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Home , Ankylosis, Articular disk, Osteoarthritis, Synovial fluid, Synovial membrane, Temporomandibular joint

Temporomandibular and Dysfunction

Kathleen Herb, DMD, MD, Sung Cho, DMD, and Marlind Alan Stiles, DMD

Corresponding author Marlind Alan Stiles, DMD open and toward arthroscopic procedures. Department of Oral and Maxillofacial Surgery, Thomas Jefferson Research continues to look toward biochemical markers University Hospital, 909 Walnut Street, Suite 300, Philadelphia, of . The interrelationship between the various dis- PA 19107, USA. orders continues to be explored. E-mail: [email protected] The (TMJ) is a compound Current Pain and Reports 2006, 10:408–414 articulation formed from the articular surfaces of the Current Science Inc. ISSN 1531-3433 temporal and the mandibular . Both sur- Copyright © 2006 by Current Science Inc. faces are covered by dense articular fibrocartilage. Each condyle articulates with a large surface area of consisting of the articular fossa, articular eminence, Pain caused by temporomandibular disorders originates and preglenoid plane. The TMJ functions uniquely in that from either muscular or articular conditions, or both. the condyle both rotates within the fossa and translates Distinguishing the precise source of the pain is a sig- anteriorly along the articular eminence. Because of the nificant diagnostic challenge to clinicians, and effective condyle’s ability to translate, the can have a management hinges on establishing a correct diagnosis. much higher maximal incisal opening than would be pos- This paper examines terminology and regional sible with rotation alone. The joint is thus referred to as as it pertains to functional and dysfunctional states of “gynglimodiarthrodial”: a combination of the terms gin- the temporomandibular joint and muscles of mastica- glymoid (rotation) and arthroidial (translation) [1]. tion. A review of the pathophysiology of the most A cartilaginous disc resides between the articular common disorders is provided. Trends in evaluation, surfaces of the temporal bone and mandibular condyle. diagnosis, treatment, and research are presented. Although other articular are composed of hyaline , this disc is composed of fibrocartilage; thus, the disc contains a much higher percentage of col- Introduction lagen, increasing its stiffness and durability. The disc does of temporomandibular disorders not have any direct vascularization or innervation; how- (TMDs) may include pain, impaired function, ever, the posterior attachment of the disc (also known as malocclusion, deviation or deflection, limited range of retrodiscal tissue) is both highly vascularized and highly motion, joint noise, and locking. Headache, tinnitus, innervated and, therefore, pertinent to the discussion of visual changes, and other neurologic complaints may joint pain. The superior lamina of the retrodiscal tissue also accompany TMDs. Because of many etiologic fac- limits extreme translation, whereas the inferior lamina tors, the diagnosis and treatment of patients with TMDs limits extreme rotation. The con- is complex. TMDs can be subdivided into muscular and trols the opening of the mandible. The superior segment articular categories. Differentiation between the two is of this muscle attaches to the anterior portion of the disc, sometimes difficult because muscle disorders may mimic and the inferior segment attaches inferior to the condyle. articular disorders, and they may coexist. Myogenic dis- As both segments contract the condyle translates anteri- orders include myalgia (myofascial pain, fibromyalgia), orly along the articular eminence, and the disc remains myospasm, splinting, and fibrosis/. Articu- interposed between the condyle and the temporal bone at lar disorders include /capsulitis, , all points of translation. trauma/fracture, internal derangement, , and neo- The joint is stabilized by three : collateral plasm. Accurate diagnosis allows for appropriate therapy (discal), capsular, and temporomandibular. These attach whether it is nonsurgical or surgical. Current trends favor to the disc at the medial and lateral poles of the man- conservative (nonsurgical) therapy, and the surgical inter- dibular condyle, as well as to the temporal fossa. These ventions have become less aggressive, moving away from ligaments limit extreme condylar movement. The capsular Temporomandibular Joint Pain and Dysfunction Herb et al. 409 surrounds the joint space and disc and acts to “TMJ disorders” became “TMDs.” For the purposes of contain the synovial fluid within the joint space. this article, we will differentiate the TMDs into articu- The capsule is lined by a . Synovial lar (joint) and nonarticular (myogenic) disorders, with tissue covers all intra-articular surfaces except for the pres- a focus on disorders most commonly encountered in sure-bearing fibrocartilage (ie, disc, condyle, eminence). clinical practice. The synovial tissue is highly innervated and