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3.1 Introduction

The complex anatomy and function of the temporomandibular joint (TMJ) and its close proximity to adjacent tissues may explain the wide spectrum of disorders involving this joint. It is often hard to identify the exact cause of TMJ pain or the factors that perpetuate the pain and dysfunction. In general, it is important to differentiate whether the symptomatology is the result of an extra-articular or intra-articular process as this can often aid in developing an appropriate differential diagnosis and treatment plan.

3.2 Making the Correct Diagnosis

A detailed pain history from the patient that addresses the onset, severity, progression, quality, radiation, and presence or absence of any aggravating and alleviating factors is crucial. A history of spontaneous or iatrogenic occlusal changes including orthodontics, orthognathic surgery, and dental prosthodontic work should be also noted. Signs such as joint noises, locking, and decrease in mandibular range of motion may all suggest an intra-articular disorder. Temporomandibular joint pain may be the result of internal derangement, inflammation of the synovial lining, other pathologies, or a combination of these. Involvement of multiple joints should alert the surgeon to the possibility of a systemic arthritide or condition. Altered sensation, unplanned weight loss, and hearing disturbances may be associated with a malignant TMJ process.

The clinical evaluation of the head and neck should include an examination of the muscles and TMJs and assessment for any asymmetry or skeletal deformity. An asymmetry of the facial skeleton, especially the mandible, might suggest a progressive overgrowth or resorption of one or both TMJs. Mandibular maximum inter-incisal opening (MIO) and excursive movements (lateral and protrusive) should accompany a thorough intraoral examination of the occlusion. Positive findings of parafunction such as signs of excessive occlusal wear facets and tongue crenations should be documented.

It is imperative that an accurate diagnosis be made prior to contemplating any nonsurgical or surgical treatment for TMJ disorders. The history and clinical examination remain the most important sources of information on which to make the correct diagnosis. Radiological imaging techniques may also be of additional help in making a correct diagnosis. In contrast to conventional imaging techniques that only provide structural information, advanced techniques like magnetic resonance scanning (MRI) and computerized tomography (CT) represent the gold standard in contemporary TMJ imaging for soft- and hard-tissue abnormalities, respectively. Additionally, nuclear imaging using radioactive isotopes offers a physiologic evaluation of the TMJ including information about active processes like inflammation, growth, or malignancy. These techniques may also allow for early detection of the condition prior to structural changes [1, 2]. Examples of this technology include single-photon emission computed tomography with technetium 99 methylene diphosphonate (SPECT/Tc-99 MDP), which gives three-dimensional images due to multiplanar imaging acquisition, and positron emission tomography (PET), which utilizes F-2-fluoro-2-deoxy-glucose, and can also be combined with CT images (PET/CT) for better anatomical correlation [3].

3.3 The Diagnostic Challenge

Identifying the correct diagnosis allows the surgeon to anticipate the natural progression of the disease as well as provide treatment directed by evidence-based guidelines. Some of the more challenging diagnostic dilemmas include the following:

  • Arthralgia as a result of the inflammatory milieu versus the disc position

  • Condylar enlargement conditions

  • Condylar resorptive processes

  • Clinical conditions mimicking TMJ closed lock

  • Open lock

3.3.1 Arthralgia

Our understanding of temporomandibular joint arthralgia has increased significantly over the last 40 years. The contribution of inflammatory cytokines to the development of arthralgia has become apparent as a result of synovial sampling. Multiple cytokines including IL-1 beta, IL-8, IL-17, CXCL-1, CCL-20, TNF-α, IFN-γ, and TIMP-1 have been identified and found to correlate with pain, response to treatment, and/or the presence of internal derangement [4, 5]. Other interleukins also present possess anti-inflammatory properties including IL-4, IL-6, IL-10, IL-12, IL-13, and OCIF/OPG [6]. The net result of the inflammatory process is the generation of reactive oxygen species including myeloperoxidase, superoxide ion, hydrogen peroxide, hydroxyl radical, and peroxynitrite anion. The result is the development of chondromalacia and degenerative joint disease. The inflammatory process also results in the release of VEGF, NGF, and FGF leading to changes in the synovial vascularity usually presenting as hyperemia and synovitis. The possibility that chronic inflammation results in a reduction of the biomechanical properties of the fibrocartilage, disc, and bone leading to disc displacement and/or degenerative changes cannot be excluded [7]. However, the potential for disc displacement in an otherwise susceptible individual to lead to inflammation and/or degeneration cannot be excluded.

