MANDIBULAR MOVEMENTThe 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.
JOINT MOTIONUntil 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 DISORDERSTemporomandibular 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
INTRACAPSULAR
capsulitis
synovitis
retrodiscitis
disc displacement, with reduction
disc displacement, without reduction
ankylosis
adhesions
joint hypermobility
EXTRACAPSULAR
myofascitis
myositis
myospasm
coronoid tendinitis
Ernest Syndrome
*Muscle splinting is a muscular response to pathology which may be initiated by intracapsular or extracapsular nociceptive events.
EXTRACAPSULAR DISORDERSPrimary 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.
INTRACAPSULAR DISORDERSThe 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).
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