Functional disorders of the temporomandibular joint (TMJ) represent a spectrum of severity that can be broadly categorized into one of two groups—hypomobility and hypermobility. This diverse group of disorders has the potential to not only affect routine daily functions, such as maintaining oral hygiene, speech, and mastication, but also can be debilitating in their severe forms. Determining the cause and any associated causative factors of the specific functional disorder is equally essential as obtaining a thorough history and physical exam. Obtaining advanced imaging, such as computed tomography (CT) or magnetic resonance (MR) scans, also enhances the surgeon’s capabilities of implementing the most appropriate treatment to minimize or even eliminate future recurrences of functional disorders.
TEMPOROMANDIBULAR JOINT HYPOMOBILITY
HISTORY AND PHYSICAL EXAM
A normal range of interincisal maxillomandibular opening ranges from 35 to 50 mm in adults. Decreases in mandibular range of motion can create obvious difficulties in daily functions, such as oral hygiene, speech, and mastication. Hypomobility results from a multitude of disorders that affect the TMJ and its associated structures. Causes of TMJ hypomobility may be broadly classified into one of three groups: trismus, pseudoankylosis, or true ankylosis. Box 47-1 lists the causes of hypomobility by group.
Repeated intraoral local anesthetic injections
Tumors involving masticatory musculature
Depressed zygomatic arch fracture
Coronoid process hypertrophy
Condylar or coronoid process neoplasms
Intracapsular fracture in pediatric patient
Medially displaced, healed fracture in adult patient
To effectively manage a patient with signs and symptoms consistent with hypomobility, a detailed history must be obtained. This should include the time course of development of symptoms, prior trauma, and any previous interventions, including surgery. Relating the history to a systematic and directed physical exam combined with appropriate radiographic studies should help direct the surgeon to a diagnosis. A number of patients may have pain and limited mouth opening related to internal derangement (ID) of the TMJ. The diagnosis and management of this group of disorders is discussed elsewhere in the text.
Imaging is often required to evaluate, diagnose, and treat TMJ hypomobility. Applying appropriate selection criteria, the surgeon may then choose among the various imaging modalities with the goal of obtaining useful information without subjecting patients to unnecessary radiation exposure or costs. The use of plain film radiography in the evaluation of the TMJ and associated structures has limited applications. Plain films depict only mineralized aspects of the joint, and superimposition of anatomic structures often makes radiographic interpretation difficult. However, if identification of overt osseous changes, condylar fractures, or presence of a joint space is the objective, then panoramic imaging may be a reasonable option. Panoramic films show gross bony erosions, osteophytes, condylar sclerosis, and tumors of the condyle or coronoid process. Panoramic radiographs also serve as good screening tools for subcondylar or coronoid fractures and coronoid elongation in addition to providing a view of the teeth and mandible. Additional plain film radiographs are useful in certain situations. An open mouth Towne’s view may reveal new or old subcondylar fractures, and a posterior-anterior cephalogram demonstrates facial asymmetry.
Advanced imaging of the TMJ is accomplished through CT scans or magnetic resonance imaging (MRI). CT scans overcome the superimposition of plain film radiography and generate high-quality images for assessment of osseous structures. CT imaging is preferable for diagnosis and treatment planning of fractures, arthritides, ankylosis, and neoplasms. Axial, coronal, and sagittal views may be obtained in addition to a three-dimensional reconstruction of all three views. El-Hakim and Metwalli showed that CT scans are effective in defining the medial and lateral extent of an ankylotic bone mass and its relation to surrounding vital structures. Contrast-enhanced CT imaging may assist in surgical planning of bony ankylosis by defining important vascular anatomy, such as the maxillary and carotid artery, and the internal jugular vein. CT scans also adequately depict skull base structures, such as the pterygoid plates and foramen spinosum, which may be intimately involved in posttraumatic ankylosis or tumor invasion.
MRI is the study of choice for defining articular disk position. Tasaki reported 95% accuracy with MRI in identification of disk position based on cadaver studies. MRI is also useful in detection of soft tissue ingrowths, fibrous ankylosis, and joint effusions that are not visible by CT. Although MRI does not highlight osseous details, cortical outlines and bony contours are still evident.
