodiscal tissue becomes perforated. This allows for direct contact of the bony articular surfaces and may or may not be associated with symptoms. The superior joint space allows for translation of the disc along the articulating temporal surface and the inferior joint space accommodates rotation of the condyle under the disc. Pathomechanical restriction of the capacity for gliding in the superior joint space has been observed to be important clinically and will be discussed later in this chapter. The disc is firm and biconcave in shape. It is comprised of fibrous tissue which is organized in sheets of antero-posteriorly oriented fibers on the superior and inferior surfaces, with thicker anterior and posterior peripheral areas made up of fiber oriented in all three directions and space (2). These fiber orientations provide for a most interesting structural design which resists displacement of the disc bodily (anteriorly and posteriorly) from the condyle during mandibular translation. Rees (89) divided the articular disc into four sections:
These discal contours provide joint stability by continual contact of all articulating surfaces during joint motion. After the approximate age of 2 years the disc is avascular and alymphatic depending on diffusion through the synovial fluid for nourishment. This avascular condition is required as pressure on blood vessels and nerves could not be tolerated. It was stated earlier that the disc is continuous laterally and medially with the joint capsule. However, it is more accurate to say that the disc is bound by firm attachments directly to the condyle. The relationship of these attachments to the capsule is an area of some debate.
The retrodiscal tissue, also known as the bilaminar zone, is an area posterior to the articular disc which is comprised of two separate layers or laminae. It extends from the superior/posterior most portion of the posterior band of the disc back to the tympanic plate and to the posterior aspect of the neck of the mandibular condyle. This structure is folded in an accordion-like fashion when the mandible is at rest or the teeth are in full contact and is stretched and extended during protrusive and mouth opening movements.
The superior stratum of the retrodiscal tissue, which is richly innervated by the auriculotemporal nerve, is a very important structure in temporomandibular joint biomechanics (121). This structure is often inappropriately referred to as a ligament. It is actually composed of elastic connective tissue which produces a passive posterior force on the articular disc during its forward movement. This traction serves to rotate the disc in a posterior direction during condylar translation (4). This arrangement adds to the stability of the joint by keeping a firm contact between the articulating surfaces. Disc movement is thus considered to be a function of disc shape and the collateral attachments which tie the disc to the condyle. Any forward movement of the articular disc during condylar translation is counteracted by elastin fibers in the superior straturn. Elastin, an extracellular tissue fiber, exhibits true elasticity (31). Injury, especially sudden injury to the temporomandibular joints during the extension phase of whiplash can produce an irreparable injury to these elastin fibers. Because elastin, unlike collagen, does not have the capacity for repair, such injuries may allow anteromedial displacement of the articular disc, especially if the lubricating capacity of the synovial tissue is lost and adhesions develop which compromise disc mobility. Following such anteromedial disc displacement the characteristic clicking in the temporomandibular joints associated with internal derangement may develop immediately or over time subject to these pathomechanical forces (107, 117).
The inferior stratum of the retrodiscal tissue is composed of loose areolar tissue made up of chiefly non-elastic collagen fibers and possibly elastin as well (36). This structure passively limits forward rotation of the disc on the condyle during translation of the mandible.
Anterior to the superior stratum but posterior to the condyle, is another vascular region termed the vascular knee. This vascular area extends throughout the retrodiscal tissues and contains numerous arteriovenous shunts. In this area, blood is shunted in and out with mandibular function (94). When the mandible translates forward, a negative pressure occurs in this area and when the condyle moves back into its normal resting position in the mandibular fossa, a positive pressure is produced. These pressure changes serve to move synovial membranes within the joint compartments, thus producing a near constant volume in the compartments during joint function. The volume of synovial fluid cannot change as quickly as the mandible moves, so therefore, the movement of blood into these arteriovenous shunts during mandibular movement helps to maintain a constant joint pressure and moves synovial fluid. In persons with a displaced articular disc, the compression of this retrodiscal tissue between the condyle and articular eminence of the temporal bone may or may not produce pain. It has been demonstrated that this area is capable of metaplastic remodeling (53) and many persons with anteriorly displaced discs do not experience pain (81). Pain is produced when inflammation and adhesions activate nociceptors. Relatively rapid disc displacement associated with inflammation is more likely to produce retrodiscogenic pain than that which occurs gradually over years. The importance of ideal disc position in a joint system which demonstrates such extreme capacity for remodeling and repair remains an issue of scientific and clinical debate to date (53).
The bony components of the temporomandibular joints are not covered with hyaline cartilage (2). These articulating surfaces are instead covered by fibrocartilage, which is a growth cartilage of a secondary type, not an articular cartilage. This fibrocartilage is capable of extensive repair and remodeling, thus resisting aging and anatomic breakdown (53). Specifically, the compact bone of the condyles and glenoid fossae are covered by layers of cartilage cells, mesenchymal tissue and fibrous tissue. While signs of degenerative joint disease (DJD) are found in the human temporomandibular joints, it is most frequently asymptomatic (47). This replacement of articular tissue with lesser quality tissue is clinically and radiographically indistinguishable from true remodeling (83) which is, by far, the more common process in the human temporomandibular joint. Clinical expression of symptoms usually follows a precipitating event such as trauma (47) and in that regard temporomandibular joint DJD is not unlike other forms of DJD. Remodeling of the temporomandibular joint articular surfaces has been associated with specific chemical mediators (I-L and tumor necrosis factor (TNF)) (64). It should be noted that articular cartilage is estrogen sensitive. In fibrous joints, such as the temporomandibular joints, estrogen stimulating chemicals have been demonstrated to accelerate DJD and estrogen repressors to slow the process (92). This may partially explain the prevalence of females in most populations of TMD patients. In fact, lower estrogen levels in post menopausal females may partially explain why TMD is less common in the elderly population.