vascularized and has regulatory, phagocytic, and secretory functions. The synovial fluid has metabolic and nutritional functions Myogenic Disorders and is essential to joint surface lubrication [2]. Within this category, MFP and MPD syndrome are The masseter, medial pterygoid, lateral pterygoid, and encountered frequently. Other muscular disorders temporalis muscles are the . The include myositis, fibrosis, tendonitis, whiplash , masseter, medial pterygoid, and temporalis are primarily and fibromyalgia. Patients suffering from MFP will have responsible for mandibular closure and bite force, whereas tenderness to palpation of two or more muscle sites. the lateral pterygoid and infrahyoid muscles are respon- Myalgias involving the muscles of mastication predomi- sible for mandibular opening. Mandibular movement is nate. MFP escalates to myofascial dysfunction when also influenced by the digastric, geniohyoid, mylohyoid, there is concomitant limitation of jaw opening [6]. stylohyoid, sternohyoid, omohyoid, sternothyroid, and MFP and MPD are intertwined. Traditionally, it was thyrohyoid muscles, which as a group coordinate complex thought that structural abnormalities (ie, dental malocclu- mandibular movements including opening, protrusion, sion, condylar malposition) led to muscular dysfunction retrusion, lateral excursion, and closure. and pain [6,7]. Muscles were thought to be under an At rest, the condyle is seated passively in the temporal increased burden in the presence of these skeletal and/or fossa with the fibrocartilage disc interposed at the most dental misalignments. As such, a “vicious cycle” model superior and anterior position of the condyle commonly was proposed: referred to as the 11-o’clock position. Mandibular open- Structural → abnormality → muscle hyperactivity ↔ ing commences with contraction of the lateral pterygoid pain ↔ mandibular dysfunction where pain and muscle and infrahyoid muscles, which rotates the condyle. hyperactivity potentiate each other and emotional stress Mandibular opening proceeds with lateral pterygoid is thought to have an additive effect [6,7]. Over time, contraction pulling the condyle forward along the artic- there has been a lack of scientific evidence to support this ular eminence (translation). The superior segment of the theory. Others have put forth a pain-adaptation model in lateral pterygoid muscle coordinates the translation of which motor behavior is altered or limited as a response to the disc with the condyle. During jaw closing the liga- pain, thus serving a protective purpose [8]. Many believe ments and retrodiscal lamina pull the condyle and disc that masticatory myalgias are instead “nonprogressive, back into resting position. self-limited, or fluctuating over time,” with a significant The TMJ receives its vascular supply from the number of patients reportedly pain free at follow-up superficial temporal, maxillary, and masseteric . examinations 1, 3, and 5 years later [8]. Innervation of the joint is provided mainly by the auric- Consideration has also been given to the prepon- ulotemporal and, to a lesser extent, the masseteric derance of female patients afflicted with TMDs. Many and posterior deep temporal . The production researchers have examined the role of estrogen in the of is also under a certain amount of etiology of masticatory myalgias [9]. The fact that the neuronal control. condition is more severe in women than in men, and that it occurs more frequently in women of reproductive age, bears further investigation. The search for causative and Temporomandibular Disorders contributing factors is ongoing. The term “TMJ pain” varies greatly in meaning among One must differentiate muscular from joint condi- clinicians, patients, and the general population. His- tions in order to appropriately treat the patient. At the torically, symptom-based classification of the disorder same time, the clinician must understand the role of MPD has been problematic. As stated by Laskin [3,4], the within the spectrum of TMDs. It has been reported that difficulty began with the introduction of a “TMJ syn- approximately 50% of all TMDs are masticatory myal- drome.” Then clinicians erroneously grouped a “variety gias or painful masticatory muscle disorders [8]. of etiologically unrelated conditions into one diagnostic MFP of the masticatory muscles is more frequently category based on the fact that they produced similar induced by stress-related parafunctional habits (ie, signs and symptoms,” and this led to “one diagnosis clenching and grinding) and rarely by mechanical causes equals one treatment.” Only later was it recognized that such as occlusal prematurities or high dental restorations. many of these patients suffered from muscle-related MFP and MPD, although considered to be muscular dis- conditions. The terms myofascial pain (MFP) and myo- orders, are thought to possibly play a causative role in fascial pain and dysfunction (MPD) evolved [5], and of the TMJ. 410 Pain Aspects of Arthritis

