Condylar Hyperplasia

Condylar hyperplasia (CH) is a generic term describing enlargement of the condyle caused by a number of different pathologies. The following sections present the classification system used by the authors to differentiate the etiology of these conditions.

Condylar Hyperplasia Type 1

CH type 1 develops during puberty as an accelerated and prolonged growth aberration of the normal condylar growth mechanism, causing mandibular prognathism. Growth is self-limiting, but the mandible can continue to grow into the mid-20s and can occur bilaterally (CH type 1A) or unilaterally (CH type 1B). These patients may have a Class I occlusion at the beginning of puberty and develop a mandibular prognathism and Class III occlusion, or they may begin with a Class III skeletal and occlusal relationship but develop a worse Class III. Not all prognathic mandibles are caused by CH; only those demonstrating accelerated, excessive mandibular growth continuing beyond the normal growth year. Either CH type 1A (bilateral) with an asymmetric rate of condylar growth or CH type 1B (unilateral) can cause progressive deviated mandibular prognathism, facial asymmetry, TMJ articular disk dislocations, TMJ pain, headaches, masticatory dysfunction, and so on.

The treatment protocol for active CH type 1 includes (1) high condylectomy, or removal of the top 4 to 5 mm of the condylar head to arrest mandibular growth; (2) TMJ disk repositioning over the remaining condyle with the Mitek anchor technique; (3) bilateral mandibular ramus osteotomies to reposition the mandible; (4) maxillary osteotomies, if indicated, to maximize function and facial balance; and (5) any indicated ancillary procedures, such as turbinectomies, genioplasty, rhinoplasty, and removal of third molars. Our studies have shown that this protocol stops mandibular growth and provides highly predictable and stable skeletal and occlusal outcomes with normal jaw function and good esthetics.

Condylar Hyperplasia Type 2

CH type 2 is caused by an osteochondroma, which can develop at any age, although two thirds of these cases arise in the teenage years. CH type 2 causes a unilateral vertical enlargement of the mandibular condyle, neck, ramus, and body, with compensatory unilateral maxillary vertical down-growth, resulting in a transverse cant in the occlusal plane. It is not self-limiting. The condyle can grow predominately vertically (CH Type 2A) or with additional horizontal exophytic growth extensions (CH Type 2B). In the more progressive tumors, a posterior open bite develops on the ipsilateral side. The overgrowth on the ipsilateral side loads the contralateral TMJ, causing disk displacement in 75% of cases.

The treatment protocol for CH Type 2 includes (1) low condylectomy, which preserves the condylar neck; (2) recontouring of the condylar neck to function as a new condyle; (3) repositioning of the articular disk over the condylar stump and repositioning of the contralateral disk, if displaced, with the Mitek anchor technique; (4) bilateral mandibular ramus osteotomies to reposition the mandible; (5) maxillary osteotomies, if indicated; (6) vertical reduction of the inferior border of the mandible on the ipsilateral side, if indicated, to improve vertical facial balance, with preservation of the inferior alveolar nerve; and (7) any indicated ancillary procedures. Our study has shown that this technique is highly predictable for eliminating the TMJ pathology, maintaining long-term skeletal and occlusal stability, and optimizing facial balance.

Condylar Hyperplasia Type 3

CH type 3 are benign, and CH type 4 are malignant conditions, that can cause condylar enlargement. They are not discussed in this chapter.

Articular Disk Dislocation

The most common TMJ pathologies are anteriorly and/or medially displaced articular disks. These conditions can initiate a cascade of events, leading to TMJ arthritis. Less commonly, the disks can become laterally and, in rare cases, posteriorly displaced. A magnetic resonance imaging (MRI) study can show the direction of disk displacement, progression of arthritic and degenerative changes, mobility of the joint components, and so on. There is generally a 4- to 6-year window during which the disks remain salvageable for repositioning, with highly predictable outcomes using the Mitek anchor technique. If the disks become nonreducing, the degenerative process proceeds more rapidly.