The mandible is suspended from the skull primarily by the temporomandibular ligaments or external lateral ligaments (36). These ligaments suspend the mandible and resist its posterior and superior displacement. Each ligament consists of two distinct portions:
The sphenomandibular ligament is also known as the internal lateral ligament (37). Classically, anatomy texts have listed its origin as the angular spine of the sphenoid and the petrotympanic fissure. However, it actually is a combination of the anterior malleolar ligament (79) which attaches to the anterior process of the malleus. This small ligament passes through the pterygotympanic fissure and the medial portion of the temporomandibular capsule and continues as the sphenomandibular ligament inferiorly and slightly laterally insert into the medial portion of the mandible. This ligament is passive during mandibular movements and maintains approximately the same amount of tension during opening and closing of the mouth (23).
The articular disc is attached to the mandibular condyle by small and firm medial and collateral attachments. While similar to ligaments, these structures are termed attachments as they join a disc to a bone rather than a bone to a bone. Being intricately involved with condylar motion these small structures limit the degree of rotation of the disc on the condylar head and contribute to disc movement during condylar translation. The lateral collateral attachment is the most common to be stretched or torn with mandibular injury, thus permitting anteromedial displacement of the articular disc which can result in clicking or even locking of the temporomandibular joints.
The stylomandibular ligament has been termed a specialized band of the cervical fascia in anatomical texts. However, it has recently been demonstrated that this structure is in fact a true ligament. This ligament serves to limit protrusive movement of the mandible (101, 102). It originates from the styloid process of the temporal bone and inserts into the medial aspect of the angle of the mandible approximately 1 cm above the inferior border between the masseter and medial pterygoid muscles.
The two basic mandibular movements are translation, which takes place in the superior joint space, and rotation which occurs in the inferior joint space. Rotation frequently occurs along a shifting axis according to translational movements. These joint actions occur during both empty mouth mandibular movements and masticatory functions. All mandibular movements occur as a result of complex muscular interactions controlled by even more complex integrated neural functions. The integration of these movements is not completely understood. Pure mandibular closure appears to involve the activation of muscle spindle afferents and golgi-tendon organs at the junction of muscles and tendons which excite, through monosynaptic reflexes, the alpha motor neurons of the motor nucleus of the trigeminal nerve. The motor nucleus also receives input from the cerebral cortex, the cerebellum, the reticular formation and other cranial nerve nuclei (21). Motor axons leave the nucleus, projecting out of the ventral pons via a small motor root that passes below the trigeminal ganglion, join the mandibular division of the trigeminal nerve and are distributed to the muscles of mastication (masseter, temporalis, medial and lateral pterygoids) as well as the tensor veli palatini, tensor tympani, anterior digastric and mylohyoid.
Mechanoreceptor afferents provide input to the mesencephalic nucleus from receptors in the periodontal tissues, tongue, palate, larynx and temporomandibular joints (20). These same afferent fibers, projecting to the mesencephalic nucleus, also synapse with cells within the motor nucleus. Therefore, jaw closure is a complex series of afferent signals to the motor and mesencephalic nuclei producing efferent activity in the muscles responsible for jaw closure. These muscles include the masseter and temporalis primarily as well as the medial pterygoids. The superior bellies of the lateral pterygoids also contract during closure and contribute to joint stability.
The jaw opening reflex, which is inhibitory to the jaw closure reflex, is mediated by the motor nucleus of cranial V through the reticular formation (20). This inhibitory reflex may also involve the spinal trigeminal tract, chiefly the pars caudalis. There is little actually known about the neural integration of these interactive opening and closing reflexes in humans. It is considered, however, that since there are no temporomandibular joint articular receptors which monitor loading, receptors in the periodontal ligaments and masticatory muscles likely serve in this capacity (108). It is known that if the jaw opening reflex dominates, then the anterior and posterior bellies of the digastric, platysma, suprahyoids (chiefly the geniohyoid, mylohyoid and stylohyoid) and inferior bellies of the lateral pterygoids are activated to open the mouth. Further, the infrahyoid muscles (sternohyoid, omohyoid, sternothyroid and thyrohyoid) fix the hyoid bone thereby assisting in mouth opening.
Even less is understood about the neuroanatomy of lateral movements of the mandible. It is known, however, that lateral movements are accomplished by simultaneous contraction of the contralateral medial pterygoid and inferior head of the lateral pterygoid in concert with the ipsilateral temporalis posterior belly. Protrusive mandibular movements represent a coordinated effort of the inferior bellies of the lateral pterygoid muscles, the bilateral anterior digastric muscles and the medial pterygoids.
Until McNamara (61) and later Mahan et al (55) demonstrated that the two bellies of the lateral pterygoid muscle actually function independently and antagonistically, temporomandibular joint motion was poorly understood. The inferior head contracts upon mouth opening and the superior head contracts with closing of the mouth. The larger inferior head originates from the lateral surface of the lateral pterygoid plate of the sphenoid and inserts into the head and neck of the condyle. When this muscle contracts along with the platysma, digastrics and suprahyoid muscles, the condyle is pulled down and across the articular eminence. Mouth opening is initiated by gravity, the relaxation of the elevator muscles, contraction of the suprahyoid muscles and stabilization of the hyoid by the infrahyoid muscles. This initial movement drops the condyle down and away from the temporal bone and produces rotation of the condyle within the fossa up to approximately 20 to 25 mm of mouth opening. This is followed by contraction of the inferior heads of the external pterygoid muscles which results in translation of the condyle and intervening disc on the articular eminence. As the mandible is moved forward the articular disc rotates posteriorly on the head of the condyle. This posterior rotation is limited by the collateral attachments which tie the disc to the medial and lateral poles of the mandibular condyle. The disc then travels anteriorly with the condyle as the mouth opens to maximum capacity. With this motion elastin fibers of the superior stratum of the retrodiscal tissue stretch exerting posterior traction on the translating disc. Throughout this entire mechanical activity a healthy articular disc remains interposed between the condyle and the articular eminence.
