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J Am Dent Assoc, Vol 132, No 10, 1402-1408.
© 2001 American Dental Association
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CLINICAL PRACTICE

Hemifacial microsomia

Etiology, diagnosis and treatment



RICHARD MONAHAN, D.D.S., KAREN SEDER, D.D.S., PRAVIN PATEL, M.D., MARDEN ALDER, D.D.S., STEPHEN GRUD, D.D.S. and MARY O’GARA, M.A.


   ABSTRACT
TOP
 ABSTRACT
DIAGNOSIS
 DENTAL CONSIDERATIONS
 TREATMENT
 SUMMARY
 REFERENCES
 
Background. Three percent of all newborns have significant structural anomalies. Hemifacial microsomia, or HFM, is the second most common facial anomaly, second only to cleft lip and palate. New therapeutic and clinical management techniques offer promising interventions that can allow many patients to have more normal childhoods at earlier ages.

Description. Due to a unilateral deficiency of the mandible and lower face, patients who have HFM have specific dental needs that require restorative, orthodontic and surgical correction.

Clinical Implications. Oral and maxillofacial malformations present diagnostic and treatment challenges unique to the dental profession. The etiology, diagnosis and treatment modalities discussed in this article can be used to help effectively rehabilitate patients who have HFM.

Hemifacial microsomia, or HFM, is the most frequently encountered form of isolated facial asymmetry.1–3 Affecting approximately one in 5,000 births and ranking second only to cleft lip and palate as the most common facial anomaly, HFM is a congenital malformation in which there is a deficiency in the amount of hard and soft tissue on one side of the face (Figure 1Go).4–6 It primarily is a syndrome of the first branchial arch, involving underdevelopment of the temporomandibular joint, mandibular ramus, mastication muscles and the ear. The affected ear may have an external soft-tissue malformation in addition to being lower set than on the contralateral side. Hearing loss may result from underdevelopment of the osseous components of the auditory system and a diminished or absent external auditory meatus. Occasionally, second branchial arch defects involving the facial nerve and facial muscles coexist with HFM. Patients who have Goldenhar’s syndrome, the most severe form of HFM, may have eye tumors and fused spines in addition to the characteristic facial asymmetry.7



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  		Figure 1. A. Frontal photograph of a child with hemifacial microsomia, showing the structural deficiency of the patient’s right mandible. B. Submental photograph in which the deformity of the external ear is evident, as well as the chiseled soft-tissue angulation caused by lack of the underlying ascending ramus and temporomandibular joint.

 
State-of-the-art diagnostic tools and clinical techniques can improve the quality of life for patients who have hemifacial microsomia at earlier ages than was ever thought possible.

While the exact etiology of HFM has not yet been determined, there are many theories based on embryologic, clinical and laboratory studies. Development of the first branchial arch, the so-called mandibular arch, is thought to be intimately involved with the occurrence of HFM.8 Formation of the mandibular arch occurs at approximately one month in utero, when the neural crest cells migrate into the vicinity of the developing tissues. Neural crest cells are precursor cells that develop early in fetal life and migrate throughout the head and neck region, stimulating local cell growth and differentiation.

Dentin is of neural crest origin. It generally is accepted that normal odontogenesis requires the presence and interaction of neural crest ectoderm and mesenchymal cells.9 Disturbances in the odontogenic process can produce abnormal or incomplete dental development.10 Maruko and colleagues9 postulated that the increased incidence of hypodontia documented in patients who have HFM may be attributed to a disturbance in neural crest cell development.