The presence of inflammation within the TMJ also appears to correlate with the presence of inflammatory biomarkers in the serum and saliva [8, 9]. The presence of inflammatory mediators within the temporomandibular joint and the correlation with pain provides an opportunity to treat these patients with anti-inflammatory medications. When patients fail to respond to systemic medication or when patients present with arthralgia and closed lock, the utility of arthrocentesis and arthroscopy becomes apparent. With few exceptions these procedures should be considered in most patients prior to any open procedure.

Although TMJ arthralgia can be explained by the presence of inflammatory mediators within the joint and/or disc position and health, the potential for peripheral and central sensitization to develop should not be underestimated [10, 11]. The presence of certain genetic polymorphisms may also predispose individuals to TMD. Furthermore multiple physiological and psychological domains may contribute to the development of TMD as well as multisystem dysregulation which is often seen in the same population [12, 13].

It seems prudent to proceed cautiously with any patient with temporomandibular joint arthralgia or closed lock first assuming that the pain is secondary to inflammation. Treatment strategies such as arthrocentesis and arthroscopy should be considered first. Arthroplasty to address disc position or structural abnormalities should be considered when the previous modalities have failed. Taking time to know the patient and carefully evaluating the response to prior surgical intervention will also allow the surgeon to develop rapport and identify comorbid psychological and physiological conditions that may make the patient a poor surgical candidate.

3.3.2 Enlarged Condyle

History

A 27-year-old adult patient was treated by an experienced surgeon with standard two-jaw orthognathic surgery. The initial preoperative clinical examination revealed an open bite on the left side. Postsurgically the occlusion was noted to be as planned, but a left-sided open bite was again noted at 24 months (Fig. 3.1a).

Fig. 3.1
figure 1

(a) Intraoral photograph of a patient showing redevelopment of a left-sided open bite approximately 12 months after two-jaw orthognathic surgery. (b) Panoramic radiograph of the same patient after the orthognathic procedure (Note: The plate in the left mandible was removed due to a postoperative infection.) (c) 3-D reconstruction of right TMJ. The condyle appears normal in morphology. (d) 3-D reconstruction of left TMJ. Note the significantly larger and lobulated condyle, which is abnormal in shape

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Diagnostic Error

The patient had a progressive facial asymmetry due to an active osteochondroma of the left TMJ, which was not diagnosed. The left condyle was significantly larger than the right side (Fig. 3.1b–d). This should have been investigated further with serial clinical examinations and an advanced imaging technique prior to jaw surgery.

Differential Diagnosis

The differential diagnosis of a unilateral enlarged condyle includes condylar hyperplasia (CH), hemimandibular hypertrophy (HH), hemimandibular elongation (HE), and osteochondroma. The clinical presentation may include a malocclusion with unilateral posterior open bite on the affected side, shifted dental midline and chin to contralateral side, canting of the occlusal plane, and progressive facial asymmetry secondary to vertical elongation of the face on the affected side. Compensatory maxillary changes can accompany the displacement of the mandibular position in long-standing cases. Although CT scans and MRI examination may be used to supplement the work-up of such condylar pathology, it may be challenging to identify the diagnosis on the basis of clinical and radiographic assessment alone. An exophytic mass and a condylar head that is lobulated suggest osteochondroma, while an enlarged and elongated condyle may suggest CH, HH, or HE. A definitive diagnosis can only be made when the clinical and radiographic features are correlated with the histopathology.

