Hemifacial microsomia (HFM) is a complex malformation syndrome with varied nomencla-ture throughout the literanomencla-ture, a large host of genetic and teratogenic associations and a wide spectrum of clinical features involving the facial skeleton and other organ systems [1]. HFM is a congenital malformation in which there is a de-ficiency in the amount of hard and soft tissues on one side of the face. It is primarily a syndrome of first and second branchial arches involving underdevelopment of the temporomandibular
joint, mandibular ramus, masticatory muscles, ears and occasionally defects in facial nerve and muscles [2].
HFM is the most frequently encountered form of isolated facial asymmetry and the second most common congenital facial anomaly after cleft lip and palate with a reported incidence between 1 : 5 000 and 1 : 5 600 live births. Males appear to be more frequently affected than females (3 : 2) and the right side is affected more often than the left side. It is usually unilateral (70%) and always
REVIEWS
Maria Mielnik-Błaszczak, Katarzyna Olszewska
Hemifacial Microsomia – Review of the Literature
Połowiczy niedorozwój twarzy – przegląd piśmiennictwa
Chair and Department of Paedodontics, Medical University of Lublin, Poland
Abstract
Hemifacial microsomia (HFM) is the most frequently encountered form of isolated facial asymmetry. It is a con-genital facial deformity involving the structures of the first and second pharyngeal arches: maxilla, mandible, external and middle ear, facial and trigeminal nerves, muscles of mastication and overlying soft tissue. Intraoral manifestations include: malocclusion, tooth discrepancies, agenesis of teeth, supernumerary teeth, enamel and dentin malformations, delay in tooth development. After cleft lip and palate, HFM is the most common cranio-facial malformation. The occurrence of HFM is between 1 in 3000 and 1 in 5600 births. Males appear to be more frequently affected than females and the right side is affected more often than the left side. Although HFM refers to one half of the face, the condition is bilateral in 31% of the cases. Due to unilateral deficiency of the mandible and lower face, patients with HFM have specific dental needs that require restorative, orthodontic and surgical correction. The treatment always requires an interdisciplinary approach including at least maxillofacial surgery and orthodontics. The article provides a discussion on the etiology, diagnosis and treatment of HFM (Dent. Med.
Probl. 2011, 48, 1, 80–85).
Key words: hemifacial microsomia, asymmetry, distraction osteogenesis.
Streszczenie
Połowiczy niedorozwój twarzy jest drugą co do częstości, po rozszczepach podniebienia pierwotnego i wtórnego, wrodzoną wadą rozwojową części twarzowej czaszki i najczęstszą przyczyną asymetrii w obrębie twarzy. Zaburzenia dotyczą struktur wywodzących się z pierwszego i drugiego łuku skrzelowego i charakteryzują się jednostronnym niedorozwojem szczęki, żuchwy, ucha zewnętrznego i środkowego, nerwu trójdzielnego i twarzowego, mięśni żucia i tkanek miękkich. Wewnątrzustnie stwierdza się: wady zgryzu, wady zębowe, braki zawiązków zębów po stro-nie zaburzenia, obecność zębów nadliczbowych, hipoplazję szkliwa i opóźnione wyrzynastro-nie zębów. Zaburzestro-nie to występuje z częstością 1/3000–1/5600 urodzeń, dotyczy częściej płci męskiej i w większości przypadków występuje po prawej stronie. W 31% niedorozwój twarzy występuje obustronnie. Leczenie pacjentów z połowiczym niedoroz-wojem twarzy jest interdyscyplinarne, wymagające współpracy lekarzy różnych dziedzin medycyny i stomatologii. W pracy przedstawiono najnowsze poglądy na temat etiologii, diagnostyki i leczenia HFM (Dent. Med. Probl.
2011, 48, 1, 80–85).
Słowa kluczowe: połowiczy niedorozwój twarzy, asymetria, osteogeneza dystrakcyjna.