TMJ pain from an articular disorder may conversely sents the condyle returning to the retrodiscal tissue and lead to MFP. This is thought to occur due to reflex mus- the disc returning to an anterior position. Many feel that cle contractions in the muscles of mastication [6,7]. This ADD with reduction does not require treatment unless is considered as a self-protective reflex and is referred to there is concomitant joint pain. as muscle “guarding” or “splinting.” Patients will pres- ADD without reduction, also known as closed lock, ent with tenderness and hyperalgesia at sites distant to will have a much different clinical presentation because the joint that mimic MFP. They may also exhibit various the condyle’s forward translation is limited by the trigger points. disc’s anterior position and is unable to reduce onto the Treatment of masticatory MFP may include phar- disc, allowing only for rotational and not translational macologic therapy (nonsteroidal anti-inflammatory movement. Patients with acute or subacute closed lock drugs, muscle relaxants, tricyclic antidepressants, anx- typically report a sudden onset of pain and inability to iolytics), occlusal appliance/splint therapy, trigger point open more than 20 to 30 mm. The patient may give a therapy (spray and stretch, injections), and physical history of joint noise that suddenly ceased with the onset therapy (mandibular ). Splint therapy is con- of signs and symptoms. Clinically, the mandible devi- sidered an adjunct to pharmacologic therapy and most ates on opening to the affected side due to the ability of appropriate when nocturnal parafunctional activities the unaffected joint to translate. Additionally, excursive can be identified. Typically, a flat-plane maxillary occlu- mandibular movements to the contralateral side are lim- sal splint designed for bilateral contact of all teeth is ited. This diagnosis of TMDs continues to present the fabricated. Such splints are thought to unload the joint clinician with a significant challenge. Establishment of by disarticulating the dentition and increasing the verti- an accurate diagnosis is necessary for effective manage- cal dimension of . By unloading the joint, there ment. The difficulty lies not in creating a distinction will be a reduction in both synovitis and masticatory between articular and muscular disorders, but in the muscle activity. Therefore, the result is a reduction in interrelation of the two entities. Although patients may symptoms. These appliances may also change condylar have isolated joint or muscular disorders, many have a position and the existing occlusal relationship, thereby component of each. Simply stated, joint disorders may reducing abnormal muscle activity and spasm. lead to muscle dysfunction, and muscle disorders may lead to joint dysfunction. This may not be possible to elicit on examination because the patient will tend to Articular Disorders guard against pain. The etiology of articular disorders may be degenera- In chronic disc displacement without reduction, the tive, traumatic, infectious, immunologic, metabolic, patient can usually recount a history consistent with acute neoplastic, congenital, or developmental. closed lock that resolved over time. Recovery of function is due to stretching the retrodiscal tissue over weeks to Articular disc displacement (internal derangement) months, restoring translational movement. Anterior disc displacement (ADD) is the most frequently MRI allows for evaluation of abnormali- encountered articular disorder. Disc displacement (also ties of the TMJ. MRI is noninvasive and avoids radiation known as internal derangement) is defined as “a distur- exposure. The disc can be visualized making diagnosis bance in the normal anatomic relationship between the possible. T1 images show a hypodense biconcave disk disc and condyle that interferes with smooth movement of between the condyle and eminence. Effusion, bone mar- the joint and causes momentary catching, clicking, pop- row edema, and soft tissue pathology are well visualized ping, or locking” [10]. Therapy is indicated if pain and with T2 imaging. Multiplane views of the TMJ are avail- significant limitation in are present. able; with high-speed MRI, dynamic studies are also The incidence of ADD is unknown. Numerous radio- available (Fig. 1). graphic, clinical, and cadaveric studies of asymptomatic The ability of the joint to adapt to biomechanical subjects have shown rates up to 30% [11]. The clinical stress and disc derangement has been a subject of debate. significance of this finding remains uncertain. In his classification system, Wilkes [12] promotes the When the articular disc becomes displaced ante- theory that internal derangement logically progresses to riorly, there is excessive stretching of the retrodiscal degenerative joint disease (DJD). Historically, surgical tissue, which then bears repeated loading force from the and nonsurgical approaches have been used to reposition mandibular condyle. This tissue has been shown to have the displaced disc, with the goal of arresting this pro- some capacity to adapt to these forces and may trans- gression [13]. In an opposing view, Milam [9] states that form into a “pseudodisc.” In many patients the disc is “the adaptive capacity of the TMJ is not infinite…some recaptured and is known as “disc displacement with individuals are… capable of mounting an adaptive reduction,” resulting in TMJ noise (clicking or popping) response to an articular disc displacement; other indi- and full translational movement of the condyle. With viduals may not adapt to these structural derangements, mandibular closure, a reciprocal (closing) click repre- and a progressive DJD may result.” Factors considered to Temporomandibular Joint Pain and Dysfunction Herb et al. 411