When mouth closing is initiated the inferior belly of the lateral pterygoid relaxes as the superior head contracts. This superior head originates from the inferior orbital rim of the sphenoid and inserts primarily into the pterygoid fovea of the condyle. A substantially lesser portion attaches to the anteromedial aspect of the capsule and to the articular disc. In a study by Bittar et al (5) the percentage of the superior head which attached to the disc was found to average approximately 2.4-6%. Contraction of the superior head theoretically helps to stabilize condylar dynamics during mouth closure and to some extent may influence disc position. Any substantial influence on disc position seems unlikely, however. The disc then effectively rotates forward as it translates posteriorly during the condyle's movement back and up into the mandibular fossa. Optimum disc position during joint movement is maintained then primarily by disc shape, although it is influenced by the collateral attachments, the retrodiscal tissue and possibly somewhat by the superior head of the external pterygoid musculature.
Temporomandibular disorders have traditionally been subclassified as intracapsular and extracapsular. Extracapsular diagnoses include myofascitis, myositis, myospasm and muscle splinting. Coronoid tendinitis and Ernest syndrome are also included in this category. Intracapsular disorders include capsulitis, synovitis, retrodiscitis, symptomatic disc displacement (with or without reduction), disc/retrodiscal perforation, ankylosis and symptomatic hypermobility (including joint dislocation). There is no specific lesion or pathology implied under the general heading of TMD, nor are there definitive symptom presentations. Many symptoms have been attributed to both intracapsular (105) and extracapsular (112) disorders yet acceptable inclusionary and exclusionary factors for some subsets of TMD are still lacking. Difficult questions have in fact been raised concerning the clinician's ability to distinguish primary myofascial TMD from arthrogenous temporomandibular joint disorders (105).
TMD DIAGNOSTIC CLASSIFICATIONS
*Muscle splinting is a muscular response to pathology which may be initiated by intracapsular or extracapsular nociceptive events.
Primary myositis and myospasm are rather rare clinical entities. Myositis presents as an acute continuous muscular pain usually following infection or trauma. The muscle will be swollen and warm to the touch. Pain-mediated limited range of motion will be specific to the involved muscle(s). Myospasm has a similar presentation, although the muscle will not be as warm to the touch or swollen. During myospasm the muscle(s) is fully contracted even at rest. Limited mandibular range of motion is pain-mediated and specific to the involved muscle(s).
When an extracapsular TMD is suspected, a myofascial diagnosis is by far the most common made. Masticatory myofascitis has the following characteristics:
It has been hypothesized that myofascitis has many potential etiologies. These include postural overload, mechanical overload, injury, elevated sympathetic activity (local or systemic) and joint, tendon and/or ligament inflammation-mediated central excitation. While masticatory myofascitis is thought to occur in a manner similar to that proposed for other muscle systems then, in the masticatory system muscle overload is thought to occur as a result of oro-facial parafunctional habits or extremely vigorous chewing. These parafunctional habits include lip biting, thumb sucking, fingernail biting and especially bruxism (63).
Bruxism consists of two activities which may be present in the same patient or which may occur separately. These activities include clenching the teeth together and grinding the tooth surfaces over each other. Clenching and/or grinding of the teeth may occur while the person is awake and/or during sleep (76). Bruxing while awake is most often considered a reaction to stress and may represent a manifestation of elevated sympathetic activity. Nocturnal clenching/grinding of the teeth may be a stress reaction (123) or may represent a manifestation of a primary central nervous system disorder or sleep disorder (88). Despite clinical acceptance of bruxism as an an etiology of TMD, it should be noted that Pullinger et al (86) found no association between tooth grinding as measured by tooth attrition and TMD except for myalgia in young males. It is interesting to note that in contrast to myositis and myospasm, which follow a clear precipitating event, masticatory myofascitis is usually cyclic (90) with no clear single etiology. Proposed etiologies such as malocclusion and bruxism have been observed to be equally prevalent in the TMD population and in the general population (18, 20, 34, 78, 84, 97, 98). It appears that cyclic expression of masticatory myofascitis may be a local expression of a systemic increase in sympathetic activity, the effects of which may vary according to the occlusal architecture and parafunctions specific to the individual. The implications of this are profound in terms of whether to treat a patient for a cyclic myofascial disorder and, if treatment is proposed, how best to go about it. Stress management and biofeedback often play a role in treatment of primary myofascitis as may management of sleep disorders (123). Intermittent use of oral orthotics (65, 120) as well as palliative physiotherapy applications (6) have been recommended. It should be noted that if muscles are not injured, they should relax in a relatively short time (within one to two days) if the stimulus for hypercontraction is removed. This principle should guide diagnoses and treatment of myofascitis. It has been suggested that sustained local symptoms of muscle hyperactivity may indicate the presence of an intramuscular inflammatory response (123). Marcel et al (58) demonstrated biochemical changes in the muscles of frequent bruxers and this data May be productive in future research of this phenomenon.
Non-muscular extracapsular TMDs include coronoid tendinitis (29) and Ernest syndrome (102, 103). These disorders involve inflammation of the temporal tendon(s) and stylomandibular ligament(s) respectively. The most common cause of both disorders is trauma especially that associated with rapid, prolonged and/or excessive mouth opening. The symptoms of temporal tendinitis (coronoid tendinitis) include both local pain (usually with attempts at mouth opening) and symptoms expressed at a distance from the inflamed tissue. These symptoms include temporomandibular joint pain, ear pain and pressure, posterior maxillary tooth pain, ipsilateral eye pain and temporal headache with extension to the occipital, posterior auricular and cervical regions. The temporalis coronoid attachment will be tender to intraoral palpation when it is inflamed. This tenderness is often mistaken for tenderness of the inaccessible external pterygoid. Reproduction of the patient's symptoms with palpation supports this diagnostic impression and elimination of symptoms with anesthetic injection confirms the diagnosis. It is not surprising that the symptoms of temporal tendinitis are similar to those of a primary temporomandibular joint intracapsular inflammation as they share the neurology of the deep temporal nerve (101). Temporal tendinitis can be found in conjunction with or separate from temporomandibular joint inflammation and differential diagnosis requires a thorough examination of the temporomandibular joint complex. While inflammation of the temporomandibular joint may cause coronoid tendon tenderness secondary to sensitization of the deep temporal nerve, the reverse is not commonly observed. In complex and resistant cases anesthetic injection often provides the most accurate diagnostic insight.
