Oral Maxillofacial Surg Clin N Am 19 (2007) 395–422

Management of Facial Asymmetry

George K.B. Sándor, MD, DDS, PhD, Dr Habil, FRCDC,
FRCSC, FACSa,b,c,d,e,f,g,*,
Taylor P. McGuire, BSc, DDS, MSc, FRCDCh,
Leena P. Ylikontiola, DDS, PhDf,g, Willy S. Serlo, MD, PhDi,j,
Pertti M. Pirttiniemi, DDS, PhDf,k
a
Graduate Program in Oral and Maxillofacial Surgery and Anesthesia, University of Toronto,
Toronto, Ontario, Canada
b
Pediatric Oral and Maxillofacial Surgery at the Hospital for Sick Children and Bloorview Kids Rehab Centre,
Toronto, Ontario, Canada
c
Mount Sinai Hospital, Toronto, Ontario, Canada
d
Regea Institute of Regenerative Medicine, University of Tampere, Tampere, Finland
e
Oral and Maxillofacial Surgery, Institute of Dentistry, University of Oulu, Oulu, Finland
f
Institute of Dentistry, University of Oulu, Oulu, Finland
g
Cleft Lip and Palate Surgery, University of Oulu, Oulu, Finland
h
Facial Cosmetic and Reconstructive Surgery, Department of Surgery, Baptist Memorial-Golden Triangle,
Columbus, MS, USA
i
Pediatric Surgery, Oulu University Hospital, Oulu, Finland
j
Department of Pediatric Surgery, Oulu University Hospital, Oulu, Finland
k
Oulu University Hospital, Oulu, Finland

No human face is perfectly symmetric in its
structure [1]. In fact, most hard and soft tissue
facial asymmetries present in the general popula-
tion exist as subconscious, innate inequities that
contribute to the uniqueness of every individual.
Alongside averageness, sexual dimorphism, and
youthfulness, symmetry has emerged as one of
the four major determinants of attractiveness
[2–4].
The causes of asymmetries affecting the face are
numerous (Box 1). Likewise, there are even more
underlying etiologic sources responsible for each
one of them. They are most easily classified by
simplistically separating them into one of three
categories: congenital, developmental, or acquired.
Congenital defects can be further subclassified
into malformations, deformations, and disrup-
tions. Malformations are those types of congenital
defects that arise because of an aberrant develop-
mental process that takes place early during
embryogenesis [5], whereas disruptions are mor-
phologic defects that arise later in the fetal period
secondary to failure of an otherwise normal devel-
opmental process [6].
Malformations, deformations, and disruptions
can be interrelated. They are not mutually exclu-
sive and they may produce asymmetries [7]. This
article describes the management of some of the
causes of asymmetries of the face.