Figure 1. MRI of the temporomandibular joint. Note the anterior location of the disc in a closed position (arrow) (A), with recapture on opening (arrow) (B), and without recapture (arrow) (C).

compromise the adaptive response include age, sex, stress, from cartilage degradation. When this ability is over- and illness [9,14]. He concludes that disc derangement whelmed, inflammation (acute synovitis) results. may exist variably as cause or effect, but does not always Inflammation of the synovial membrane is an early progress to disease. sign of DJD [20]. Inflammatory and pain mediators Although patients without internal derangement have been identified in TMJ synovial fluid [21,22]. may develop (OA) [15], a complex two- Chemical breakdown of degenerative byproducts is way relationship exists. Controversy continues as to thought to stimulate the production of inflammatory whether disc derangement is a cause or a result of DJD; and pain mediators (prostaglandin E2 and leukotri- however, scientific evidence strongly supports the latter ene B4, among others) through the arachidonic acid conclusion [15–18,19•]. cascade. Prostaglandin E2 is a powerful vasodilator and leukotriene B4 attracts inflammatory cells. Their Capsulitis and synovitis presence creates acute synovitis pain and stimulates Inflammation of the capsular ligament may manifest further damage from cytokines and proteases. For this with swelling and continuous pain localized to the reason and for joint lavage joint. Movements that stretch the capsular ligament and lysis of adhesions are believed to have a therapeutic cause pain with resultant limitation of such move- effect [23–25]. These procedures remove particulate ment. Significant inflammation may increase joint fluid debris and pain mediators, aiding reduction of joint volume. When this occurs, one may see an ipsilateral inflammation and pain. Results are similar with and posterior open bite (lack of contact between maxillary without disc repositioning [23]. Lysis of adhesions may and mandibular teeth) secondary to inferior displace- improve range of motion. injections are also ment of the condyle [7]. Similarly, inflammation due to used to reduce synovial inflammation and pain. Recent trauma or abnormal function may affect the retrodiscal investigations have looked at intra-articular morphine tissue. Edema in this area may cause anterior displace- for sustained pain relief in patients [26]. Research is ment of the condyle and an acute malocclusion with now focusing on the role of biochemical mediators in painful limitation of mandibular movements. the development and progression of TMJ pain and dys- The highly innervated and vascularized synovial function [19•,22] and the identification of biochemical membrane digests debris and pain mediators released “markers” of TMJ disease [14]. 412 Pain Aspects of Arthritis

Figure 2. MRI of the right temporomandibular joint. Note the anterior disc (arrow on left) dislocation and condylar head (arrow on right) degenerative changes.