Ernest syndrome is an inflammatory disorder of the stylomandibular ligament (103). Symptoms are similar to temporal tendinitis except that mouth opening will not produce pain at the coronoid process and throat pain may be present. A diagnostic impression is developed by history, location of tenderness and symptom reproducibility during palpation. Diagnosis once again is confirmed by anesthetic injection.
Muscle splinting, while usually listed under extracapsular disorders, is a unique phenomenon. The diagnosis of muscle splinting implies a protective muscular response to pathology (122) which may be intracapsular (e.g. synovitis) or extracapsular (e.g. temporal tendinitis). The characteristic signs and symptoms of masticatory muscle splinting are limited range of motion which is specific to the protected region, pain with mandibular movement (primarily mouth opening) with little or no muscular pain at rest and a sense of weakness and/or fatigue in the involved muscles. Muscle splinting is frequently mistaken for a primary muscular disorder because of these signs and symptoms. If muscle splinting is present, the primary pathology stimulating splinting should be identifiable. The primary focus of irritation is usually capsular/ intracapsular inflammation, coronoid tendinitis or muscle injury. Primary myofascitis will not cause muscle splinting. It should be noted that muscle splinting will much more dramatically limit mouth opening than protrusive or lateral mandibular movements.
The terms intracapsular and arthrogenous when applied to TMD indicate that the driving force behind the expression of symptoms is found within the temporomandibular joints proper. While it has been understood for decades that pathologic changes within the temporomandibular joints could result in local symptoms (119), debate has continued over what association, if any, intracapsular disorders have with myofascial presentations and other symptoms expressed at some distance from the joints themselves. One school of thought holds that intracapsular disorders are a subclassification of TMD separate from, however related to, masticatory myofascitis and other muscular influences. Research by Vallerand and Hall (113), Montgomery et al (68), Danzig et al (17), Mosby (70) and Steigerwald et al (105) indicates that temporomandibular joint pathology may in fact produce reactive myofascial presentations in the head, neck and shoulder musculature as well as other symptoms including dizziness, tinnitus and hearing loss (14). The reactive muscular component will demonstrate hypertonicity and tenderness and may well produce tertiary sites of pain when trigger points are produced and/or activated in the involved muscles. This trigeminal affect on the cervical region was also noted by Miralles et al (67) relative to the influence of stabilizing oral orthotics on the sternocleidomastoid musculature. Variations in jaw posture have also been observed to effect the sternocleidomastoid and upper trapezial musculature (124).
PATHOMECHANICS, PATHOPHYSIOLOGY AND PATHONEUROLOGY OF ARTHROGENOUS DISORDERS
The temporomandibular joints are ideally constructed for adaptation, remodeling and repair. Theoretically, this is necessary as this joint system is arguably one of the most active and complex in the body and must adapt to shifting occlusal, postural, functional and parafunctional influences over the lifetime of the individual. Symptoms of the joint-specific intracapsular or arthrogenous TMD may be confined to the joint system or demonstrate complex neuro-myogenous referral patterns. Symptoms of arthrogenous TMD develop when inflammation and biochemical degradation within the joint exceed the capacity for repair (100) and/or when adhesions form within the joints interfering with disc and/or joint mobility (71). Degenerative joint disease (DJD) is defined as replacement of normal articular tissues with tissue of lesser quality (47). While this has been observed in human temporomandibular joints, it is observed in both symptomatic and no symptomatic joints and does not identify a specific clinical entity (47). DJD of the temporomandibular joints does not have a specific etiology and the temporomandibular joints have not demonstrated a tendency toward progressive deterioration and symptom expression. The only component of the temporomandibular joints that has been histological observed to degenerate rather than remodel when the disc is displaced is the disc itself (53).
SENSITIZATION OF NOCICEPTORS IN THE TEMPOROMANDIBULAR JOINTS
Small (group III and IV) receptors are the most numerous receptors in the human temporomandibular joint (49). These fibers are sensitized by inflammation and mechanical deformation such as capsular swelling (108). This decrease in the neural threshold of stimulation may result in neural firing in response to what would otherwise be considered non-noxious stimulation (15, 95). This may explain why patients with articular driven disorders tend to have rather constant symptom expression with fluctuations in intensity when compared with primary myofascial disorders which tend to be truly cyclic. If nociceptors within the temporomandibular joints are stimulated, pain may be experienced locally and/ or along other pathways of the trigeminal nerve (137). Capsular swelling and/or deformation may sensitize mechanoreceptors as well and flood the trigeminal system leading to central sensitization and neuroplasticity (99, 114). This may result in stimulation of other components of what is referred to as the trigemino-cervical complex which includes cranial nerves V, VII, IX, X, XI and XII as well as cervical nerves I through IV (56). This can result in a diffuse spread of symptoms according to the complexity of this system and its interaction with higher level CNS centers. One of the results of this process appears to be elevated activity of the sympathetic nervous system. Research by Hubbard et al (43) has indicated that elevated sympathetic activity, whether local or systemic, may affect the spindle cells of the muscles causing trigger point activation, muscle shortening and local muscle tenderness. Muscles which can be affected by this process include the masticatory muscles (9,30) as well as the intrinsic cervical muscles, the sternocleidomastoideus and upper trapezius (70,105). The reactions and symptoms of the neck and shoulder muscles may be ipsilateral, contralateral or bilateral to the involved joint. This was demonstrated clearly by Danzig et al (17) who investigated the impact of anesthetic injected into symptomatic temporomandibular joints on muscles of the neck and upper shoulder region. It is interesting to note that in Mosby's study (70) it was observed that muscular response to temporomandibular joint pathology was greater in the sternocleidomastoid, upper trapezial and cervical musculature than in the masticatory muscles.
