PATHOMECHANICS, PATHOPHYSIOLOGY AND PATHONEUROLOGY OF ARTHROGENOUS DISORDERSThe 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 JOINTSSmall (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 TMDTo 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.
TMD EXAMINATTONThe 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.
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 MOTIONMandibular 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:
Mouth opening. Mouth opening is generally considered normal at 40 to 50 mm. This should be an unstrained vertical movement and is measured from the lower edge of the upper central incisors to the upper edge of the lower central incisors. If overbite (vertical incisal overlap) exceeds 1 to 2 mm add the excess to the overall measurement.
Lateral mandibular movement or laterotrusion is measured from maxillo-mandibular midline (allowing for asymmetry) to the extreme of both right and left lateral mandibular movement. The mouth is slightly open so that the teeth do not touch during this test. This movement should be unstrained and should not require an excess of mouth opening. Normal range is 10 to 12 mm to each side.
Protrusion (forward movement): The mandible can normally be protruded 10 to 12 mm from the point of maximum occlusal contact. This should not require an excess of mouth opening. It should be noted that during protrusive, as with lateral movements, the mouth is slightly opened to avoid tooth-to-tooth contact.
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.
If mouth opening is limited at 26 to 32 mm and not modifiable, one should suspect disc dislocation (disc displacement without reduction). In this case protrusion will be limited at approximately 4 to 8 mm. If the disc(s) are also medially dislocated, laterotrusion (side-to-side movement) will be limited to the side opposite the involved disc at approximately 4 to 8 mm. Other causes of non-modifiable limited mandibular movement include joint ankylosis which may be fibrous or bony and hypertrophy of the coronoid processes. Limitations produced by these pathologies are frequently more extreme than disc dislocation.
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.
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