Dent. Med. Probl. 2011, 48, 1, 80–85
asymmetrical if it exhibits bilaterally. Although “hemifacial” refers to one half of the face, the con-dition is bilateral in 31% of cases, with one side be-ing more affected than the other. In 48% of cases, the condition is part of a larger syndrome such as Goldenhar syndrome [3–6].
HFM was first described by German physi-cian Carl Ferdinand Von Arlt in 1881. Gorlin et al. used the term HFM to describe patients with uni-lateral microtia, macrostomia and malformation of mandibular ramus and condyle, whereas Gold-enhar syndrome was described as a variant with vertebral anomalies and epibulbar dermoids. The name craniofacial was proposed by Converse et al. when cranial deformities were included. Other synonyms include first arch syndrome, first and second branchial arch syndrome, otomandibular dysostosis, oculo-auriculovertebral dysplasia and lateral facial dysplasia [7].
The clinical picture of HFM varies from a little asymmetry in the face to severe under-develop-ment of one facial half with orbital implications, a partially formed ear or even a total absence of the ear. The chin and the facial midline are off-centred, and deviated to the affected side. Often, one corner of the mouth is situated higher than the other, giv-ing rise to an oblique lip line. Other asymmetric symptoms are the unilateral hypoplastic maxillary and temporal bones, a unilateral shorter zygomatic arch and malformations of the external and inter-nal parts of the ear. Auditory problems (conduc-tion deafness) as a result of malforma(conduc-tions in the middle ear and facial nerve dysfunction (temporal and zygomatic branch of the facial nerve) are very common in these patients: 30–50% of the patients have auditory problems [8]. Intra-oral structures can also be affected in this condition: agenesis of third molar and second premolar may be pres-ent on the affected side, as well as supernumerary teeth, enamel malformations, delay in tooth devel-opment and hypoplastic teeth [9]. The masseter, temporal and pterygoid muscles, and the muscles of facial expression are hypoplastic on the affected side. The degree of under-development of the bone is directly related to the hypoplasia of the muscle to which they are attached [10]. In most cases, there is an under-developed condyle, but aplasia of the mandibular ramus and/or condyle, with the absence of one glenoid fossa also sometimes oc-curs. In these cases, the maxilla is hypoplastic at the affected side [5]. Moreover, patients with HFM often reveal asymmetric development of mastica-tory system muscles as well as agenesis of salivary glands and rarely palate clefts.
Owing to the various clinical manifestations of the disorder, many classifications have been de-veloped to help categorize these patients. The two
most frequently used classifications are the skel-etal–auricular–soft tissue (SAT) and the orbital asymmetry–mandibular hypoplasia–ear malfor-mation–nerve dysfunction–soft tissue (OMENS) deficiency classification [11, 12].
The OMENS classification (O – orbital distor-tion; M – mandibular hypoplasia; E – ear anoma-ly; N – nerve involvement; and S – soft-tissue defi-ciency) is the most comprehensive and, therefore, one of the most commonly used systems. It encom-passes the skeletal and soft-tissue abnormalities, as well as facial nerve and extracranial problems. It is common for patients who have a syndrome associ-ated with the first branchial arch to have extracra-nial abnormalities, such as heart and pulmonary defects, as these systems develop simultaneously with the first arch [13, 14].