THE NEURAL ANATOMICAL BASIS FOR MUSCULAR CO-CONTRACTION AND REFERRED PAIN IN ARTHROGENOUS TMD
To fully appreciate the impact of pathomechanical and pathophysiologic influences on symptom expression beyond the experience of local temporomandibular joint pain, one must consider the central connections of the joint receptors. The nucleus caudalis of the trigeminal system receives nociceptive input from the oro-facial region (10, 38). This nucleus extends down to at least the level of C3 in the spinal cord and convergence from cervical nerves influences this region (7). Interneurons in this region relay information to higher order centers as well as to other cranial nuclei (21). This area may become sensitized as a result of temporomandibular joint-specific neural influences (99, 114). Bradykinin and substance P spillover may then influence regional cervical nerves and stimulate reactions in the associated cranial nuclei and there higher order centers. The most likely cranial nuclei to be affected include CR VII, IX, X and XI (124) as well as other regions of cranial V including its motor nucleus (9, 99). This process of joint receptor sensitization leading to interneuronal activation with subsequent sensitization and neuro-plastic central reactions may explain the plethora of symptoms peripheral to the temporomandibular joint primary pathology. This includes myofascial presentations of the masticatory and cervical regions which are often clinically mistaken for primary processes. Another frequently misinterpreted symptom is masticatory muscle splinting which can occur secondary to joint pathology (122). The clinical implications of such misinterpretation cannot be overstated.
It is a well accepted principle that the site of pain and the source of pain are different in many disorders (77). The classic example of this is causalgic pain experienced in a missing limb. Trigger point pain also represents a condition which presents with the pain site separate from the pain source (111). These complex clinical entities cause substantial diagnostic difficulties. There are, however, clinical signs which aid in exposing the source of pain. Trigger points for example will produce a typical pain pattern when they are aggressively palpated and/or stretched. The area of pain, if it is truly produced by a trigger point, will be non-tender unless there is some other local pathology or tissue reaction present. Trigger point pain is classically reduced or eliminated with anesthetic injection at the source of pain while injection of the site of referred pain does not impact the pain presentation (77). The most common peripheral symptoms produced by temporomandibular joint pathology result from neural stimulation of muscle activity which produces hypertonic and tender muscles (105). This includes the masticatory and/or cervico-trapezial regions. Trigger points may then arise from these affected muscles producing tertiary locations of pain expression or other symptoms including dizziness and tinnitus. The site of referred pain and the source of pain may thus become even more obscured as the trigger points which now appear as the source of pain are actually second level pain initiators activated by muscular response to the primary joint pathology.
Symptoms local to the dysfunctional temporomandibular joints include temporomandibular joint pain, painful clicking in the temporomandibular joints and limited capacity for mandibular movement beyond the tolerance of the patient (42). Local symptoms of temporomandibular joint pathomechanics are just that ... symptoms. That is, there must be some noxious experience reported by the patient or some restriction in desired capacity for mandibular function for a disorder to be present. There are no signs of joint dysfunction which are predictive of symptom expression except in their extremes. This includes clicking and other temporomandibular joint noises, deflection and/or deviation of mandibular movement from the midline and less than optimal mandibular range of motion. All of these findings are present in the patient and non-patient populations studied and despite theories to the contrary, none are predictive of eventual expression of pain or limited mandibular capacity (19). The findings of temporomandibular joint noise, altered mandibular tracking and/or limited mandibular range of motion do not constitute symptoms and do not indicate the presence of a temporomandibular disorder unless they are specifically noxious to the patient or are associated with symptoms for which the patient is seeking care and which are traceable back to the region.
The examination of this region involves six component procedures. Many portions of the examination are integral to evaluation of any synovial joint system. However, the craniomandibular region also has characteristics which are unique and require special investigation.
The six parts of the TMD examination include:
Without question the most important aspect of the clinical TMD examination is the case history as this will establish the background against which clinical findings can be interpreted. This is true of all musculoskeletal disorders. The case history will help the clinician to decide if a TMD is present and if so will help to answer questions concerning etiology and perpetuating factors which may interfere with successful case management. In taking the case history one should keep in mind that the etiologies of TMD remain in question.
Trauma has been clearly established as a precipitating factor for TMD (82, 85). There are two types of overt trauma which are known to precipitate a TMD. The first is direct trauma such as a blow to the mandible (35, 42). The second type is indirect trauma usually associated with a "whiplash injury" (8, 11, 16, 27, 32, 35, 41, 50, 51, 57, 91, 93, 96, 104, 116, 117). Indirect trauma has also been associated with protracted and/or excessive mouth opening (35) such as may occur during oral intubation, a prolonged dental visit or third molar extraction. When a clear precipitating event such as trauma does not predate the onset of a TMD, other historical data which may shed light on a possible etiology should be investigated such as: dental history, orthodontic history, prior traumas, rheumatologic and medical history, family history and parafunctions such as bruxism.
MANDIBULAR RANGE OF MOTION
Mandibular range of motion is generally best measured with the patient seated comfortably. A disposable millimetric ruler is recommended for hygiene and accuracy. Three mandibular movements are measured and recorded:
Patients who demonstrate restricted ranges of motion which are mechanical in nature should prompt a referral to a specialist in the treatment of temporomandibular disorders especially if the onset is sudden and/or follows trauma. Restricted range of motion is a complex affair and may be a sign of such disorders as disc dislocation accompanied by ligament damage, muscle splinting, ankylosis and/or frank myospasm. If a restricted active range of motion is noted, an attempt may be made to assist movement manually. This is known as assisted active range of motion. Active assisted range of motion may be coupled with proprioceptive neuromuscular facilitation (p.n.f.) techniques to minimize neuromuscular restriction. This is accomplished by having the patient contract the restricting muscle against resistance and then subsequently attempting movement with manual assistance in the desired direction. This technique can be used for all three mandibular movements, but is most commonly used to test restricted mouth opening. This test should be performed gently and carefully.