Management Considerations

The first step in the treatment is to decide whether the enlarged condyle is still active and growing. If inactive, the patient can be treated with traditional orthognathic surgery with a realistic expectation of stability. If still active based on clinical, radiographic, or scintigraphic/PET scanning, it becomes important to make the correct diagnosis in order to determine the most appropriate surgical treatment. High condylectomy is a procedure in which 3–5 mm of the superior aspect of the condylar head is removed in an attempt to remove the cartilaginous cap. This is potentially a reasonable treatment choice to arrest active condylar hyperplasia but would not be appropriate for osteochondroma. Low condylectomy may be the treatment of choice in situations where the lesion involves the superior region of the condyle [14]. It has the advantage of preserving a portion of the joint while avoiding the need for joint reconstruction. However, there is little long-term data to support this approach. Resection of the condyle or osteochondroma involves a complete condylectomy, and while this eliminates all growth-related pathology, it does require either autogenous or alloplastic reconstruction [15].

3.3.3 Small Condyle

History

A 22-year-old patient was referred by her dentist to an orthodontist for evaluation and management of a worsening class II, open bite deformity which was also associated with TMJ pain and dietary limitations. She underwent a combined orthodontic and two-jaw surgical treatment with good results (Fig. 3.2a, b). Several months after debanding, she started to develop an anterior open bite again. Ultimately, there was significant degenerative change within bilateral TMJs (Fig. 3.2c) due to continued condylar resorption resulting in progressive mandibular retrusion (Fig. 3.2d, e).

Fig. 3.2
figure 2

(a, b) Intraoral views of the 8-month postoperative occlusion of a patient (immediately after removal of orthodontic appliances) who underwent combined orthodontic and orthognathic surgical treatment for correction of an open bite, class II skeletal and occlusal deformity. (c) Sixteen-month postoperative panoramic radiograph showing advanced bilateral resorption of condyles. (d, e) Relapse has occurred 4 months later due to continued TMJ condylar resorption

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Diagnostic Error

The patient had pre-existing, active TMJ condylar degeneration which was a source of the developing open bite and a progressive class II dentofacial deformity. In the presence of an active resorptive disease process, relapse and redevelopment of the malocclusion should have been expected.

Differential Diagnosis

Evidence of condylar resorption in a young person manifested by a progressive change in occlusion or radiographic evidence of TMJ degeneration should alert the surgeon to the potential for progressive condylar resorption (PCR) or a systemic arthritide unless proven otherwise. Specific causes of condylar degeneration include rheumatoid arthritis, internal derangement, use of steroids, trauma, systemic autoimmune/connective tissue (CT) diseases (e.g., lupus, psoriasis, scleroderma), orthodontic treatment, and orthognathic surgery [16, 17].

Management Considerations

The etiology and pathogenesis of condylar resorption remains unclear. It may be classified into primary (idiopathic) and secondary (known etiology) depending on the presence of predisposing factors [18]. In PCR, the patient usually presents with a progressively retruded chin, mild TMJ pain with and open bite deformity. In contrast, many patients with TMJ resorption due to CT disease have significant preauricular joint and myofascial pain. Connective tissue diseases that can affect the TMJ are broadly divided into rheumatoid arthritis (RA) and the seronegative spondyloarthropathies. The latter can include conditions such as psoriatic arthritis, lupus arthritis, scleroderma, ankylosing spondylitis, arthritis associated with inflammatory bowel disease, and reactive arthritis. Juvenile idiopathic arthritis can be positive or negative for rheumatoid factor and also affects the TMJ in younger individuals leading to destruction of the condylar growth center with subsequent disturbances in mandibular growth [19, 20]. The metabolic diseases of gout and pseudo gout are also similarly known to affect the TMJ. The effects of these systemic autoimmune/CT diseases on the TMJ may induce a plethora of characteristic radiographic (MRI) findings such as abnormal disc position, abnormal disc morphology, osseous changes in the mandibular condyle, deformity of the articular eminence, and glenoid fossa, besides an abnormal bone marrow signal of the mandibular condyle [21]. If a patient is suspected to be having TMJ disorder secondary to a CT disease, rheumatology consultation is recommended.