The most useful in clinical practice are the Pruzansky’s and Kaban’s classifications. Pruzan-sky [15] in a classic paper published in 1969 de-scribed a system that presented a simple workable mandibular classification based on three different types of mandibular deformities. In Pruzansky’s system a grade I mandible is a small mandible with a normal TMJ. In essence, it is a normally shaped miniature mandible with a normal glenoid fossa and well-developed muscles of mastication. Pruzansky’ grade II mandible has a functioning TMJ with a misshapen condyle and a ramus that is short and abnormally shaped. The muscles of mastication are somewhat deficient. In Pruzan-sky’s grade III mandible, the ramus, and glenoid fossa are absent and there is no TMJ – in essence, agenesis of the ramus. There is also significant soft tissue deformities. The mandible may end abruptly in the molar region. In the Pruzansky system, the distortion of the adjacent facial skeleton is directly related to the degree of mandibular deformity [15]. In Kaban’s [16] modification of Pruzansky’s grad-ing system, type I and type III are essentially un-changed, but the type II deformity is separated into IIA and IIB. In a Kaban type IIA, the TMJ, ramus and glenoid fossa are hypoplastic, malformed and malpositioned, but the deformed joint is adequately positioned for symmetric opening of the mandible. In the type IIB the joint is malpositioned inferiorly and medially and will not function as a TMJ for adequate symmetric opening of the mandible. In the type IIA, the degree of hypoplasia of the man-dibular musculature is closer to normal than in the type IIB. In the type III deformity of the neu-romusculature is very deficient [16]. In the United States the Kaban’s modification of Pruzansky’s system is the system most widely used in publica-tions. Although other methods of classification have been reported in the literature, Pruzansky’s remains the most frequently used.
In normal growth, forces exerted by the de-veloping mastication muscles contribute to the formation of the facial skeleton. The functional matrix theory states that craniofacial skeletal de-velopment is influenced by the sum of functions of the attached neuromuscular envelop and the needs of the associated visceral spaces [17]. Enlow and Poston [18] 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. In more severe cases, entire portions of the mandible, such as the condyle and ramus, fail to develop, and, thus, ac-centuate the clinical presentation. The combined deficiencies of the soft-tissue and osseous struc-tures of the maxillofacial region result in the clini-cal manifestations characteristic of HFM.
Etiology
While the exact etiology of HFM has not yet been determined, there are many theories based on embryologic, clinical and laboratory studies. The pathogenesis HFM is incompletely understood. Poswillo described an animal phenocopy result-ing from embryonic hemorrhages from a defective stapedial artery in the region of the first and sec-ond branchial arches [19]. Johnston [20] proposed the hypothesis that a deficiency in neural crest cell migration to the region of the first and second pharyngeal arches explains the pathogenesis of HFM and microtia. More recently (2002), a report of a transgenic mutation of a locus termed Hfm (B1 to B3 on chromosome 10) in a mouse model seems to provide insight into the pathogenesis of HFM [21]. In particular, the model supports the hypothesis that at least some of the anomalies associated with HFM have a genetic basis medi-ated via mesenchymal disruptions and possibly embryonic hemorrhages. Another genetic study suggested a chromosomal locus termed far to be involved [22]. Mice with the far mutation demon-strated hemimaxillary hypoplasia. A single gene process that could interfere with cartilaginous mandibular development had been postulated previously based on embryonic experiments plus stochastic modeling.
A widely accepted theory for the pathogenesis of HFM is that hemorrhage associated with the formation of the stapedial arterial system during embryogenesis disrupts normal development of the first, and also second, arch derivatives [23]. The evolution of this theory is instructive. It was initially based on an understanding of the
em-bryonic development of the stapedial artery. Sub-sequently, a teratogen-induced and a genetically engineered animal phenocopy of HFM have been created; both reveal hematomas of the stapedial artery as the first pathologic event.