Restricted range of motion may be pain and/or mechanically mediated. Restricted movement that is muscular/neuromuscular in origin may be temporarily modified with p.n.f , massage and physiotherapy. Mechanical restriction (disc, adhesion, ankylosis) is minimally modifiable, if at all, with musculoskeletal therapy. Pain-mediated restriction may indicate muscle splinting secondary to primary tissue inflammation. Differentiating primary muscle disorders from muscle reactions to joint pathology is a critical step in the diagnostic process. Misinterpretation can lead to misdirected treatment.
While there are no range of motion limitations which enable the doctor to make an absolute diagnosis, there are guidelines. The following should help you to develop a diagnostic index of suspicion.
Limited mouth opening with full protrusion indicates a neuromuscular/muscular problem (see palpation exam for differential). The mechanical processes of ankylosis and/or coronoid hypertrophy will limit movement in all directions specific to the involved joint(s) and will be entirely non-modifiable with physical techniques (manipulation, physiotherapy, massage). Keep in mind that with restrictions below 25 mm you cannot know if the discs are displaced/dislocated because they cannot limit condyle movement until that point. Disc dislocation (displacement without reduction) will more profoundly affect protrusion than opening. Limited mouth opening with normal protrusion is almost never a disc-mediated phenomenon.
Ideal mouth opening should be unstrained and appear as a vertical movement with no deviation/deflection from the midline. Attempts at protrusive movement should, as well, be unstrained and free from any lateral movement from the vertical midline. Attempts at lateral movement should be unstrained and free from attempts on the part of the patient to open the mouth in order to achieve lateral movement.
Deviation is defined as movement of the mandible away from the midline during opening and/or protrusion without return to center during the movement. Deflection is defined as movement of the mandible away from midline followed by a return to center. As with limited range of motion deviation and deflection may be the result of muscular, neuromuscular or mechanical factors. As previously stated, muscular/neuromuscular influences may be modified with massage, physiotherapy and p.n.f , while mechanical factors are minimally modifiable and produce more of a repetitive, identical or similar pattern.
Joint mediated deviation may indicate disc dislocation (anterior/medial), capsular adhesion or ankylosis. The deviation will occur to the side of the pathology ("the chin will point to the problem"). Deviation to the same side during mouth opening and protrusion is virtually pathognomonic of a mechanical dysfunction on the side of the deviation.
Mandibular deviation has been documented in the nonsymptomatic population (39). Incidental findings of mandibular deviation without related symptoms (local or peripheral) are generally monitored rather than treated. If this finding arises or develops during the continuum of symptoms following trauma and is associated with limited opening and protrusion, it signals the possibility of a serious joint pathology/injury. This condition is unlikely to remit spontaneously and very well may fail conservative management. A second opinion with an oral and maxillofacial surgeon is suggested for temporomandibular joint injury when symptoms are coupled with mandibular deviation and/or signs of locking. This is especially important now that minimally invasive arthroscopic surgical techniques are available and have proven to be effective for these conditions (42, 68, 71, 105). The more aggressive surgical intervention of arthrotomy has also been shown to be effective for advanced therapy resistant joint-specific disorders (119).
Mandibular deflection may result from disc displacement with reduction and/or muscular influences. Disc displacement may or may not be accompanied by adhesive restriction of disc mobility. The more repetitive and non-modifiable the deflection pattern the more likely that it results from disc displacement and that the disc is adhesively restricted and possibly morphologically altered. This condition may be unilateral or bilateral.
Two basic deflection patterns are seen. The first is termed a "C" type deflection and indicates a unilateral disc displacement on the side of deflection. This would indicate that while the disc is displaced forward of the condyle and may be adhesively restricted from translation in the superior joint space, it is not folded or dysmorphic enough to prevent full condylar translation. During mouth opening the chin will move to the side of the displacement and then return to center. The other major deflection pattern is termed an "S" or "Z" type of deflection indicating a bilateral displacement. This type of deflection pattern occurs when both discs are displaced forward, one more than the other (the second deflection indicates the more anteriorly displaced disc). If both discs are equally dislocated or displaced there may be no deviation or deflection, but rather limited mouth opening at 26 to 32 mm of opening (bilateral disc dislocation) or simultaneous clicking/popping in the temporomandibular joints bilaterally (bilateral disc displacement).
Deflections are frequently associated with joint noises such as clicking/popping in the temporomandibular joints. The noise will usually occur at the apex of the deflection on the side of the displaced disc. It should be kept in mind that the disc may be ideally positioned (not displaced), but adhesively restricted. This can result in altered disc dynamics with deflection toward and clicking/ popping in the involved joint. In cases where clicking and deflection are caused by joint pathology other than disc displacement, conflict between clinical exam findings and an MRI of the joint(s) may result. (See special tests section).
Temporomandibular joint noises were once considered almost pathognomonic of temporomandibular disorders. New thought has led us to believe, however, that many joint noises present with mandibular movement may be part of the natural history of asymptomatic joints (83). These noises may be the result of remodeling and accommodation processes which take place over time or the result of specific architectural predispositions such as superior/posterior condyle positioning. Clicking in the temporomandibular joints has been identified in greater than 40% of the asymptomatic population (39). Any joint noises arising or increasing within three months of trauma, such as whiplash, and/or which are associated with continuing symptoms should be considered important (107). Joint noises do not identify the presence of a temporomandibular disorder, but help to classify the type of disorder when symptoms are present (52).
Auscultation of the temporomandibular joints can be performed with light digital palpation or use of a stethoscope. Joint vibration analysis (JVA) machines are sometimes used to record joint noises. These machines can accurately record many characteristics of temporomandibular joint noises (45, 46). The data gained from JVA needs to be interpreted in light of the history and entire clinical exam however before an accurate diagnosis can be made.