If the resorption occurs in a bilateral fashion, there is a symmetric posterior shift of the mandible with class II skeletal and dental malocclusion. On the other hand, asymmetric bilateral or unilateral disease processes may result in a dental and skeletal mandibular midline shift, contralateral posterior open bite, and ipsilateral cross bite. Irrespective of the etiology, it is critical to determine whether the disease is active or not by a thorough history and serial clinical and radiographic evaluations. Computed scans and MRI provide static information and cannot provide information about disease activity. A technetium 99 MDP study can be useful in determining metabolic activity in the condyles. The treatment of TMJ condylar resorption remains controversial and will depend on the extent and stage of the disease. Although it may occasionally be self-limiting, it can be reactivated by orthodontics or orthognathic surgery [22,23,24]. Most clinicians agree that the TMJs must be stable prior to any orthognathic surgery. Potential treatments for patients with active PCR patients include the following: (1) observation for disease arrest (“burn out”) followed by maxillary orthognathic surgery to close the open bite and/or chin camouflage surgery to improve facial profile, (2) TMJ replacement with autogenous tissues (most commonly costochondral grafts) with delayed orthognathic surgery, and (3) TMJ replacement with alloplastic joints with delayed or concomitant orthognathic surgery.

3.3.4 Clinical Conditions Mimicking TMJ Closed Lock

History

A 48-year-old adult patient had a history of progressively decreasing mouth opening over a period of 10 years with no TMJ pain and mild unilateral, left-sided temporal and masseter tenderness. When he presented initially to a local surgeon, he had a maximal inter-incisal opening of 16 mm. A preoperative panorex was unremarkable, and the surgeon prescribed NSAIDS and muscle relaxants and referred him for physical therapy without much success. A TMJ MRI was next obtained which showed bilateral internal derangement. The patient underwent bilateral TMJ arthrocentesis with no improvement.

Diagnostic Error

The etiology of the limited opening in this patient was a unilateral osteochondroma of the coronoid process, which was not diagnosed. The lack of joint pain and long-standing history should have alerted the clinician to other causes of limited opening. A CT scan may have been more beneficial than a MRI (Fig. 3.3a, b).

Fig. 3.3
figure 3

(a) Axial CT scan showing an osteochondroma of the left mandibular coronoid process. (b) Coronal CT scan showing osteochondroma of the coronoid area which was causing impingement on the zygomatic arch during mandibular translation. (c, d) Other osseous etiologies of refractory trismus include TMJ ankylosis (c) and coronoid hyperplasia (d). (e) MRI image demonstrating closed mouth position with anteriorly displaced disc (white arrow). (f) Open mouth view of same patient showing limited mandibular translation and no mobility of displaced disc, which remains in the same position (beneath the articular eminence) as in the previous figure (white arrow)

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Differential Diagnosis

Intra-articular TMJ disorders such as internal derangement, fibrous adhesions, and fibrous or bony ankylosis should be considered (Fig. 3.3c). Extra-articular conditions like coronoid hyperplasia (Fig. 3.3d) and neuromuscular disorders should also be considered.

Management Considerations

Prior to attempting any surgical treatment, it should be determined whether the hypomobility is intra-articular or extra-articular. The latter is a result of fibrosis and scarring of the muscles and soft tissues or mechanical impingement that is independent of the TMJ. This includes prior soft tissue trauma or surgery, radiation therapy [25, 26], depressed zygomatic arch fracture [27], myositis ossificans traumatica [28], severe facial burns, and coronoid hyperplasia [29]. The treatment of these conditions includes correction of the causative factor if possible and early aggressive physical therapy to improve the mandibular range of motion.