In patients in whom the TMJ condition has been present for longer than 6 years, significant TMJ degeneration is present, multiple other joints are involved, other systemic diseases are present, or the patient has a history of recurrent infections (e.g., urinary tract, gastrointestinal tract, and respiratory tract), these factors may indicate that a total joint prosthesis may provide a more predictable treatment outcome. If the disks meet the requirements for salvage, the treatment protocol is (1) TMJ articular disk repositioning and ligament repair with Mitek anchors; (2) bilateral mandibular ramus osteotomies to reposition the mandible; (3) multiple maxillary osteotomies, if necessary; (4) any indicated ancillary procedures. When displaced disks are repositioned, the condyle and mandible usually are displaced downward and forward, and in patients with Class I occlusions to begin with, this displacement can create posterior open bites and an end-on incisor relationship. Mandibular ramus osteotomies may be indicated to maintain a good occlusion and allow the mandibular ramus and condyle to move inferiorly and forward to accommodate the repositioned articular disk within the joint space.

Adolescent Internal Condylar Resorption (AICR)

AICR is one of the most common TMJ conditions seen in teenage females (8 : 1 female to male ratio). This hormonally mediated condition is initiated as the adolescent enters the pubertal growth phase, usually between the ages 11 and 15 years. Our hypothesis is that the female hormones released during pubertal growth stimulate female hormonal receptors in the TMJ tissues. This results in a hyperplasia of the synovial cells, which produce chemical substrates that break down the ligaments supporting the disks in place, allowing the disks to become anteriorly displaced. The tissue then surrounds the condyle, and the chemical substrates cause the condyle to resorb; however, the fibrocartilage on the condyle and fossa remains intact as the condyle shrinks. At least 25% of these patients have no symptoms, but they nevertheless have a pathologic condition that causes the condylar resorption. These cases are best treated within 4 to 6 years after the onset of the TMJ pathology. The condition usually occurs bilaterally.

The treatment protocol for salvageable disks is (1) bilateral TMJ articular disk repositioning and ligament repair with Mitek anchors; (2) bilateral mandibular ramus osteotomies to advance the mandible in a counterclockwise direction; (3) multiple maxillary osteotomies to advance the maxilla in a counterclockwise rotation; (4) ancillary procedures if indicated, such as genioplasty, turbinectomies, rhinoplasty, and removal of third molars. This treatment protocol produces highly stable and predictable results. If the disks are nonsalvageable, patient-fitted total joint prostheses are indicated (these are discussed later in the chapter).

Reactive Arthritis (Seronegative Spondyloarthropathy)

Reactive arthritis is an inflammatory process that can occur in TMJs with or without displaced articular disks and with or without condylar resorption. It usually is related to bacterial or viral pathology. The condition is most commonly seen in females and does not usually begin until the late teenage years or later. Preliminary studies have identified bacterial species from the Chlamydia and Mycoplasma families. These bacteria live and function as viruses, stimulating the production of substance P, cytokines, and tumor necrosis factor, which are pain modulators and contribute to the degenerative process in the TMJs. Other bacterial and viral elements also may be causative factors. An MRI study may show displaced disks, inflammation, and progression of disk and condylar degeneration. Patients with localized TMJ reactive arthritis with displaced but salvageable disks may respond well to joint débridement, articular disk repositioning with Mitek anchors, and appropriate orthognathic surgical procedures to correct the coexisting dental facial deformity. In more aggressive forms of the disease or with polyarthropathy, TMJ patient-fitted total joint prostheses with fat grafts may be indicated.

TMJ Ankylosis

TMJ ankylosis usually develops as a result of trauma, inflammation, sepsis, and/or systemic diseases, resulting in severely limited jaw function and oral hygiene and nutritional problems. When this condition occurs during the growing years, it can severely affect jaw growth and development, resulting in significant dentofacial deformities, malocclusion, and airway compromise.

The most predictable treatment protocol is (1) release of the ankylosed joint and removal of the heterotopic and reactive bone with thorough débridement of the joint and adjacent areas; (2) reconstruction of the TMJs with a patient-fitted total joint prosthesis (and, if indicated, advancement of the mandible) ; (3) coronoidotomies or coronoidectomies if the ramus is significantly advanced or vertically lengthened with the prosthesis; (4) autogenous fat grafts harvested from the abdomen or buttocks and packed completely around the articulating area of the prosthesis ; (5) additional orthognathic procedures, if indicated, such as a contralateral sagittal split osteotomy and/or maxillary osteotomies; and (6) any indicated ancillary procedures. In these cases, it is vital to place fat grafts around the articulating portion of the prosthesis to prevent the recurrence of heterotopic and reactive bone.