During the standard TMD examination the doctor should place the stethoscope and/or the finger tips of the second and third digits lightly over the lateral poles of the temporomandibular joints. This contact should be no heavier than light skin contact to preclude putting pressure on the lateral poles of these joints. The doctor instructs the patient to fully open and then close the mouth. The patient is then subsequently instructed to protrude, retrude and laterotrude the mandible. Various joint noises may be heard and should be recorded. Joint noises are usually referred to as clicking, popping and crepitus. Clicking/popping in the temporomandibular joints which occurs within the normal range of motion (less than 40 to 50 mm) most frequently occurs as a result of disc displacement and/or adhesions. This second cause (adhesions) is important to remember because it clinically mimics disc displacement, but may be interpreted as a normal joint on an MRI (see special tests). Persistent joint noise coupled with continued symptoms and joint tenderness is an important clinical finding whether it results from disc displacement or adhesions. Clicking/popping in the temporomandibular joints is often thought to occur as a result of "spasm" or incoordination of the superior heads of the external pterygoids. This is very unlikely however as research has shown that this muscle has little or no mechanical advantage over the disc (5). Intermittent clicking which seems stress/clenching related is more likely due to hypertonicity of the elevator muscles during joint movements. The strong possibility of concurrent disc complex instability, adhesions and/or disc displacement exists in these cases.
You may notice that deflection is present without clicking during the examination. While this may be a muscular affect, you should challenge this finding by modifying your examination procedure. To do this, lightly grasp the chin and guide the mandible through a straighter course of opening and protrusion. Muscular influences on deflection are minimized then and clicking/popping and even intermittent locking may be observed.
Clicking and deflection are usually coordinated manifestations of the same event, i.e. discal and/or adhesive interference with condylar translation. As such, uncomplicated clicking usually occurs at the apex of mandibular deflection toward the involved joint. Variations on this theme may occur, however. The most important of these is encountered when deviation to one side is accompanied by clicking on the opposite side. The doctor may misinterpret this clicking as indicative of the primary problem, especially as this may be the more painful side. It is the side toward which the mandible deviates which is more profoundly deranged, however, especially if deviation occurs during both protrusion and mouth opening lack of treatment of the side toward which the mandible deviates will undermine any attempt to treat the side productive of the clicking.
Crepitus may be detected during auscultation. This is described as a "ground glass" sound and signals the possibility of discal or, more commonly, retrodiscal perforation (43). If this is present in a symptomatic joint, it identifies an advanced problem which may prove difficult to manage even with surgical techniques. While conservative care is appropriate and may prove successful, early referral for surgical consultation is recommended if clear and steady progress is not achieved. Crepitus may or may not be associated with deflection, deviation and/or decreased range of motion. As with clicking, crepitus may be present without symptoms if there is no associated inflammation. These cases are generally monitored rather than treated unless there is a report of shift in facial contour or occlusion. If alteration of facial contour and/or a shift in occlusion is reported by the patient, they should always be referred for an expert opinion.
Noises described as popping or clunking may occur at the widest point of mouth opening (generally 50+mm). These sounds occur as the condyle passes over the temporal eminence. This indicates joint hypermobility. This may be a manifestation of general ligament laxity or of local ligament damage/degradation. This hypermobility is clinically more significant if the temporal eminence is steep (like a vertical wall). Temporomandibular joint hypermobility has been observed in the asymptomatic population. Coupled with symptoms however it calls for strict patient compliance with instructions to limit full mouth opening. If hyper-translation is allowed to continue after inflammation has begun, substantial joint damage and even non-reducing joint dislocation may occur as pathology progresses.
As a final point in this section the issue of the "posterior disc" should be addressed. This was a popular concept before accurate imaging techniques alerted us to the prevalence of the anterior/medial disc displacement. As it turns out the posterior disc is a very uncommon occurrence and when it is observed it is usually a transient position which occurs during functional mandibular movements. That is, if the disc is prevented from translating by adhesions in the superior joint space, the condyle may click onto and past the disc causing a momentary posterior disc positioning. In these cases generally the closing click is louder than the opening click. This finding implies that not only is the disc non-mobile, but that the collateral attachments of the disc to the condyle are weakened allowing the condyle to move both forward of and posterior to the disc during these respective condylar movements. In contrast to this, the anteriorly displaced disc that is not adhesively restricted and has intact collateral attachments presents almost invariably with an opening click that is louder than the closing click (the closing click may in fact be inaudible). The dysfunctional posterior disc phenomenon may also occur secondary to changes in disc shape. In our experience patients presenting with a dominant closing click have a poor prognosis for success with conservative care. While conservative care may be tried and very well may succeed, there is no scenario in which thrusting the mandible in an A-P direction to seat the condyle under a posterior disc is appropriate.
Palpation is perhaps the most undervalued and misunderstood of the TMD exam procedures. Palpation findings for muscles, joints, ligaments and tendons are often considered equally reliable or unreliable and lumped under the heading of "subjective" data. In fact, with regards to muscles and joints, inter-examiner and serial intra-examiner reliability is different for each tissue. This includes studies of the cervical, lumbar and masticatory regions (19, 44, 60,90).
The effectiveness of palpation for differentiating patients from non-patients has not been thoroughly validated. The following statements represent the reliable information derived from skilled palpation:
Many difficult questions are now being asked which challenge our ideas about myofascial disorders. In the field of TMD this is very troublesome as a "myofascial" diagnosis is one of the most commonly assigned in clinical practice. Results from four surgical studies and two temporomandibular joint anesthetic injection studies challenge the idea that we can identify myogenous disorders exclusively by the presence of muscular tenderness to palpation. These studies have demonstrated remission of both masticatory and cervical myofascial tenderness when the temporomandibular joints are injected with an anesthetic and/or operated (17, 68, 70, 105, 113). This is not to say that all myofascial presentations are driven by joint inflammation, but rather that muscle tenderness alone cannot rule in a true primary myogenous disorder, cannot rule out an arthrogenous disorder and cannot rule in a mixed arthrogenous/ myogenous disorder as the arthrogenous disorder is capable of driving the entire muscular component (105). Joint tenderness as an isolated finding may not be an accurate inclusionary factor for symptomatic capsulitis as it has been noted that joint receptor discharge increases with muscle activity (66). In fact, comparing locations, patterns and relative degrees of tenderness in the muscles and joints of the head and neck may give us the most useful diagnostic impression (105). It should be noted that the presence of cervical muscle tenderness in patients expressing symptoms in the head and neck has been identified as indicating a high probability of TMD (40, 109, 115).