Trismus is defined as a spasmodic contraction of jaw muscles resulting in forceful jaw closure and difficulty opening the mouth. Trismus results from inflammation or irritation causing involuntary sustained spasms of the muscles of mastication. True trismus differs from the voluntary resistance to mouth opening and muscle guarding secondary to pain as seen in ID. Trismus is commonly acute in onset and may be painful. The history, symptoms, and physical exam often indicate the cause(s) of trismus. Clearly identifiable sources, such as odontogenic infection, recent and repeated local anesthetic injections, maxillofacial trauma, preexisting myofascial pain dysfunction syndrome, or recent ingestion of phenothiazine drugs, should be investigated. Some patients report a history of chronic muscle splinting as a result of myofascial pain induced by parafunction, malocclusion, or prolonged jaw positioning. Over time they may develop a secondary myospasm with involuntary restricted mouth opening. These patients are best treated with removal of causes, continued motion within painless limits, occlusal disengagement, splint therapy, and possible prescription of muscle relaxants. Muscular contusion resulting from trauma or myositis following multiple local anesthetic injections is treated with moist heat, nonsteroidal antiinflammatory medications, massage, and soft diet.
Maxillofacial infections causing trismus require prompt incision and drainage, extraction of offending teeth, and directed antibiotic therapy. Regardless of the cause of acute trismus, patients require frequent follow-up appointments to assess progress. A regular regimen including range-of-motion exercises and physical therapy should be initiated to regain interincisal opening. Patients who continue to consistently posture their mouths closed often develop limited opening that is challenging to resolve.
With a more gradual onset, painless trismus is worrisome for neoplastic invasion. The literature reports several cases of nasopharyngeal carcinoma presenting with trismus as the only symptom. Neoplasms of the oral tissues, such as squamous cell carcinoma of the tonsillar pillar or tongue base, may also cause limited mouth opening. Any tumor arising from structures surrounding the TMJ, such as the parotid gland or parapharyngeal space, can produce trismus through invasion of the muscles of mastication. Another rare but important cause to consider is temporal or giant cell arteritis (GCA). Nir-paz reported in a retrospective review of patients admitted and diagnosed with GCA that 6.8% noted reduction in jaw opening. The limited opening was frequently associated with jaw claudication.
Pseudoankylosis has varying degrees of limited mouth opening and is most commonly secondary to prior soft tissue or muscle injury resulting in fibrosis and scarring. Restriction of mandibular movement is independent of the TMJ. Patients typically experience painless mouth opening until reaching the point of restriction. A solid, distinct limitation point is unusual. A slight increase in interincisal opening is often attainable with a gradual scissoring motion of the thumb and index finger or use of a Therabyte device. Historical clues to diagnosis include prior trauma or surgery, previous radiation, timing of onset, or changes in occlusion or symmetry. A complete intraoral and extraoral exam may reveal the source of restriction, such as a dense scar band, fibrosed muscle of mastication, or coronoid impingement.
If acute pain with limited mouth opening is the initial presentation, a subcondylar fracture or depressed zygomatic fracture should be suspected. The patient with a displaced subcondylar fracture usually has a contralateral posterior open bite and deviates to the side of the fracture on opening the mouth. Similarly, patients with depressed zygomatic arch fractures deviate toward the affected side while opening their mouth, but will come to an abrupt stop when the coronoid process contacts the collapsed arch. Plain films, such as panoramic or open mouth Towne’s views, may reveal subcondylar fractures. However, CT imaging gives more detailed information about the location of the displaced segment and also clearly exhibits fractures of the zygoma and midface. Appropriate reduction and treatment of fractures usually corrects the hypomobility. Rikalainen et al reported a series of 379 surgically treated zygomatic fractures in which 36 cases were complicated by restricted mouth opening during the recovery period. The cause was believed to be extracapsular fibrosis. Thus the surgeon must stress postoperative physical therapy to prevent fibrosis and regain the preinjury range of motion.
If a depressed fracture of the zygoma or a displaced coronoid fracture is either unrecognized or not treated in the acute setting, extraarticular ankylosis may occur. Fusion of the coronoid process to the zygoma appears to result from organization and calcification of a traumatic hematoma formed at the time of injury.