McKenzie [24], building on earlier embryologic observations, postulated that abnormal develop-ment of the stapedial artery could explain the constellation of abnormalities in HFM, or what he called the first arch syndrome. During em-bryonic weeks 3 to 5, the blood supply to the first arch depends on the successive relay of three ves-sels: the first aortic arch, then the stapedial artery (a second arch derivative), and finally the defini-tive blood supply from the external carotid artery. He reasoned that any disruption of this sequence, which needed to be precisely timed and coordinat-ed, could result in ischemia to embryonic tissue during a critical period of rapid growth and differ-entiation [24]. Poswillo [23] was successful in cre-ating a phenocopy of what he called the first and second branchial arch syndrome in the offspring of mice and monkeys administered the teratogens triazene and thalidomide, respectively. Micro-scopic examination of affected embryos revealed hematomas surrounding the anastomoses of the developing stapedial artery. Poswillo [23] hypoth-esized that variations in the size and shape of the hematoma would explain the phenotypic variabil-ity; the larger the hematoma, the more structures would be involved and the longer the time for the hematoma to resorb, and thus the less time for the embryonic tissue to repair and redifferentiate. Most recently, investigators have created a trans-genic mouse line with an insertional mutation that results in a phenocopy of HFM, including microtia and malocclusion. The mutation was the deletion of a 23 kb segment on mouse chromosome 10, which the investigators have designated Hfm, for hemifacial microsomia-associated locus. These genetically engineered mice also showed rupture of the stapedial vasculature as the first pathologic event, lending further credence to the theory of stapedial artery rupture and resultant hematoma and ischemia first formulated nearly four decades earlier. It seems likely that the cervical vertebral anomalies long associated with HFM also have, as their fundamental pathogenesis, abnormalities of the early vasculature. This would be in keep-ing with experiments showkeep-ing the relationship between congenital vertebral abnormalities of for-mation and segmentation with abnormal interseg-mental artery development [25, 26].
Laboratory studies suggest that an early loss of neural crest cells may be the specific factor re-sponsible for the clinical presentation of HFM. 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) also have been associated with an early loss of neural crest cells. 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 pre-sentation. Increased incidence within families has been documented, which suggests the possibility of genetic inheritance [27, 28]. For unaffected par-ents with one child affected with HFM, the chance that the second child has the same condition ap-pears to be lower than 1%. Parents affected with HM have approximately a 3% chance of passing the condition on to their offspring. The condition seems to have a multifactorial origin and is hetero-geneous in its clinical appearance [29].
Diagnosis
The diagnostic work-up of each patient must establish the extent of the anatomical deformity and the associated degree of functional impair-ment. A panoramic radiograph provides an ex-cellent overview of the osseous structures of the mandible and maxillofacial complex.
Since a cleft palate often is associated with HFM, an occlusal radiograph is needed to depict the osseous integrity of the palatal vault. The re-lationship of the mandible and maxilla to the cra-nial base can be established initially with a lateral cephalometric radiograph. A frontal skull radio-graph (posterior-anterior view) can be used to de-pict the degree of osseous asymmetry of the face. Computed tomography, or CT, can provide both a three-dimensional rendition of the soft tissue of the face and an image of the underlying bone [3]. Recently, Gateno et al. [30] 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. Information on comparative muscle development can be assessed through CT or magnetic resonance imaging on a case-by-case basis. These diagnostic imaging modalities contribute to a structural assessment of the patient [31]. The differential diagnosis of this condition includes Pierre Robin syndrome, Moe-bius syndrome and Treacher Collins syndrome.
The results of the study of Keogh et al. con-firm the hypothesis that a significant subgroup (40%) of patients with microtia and clinically iso-lated ear malformation exhibited underappreciat-ed skeletal and soft-tissue findings consistentwith a diagnosis of HFM. Therefore, by using microtia as a clinical marker, the physician can earlier iden-tify patients with HFM, even if the HFM in some
patients becomes apparent later in childhood. The HFM can be difficult to recognize in infancy because prominent buccal fat pads tend to mask underlying mandibular asymmetry and because infants have no teeth to assist with examination of jaw position. However, mandibular deformity can become progressively more visible with age owing to asymmetrical skeletal growth plus con-comitant thinning of the buccal fat pads. In this series, some patients were diagnosed only after the facial structures had matured from infancy to early childhood.