Palpation of the masticatory and cervical/upper shoulder regions is necessary and important in the TMD examination. These tests are necessary to satisfy the demands of standard of care and can provide useful information in the following ways. First, identification of trigger points and muscle hypertonicity provides targets for treatment in true non-arthrogenous myofascial conditions (112). Second, certain patterns of muscle tenderness and hypertonicity can be informative diagnostically when temporomandibular joint tenderness is present concurrently (105). Third, when temporomandibular joint pathology is suspected of being the driving force behind the symptoms, specific areas of muscle tenderness and hypertonicity can serve as target areas for anesthetic temporomandibular joint injections and/or joint-specific treatment trials (17, 105, 107).
TEMPOROMANDIBULAR JOINT PALPATION - TECHNIQUE
IMPORTANT PALPATION FINDINGS
TMD PROVOCATION TESTS (CHALLENGES)
History, range of motion, tracking, auscultation and palpation will give you 95% of the information you need to develop an accurate diagnostic impression. To challenge this impression, provocation tests may be used. Keep in mind that the goal of these tests is to provoke a response from the patient when injured/damaged tissue is stressed. Thus, by definition these tests will aggravate the pathology. Use them sparingly and with discrimination. If these tests are used repeatedly, healing may be undermined. These tests may be performed during the initial examination and should only be repeated if the response to conservative care has been poor and a surgical referral is being considered.
In summary, provocation tests can help to clarify the diagnostic impression. As the tests are provocations of potentially damaged tissues they should be performed carefully and not repeated routinely. They should be used during reexamination only if the case is not progressing satisfactorily and the diagnosis needs to be challenged. These tests are indicators of diagnostic probability and do not stand alone as definitive.
Numerous radiographic examinations are available for the temporomandibular joints. It is advised here that any radiographic evaluation of the temporomandibular joints be interpreted by a specialist in the field of TMD. The most frequently ordered studies include tomograms, transcranials and the panelipse. These films have specific uses and limitations and are ordered generally when fracture and/or pathology is suspected or specific treatment regimens demand information about anatomic or other joint characteristics. While an in-depth presentation on radiology is beyond the scope of this chapter, a few pertinent diagnostic correlations should be mentioned.
Special tests are generally ordered when it is necessary to confirm the diagnostic impression. These tests all have specific uses and limitations. They are useful in classifying the temporomandibular disorder rather than establishing the presence or absence of a disorder. The following is an overview only.
DIAGNOSTIC CONFIRMATION OF TMD
As the onset of a TMD is not predictable, these disorders should be viewed as beginning with the onset of symptoms. These symptoms may be local to, or occur at some distance from, the involved tissue. If TMD is suspected, the first order of business is to identify the location of the dysfunctional tissue e.g. intracapsular versus extracapsular, as this will most clearly define the immediate appropriate treatment plan. If both intracapsular and extracapsular findings are present, one should try to ascertain which is more likely to be driving the other. Consideration should then be given to the patient's history with an eye to the most likely precipitating event as this will profoundly influence the proper treatment and prognosis (e.g. chronic insidious versus acute traumatic). Finally, any factors which may have predisposed the patient to the onset of the disorder or threaten to perpetuate its expression should be recorded. This, once again, is not unlike the appropriate diagnostic workup for spinal, paraspinal and other musculoskeletal disorders, although an expanded data basis specific to TMD is necessary. For example, such issues as malocclusion, developmental oro-facial anomalies, oro-facial parafunctional habits, sleep disorders and specific dental health history will need be considered with TMD.
An appropriate clinical
diagnostic impression then should include symptoms expressed, location
of injured or dysfunctional tissue, potentially perpetuating factors and
probable etiology. These considerations are essential for intervention,
management and/or referral.
A SUMMARY OF SPECIFIC DIAGNOSES
*Note: Pain with resisted mouth closure or resisted protrusion may irritate capsulitis and produce joint pain because the superior head of the external pterygoid attaches to the capsule.
*Note: These last two tests may stimulate inflamed retrodiscal tissue especially if the disc is displaced anteriorly. This is sometimes termed retrodiscitis. Synovitis is necessarily concurrent with retrodiscitis and there may be little clinical value in distinguishing the two.
Audible, visible and/or palpable movement of the condyle(s) past the temporal eminence. If unilateral, the condition may be secondary to contralateral joint hypomobility.
*Joint dislocation represents a combination of joint hypermobility and elevator muscle spasm. The patient presents with exaggerated mouth opening and mandible protruded. The condition may self-reduce or dislocation may be non-reducing. Reduction is best accomplished with manipulation under anesthesia to minimize joint damage.
MASTICATORY MYOFASCITIS (MYALGIA, M.P.D.)
Temporomandibular disorders are a subclassification of musculoskeletal disorders and produce symptoms both local to the craniomandibular region and at some distance from the area. Temporomandibular disorders are generally subclassified as intracapsular and extracapsular and may be thought of as primary myofascial disorders and inflammatory or mechanical disorders of joints, ligaments, tendons and muscles. Symptom complexes vary greatly and frequently represent the reflexive influence of craniomandibular pathology on the central nervous system. Central nervous system sensitization and altered neuroplasticity may result in a spread of neural activity throughout the triggering-cervical complex. Reactive muscle contraction and associated trigger point expression may produce pain and other symptoms throughout the head, neck, upper back and upper extremities.
Accurate diagnosis of the patho-etiology behind the production of TMD symptoms will result in improved treatment results. Early identification of arthrogenous disorders coupled with more accurate delivery of therapy may serve to prevent the progression of temporomandibular joint degradation and stem the development of resultant chronic pain presentations.
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