Occasionally, blunt trauma to the maxillofacial skeleton may cause sufficient injury to the soft tissues to initiate pseudoankylosis in the absence of facial fractures. Thoma first described myositis ossificans traumatica (MOT) in 1958 as a condition caused by calcification and ossification of a traumatic intramuscular hematoma. Although a rare occurrence in the head and neck, multiple cases of MOT have been described in the literature, with causes ranging from anesthetic injection to severe blunt trauma. Although the specific pathophysiology of MOT is unknown, the widely accepted theory involves an aberrant healing process. Experts believe that either extraosseous cells undergo metaplasia when exposed to BMP traumatically displaced into soft tissues or proliferating vascular granulation tissue undergoes metaplasia to form bone-forming cells. The masseter muscle is most commonly involved in MOT, but cases affecting the temporalis, genioglossus, buccinator, and medial pterygoid muscles have been described. Usually, there is scant evidence of ossification until limited mouth opening occurs. Symptoms generally do not appear until 3 to 6 weeks after the trauma. Calcification may only be visible on CT or MRI images. Histologic findings consist of newly formed lamellar bone within muscle fibers, resembling callous formation in a healing fracture. MOT has a high rate of recurrence regardless of treatment. Therefore the literature advocates aggressive intervention including dissection and surgical release of the affected muscles, excision of ossified fibers, and often coronoidectomy. Other treatment modalities, such as physiotherapy, magnesium, and the bisphosphonate, Didronel, have been reported, but appear to have minimal efficacy.
Mandibular hypomobility is a common complication in patients treated with radiation therapy for head and neck malignancies. Reported prevalence ranges from 5% to 38% based upon varying criteria used to define limited mouth opening and a preponderance of retrospective studies. Pseudoankylosis occurs secondary to fibrosis, contracture, and spasm in the muscles of mastication exposed to radiation. Limited mouth opening often evolves slowly and is usually painless. The onset of hypomobility occurs approximately 9 weeks after radiation and continues to progress rapidly for 9 months. There may be a continual protracted decline in the range of motion over subsequent years. The extent of fibrosis appears to be correlated with the total dose of radiation and the amount of radiation directed to the TMJ and pterygoid muscles. Dijkstra et al performed a systematic review of clinical studies evaluating radiation-associated trismus and methods of intervention. They reported that exercises using a Therabyte appliance or tongue blades significantly increased the range of motion in the short term. In addition, a modest short-term benefit to mouth opening was seen with pentoxifylline or microcurrent electrotherapy. When attributing mandibular hypomobility to effects of radiation treatment, the physician must ensure that trismus secondary to cancer recurrence is not overlooked.
Although uncommon, a variety of neoplastic processes involving the mandibular condyle and coronoid process have been described and may lead to extracapsular hypomobility. Patients typically have gradual onset of painless limited mouth opening and deviation to the affected side. Most primary neoplasms involving the TMJ or coronoid process are benign. Neoplasms reported in the literature include synovial or ganglion cysts, osteomas, chondromas, osteochondromas, giant cell granulomas, osteoblastomas, and hemangiomas. Although exceedingly rare, primary malignancies, such as an osteosarcoma, of the TMJ have been reported. Metastasis of malignancies to the mandible is rare and involvement of the condyle even more unusual because of the paucity of marrow. Nonetheless, Miles et al recently described a case of breast adenocarcinoma metastatic to bilateral TMJs that presented with limited mouth opening many years after initial treatment. By the time the neoplasm or disease causes symptoms, the lesion may be visible on simple a panoramic radiograph. However, appropriate further imaging with CT or MRI is usually indicated. Treatment of neoplasms or neoplastic-like conditions of the condyle or coronoid process typically involves surgical resection of the lesion and reconstruction if necessary. Further surgery, chemotherapy, or radiation treatment may also be required depending on the specific pathologic condition.
Coronoid hyperplasia is a rare condition leading to limitation of mandibular motion as a result of unnatural contact of the elongated coronoid process with the posterior surface of the zygomatic bone. Hyperplasia of the coronoid process is often bilateral and displays a gradual, painless decrease in both mandibular opening and protrusion. Symptoms often appear around the age of puberty, and the condition is more commonly seen in men. Unilateral coronoid hyperplasia is thought to have a traumatic cause. The pathophysiology of bilateral cases remains unknown, but some theories include heredity, an endocrine source, or hyperactivity of the temporalis muscle. In some instances, affected individuals are unaware of the decreased mouth opening, and the hyperplasia is discovered only after a patient is unable to have dental treatment or becomes a difficult intubation. Although the enlarged coronoid processes are usually visible on panoramic radiograph, CT scans are the preferred images for defining the exact coronoid shape and confirming impingement at the level of the zygoma. Coronoidectomy via an intraoral approach is the treatment of choice for coronoid hyperplasia. Vigorous postoperative physical therapy is imperative in establishing a normal range of mouth opening. Patients should also be monitored for recurrence of coronoid process overgrowth as it has been described in the literature and in personal accounts.