Congenitally Deformed/Absent TMJ (Hemifacial Microsomia, Treacher Collins Syndrome)

Hundreds of congenital syndromes can cause facial deformity. Hemifacial microsomia (HFM) is one of the more common syndromes and may present with features such as unilateral hypoplasia or aplasia of the mandibular condyler, ramus, and body and hypoplasia of the maxilla, zygomatic orbital complex, and temple bone, with decreased ipsilateral facial height, a retruded mandible deviated toward the ipsilateral side, Class II malocclusion with a transverse cant to the occlusal plane, and significant ipsilateral soft tissue deficiency. The treatment protocol for these patients includes (1) ipsilateral mandibular ramus and TMJ reconstruction with a patient-fitted total joint prosthesis; (2) contralateral disk repositioning if the disk is displaced; (3) contralateral sagittal split osteotomy; (4) maxillary osteotomies to advance and transversely level the maxilla; (5) placement of fat grafts around the TMJ prosthesis; and (6) any indicated ancillary procedures. It is best to perform these procedures in females at the age of 15 and in males at the age of 17 to 18 to prevent adverse effects of growth from the normal side. If done earlier, secondary orthognathic surgery may be indicated.

Connective Tissue and Autoimmune Diseases (CT/AI)

CT/AI diseases can affect the TMJs. Such diseases include juvenile idiopathic arthritis (JIA), juvenile rheumatoid arthritis (JRA), rheumatoid arthritis (RA), psoriatic arthritis, ankylosing spondylitis, Sjögren’s syndrome, systemic lupus erythema, scleroderma, mixed connective tissue disease, and others. Multiple systems are usually involved, although with JIA, occasionally only the TMJ joints are involved. Peripheral joints are usually symmetrically inflamed, resulting in progressive destruction of articular structures. Facial deformity can occur with involvement of the TMJs. In growing patients, clinical and radiographic features include a retruded mandible, maxillary AP and posterior vertical hypoplasia, progressively worsening facial and occlusal deformity, high occlusal plane angle facial morphology, Class II occlusion, anterior open bite, and TMJ symptoms, such as noise, pain, and jaw dysfunction. MRI features include loss of condylar vertical dimension, significant mediolateral condylar narrowing, possible anteroposterior mushrooming of the condyles, and resorption of the articular eminence. Articular disks usually are in position but are surrounded by a reactive pannus that eventually destroys the disk and also causes condylar and articular eminence resorption.

The treatment protocol for these conditions is (1) bilateral TMJ reconstruction and mandibular counterclockwise ad­­vancement with patient-fitted total joint prostheses; (2) bilateral coronoidotomies or coronoidectomies; (3) harvesting of autogenous fat grafts from the abdomen or buttock and packing of these grafts around the articulation aspect of the prostheses; (4) maxillary osteotomies to advance the maxilla in a counterclockwise direction; and (5) additional adjunctive procedures if indicated. It is best to treat females at 14 to 15 years and males at 16 to 17 years, when most of the normal facial growth is complete.

Other End-Stage TMJ Pathology

Other TMJ end-stage conditions may include (1) advanced reactive arthritis or osteoarthritis; (2) neoplasms; (3) multiply operated TMJs; (4) failed TMJ alloplastic implants; and (5) failed autogenous tissue grafts. Patients with these TMJ pathologies would benefit from TMJ reconstruction and, when indicated, mandibular advancement using patient-fitted total joint prostheses and other indicated orthognathic surgical procedures.

Step 1:

Access to the TMJ

After patient preparation, a Tegaderm dressing is placed over the mouth and nose to isolate them from the TMJ surgical areas. An endaural or preauricular incision is made to provide TMJ access. When dissection to the lateral capsule has been performed, 1.5 mL of local anesthetic is injected into the superior joint space. A #15 blade is used to open the superior joint space, and the lateral capsule is released along the articular eminence. An incision is made just above the lateral pole of the condyle and extended posterior to enter the lower joint space.

Step 2:

Disk Repositioning

Excessive bilaminar tissue covering the top of the condyle is excised forward to the posterior border of the articular disk. The disk is mobilized by freeing up the anterior attachment along the anterior slope of the articular eminence and elsewhere, as required; the disk then is repositioned passively over the condyle. The lateral pterygoid muscle attachment generally is maintained to provide anterior stability to the disk ( Figure 133-1, A ).