Laboratory studies suggest that an early loss of neural crest cells may be the specific factor responsible for the clinical presentation of HFM.11,12 Additional problems associated with HFM, such as cleft palate (seen in as many as 10 percent of the cases) and cardiac anomalies (seen in as many as 50 percent of the cases)2,7 also have been associated with an early loss of neural crest cells.13 The extent of the neural crest cell loss is reflected in the degree of severity of the facial deficiency and, therefore, is thought to dictate the severity of the clinical presentation.14 Increased incidence within families has been documented, which suggests the possibility of genetic inheritance.5

Owing to the various clinical manifestations of the disorder, many classifications have been developed to help categorize these patients.15–18 The OMENS classification (O = orbital distortion; M = mandibular hypoplasia; E = ear anomaly; N = nerve involvement; and S = soft-tissue deficiency) is the most comprehensive and, therefore, one of the most commonly used systems.19 It encompasses the skeletal and soft-tissue abnormalities, as well as facial nerve and extracranial problems.20,21 It is common for patients who have a syndrome associated with the first branchial arch to have extracranial abnormalities, such as heart and pulmonary defects, as these systems develop simultaneously with the first arch.

In normal growth, forces exerted by the developing mastication muscles contribute to the formation of the facial skeleton.22,23 The functional matrix theory states that craniofacial skeletal development is influenced by the sum of functions of the attached neuromuscular envelop and the needs of the associated visceral spaces.24 Enlow and Poston25 demonstrated that mandibular growth is dependent on the mastication muscles and the eruption dentition. In patients who have HFM, the associated muscles may be smaller and underdeveloped, thereby adversely affecting the maturation of the facial bones.26–28 In more severe cases, entire portions of the mandible, such as the condyle and ramus, fail to develop, and, thus, accentuate the clinical presentation. The combined deficiencies of the soft-tissue and osseous structures of the maxillofacial region result in the clinical manifestations characteristic of HFM.


   DIAGNOSIS
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 ABSTRACT
 DIAGNOSIS
DENTAL CONSIDERATIONS
 TREATMENT
 SUMMARY
 REFERENCES
 
A team approach is necessary to coordinate and deliver optimal treatment in complex HFM cases. The diagnostic work-up of each patient must establish the extent of the anatomical deformity and the associated degree of functional impairment.

A panoramic radiograph provides an excellent overview of the osseous structures of the mandible and maxillofacial complex. Since a cleft palate often is associated with HFM (Figure 2AGo), an occlusal radiograph is needed to depict the osseous integrity of the palatal vault (Figure 2BGo). The relationship of the mandible and maxilla to the cranial base can be established initially with a lateral cephalometric radiograph. A frontal skull radiograph (posterior-anterior view) can be used to depict the degree of osseous asymmetry of the face.



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  		Figure 2. A. Clinical photograph of a cleft palate in a patient who has hemifacial microsomia. B. Occlusal radiograph showing osseous outline of the margins of a unilateral palatal cleft (arrows).

 
Computed tomography, or CT, can provide both a three-dimensional rendition of the soft tissue of the face (Figure 3AGo) and an image of the underlying bone (Figure 3BGo). Recently, Gateno and colleagues29 successfully used three-dimensional CT data and virtual reality software to simulate surgical treatment plans that alter both the size and shape of the mandible.



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  		Figure 3. A. Three-dimensional computed tomographic, or CT, image of a patient who has hemifacial microsomia. Note the diminished external ear and apparent concavity of the soft tissue on the affected side. B. CT image of the underlying bone after the soft tissue was removed using a computer. The middle portion of the zygomatic arch and the external auditory meatus are absent. The angle of the mandible and the temporomandibular joint area are extremely underdeveloped.

 
Information on comparative muscle development can be assessed through CT (Figure 4Go, page 1406) or magnetic resonance imaging on a case-by-case basis. These diagnostic imaging modalities contribute to a structural assessment of the patient. They also help establish the degree of anatomical malformation and the relationship of the deformity to the adjacent craniofacial skeleton. In addition, comparing preoperative and postoperative CT scans can be a reliable diagnostic method for confirming treatment effectiveness.30



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  		Figure 4. Computed tomographic data manipulated to illustrate the relative development of the masseter muscle. A. The normal side shows the broad insertion of the muscle from the angle of the mandible onto the full length of the intact zygomatic arch. B. The affected side shows that the muscle is diminished in both length and width as it clings to the underdeveloped mandible; it has a reduced area of insertion on the deficient zygomatic arch.