Mandibular hypomobility following surgical procedures or injuries occurs infrequently, but is a recognized cause of pseudoankylosis. In some instances, such as cicatricial scarring of the lips after a severe burn, the source of restricted mouth opening is obvious. More commonly the patient must be questioned regarding a history of a craniotomy, skull base surgery, temporal fossa procedures, or extensive intraoral incisions to make the correct diagnosis. In a review of adult patients undergoing elective frontotemporal craniotomy, Kawaguchi et al reported an incidence of limited mouth opening less than 25 mm in 33.3% and 20.5% two weeks and one month, respectively, after operation. Possible causes of pseudoankylosis following transtemporal neurosurgery or procedures involving the temporal fossa include postincisional scar formation in muscle, Volkmann’s contracture secondary to muscle devascularization, and hematoma organization. The fibrosis and contracture of the temporalis muscle develops within several weeks of surgery and usually resolves within 6 to 12 weeks.
On physical exam after multiple intraoral procedures, a dense scar band may be palpable intraorally on terminal mandibular opening. If the range of motion does not improve with physiotherapy, localized release of scar bands may be necessary. Active and passive jaw exercises initiated shortly after surgery aide to prevent persistent hypomobility. If patients require additional operative intervention, limited mouth opening may cause anesthetic complications and difficult intubation even if pseudoankylosis is short term. When the diagnosis of limited mouth opening is delayed, the efficacy of physical therapy steadily declines. Patients experiencing persistent hypomobility are treated with coronoidectomy and temporal muscle release.
Various types of ankylosis have been classified based on the type of tissue involved (bony, fibrous, or fibro-osseous) and the extent of fusion (incomplete, complete). The mildest form of true ankylosis is dense adhesions of the TMJ. As the adhesions progress, the fibrous ankylosis obliterates the superior joint space and mandibular opening may be severely restricted. In the most severe scenario, there is bony union between the condyle and the glenoid fossa. Topazian and Sawhney have proposed further categorization schemes in attempts to aide diagnosis and treatment. Sawhney lists four types of ankylosis :
Type I—decreased joint space with dense fibrous adhesions
Type II—decreased joint space with dense fibrous adhesions, which also exhibits lateral “lipping” and bony bridges
Type III—broad areas of bony bridging from the lateral ramus to the zygomatic arch
Type IV—complete bony fusion
Topazian describes three subtypes of ankylosis :
Stage I—ankylotic bone limited to the condylar process
Stage II—ankylotic bone reaches the sigmoid notch
Stage III—ankylosis extends to the coronoid process
Trauma is the most frequent cause of true ankylosis followed by infection and systemic disease. In the case of trauma, it is believed that hypomobility follows formation of an intraarticular hematoma with subsequent scarring and abnormal bone formation. Alternatively, displaced fracture segments producing mechanical obstruction or extended immobilization following treatment with maxillomandibular fixation may contribute to ankylosis. In children, a fall with blunt trauma to the chin may result in an intracapsular fracture that can lead to ankylosis. If fractures remain undetected at the time of injury and proper follow-up and physiotherapy are not pursued, the child may develop a significant growth disturbance as a result of hypomobility. Abnormal development may result from damage to articular cartilage of the condyles and disruption of the growth activating functional matrix. Bilateral fractures can lead to limited mouth opening and retrognathia in adolescence and adulthood.
Shifts in dental midline and a shortened ramus and deficient mandibular angle on the affected side resemble changes seen in hemifacial microsomia. Unilateral mandibular growth disturbance can secondarily affect midfacial anatomy leading to cants of the maxillary occlusal plane and malformations of the piriform rims and bony orbits. In addition to growth and aesthetic considerations, hypomobility in children initiates potential problems with chewing, speech development, oral hygiene, and access to oral care.
When posttraumatic ankylosis occurs in adult patients, a medially displaced condylar fracture is often discovered. Patients have limited mouth opening, decreased translation, and possible deviation with function, but are usually not affected with the asymmetry and aesthetic compromise suffered by children.
TMJ infections from local or systemic sources are the reported cause of ankylosis in 10% to 49% of patients. The most frequent source is contiguous spread from otitis media, mastoiditis, or odontogenic infection. With current widespread use of aggressive antibiotic therapy for infections, cases of infection-induced ankylosis are increasingly rare. However, in underdeveloped countries where access to appropriate drug therapy is limited, an infectious cause is still of concern. Though uncommon, spread of infection to the TMJ via the hematogenous route has been described in systemic cases of tuberculosis, gonorrhea, and scarlet fever.