Frontal plagiocephaly

* Corresponding author. The Hospital for Sick Chil-

The term plagiocephaly, from the Greek
dren, S-525, 555 University Avenue, Toronto, Ontario, plagios (oblique) and kephale (head), means
Canada M5G 1X8. distortion of the head, and refers clinically to
E-mail address: george.sandor@utoronto.ca craniofacial asymmetry [8]. It is a descriptive
(G.K.B. Sándor). term that is used by clinicians to describe a specific
1042-3699/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.coms.2007.05.001 oralmaxsurgery.theclinics.com
396 SÁNDOR
Box 1. Some causes of facial asymmetry
Deformational plagiocephaly
Synostotic plagiocephaly
Clefting conditions
Hemifacial hyperplasia
Hemifacial atrophy
Hemifacial microsomia
Costochondral graft overgrowth
Condylar and hemimandibular
hyperplasia
Idiopathic condylar hypoplasia
Traumatic condylar hypoplasia
Torticollis
Hamartomas
Vascular malformations
Neoplasms
morphology of upper facial asymmetry found in
affected patients [9]. All patients who present for
consultation with an abnormally shaped head
require careful evaluation because the treatment
of plagiocephaly varies significantly according to
the underlying cause. There are two main causes
of plagiocephaly: deformational plagiocephaly
(DP) and craniosynostotic plagiocephaly (CP).
Infantile plagiocephaly is most commonly
caused by positional deformation of the skull.
Although there has been a major decrease in the
incidence of sudden infant death syndrome since
the American Academy of Pediatrics released its
recommendation in 1992 that infants be placed
down for sleep in a non-prone position [10], the
incidence of DP has increased dramatically with
a concurrent increase in the incidence of torticollis
[9,11,12]. In particular, infants who require new-
born intensive care, particularly premature in-
fants, are more prone to DP and ipsilateral
dolichocephaly. Fortunately, the former can be
prevented or minimized by proper positioning
[12]. Similarly, DP can often be treated success-
fully with cranial molding-helmet therapy alone
[13]. Craniosynostotic plagiocephaly is less com-
mon. It should always be considered in the differ-
ential diagnosis, as its functional implications and
treatment considerations are different.
Craniosynostosis, a premature fusion of cra-
nial sutures, can arise as an isolated, sporadic,
nonsyndromic congenital defect or as part of
a larger craniofacial syndrome. Each of these, in
turn, may be divided by origin into primary or
secondary. The current primary craniosynostosis
et al
hypothesis suggests that the overproduction of
bone at the suture is the cause of the craniosy-
nostosis, with closure of the affected suture di-
rectly affecting subsequent brain and cranial
growth secondarily through altered intracranial
pressure (primary suture fusion model) [14]. The
secondary craniosynostosis hypothesis attributes
decreased cranial base growth or abnormal brain
growth as the underlying cause of the craniosynos-
tosis (cranial base, secondary brain parenchyma
models, respectively) [14]. In the more common pri-
mary cases, premature fusion inhibits normal skull
growth in a direction perpendicular to the orienta-
tion of the fused suture as described by Virchow’s
Law [15]. This process, in turn, leads to skeletal
compensation and abnormal craniofacial growth
at adjacent sutures.
The importance of symmetric cranial vault
expansion cannot be overstated, as elevated
intracranial pressure (ICP) is the most significant
functional problem associated with untreated cra-
niosynostosis [15,16]. One third of patients who
have craniofacial dysostosis syndromes and about
15% to 20% of children who have single-suture cra-
niosynostosis have a documented increase in ICP
[17,18]. Multiple-suture craniosynostosis has
a worse neurologic prognosis than single-suture
craniosynostosis [18]. Isolated craniosynostosis
still has been shown to be associated with a three-
to fivefold increase in risk for cognitive deficits or
learning/language disabilities [19]. The causal basis
for this association is unclear. No particular
calvarial suture (sagittal, metopic, left or right uni-
lateral coronal) has yet been associated with
a higher risk for problems [19]. Furthermore, per-
sistent postoperative raised ICP has been described
in 6% to 15% of patients who have craniofacial
dysostosis [17]. There are multifactorial causes of
increased ICP in both types of patients, which in-
clude altered cerebral perfusion pressures (CPP),
upper airway obstruction, and hydrocephalus
[15,17]. Hydrocephalus is rarely observed in non-
syndromic craniosynostosis, and in these cases is
usually attributable to coincidental disorders. Con-
versely, it is a common feature of syndromic cranio-
synostosis, affecting at least 40% of patients who
have Crouzon, Pfeiffer, or Apert syndrome [20].
At the present time, the underlying mechanisms
and overall proportionate effect of each on raised
ICP remains uncertain. Decreased CPP as a conse-
quence of elevated ICP is believed by some to be the
one most responsible for the neurologic, cognitive,
and ophthalmologic sequelae exhibited frequently
by these children, however [21].
 MANAGEMENT OF FACIAL ASYMMETRY
The prevalence of all forms of craniosynostosis
has been estimated to be 1 in 1000 live births [22],
with most cases arising as sporadic occurrences of
unknown cause [15,23]. Syndromic craniosynosto-
sis is usually genetic, presenting with autosomal
dominant or recessive patterns, depending on the
specific syndrome [15]. Craniofacial dysostosis is
another term that should not be used incorrectly
in place of craniosynostosis, because the former
encompasses abnormalities of not only the cranial
sutures but also abnormal development of the
cranial base and facial bones because of other
affected sutures [15,16]. Current treatment algo-
rithms for syndromic/nonsyndromic craniosynos-
tosis and craniofacial dysostoses all make use of
surgery, but the specific indications, timing, and
exact techniques used for the reconstruction of
each can vary widely from patient to patient and
center to center [9,15,16,24,25].
Classification
The classification of craniosynostosis is based
on cranial vault morphology. As such, skull shape
is representative of the underlying fused sutures
only and not of the cause. Synostotic frontal
plagiocephaly arises because of the premature
closure of one of the coronal sutures (Fig. 1A).
The fusion of an ipsilateral frontal bone to its ad-
jacent parietal bone results in the formation of
one single large segment of calvaria with restricted
growth potential. Osseous compensation for rapid
infantile brain growth in the face of this problem
then takes place at all remaining patent sutures,
but is most prevalent along both sides of the con-
tralateral coronal suture [15].
Patient evaluation
Craniosynostotic plagiocephaly, which war-
rants surgical correction, is documented clinically
and radiographically and must be accurately
differentiated from DP. Although differentiation
by physical examination between synostotic fron-
tal plagiocephaly and DP is possible for an
experienced observer, inexperienced clinicians
may have difficulty making an anatomically
accurate diagnosis [26].
Classic isolated synostotic frontal plagioce-
phaly results in a predictable craniofacial mor-
phology in affected patients. A focused clinical
examination usually reveals the ipsilateral supra-
orbital rim and orbit to be superiorly and poste-
riorly displaced, with concomitant widening of the
palpebral fissure, flattening of the forehead, and
397
deviation of the nose to the flattened side (Fig. 1B)
[9,15]. Contralateral displacement of the chin and
anterior fontanelle are also commonly exhibited,
which further enhance the degree of facial asym-
metry. Various adjunctive methods used to aid
clinicians further in diagnosis and treatment plan-
ning include digital and standard anthropometry
[26–28], serial standardized digital photographs
[27,29], direct head circumference measurements
[29], and thermoplastic [30] and manual plaster-
casting techniques [31]. Many centers are also
developing and using newer three-dimensional
(3D) clinical imaging technologies in an attempt
to further enhance this process [31].
The regular use of conventional skull
radiographs has decreased substantially as high-
resolution CT scans, including 3D osseous surface
reformations with stereolithic skulls, have become
a standard element in the evaluation of craniofa-
cial anomalies in many centers (Fig. 1C). CT stud-
ies have shown that the endocranial base
dysmorphology of patients who have plagioce-
phaly is cause-specific for synostotic frontal and
posterior synostosis as compared with DP [32].
Consequently, 3D-CT endocranial base images
are often used to assist in the differential diagnosis
of plagiocephaly [33]. When initial clinical and
radiographic examinations performed are sugges-
tive of nonsyndromic synostotic frontal plagioce-
phaly, prospective patients are then jointly
reviewed by a team consisting of a pediatric sur-
geon, pediatric neurosurgeon, pediatric ophthal-
mologist, radiologist, and craniomaxillofacial
surgeon.
Treatment
The timing of surgery in infants is most often
dictated by the absence or presence of docu-
mented increases in ICP. Without evidence of
increased ICP, our group’s preference is to delay
definitive reconstruction until the child is between
12 and 24 months of age. Earlier intervention,
between the ages of 2 and 9 months, is commonly
performed in infants who have increased ICP
attributable to the tripling of intracranial volume
that occurs with normal unobstructed brain
growth over this time frame [15,34,35].
The overall goal in the treatment of nonsyn-
dromic synostotic frontal plagiocephaly is to
restore facial symmetry and balance to the cra-
niofacial complex by focusing on the distortions
of the forehead and orbits. Achieving this there-
fore requires the surgical manipulation and
398 SÁNDOR et al

