Evaluation and treatment of the adult patient presenting with facial asymmetry

Craniofacial microsomia (congenital)

After cleft lip and palate, craniofacial microsomia is the second most common congenital anomaly of the head and neck region. The condition affects multiple tissue planes—the underlying skeleton, the overlying facial musculature, and the subcutaneous tissue—to varying degrees of deficiency. In the vast majority of the cases, the condition is unilateral; however, in 10% to 15% of the cases, there is bilateral involvement (bilateral craniofacial microsomia). When present in the bilateral form, the two halves of the face are differentially involved, and the face is asymmetrically affected. ^,

The OMENS-Plus classification that evolved from a series of proposed classification schemes by David and Cooter, Vento et al., and Horgan et al. The acronym stands for orbit, mandible, ear, nerve, and soft tissue, with each variable assigned a severity index ( Table 41.2 ). The “plus” indicates the extracranial involvement. The more recent pictorial classification of OMENS by Horgan et al. is an excellent visual tool. Compared with the simpler Pruzansky classification, the more comprehensive classifications are not as clinically practical in guiding treatment planning. However, they have the benefit of ensuring that all of the components of the anomaly are assessed and objectively noted for management.

Even though the extent of the deformity may include the entire hemicraniofacial skeleton, the mandibular deformity is considered the cornerstone. Asymmetrical mandibular growth and development are present in the vast majority as the initial presentation for clinical assessment and management. The mandible plays a pivotal role in progressive distortion of the facial skeleton on the affected side, with secondary compensation on the contralateral side. The hypoplastic mandible results in multiplanar deficiency of the hemimaxilla and obliquity of the occlusal plane by restricting the normal downward vertical growth of the maxilla. Correction of the mandibular–maxillary relationship does not necessarily correct the upper midfacial involvement, and additional procedures may be necessary to achieve facial symmetry.

Unilateral condylar hyperactivity (developmental)

Many authors have used the term unilateral condylar hyperplasia; however, the term unilateral condylar hyperactivity, suggested by Obwegeser, is more appropriate because it more accurately encompasses the various clinical presentations seen.

Idiopathic overgrowth of the mandibular condyle is unilateral, presents itself during pubertal growth as a developing mandibular asymmetry, and is self-limiting by adulthood. It is not evident at birth. The asymmetry becomes increasingly more noticeable in later childhood through adolescence. Often, it is useful to ask the parents to bring annual school photographs to review the progression of the asymmetry, and this helps confirm the diagnosis.

The underlying etiology remains unclear and may be varied, but the final outcome is a dysregulation in growth that occurs within the cartilaginous region of the condylar head. During this active period, technetium-99 scintigraphy can confirm condylar hyperactivity compared with the contralateral unaffected condyle. Although the nuclear scan does not provide insight into the etiology, its value is that a negative result on it confirms that growth is complete, and thus surgical intervention can be initiated.

Idiopathic asymmetry

Many patients present with minor to moderate facial asymmetry without an obvious etiology. These patients may have an extremely mild case of craniofacial microsomia, asymmetry at the extreme of normal variation, or an asymmetry that might be considered normal but bothers the patient. These patients are typical treated with less-invasive procedures to meet their goals.

Traumatic (acquired)

Perhaps the most common cause of dentofacial skeletal asymmetry is trauma. The asymmetry can affect any component, depending on the original fracture pattern, from isolated fractures to panfacial fractures. In the upper midface, posttraumatic nasal asymmetries and residual malar asymmetries are common. In the lower face, traumatic injuries to the mandible, of which nearly 25% involve the condyle, are among the more common causes of facial asymmetry in children and young adults. Complications from either lack of treatment or unsatisfactory outcomes of treatment include skeletal facial asymmetry, occlusal crossbite, lateral gnathism, various degrees of restricted motion to complete ankylosis, and osteoarthritis. In many cases, the early trauma goes unnoticed by the family and medical attention is not sought; and when medical attention is sought, the condylar injury is undiagnosed at the time of the assessment. The hemarthrosis that occurs with condylar compression injuries is often difficult to diagnose and becomes evident with restriction and ankylosis as functional asymmetry progresses. With condylar neck fractures, medial displacement by the lateral pterygoid muscle occurs, affecting the temporomandibular joint (TMJ) kinematics and the posterior mandibular height on the affected site. The condylar head remodeling adapts to maintain TMJ function. The extent to which subsequent facial development can remain symmetrical within an acceptable tolerance depends on the timing of the insult in the growth and development of the child and the extent of the injury. For additional information, the reader is referred to Chapter 42 , which discusses posttraumatic reconstructive strategies in depth.

Parry-Romberg disease (acquired)

Of the facial asymmetries, those caused by Parry-Romberg disease are characterized by a striking “sunken” appearance to the affected side of the face. There is a sharp demarcation from the normal hemiface. Frequently, there is a soft tissue crease in the forehead, a coup de sabre, which is a characteristic hallmark of the disease. The disease is progressive in nature, with atrophy of the skin, subcutaneous tissue, muscle, and dentoosseous framework in its severest forms. Intraoral findings of the atrophic process may involve the alveolar process, the palate, and the tongue on the affected side. In nearly 35% to 40% of the patients, the orbital region and the eyelid adnexal structures are involved, resulting in enophthalmos with loss of periorbital fat, eyelid atrophy with ptosis, and loss of eyelashes and eyebrow hair. Visual acuity may be affected, with involvement of the retina and the optic nerve. ^,

The etiology of Parry-Romberg disease remains unknown. It begins insidiously in childhood to midadolescence, with relentless progression until it stabilizes typically in adulthood. The duration of the active phase of the disease process varies significantly, extending from 2 years to up to over a decade. Any orthodontic–skeletal and soft tissue reconstruction must take into account this variability in the duration of the active phase. Although there is little correlation between the severity of the soft tissue involvement and age at onset, the effect on dentoskeletal involvement does correlate with the age of the patient. In an overwhelming 85% of patients with osseous involvement, the disease could have started before age 9 years. With skeletal involvement of the maxilla and the mandible, the dental arch alignments are affected, and there is typically a lateral open bite on the affected side.