Systemic inflammatory and rheumatologic diseases cause approximately 10% of ankylosis cases. Although ankylosis is not typical of TMJ involvement in these diseases, it has been described in patients with psoriatic arthritis, ankylosing spondylitis (AS), and rheumatoid arthritis. Psoriasis is a chronic dermatologic disease, which affects approximately 1% to 2% of the population. In patients with psoriasis, the incidence of arthritis is only about 5% to 7%, and inflammation is rarely seen in the TMJ. To label a case as psoriatic arthritis of the TMJ, the patient must carry a diagnosis of psoriasis, have erosive polyarthritis, and have a negative test result for rheumatoid factor. Common clinical signs of psoriatic arthritis include stiffness, crepitus, and tenderness. Less frequently, limited mouth opening and ankylosis are seen. As in other affected joints, psoriatic arthritis of the TMJ is characterized by fibrosis, and lesions are mostly erosive-productive and osteoporotic after inflammation resolves. Radiographic signs may show flattening, erosion, or positioning changes.
Ankylosing spondylitis (AS) is a chronic, progressive inflammatory disease that primarily affects the axial skeleton including the spine and adjacent soft tissues. The sacroiliac joint is involved uniformly. AS usually affects men in the third decade and is associated with HLA-B27 in 88% to 96% of cases. The reported incidence of TMJ involvement ranges from 1% to 50%. Patients may have symptoms of stiffness, pain, and a decreased range of motion. The onset and degree of TMJ involvement often parallels the extent of spinal and peripheral joint disease. TMJ ankylosis secondary to AS develops infrequently, and only 12 cases have been reported according to a literature review and case report published by Benazzou et al in 2005. Radiographic evidence of a TMJ pathologic condition includes abnormal condylar shape, erosions, decreased translation, disk abnormalities, and osteophytes. However, radiographic signs are not always correlative with clinical symptoms.
Rheumatoid arthritis is an inflammatory polyarthritis that characteristically has symmetric bilateral proliferative synovitis of large joints. TMJ involvement is seen in 33% to 70% of patients. Of patients with a TMJ pathologic condition, 75% show bilateral disease. TMJ symptoms and signs of tissue destruction generally develop late in the disease process. In several studies, insufficient systemic control of the inflammatory mediator TNF-α has been associated with TMJ pain and destruction. With advanced disease, patients may develop a decreased range of motion, limited bite force, myofascial pain, and joint damage. Interestingly, patients without clinical signs or symptoms of TMJ involvement may have positive MRI or CT findings. Common radiographic findings include a decrease in joint space, mandibular and temporal subchondral cysts, condylar degeneration and resorption, condylar shape and height anomalies, erosion, and demineralization. As a result of loss of condylar and ramal height, malocclusion and open bite often develop. As bone erosion progresses, the joint space fills with fibrous tissue, and infrequently, ankylosis ensues.
Juvenile idiopathic arthritis (JIA), formally called juvenile rheumatoid arthritis (JRA), is a chronic inflammatory disease with onset before age 16 and lasting greater than 6 weeks. TMJ involvement reportedly occurs in greater than 50% of affected children and is often bilateral. The highest prevalence of TMJ destruction occurs in children with an early onset and a polyarticular course. Clinical symptoms of pain, stiffness, and functional limitation have been shown to be unreliable predictors of TMJ involvement in JIA children, and often TMJ destruction develops without any symptoms. A recent survey by Twilt et al found that the absence of translation during maximal mouth opening, asymmetric opening, and crepitation detected on orthodontic examination were good predictors of radiographic TMJ involvement. Early and progressive damage of the condyle secondary to JIA subsequently affects mandibular growth and development. Patients develop characteristic retrognathia, posterior rotation of the mandible, and subsequent anterior open bite deformity. Hypomobility and difficulty with chewing are consequences. Control of the systemic disease with antiinflammatory medications and immunomodulating drugs are the primary efforts to halt the disease process. However, some authors describe improvement in pain and mouth opening of JIA patients after TMJ injection with corticosteroids.