Fig. 1. (A) Preoperative 3D CT scan showing fusion of the right coronal suture in this child who has craniosynostotic
plagiocephaly. (B) Frontal photograph of an 18-month-old girl who has right-sided craniosynostotic plagiocephaly.
Note the displacement of the chin toward the left. (C) Stereolithic skulls of patients who have plagiocephaly. These
models are useful for surgical planning of complex craniomaxillofacial conditions. (D) Elevation of frontal bone flap.
(E) Fronto-orbital bandeau is removed, trimmed, and scored to permit bending. The resorbable fixation is applied to
the inner surface of the bandeau to increase its stability and keep most of the fixation material hidden. (F) The radiating
triangles are cut from the frontal bone flap and adapted to eliminate the preoperative asymmetry. The resorbable fixation
material can be softened in a warming bath to permit more accurate adjustments in contour. (G) The triangles adapted
and fixated to the fronto-orbital bandeau. (H) Specially designed bone collector or suction trap to harvest bone slurry
during cranioplasty procedures (CSMT, Mississauga, Canada). (I) The remaining osseous gaps are grafted over with
bony fragments or slurry collected using a suction trap. The sheet-like resorbable fixation material acts like a membrane
to help promote bony regeneration. (J) Final readaptation of pericranium after use of fibrin glue to keep bone slurry in
calvarial defects. (K) Closure of the scalp with zigzag incision to allow cranial reshaping without soft tissue tension. (L)
Immediate postoperative frontal view of corrected cranial asymmetry.
 MANAGEMENT OF FACIAL ASYMMETRY 399