Treatment
The treatment of patients with hemifacial mi-crosomia is complicated and long-lasting, therefore it requires co-operation between many special-ists from medical and dental fields. In designing a course of treatment, the dental occlusion must be considered in conjunction with the underlying skeletal condition. Orthodontic therapy begins with removable orthodontic appliance (function-al appliance) and when secondary dentition ap-pears it is possible to continue the treatment using fixed orthodontic appliance to restore proper oc-clusal plane. The surgical intervention is needed to lengthen the mandibular ramus and corpus which will reduce facial asymmetry. There are es-sentially two approaches: either an early (during growth) or a late (after the active growth period) surgical intervention. In the early approach, either the conventional surgical procedure or the distrac-tion technique are possible. During the conven-tional surgical procedure, the deficient ramus of the mandible is partly replaced by an autologous costo-chondral bone graft. A costo-chondral bone graft is preferred as it still has a growth potential that makes it comparable to the non-affected side. A costo-chondral graft provides length to the ra-mus, as well as a joint; it also acts as a growth cen-tre. The chin should be re-positioned in the centre of the face during this procedure. For most chil-dren, a single operation is sufficient to correct the asymmetry. The problem with some grafts, how-ever, is that they show over-growth. In some cen-tres the use of the distraction technique is the early procedure of choice. The late procedure consists of either a classical osteotomy (i.e. bimax surgery with canting the maxilla in combination with advance-ment of the mandible and lengthening the ramus) or a bimaxillary distraction osteogenesis (Ortiz-Monasterio method) [8, 32–34]. Use of an alterna-tive procedure called distraction osteogenesis has become widely accepted. It is a process in which new bone is formed between the surface of bone
segments that gradually are separated by incre-mental traction. This gradual method of creating bone after a surgical corticotomy – sectioning of the cortical plates – was first described by Gavriil A. Ilizarov [35, 36], an orthopedic surgeon, in 1985 and has gained wide applicability in the area of craniofacial deficiencies. Distraction osteogenesis has become a widely accepted procedure in ortho-pedics and has been applied to treat the skeletal de-formities and severe bony defects in the craniofacial complex. With this procedure, bone volume can be increased by gradual traction of a fracture cal-lus formed between osteotomized bony segments. Bone lengthening by osteotomy and distraction os-teogenesis of long bones was first described in 1905 by Codvilla and popularized by Ilizarov. Mandibu-lar lengthening by gradual distraction was reported in 1973 by Snyder et al. [37] who used an extraoral device in a canine study; new bone formation at the elongated site was demonstrated later by Karp et al. [38]. In 1992, McCarthy et al. [39] successfully elongated the mandible by up to 24 mm. This pro-cedure 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 histogen-esis. This concomitant expansion of the soft-tissue functional matrix allows for multidimensional ex-pansion of the lower jaw. Under the influence of
tension produced by distraction, active histogenesis occurs in skin, fascia, blood vessels, nerves, mus-cle ligaments and periosteum. Ortiz-Monasterio et al. [34] first reported and popularized the tech-nique of combined maxillomandibular distraction in adults to avoid “occlusal disasters”. According to this technique, the hypoplastic maxilla is dis-tracted in conjunction with the mandible, after a Le Fort I corticotomy is performed at the time of the mandibular corticotomy and using intermax-illary fixation with elastic bands. Satoh et al. [40] performed a combined maxillomandibular dis-traction in children in the mixed dentition phase (7 to 12 years old) using a rigid intermaxillary fixation for 1 hour followed by a soft intermaxil-lary fixation with elastics. The main advantages of simultaneous maxillo-mandibular distraction are the immediate correction and horizontalization of the occlusal cant and the shortening of the dura-tion of orthodontic treatment. Disadvantages are essentially the need for intermaxillary fixation and possible injury to the unerupted upper molars.
Successful treatment of hemifacial microso-mia calls for close coordination among the pa-tients’ dental care providers, dental specialists and medical care providers. From maintenance thera-py to intricate orthodontic, pediatric, restorative, prosthetic and surgical procedures, all aspects of clinical care must be maximized to provide these patients with optimal treatment.
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Address for correspondence:
Katarzyna Olszewska
Chair and Department of Paedodontics Medical University of Lublin
Karmelicka St 7 20-081 Lublin Poland E-mail: catieol@interia.pl Received: 10.12.2010 Revised: 28.12.2010 Accepted: 31.01.2011
Praca wpłynęła do Redakcji: 10.12.2010 r. Po recenzji: 28.12.2010 r.