Orthognathic surgery, primarily mandibular advancement or setback, has been reported to cause or exacerbate hypomobility. Proposed mechanisms include fibrous ankylosis secondary to increased pressure on the TMJ, atrophy of the muscles of mastication, soft tissue scarring, and condylar torque causing disk impingement. With widespread use of rigid fixation in orthognathic surgery, long periods of maxillomandibular fixation that contribute to muscular atrophy are unusual. Occasionally, patients may develop excessive fibrosis and scar banding at the sites of intraoral incisions for mandibular osteotomies. Limiting the amount of lateral and superior stripping of the mandible may prevent this outcome. If limited mouth opening and tight intraoral scar bands are noted postoperatively, patients should be placed on a regular regimen of physical therapy. However, if mouth opening does not improve, scar excision may become necessary.
Most surgeons agree that careful positioning of the mandibular proximal segment at the time of surgery is essential to preserve healthy TMJ function and achieve a stable occlusion. Some authors suggest that rigidly fixating the mandible produces increased torque on the condyle with potential adverse effects on the TMJ. However, multiple recent studies comparing TMJ symptoms and mouth opening between patients treated with rigid fixation or wire osteosynthesis following mandibular osteotomy found no significant long-term effects with either method. Van Sickels et al showed that a posterior and superior change in condylar position occurred following mandibular advancement whether using rigid fixation or wire osteosynthesis. No particular factor identified in the study could be attributed to the change, and the authors proposed that remodeling and adaptation of the condyles occurs as a result of changes in the mechanical load. This appears to be a probable scenario because different surgeons use numerous methods to position the proximal segment and persistent hypomobility after orthognathic surgery is rare.
Patients who have prolonged limited mouth opening and fail to respond to physiotherapy should be assessed for presence of a true intraarticular source. Whether or not these patients had preexisting TMJ dysfunction, arthrocentesis may be therapeutic for cases of hemorrhage, edema, or fibrosis in the superior joint space. In the rare case of hypomobility caused by severe condylar torque that does not improve with function and joint adaptation, reoperation with proximal segment repositioning is a viable option to consider.
It is not uncommon for true ankylosis to be preceded by prior TMJ surgery. Patients beginning with pain and limited mouth opening as a result of an internal derangement may undergo an arthrocentesis, arthroscopy, or arthroplasty. When appropriate postoperative exercises, physiotherapy, and follow-up care are not obtained, the patient often returns only after hypomobility has progressed to the point of interfering with daily function.
As always, a thorough history and physical examination leads the surgeon to suspect intracapsular ankylosis as the source of hypomobility. With fibrous ankylosis, the condyle on the involved side or sides is typically limited to rotational movement along the lower border of the articular disk. No translation occurs on the fibrosed side as a result of adhesions between the disk and fossa. Depending on whether unilateral or bilateral fibrous ankylosis exists, the patient will usually open his mouth only 15 to 25 mm and may have deviation toward the side of ankylosis. At the other extreme, a patient with bilateral bony ankylosis may show a nominal mouth opening of 5 to 7 mm and an inability to perform protrusive and excursive movements. Intracapsular ankylosis most often occurs in the intermediate fibro-osseous form, and patients exhibit limited mouth opening and decreased translation. Minimal movement of the lateral pole of the affected condyle is appreciated on palpation. The muscles of mastication and perimandibular soft tissues are secondarily affected by the hypomobility. Thus shortening of the pterygomasseteric sling and the sphenomandibular and stylomandibular ligaments may be noted. After a prolonged inability to open the mouth, repetitive isometric contraction of the temporalis muscle can lead to muscle hypertrophy and subsequent elongation of the coronoid process. Pain may not be a key element of the ankylosed joint, but the contralateral joint occasionally displays tenderness, clicking, and popping as a result of compensatory abnormal movements.
A screening panoramic radiograph may demonstrate condylar deformity, narrowing or irregularity of the joint space, or obliteration of normal bone anatomy. However, CT scanning in multiple planes with the option of three-dimensional reconstruction is the method of choice for evaluation of true ankylosis. CT imaging provides detailed information regarding the dimension of ankylosis and allows preoperative planning to enable complete excision. Failed surgical attempts often result from unrecognized ankylosis of the superior medial condyle to the skull base.
After appropriate imaging investigation and determination of unilateral or bilateral involvement, options for treatment of ankylosis are considered. Treatment goals uniformly aim to prevent disease progression, restore mandibular form and function, and diminish patient suffering and disability. However, no single method produces uniform success.