Fig. 1 (continued)

repositioning of multiple osseous regions, includ- 2. Bilateral fronto-orbital advancement/model-

ing the affected orbit, bilateral supraorbital ridge,
forehead, and temporoparietal regions. Although
the technical aspects of every reconstruction vary
from individual to individual, most craniofacial
surgeons reshape and reposition the calvaria and
orbit using one of three procedures first intro-
duced by Tessier in 1967:
1. Unilateral fronto-orbital advancement
(‘‘canthal advancement’’)
ing without nasal osteotomies and
straightening
3. Bilateral fronto-orbital advancement/model-
ing with closing wedge nasal osteotomy
[36,37].
Of the three different surgical techniques, the
results achieved by the bilateral approach are
most often considered better than those attained
with the unilateral techniques [38,39]. In addition,
400 SÁNDOR
osteotomies of the nasal bones are recommended in
the cases of older children who have severe nasal de-
viation associated with dislocation of the nasoeth-
moidal complex [39]. Many modifications of these
basic osteotomy approaches have been imple-
mented since they were first described. More re-
cently, distraction osteogenesis has also been used
for the correction of plagiocephaly [40] and other
types of craniosynostosis [41], on its own and in
conjunction with conventional osteotomies [42].
When surgically correcting nonsyndromic synos-
totic frontal plagiocephaly, our preference is the
‘‘Daisy Petal’’ [43] or ‘‘Sunrise’’ [44] or what our
team refers to as the triangle modification of the bi-
lateral fronto-orbital advancement.
Using a zig-zagged coronal incision, access to
the frontoparietal and orbital regions is obtained.
This incision allows the possibility of multiple
‘‘V’’ to ‘‘Y’’ advancements to accommodate the
alterations of head contour produced by the
osteotomy. The zig-zagged coronal incision also
results in a more esthetic result than a straight
incision. A craniotomy is performed to allow for
the removal of the bilateral frontoparietal regions
of the calvaria (Fig. 1D). A standard bilateral
fronto-orbital bandeau is then removed, adjusted,
and advanced for later fixation to the stable pos-
terior calvaria using resorbable osteosynthesis
plates (Fig. 1E). Next, the flattened frontal bone
is cut with oblique radial osteotomies starting at
the bregma into numerous triangles (Fig. 1F).
The triangles are rotated axially in a medial direc-
tion (Fig. 1G). Internal table corticotomies are
performed to recurve the flattening and to obtain
a proper curve in the coronal plane. The remain-
ing osseous gaps are then grafted using remaining
calvarial bone slurry harvested with a specially
designed suction trap, shown in Fig. 1H (CSMT,
Mississauga, Canada) [45]. All bone fragments
are fixated to each other using resorbable osteo-
synthesis plates (Fig. 1I). At the completion of
this procedure, fibrin glue is placed over the
grafted sites and the pericranium is treated care-
fully to obtain a better adaptation of the new
bone shape (Fig. 1J). On final layered closure of
the incision, this technique creates a stable unit
that provides immediate improvements in cranio-
facial symmetry to the frontoparietal regions
(Fig. 1K, L).
Torticollis
Torticollis is a condition of unknown cause,
consisting of a unilateral tilt of the neck to one
et al
side caused by the development of a fibrous
band in the sternocleidomastoid (SCM) muscle
[7]. This condition is usually unilateral and re-
sults in the development of a cervicofacial asym-
metry with the interpupillary plane slanted
downward and the chin deviated to the side of
the affected SCM muscle (Fig. 2A, B). The con-
dition has been treated in the past with a stepped
myotomy and lengthening of the SCM muscle
but this has a tendency to recur. Our group sup-
ports the excision of the entire SCM muscle and
its band from its origin to its insertion. Failure
to correct torticollis may result in the develop-
ment of a future more significant facial asymme-
try. Torticollis may also be associated with
other intracranial findings, such as intracerebral
cysts and hydrocephalus (Fig. 2C) [35]. We rec-
ommend that in cases with torticollis that have
not been present in the neonatal period MRI
evaluation should be done to exclude such
lesions.
Unilateral clefting conditions
Unilateral clefting syndromes, by their very
nature, can cause profound facial asymmetries.
The exact nature of the deformity depends on the
location and extent of the cleft. With respect to
the production of facial asymmetries it is the
location of the cleft relative to the midline that is
of importance. Nonsyndromic unilateral cleft lip
with or without cleft palate is the most common
cause of congenital asymmetry of the craniomax-
illofacial skeleton. It occurs with an incidence of
0.77 per 1000 births, more commonly on the left
side and in males [46]. The unilateral cleft lip de-
formity has effects on the facial skeleton and nasal
structure that go far beyond the lips. Even in the
repaired state unilateral cleft patients may exhibit
striking asymmetries of their noses (Fig. 3) and
may require secondary cleft lip rhinoplasties [47].
Hemifacial hyperplasia
Hemifacial hyperplasia is a rare sporadic
developmental condition that can lead to pro-
nounced facial asymmetry that grows with the
patient throughout childhood (Fig. 4A). Both soft
tissue and hard tissue structures can be affected, in-
cluding the cartilage, facial bones, and teeth
(Fig. 4B). Hemifacial hyperplasia is a segmental
form of congenital hemihyperplasia that may be
complex, involving half the body. Although the
 MANAGEMENT OF FACIAL ASYMMETRY 401