The arthritides placement or perforation. This continues into the later Arthritis of the TMJ has many etiologies: frequently stages, and patients may develop crepitation secondary OA and (RA) and less often infec- to bone exposure. Pain and formation result in tious, metabolic (), or immunologic (ankylosing limitation of joint movement. Dijkgraaf et al. [32] found spondylitis, ). DJD, also known as OA, has a that “in many patients, the signs and symptoms of TMD multifactorial pathogenesis including biomechanical, are attributable to osteoarthritis.” The authors place less biochemical, inflammatory, and immunologic insults. emphasis on the stage of internal derangement and more Excessive and repetitive mechanical stress has been impli- emphasis on both the stage of cartilage degradation and cated [19•]. Inflammatory mediators and waste products grade of synovitis. may play a role in DJD [27–42]. Inflammatory states Panoramic is an excellent screening cause changes in the of synovial fluid, which tool for the presence of bony degenerative changes. changes its ability to nourish the articular cartilage, thus In addition to identifying disc displacement, MRI is changing cartilage metabolism. useful in the diagnosis of joint effusion, osteoarthritic OA is classified as primary (no known predisposing changes, bone marrow abnormalities of the mandibu- factors) or secondary (associated with known abnor- lar condyle, retrodiscal tissue changes, and malities or ). Primary OA symptoms begin in the (Fig. 2) [43,44]. fifth to sixth decade. Secondary OA produces symptoms TMJ arthroscopy now allows clinicians to visualize at an earlier age. degenerative changes of both the articular cartilage and In contrast to the other arthritides, OA symptoms disc at early stages [20]. Arthroscopy is considered to will not necessarily be present in other . Patients be the “gold standard” in the diagnosis of OA because suffering from OA complain of increasing pain during degenerative changes are visualized earlier than with increased function and load bearing throughout the radiographic techniques. day. Joints are tender and will exhibit decreased range RA is a chronic systemic inflammatory disease of motion. may indicate loss of articular carti- affecting the joints and other organs. A childhood form, lage. Patients may have referred pain to head and juvenile RA, also exists. The etiology is unknown, but an regions. Radiography may reveal joint space narrowing, autoimmune component has been identified (rheumatoid formation, condylar head flattening, and factor). Of the patients who test positive for rheumatoid subchondral bone cysts. factor, 50% to 75% will develop TMJ involvement [45]. In the osteoarthritic joint, there is progressive soft- The age of onset is younger (fourth to sixth decade) than ening and loss of cartilage, which Quinn [20,31] calls that seen with OA. In contrast to OA, patients with RA chondromalacia (softening of the articular cartilage) typically have morning stiffness that lasts for more than of the TMJ. It is thought that repeated stress-related an hour, but report improvement of mobility with func- microtrauma (ie, ) eventually overloads the tion throughout the day. They complain of deep, dull joint’s articular cartilages leading to compression and preauricular pain that worsens with function. Patients shearing of cartilage. injury stimulates may also report fever, malaise, and fatigue. They will release of proteolytic enzymes and other collagenases. eventually experience decrease in jaw mobility, joint Eventually, there is loss of water and loss of cartilage destruction, and fibrous . Patients may progress resilience [20,30–33]. to loss of mandibular ramus height, retrognathia, and Four stages of TMJ OA are based on the amount of open bite. Patients will have symptoms long before there cartilage degeneration and the grade of synovitis. In stage is radiographic evidence of disease. Early imaging with 2, the early stage, patients may report pain and limited MRI may be beneficial to evaluate disc morphology and range of motion. Joint noise may occur due to disc dis- pathologic changes. Temporomandibular Joint Pain and Dysfunction Herb et al. 413

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