In cases limited to fibrous ankylosis or minimal lateral osseous bridging, lysis of all joint adhesions and removal of laterally fused and exophytic bone are advocated. Conservative recontouring of the fossa and condyle is completed with attempts to preserve any healthy-appearing articular cartilage. If a portion of salvageable disk remains, this can be mobilized and reduced. Long et al advocate disk preservation and suggest suturing the disk remnant to the TMJ capsule or a flap of temporalis fascia. They reported using this technique in 21 patients with a preoperative mandibular interincisal opening (MIO) of 0 to 15 mm increasing to 25 to 45 mm postoperatively. No recurrences were noted after 1 to 7 years of follow-up.
Frequently, intraarticular ankylosis occurs in more extensive forms and requires an aggressive excision of the ankylotic element. Gap arthroplasty is the simplest surgical method described to treat significant fibro-osseous and complete bony ankylosis. In performing a gap arthroplasty, the surgeon removes a portion of bone sufficient to allow free movement of the mandibular stump. The gap created lies inferior to the biologic site of articulation and thus alters the mechanics of mandibular opening. Roychoudhury et al reported a 2% recurrence rate and mean increase in mandibular opening from 3 mm to 30 mm 36 months postoperatively after gap arthroplasty in a mostly pediatric population. Approximately 30% of the patients developed unstable occlusion that improved over time, and patients with bilateral ankylosis frequently acquired an anterior open bite after the minimum 15-mm gap arthroplasty.
Once release of fibro-osseous ankylosis is completed, the surgeon should mobilize the mandible to determine if adequate mouth opening has been accomplished. If the range of motion is unacceptable, additional actions are often necessary. Kaban et al promote dissection and stripping of the temporalis, masseter, and medial pterygoid and ipsilateral coronoidectomy to address the secondary soft tissue contribution to hypomobility. When MIO remains insufficient, the surgeon may consider contralateral coronoidectomy or arthroplasty.
Since reankylosis is reported to occur in up to 50% of cases after gap arthroplasty, placement of an interpositional material between the condylar stump or ramus and the skull base (interpositional arthroplasty) is usually advocated. The choice of interpositional material may affect long-term results, and the use of a multiplicity of autogenous and alloplastic products have been used. Common autogenous sources include dermis, full-thickness skin graft, temporalis muscle, fascia, and auricular cartilage. Alloplastic interpositional materials, such as silicone, acrylic, polymethylene, ceramic, and various metals have been described. Proponents of autogenous materials cite the possible migration, fragmentation, and foreign body reaction that can occur with alloplasts. In a study of 38 patients treated with condylectomy and placement of silicon blocks or sheets as interposition material, Ortak et al reported a 7.8% incidence of infection.
After sufficient resection of ankylotic bone and fibrous tissue, the resulting gap is frequently too large to provide appropriate posterior vertical support and a stable occlusion. Therefore joint reconstruction is preformed primarily or secondarily to reestablish mandibular function. Options for reconstruction include an autogenous graft, alloplastic prosthesis, or distraction osteogenesis.
The literature cites the use of fibula, metatarsal, sternoclavicular, and iliac crest grafts as methods of reconstruction, yet the most often used and most extensively studied is the costochondral graft. Advantages of costochondral grafts include biologic compatibility, remodeling capability, and growth potential. Disadvantages consist of donor site morbidity, fracture, resorption, increased operating time, reankylosis, and unpredictable growth. Although the incidence of adequate growth, overgrowth, insufficient growth, or even resorption with costochondral grafts is unknown, it continues to be the favored reconstructive choice in children. Medra recently published a review of patients treated with costochondral graft reconstruction after condylar resection for ankylosis. Eighty-five grafts (25 unilateral, 30 bilateral) were followed for 7 to 10 years and showed reankylosis in 6%, resorption in 25%, overgrowth in 4%, and favorable remodeling in 59%. Fifty-eight percent of patients showed MIO greater than 25 mm, 18% between 5 to 25 mm, and 24% less than 5 mm. Although most surgeons use a short period of maxillomandibular fixation following costochondral grafting because of the soft character of the bone, there is universal recommendation for early release and initiation of jaw-opening exercises. Aggressive physiotherapy should be maintained for 6 months to a year postoperatively. If a range of motion comfortable to the patient is present at 1 year after surgery, a reasonable exercise regimen of passive and active motion may be maintained indefinitely.