Fig. 2. (A) Left-sided torticollis with fibrous band in left sternocleidomastoid muscle, occlusal plane canted down to the
left, and chin point deviation to the left. (B) Posteroanterior (PA) cephalogram in a patient who has left-sided torticollis
showing severe head tilt to the left and a downward cant of the occlusal plane to the left. (C) Intracerebral cyst found in
patient who had torticollis.

condition is generally unilateral, a limited bilateral
crossover can occur in hemihyperplasia [48]. There
is an association of Wilms tumors of the kidney in
patients who have hemifacial hyperplasia, along
with other possible findings such as nevi, pigmenta-
tion, and telangiectasia of the skin; unilateral en-
largement of the cerebral hemisphere; seizures;
mental retardation; and conductive hearing loss
[48]. A tumor surveillance protocol with abdominal
ultrasound examinations is recommended for chil-
dren who have congenital hemihyperplasia to rule
out rare Wilms tumors [49]. The correction of the
facial deformities may require the harmonious se-
rial reduction of both hard and soft tissue elements
after growth cessation.
Hemifacial atrophy
Hemifacial atrophy is a rare condition of
unknown cause also known as Parry-Romberg
syndrome. It is a progressive condition that results
in severe atrophy of all of the hard and soft tissues
of one side of the face to varying degrees
(Fig. 5A, B). Some believe that it is the result of
the interruption of the trophic effects of the supe-
rior cervical ganglion, because the condition has
been produced by cervical sympathectomy in the
rat model [50]. It is associated with Jacksonian ep-
ilepsy with partial unilateral focal seizures,
alopecia on the affected side, and cutaneous
pigmentation changes. It has been associated
with systemic lupus erythematosus, coup de sabre
scleroderma, Rasmussen encephalitis, and Lyme
disease. Once the progressive nature of the condi-
tion has stabilized, management has included
both hard tissue and soft tissue augmentations
to mask the effects of the localized atrophy.
Such procedures have included silicone and fat
injections, hydroxyapatite and coral granule aug-
mentations [51], alloplastic implants, and free
402 SÁNDOR
Fig. 3. A 36-year-old patient who has cleft lip and palate
with profound residual nasal asymmetry that distorts the
symmetry of the rest of the face.
tissue transfers of fat using omentum or latissimus
dorsi, for example. The results have been variable.
Hemifacial microsomia
Hemifacial microsomia (HFM) is an umbrella
term that encompasses a group of variably ex-
pressive asymmetric craniofacial malformations.
These malformations are ultimately derived from
aberrations of development of derivatives of the
Fig. 4. (A) A 24-year-old who has hemifacial hypertrophy of left side of face. Note the maxillary dental midline has
shifted to the right. (B) Stereolithic skull showing the underlying bony deformity in hemifacial hyperplasia that contains
hyperplastic soft and hard tissues.
et al
first and second branchial arches [5,52]. HFM on
its own commonly presents with an extremely var-
iably asymmetric unilateral or bilateral hypoplasia
of the orbits, maxilla, mandible, ear, cranial
nerves, and related soft tissues (Fig. 6A, B). Mal-
formations during early embryonic life involving
other structures derived from the first and second
branchial arch do, however, potentially result in
a wider spectrum of anomalies that encompass
diverse and heterogeneous phenotypes within the
oculoauriculovertebral spectrum (OAVS) [53].
Other clinically descriptive terms used to describe
HFM may include otomandibular dysostosis,
lateral facial dysplasia, first and second branchial
arch syndrome, unilateral intrauterine facial
necrosis, unilateral craniofacial microsomia, and
oculoauriculovertebral dysplasia [54].
HFM is second only to nonsyndromic cleft lip
and palate as the most common congenital
anomaly affecting the craniofacial region [5]. It
is found to occur with an estimated incidence of
1 in 3500 to 5600 live births with a slight 3:2
male predominance [5]. Most patients are of
normal intelligence. Although bilateral cases do
occur, 70% to 85% of the cases are unilateral,
most commonly involving the right side. Clefting
may also occur in patients who have HFM, with
up to 23% [55] of patients demonstrating a macro-
stomia compared with a lower 10% to 15% inci-
dence of cleft lip and palate [54,55]. Many
patients also have external ear deformities ranging
from ear tags to microtia and anotia.
 MANAGEMENT OF FACIAL ASYMMETRY 403

