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Temporomandibular Joint Pain and Dysfunction

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Temporomandibular Joint Pain and Dysfunction Temporomandibular Joint Pain and Dysfunction Kathleen Herb, DMD, MD, Sung Cho, DMD, and Marlind Alan Stiles, DMD Corresponding author Marlind Alan Stiles, DMD open arthroplasty 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 disease. The interrelationship between the various dis- PA 19107, USA. orders continues to be explored. E-mail: [email protected] The temporomandibular joint (TMJ) is a compound Current Pain and Headache Reports 2006, 10:408–414 articulation formed from the articular surfaces of the Current Science Inc. ISSN 1531-3433 temporal bone and the mandibular condyle. Both sur- Copyright © 2006 by Current Science Inc. faces are covered by dense articular fibrocartilage. Each condyle articulates with a large surface area of temporal bone 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 mandible 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 anatomy 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 cartilages are composed of hyaline cartilage, 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 Signs and symptoms of temporomandibular disorders not have any direct vascularization or innervation; how- (TMDs) may include pain, impaired jaw 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 lateral pterygoid muscle 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/contracture. Articu- interposed between the condyle and the temporal bone at lar disorders include synovitis/capsulitis, joint effusion, all points of translation. trauma/fracture, internal derangement, arthritis, and neo- The joint is stabilized by three ligaments: 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 ligament 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 membrane. 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 muscles of mastication. The include myositis, fibrosis, tendonitis, whiplash injury, 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 arteries. 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 nerve and, to a lesser extent, the masseteric derance of female patients afflicted with TMDs. Many and posterior deep temporal nerves. The production researchers have examined the role of estrogen in the of synovial fluid 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
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