Alloplastic materials represent a biomechanical versus biologic solution for reconstruction of the TMJ. Proposed advantages of alloplastic reconstruction include avoidance of donor site, decreased operating time, immediate return to function, and good reproduction of anatomic contours. In addition, alloplastic options are frequently favored in patients with systemic, inflammatory, autoimmune diseases or local resorptive TMJ pathologic conditions for whom autogenous grafts are contraindicated. Some surgeons think that the decreased vascularity and extensive scarring found in patients with multiple surgeries compromise the success of autogenous grafts and therefore opt for alloplastic prostheses in these patients. High cost, wear and failure of materials, variable long-term stability and/or screw loosening, lack of growth, and history of foreign body giant cell reactions are quoted disadvantages of alloplasts. A total TMJ prosthesis was first described in the 1970s, and various forms including the Proplast-Teflon containing Vitek-Kent and Silastic implants were used in the late 1970s through 1980s. These devices were removed from the market secondary to documented bony erosions, fragmentation, poor biocompatibility, and giant cell reaction. Attempts to reconstruct the TMJ with alloplastic condylar replacement have demonstrated fossa erosion and heterotopic bone formation. Currently, three complete TMJ prostheses are FDA approved for use in America. The W. Lorenz TMJ Replacement System is a stock prosthesis consisting of a high-molecular-weight polyethylene fossa and a cobalt-chromium-molybdenum condyle with titanium plasma coating on the ramal surface. The prosthesis underwent a 10-year clinical trial before approval in January 2006, but has been used in Canada, Europe, and South America for a number of years. Surgeons are required to undergo a training period before being approved to place the device.
The second FDA-approved system is the TMJ Concepts custom-made prosthesis that was developed in 1989 by Techmedica, Inc. and approved for use in July 1999. TMJ Concepts are CAD/CAM devices made of a titanium mesh and ultra–high-molecular-weight polyethylene fossa and a titanium alloy mandibular shaft with a chromium-cobalt-molybdenum condyle. Wolford evaluated 38 patients (69 TMJs) treated with TMJ Concepts devices and followed for 60 to 96 months. He reported statistically significant improvement in interincisal opening, pain level, and jaw function postoperatively and long-term stability of occlusion. However, this study included patients with varying indications for joint reconstruction and was not limited to the treatment of ankylosis. Complications discussed included loosening of screws in one patient and heterotopic bone formation in five patients.
The Christensen TMJ Arthro-Chrome Condylar Prosthesis is available as a stock device or in a patient-specific model marketed by TMJ Implants, Inc. The entire condylar prosthesis, fossa-eminence component, and retaining screws are manufactured from a cobalt-chromium-molybdenum alloy. The Christensen system was previously on the market as a preamendment Class III device. After changes in FDA requirements, the manufacturer submitted an application and received premarket approval for the prosthesis in January 2001. 93 Preclinical data demonstrated an estimated fatigue limit of 130 lb for the prosthesis, and it is not recommended for use in patients with a history of muscle hyperfunction. TMJ Implants, Inc. published the results of a prospective study of 43 subjects implanted with the device. They report significant increases in interincisal mouth opening, decreases in pain, and less dietary restriction in subjects 36 months after surgery.
A more recently described option for reconstruction of the TMJ after resection of ankylosis is distraction osteogenesis. Kaban et al modified his original protocol with substitution of distraction versus costochondral grafting when practical. The placement of the distraction device occurs after release of ankylosis, joint mobilization, and repositioning of a disk remnant or the placement of the surgeon’s choice of interpositional material. The distal portion of the mandible may be recontoured to adapt to the glenoid fossa. A bicortical mandibular osteotomy is created distally, the distraction device fixated, and segment mobility verified. Depending on the surgeon’s preference, distraction begins 1 to 5 days postoperatively and proceeds at a rate of 1 mm per day. After achieving the desired amount of lengthening, a 4- to 6-week consolidation phase is completed before removal of the distraction appliance. Reported advantages of distraction osteogenesis are avoidance of a donor site, immediate physiotherapy, possible soft tissue augmentation, and simultaneous correction of any associated mandibular deformity. Disadvantages include a second surgery for device removal, the need for patient compliance, the inability to precisely control distraction vector, scars from extraoral devices, and an occasional resultant open bite deformity.
The treatment of true ankylosis of the TMJ is a difficult undertaking with many potential complications regardless of technique. Reankylosis and continued hypomobility are the most commonly cited adverse outcomes. Thorough resection of ankylotic tissue, the replacement of displaced disk tissue or insertion of interpositional material, and a rigorous postoperative physiotherapy program may decrease the incidence of these problems. Kaban et al state that an average interincisal mouth opening of greater than 35 mm is rare after surgery for correction of TMJ ankylosis. Many patients are satisfied when 30 mm of opening is attainable.