Fig. 5. (A) Frontal photograph of an 18-year-old woman who has hemifacial atrophy of the right upper third of the face
involving the frontal, right periorbital, and right zygomatic areas. (B) Coup de sabre–like deformity near glabellar region
outlined with marking pen. Note preexisting craniotomy scar for neurosurgical treatment of focal epileptiform seizures.
In its worst presentation patients who have hemifacial atrophy may exhibit Rasmussen encephalopathy with atrophy of
one hemisphere.

The true pathophysiologic basis underlying
this condition is not yet fully known, but two
important concepts are recognized. First, based
on experimental evidence and clinical observa-
tions, HFM is still believed to be one of several
structural anomalies that are postulated to result
from vascular disruption [56], with rupture of the
stapedial artery still playing a central role [57].
A second cause may be abnormal migration of
neural crest cells, because HFM may occur in
conjunction with cardiac anomalies or other cra-
niofacial morphologic malformations belonging
to the OAVS spectrum [55,58].
Classification
The wide variation of hard and soft tissue
defects reported with HFM has led to the
development of diverse classification systems. A
comparative chronologic synopsis of these systems
can be found in Table 1 [59–61].
Most clinicians agree that a useful HFM classi-
fication system must be centered on a functional
temporomandibular joint (TMJ) and the mandible
because these components are of prime importance
among all other defects when it comes to reestab-
lishing form and function. As such, the Kaban-
HFM system seems well suited to be applied to
treatment planning and surgical management.
From a reconstructive perspective, types I and
IIA are similar because both have a functional
TMJ. Types IIB and III are more akin to each other
because the TMJ apparatus, mandible, and related
musculature are either severely malformed, totally
absent, or inadequately positioned and often re-
quire alternative reconstructive techniques in an
attempt to reconstitute normal form and function
(Tables 2 and 3).
Patient evaluation
The successful management of HFM-induced
facial asymmetry requires the attainment of accu-
rate clinical, photographic, and radiographic
records. Qualitative and quantitative hard and
soft tissue measurements of the facial skeleton,
overlying soft tissue, and dentoalveolar structures
must be obtained by analyzing the patient in all
three planes of space. The auditory and facial
nerve function must also be evaluated. Standard-
ized facial photographs, including a right and left
three-quarter oblique and a submentovertex view,
are taken. Additionally, frontal views of the
patient at rest, in full smile, and while biting on
a wooden tongue blade or a Fox plane are
obtained to assess occlusal canting relative to
the interpupillary plane (Fig. 7A). Intraoral
records should include study models mounted on
a semiadjustable articulator and intraoral photo-
graphs of the occlusion and maxillary and man-
dibular arches. Plain film radiographs (frontal
and lateral cephalogram, panoramic, and
404 SÁNDOR et al