An acute intra-articular cause of limited opening may include closed lock secondary to internal derangement. Patients often present with limited inter-incisal opening and deviation to the affected side. Clicks are rarely encountered on exam, but patients may give a past history of them since there is often anterior disc displacement without reduction at the time of presentation (Fig. 3.3e, f). Pain is elicited when attempting to increase the opening by stretching or forcing. Treatment may include arthrocentesis or arthroscopy. An anchored disc may also cause limited opening despite normal disc position.

Long-term limited opening should alert the surgeon to multiple potential causes. The treatment of bony ankylosis varies according to the degree of ankylosis, surgeon experience, and preference. A variety of surgical techniques have been described in the literature with no single method proven to be ideal. This includes gap arthroplasty, interpositional arthroplasty, and TMJ reconstruction using autogenous or alloplastic replacements. Fibrous ankylosis may be amenable to be more conservative surgical management [30].

3.3.5 Increased or Normal Mouth Opening with Locked Jaw

History

An 18-year-old patient presented to the emergency room with a TMJ open lock condition. He gave a history of recurrent open locks during range of motion movements multiple times during the last 3 months, all of which were self-reducible. A CT scan was obtained and the patient was diagnosed as having a TMJ dislocation. The “dislocated mandible was reduced” under intravenous sedation by the ER physician. He was then referred to a specialist for follow-up.

Diagnostic Error

The clinician failed to diagnose the condition appropriately. The history of recurrent yet “self-reducible” open locks should have alerted the physician that the etiology was unlikely to be dislocated condyle out of the fossa and trapped anterior to the eminence. The CT scan obtained at the time of the locking (Fig. 3.4b) reveals that the condyle was not dislocated out of the fossa.

Fig. 3.4
figure 4

(a) CT scan demonstrating true condylar dislocation with the mandibular condyle displaced beyond the anatomic limits of the glenoid fossa and is trapped anterior to the articular eminence. (b) CT scan showing that the mandibular condyle remains within the anatomic limits of the glenoid fossa and is not trapped anterior to the articular eminence

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Differential Diagnosis

Open lock may be the result of either dislocation of the condyle (Fig. 3.4a) or a disc-condyle issue. In the former, there is usually hypermobility with steep articular eminence where the condyle gets trapped anterior to the fossa on wide opening, while in the latter, the condyle stays in the fossa (Fig. 3.4b) but translates anterior to the disc, which prevents closure.

Management Considerations

In TMJ condylar dislocation, the condyle is anterior and superior to the articular eminence on CT scan, and this condition is often accompanied by spasm of the muscles of mastication. Dislocation can be classified into acute or chronic, partial or complete, dislocation. Acute cases are typically managed by manual reduction and analgesics. On the other hand, chronic dislocation is managed by different nonsurgical and surgical options. Surgical treatment generally aims at either augmenting (to prevent dislocation) or removing the mechanical obstacle (to allow self-reduction).

In contrast to this scenario, there are some patients where the open lock condition occurs within the expected range of condylar motion [31]. In these cases, the occurrence of open lock is often spontaneous, and usually there is no associated history of joint laxity, neurologic disorders, and other factors that predispose to condylar dislocation [22]. On radiographic examination, the eminence is shallow and the condyle is located inferior to rather than in front of and superior to the eminence (Fig. 3.4b). The obstruction, which is not visible in plain radiographs or CT scans, may be demonstrated on TMJ MRI scans (esp. dynamic cine MRI) which show that the condyle is located in front of the anterior band of the disc in an open lock position and is unable to return posteriorly into the fossa due to mechanical obstruction by the disc. These cases can usually successfully be managed by arthrocentesis or disc-related surgical procedures.