 
Since ossicles of the ear are derived from Meckel’s cartilage—the precursor of the mandible—patients who have HFM routinely have hearing deficiencies on the affected side. Unfortunately, hearing loss present at birth can contribute to language impairment and learning difficulties in many cases.31,32 The speech patterns of some children who have HFM simply may be manifestations of unilateral hearing loss caused by failure of the external auditory meatus to develop, a condition known as a unilateral atresia. This scenario, however, can be more complicated in HFM cases in which the patient also has a cleft palate, as the integrity of the muscles contributing to the palate also are involved in equalizing the air pressure of the ear; the tensor veli palatini muscle of the soft palate plays a major role in opening and closing the eustachian tube of the middle ear. Chronic otitis media—recurrent infections affecting the already compromised middle ear—is another challenge faced by patients who have a cleft palate.

The anatomy and responsiveness of the soft palate become concerns as well. If the length or function of the soft palate is affected adversely by either the osseous cleft or a resultant asymmetry of the involved muscles, velopharyngeal incompetence—the inability to close off the oropharynx from the nasopharynx—results in varying degrees of speech distortion. This complex array of structural problems makes hearing and speech assessment imperative. The audiologist and the speech pathologist are integral parts of the diagnostic team. Hearing evaluation, phonics tests, laryngoscopic inspection and vocalization analysis help establish each patient’s anatomical, neurological and functional status. This information is crucial in determining the appropriate course of rehabilitation.

While the expertise of the general practitioner and orthodontist are essential in establishing and maintaining maximum oral health, the maxillofacial prosthodontist, pediatric dentist and periodontist are involved in the diagnostic process, depending on the specific needs of each patient. Since there can be a psychological, as well as a physical, impact on patients who have significant craniofacial anomalies, a psychologist is needed to establish each patient’s social and emotional statuses. The team approach to clinical assessment helps the team develop a realistic treatment plan that can address the goals and expectations of the patient and his or her family.

The diagnostic evaluation of HFM requires the expertise of both the medical and dental communities. The members of a cleft palate/craniofacial team represent a broad spectrum of the health care profession. Each member needs to work closely with the patient’s primary dental and medical health care providers and make vital contributions to the overall success of every case.


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 REFERENCES
 
Malocclusions are prevalent in the HFM population in a degree proportional to the patients’ skeletal discrepancies. Typically, the side of the face affected by HFM has significant dental crowding, inclination of the anterior teeth toward the affected side and an unilateral crossbite.33,34 Tooth development may be delayed on the affected side.35,36

Patients who have HFM are five times more likely to have missing teeth than is the general population.37,38 In a recent study using the panoramic radiographs of 125 patients who had HFM, researchers found a 25 percent prevalence of congenitally missing teeth9 vs. a less than 10 percent reported frequency of congenitally absent teeth in the unaffected patient population.39 An increased dental agenesis has been noted when the skeletal malformation is more severe.40 Enamel hypoplasia has been documented in the primary incisors on the affected side, suggesting that the primary dental enamel may serve as a developmental marker for the timing of the events leading to the condition.41


   TREATMENT
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SUMMARY
 REFERENCES
 
In designing a course of treatment, the dental occlusion must be considered in conjunction with the underlying skeletal condition. Typically, a combined surgical-orthodontic approach is taken.42 In the past, growth-directing devices known as functional appliances were used to encourage growth and minimize the extent of orthognathic surgery needed once the child had finished growing.

In nongrowing adult patients, skeletal deformities such as maxillomandibular hypoplasia, facial asymmetry, congenital micrognathia and HFM traditionally were treated with osteotomies followed by acute orthopedic movement and osseous fixation.43–47 Unfortunately, the inherent risk of relapse caused by the inability of muscles to be acutely stretched often compromised the results.48 In addition, poor soft-tissue adaptation could lead to compromised function and esthetics.49 When autogenous costochondral grafting was used in more severe deformities, infection, pain and donor site morbidity posed important postoperative concerns.50

Use of an alternative procedure called distraction osteogenesis has become widely accepted.51–55 It is a process in which new bone is formed between the surface of bone segments that gradually are separated by incremental traction. This gradual method of creating bone after a surgical corticotomy—sectioning of the cortical plates—was first described by Gavriil A. Ilizarov, an orthopedic surgeon, in 198856,57 and has gained wide applicability in the area of craniofacial deficiencies.58–61