Fig. 6. (A) Preoperative photograph of an 18-year-old man who has right-sided hemifacial microsomia classified as type
IIA. (B) Lateral profile photograph showing partially reconstructed right ear affected with microtia. (C) Preoperative
panoramic radiograph of patient in Fig. 5A, B. (D) Preoperative PA cephalogram of patient in Fig. 5A, B. (E) Preop-
erative lateral cephalogram of patient in Fig. 5A, B. (F) Le Fort I osteotomy to correct occlusal cant by impacting the
maxilla on the left side and extruding the maxilla on the right side. (G) The gaps left by extruding the maxilla are grafted
using bone harvested from the iliac crest. Rigid fixation has been applied to the osteotomy site and bone grafts. (H) An
inverted ‘‘L’’ osteotomy was chosen to help reposition the mandible on the right making the vertical length of the ramus
longer and placing the inferior segment laterally with an iliac crest one graft over top to minimize the concave defect in
the right angle region of the mandible. (I) Postoperative panoramic radiograph showing the healed fragments and their
hardware. A differential impaction and extrusion using a Le Fort I osteotomy of the maxilla was used. The right man-
dible was treated with an inverted ‘‘L’’ osteotomy and bone graft on the lateral aspect of the ramus of the mandible with
left-sided sagittal split osteotomy. A genioplasty was performed to place the asymmetric chin into the midline. (J) Post-
operative PA cephalogram showing the laterally and inferiorly repositioned angle of the mandible. (K) Postoperative lat-
eral cephalogram showing the new anteroposterior position of the jaws. (L) Postoperative frontal photograph. Note the
newly filled-out right-angle region of the mandible. (M) Postoperative profile view photograph showing the jaw line.

a submentovertex) are often still obtained, but
3D-CT reconstructions and stereolithic skulls
(Fig. 8A, B) illustrating the finer elements of the
patient’s hard and soft tissue defects are quickly
becoming the standard of care [62–64].
General treatment principles
The overall strategy for patients who have HFM
varies considerably. All comprehensive phased
treatment plans are individually developed based
on each patient’s age, physical examination, and
assessment of photographs, radiographs, mounted
models, and classification. There are, however,
some important concepts to appreciate:
The extent and rate of progression of facial
asymmetry that develops in HFM depends
directly on the pre-existing skeletal morphol-
ogy [65].
 MANAGEMENT OF FACIAL ASYMMETRY 405

Fig. 6 (continued)

Untreated HFM affects the development of the
maxilla because normal vertical growth of
the ipsilateral maxilla is restricted by the
poorly developed vertical growth of the cor-
responding mandible.
Regardless of the skeletal type present, the
end-stage deformity can be reduced by early
childhood intervention because HFM is
a progressive condition affected by growth
[66].
406 SÁNDOR et al

Fig. 6 (continued)

Treatments vary along a wide spectrum from
the use of functional dentoalveolar orthope-
dic appliances to total TMJ reconstruction.
Additional surgical procedures to correct
secondary osseous and soft tissue defor-
mities are commonly required.
Management of hemifacial microsomia type I
Treatment begins preferably in the primary or
early mixed dentition stage with the introduction
of a functional dentoalveolar orthopedic appli-
ance. The goals at this early stage are to maximize
appositional mandibular bone growth on the
affected side in an anterior and inferior direction
by exerting tension on the attached muscles and
soft tissues [67,68].
In postpubescent HFM-type I adolescents and
adults who do not have prior orthodontic or
surgical interventions, conventional double-jaw
orthognathic surgery and bone grafting may
be required to correct the deformity. Le Fort I
osteotomy is required to address the canted
occlusal plane, while at the same time allowing
for optimal maxillomandibular horizontal or
vertical positioning and final incisor tooth show.
Concomitant mandibular osteotomies may consist
of either bilateral sagittal split ramus osteotomies
or bilateral vertical ramus osteotomies or an