Principles of dental traction for the correction of skeletal deficiencies have been practiced since the 18th century, when Pierre Fauchard first described the use of the expansion arch.62 Distraction osteogenesis has been applied recently to the advancement of severe retrognathia in patients who have Pierre Robin sequence, thus avoiding the need for a tracheostomy procedure to reduce obstructive sleep apnea.63 Figueroa and Polley64 have used distraction osteogenesis to correct mid-face hypoplasia of the maxilla in patients who have craniofacial deformities. Improving facial balance and esthetics after distraction of the maxilla has been demonstrated by Ko and colleagues.65 With the multitude of applications in the oral and maxillofacial region, it is important for the dental practitioner to have an appreciation of the physical and biological processes involved in distraction osteogenesis.66

Distraction osteogenesis involves a corticotomy with minimal disruption of the periosteum and endosteum. New bone then is created by the gradual separation of the two bony segments that have been surgically severed.67 They are separated and advanced daily until the desired length is achieved. This procedure allows for the development of viable new bone with the same characteristics as the adjacent bone.

Traction forces applied to bone also create tension in the soft tissue, initiating a sequence of adaptive changes termed distraction histogenesis.68,69 This concomitant expansion of the soft-tissue functional matrix allows for multidimensional expansion of the lower jaw.70 Under the influence of tension produced by distraction, active histogenesis occurs in skin, fascia, blood vessels, nerves, muscle ligaments and periosteum.71–77 Because the lengthening procedure progresses slowly over several weeks, the soft tissue is able to stretch and adapt gradually without loss of sensation. For patients who have HFM, this secondary gain is significant because they lack both bone and overlying soft tissue.78


   SUMMARY
TOP
 ABSTRACT
 DIAGNOSIS
 DENTAL CONSIDERATIONS
 TREATMENT
 SUMMARY
REFERENCES
 
Successful treatment of complex craniofacial malformations calls for close coordination among the patient’s dental care provider, dental specialists and medical care providers. State-of-the-art diagnostic tools and clinical techniques can improve the quality of life for patients who have HFM at earlier ages than was ever thought possible. From maintenance therapy to intricate orthodontic, pediatric, restorative, prosthetic and surgical procedures, all aspects of clinical care must be maximized to provide these patients with optimal treatment. While the challenges are significant, the rewards of improving the quality of life of patients who have HFM are immeasurable.


   FOOTNOTES
 

Dr. Monahan is an associate professor and the director, Division of Radiology, College of Dentistry, University of Illinois, Chicago; an associate professor, Department of Dental Diagnostic Science, University of Texas Health Science Center, San Antonio; and a clinician/consultant, Shriners Hospital for Children, Chicago. Address reprint requests to Dr. Monahan at 30 N. Michigan Ave., Suite 1329, Chicago, Ill. 60602.


Dr. Seder is in private practice of orthodontics, Chicago; a member of The Northwestern University Cleft Lip and Palate Team, Chicago; and a clinician/consultant, Shriners Hospital for Children, Chicago.


Dr. Patel is the chief, Plastic Surgery Services, Shriners Hospital for Children, Chicago; an attending plastic surgeon, Children’s Memorial Hospital, Chicago; and an assistant professor, Division of Plastic Surgery, Northwestern University Medical School, Chicago.


Dr. Alder is a professor and the director, Digital Imaging Analysis Lab, Department of Dental Diagnostic Science, University of Texas Health Science Center, San Antonio; and a clinician/consultant, Shriners Hospital for Children, Chicago.


Dr. Grud is in private practice of orthodontics, Berwyn, Ill., the orthodontic consultant to The Northwestern University Cleft Lip and Palate Institute, Chicago; and a clinician/consultant, Shriners Hospital for Children, Chicago.


Ms. O’Gara is an associate professor, Division of Surgery, Northwestern University Medical School; and a clinician/consultant, Shriners Hospital for Children, Chicago.


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