Table 1
Overview of available hemifacial microsomia classification systems
Author Date introduced HFM classification system
Kaban et al [59] 1981 Types I, II (A & B), and III:
Designed to relay the underlying types of skeletal deformity based on the
mandible and the TMJ as a center of reference
David et al [60] 1987 SAT system:
Acronym used to highlight the three major anatomic components that are
altered in HFM
‘‘S’’ for skeletal malformations, ‘‘A’’ for auricular involvement, ‘‘T’’ for tissue
defects
Modeled after the TMN classification of tumors
Vento et al [61] 1991 OMENS system:
Expanded on ‘‘SAT’’ with acronym describing the five major manifestations
‘‘O’’ for orbital distortion, ‘‘M’’ for mandibular hypoplasia, ‘‘E’’ for ear
deformity, ‘‘N’’ for nerve defects, ‘‘S’’ for soft tissue deficiencies
Each category is totally independent and the degree of deformity, including
normal, is rated for each group
Abbreviations: TMJ, temporomandibular joint; TMN, Tumor, Node, Metastasis.
 MANAGEMENT OF FACIAL ASYMMETRY 407

ipsilateral vertical ramus osteotomy with a contra-

Rudimentary to absent
Masseter and medial
lateral sagittal split osteotomy (Fig. 6C–H). Re-
gardless of the osteotomy design, mandibular
movements usually make up the asymmetric cor-

Rudimentary
rection, including advancement on the affected
pterygoid

Type IIA HFM commonly displays hypoplastic morphology with increasing malformation; TMJ is usually positioned symmetrically for opening
side and setback on the unaffected side. Antero-
posterior position and final vertical adjustments
Present but underdeveloped; may contain fatty infiltration

are subject to the Le Fort I performed for the

As with Type I with increasing severity of hypoplasia occlusal plane leveling and incisor show. The se-

Hypoplastic to absent; not attached

lection of a vertical ramus versus a sagittal split
osteotomy design primarily depends on the degree
of asymmetry correction required to align the
maxillary and mandibular midlines with facial
midline. Finally, a genioplasty may also be per-
formed to level and reposition the chin back to
Lateral pterygoid

No articulation between the condyle and glenoid fossa seen; TMJ is displaced inferiorly, medially, and anteriorly
Masticatory muscle morphology

the facial midline vertically (Fig. 6I–M).

to condyle

Management of hemifacial microsomia type IIA

Absent

Similar to HFM-type I, treatment of patients

who have type IIA commences in early childhood
with the use of a functional dentoalveolar ortho-
Rudimentary

pedic appliance. In such cases surgical vertical

Hypoplastic
Temporalis

mandibular lengthening is usually required to

Type I HFM commonly displays hypoplastic morphology with little to no malformation

adequately correct the asymmetry because the

mandibular hypoplasia is more severe. Fortu-
nately, early intervention occasionally precludes
the need for a compensatory Le Fort I osteotomy.
Present; more malformed

Adults who have HFM-type IIA, however, almost

always require a bimaxillary or double-jaw or-
varying degrees

thognathic approach identical to that used for

than Type I

patients who have HFM-type I for 3D surgical

Gonial angle

Preserved to

correction of their underlying facial asymmetry.

Absent

Absent

Management of hemifacial microsomia type IIB

Childhood treatment of patients who have
Osseous and muscular morphology of hemifacial microsomia

HFM-type IIB begins once again with functional

Coronoid

dentoalveolar orthopedic appliances. Attempts to

process

Present

Present

Present

Absent

maximize affected maxillary and mandibular

growth and to decrease dentoalveolar compensa-
tions are received with the understanding that
Rudimentary

they are less effective at alleviating the overall

Hypoplastic,
and cone

asymmetry because of the severity of the un-

Small but
present

shaped
Condyle

Absent

derlying defects. Consequently, an initial surgical

Mandibular morphology

procedure may be performed during the mixed

dentition stage when midface asymmetry begins to
occur. The absence of a functional TMJ with no
Hypoplastic to
Glenoid fossa

articulation and no translation (see Tables 2 and 3)

Hypoplastic

requires that the rudimentary, malpositioned

absent

Absent

Absent

one be removed. A new TMJ is then simulta-

neously fabricated in a newer, more ideal location
to allow for symmetric joint function. Autogenous
reconstruction consisting of costochondral and il-
Table 2

Kaban

iac crest grafts are preferred to alloplasts and are

type

IIA

IIB

III

used to construct a new glenoid fossa and

I
408 SÁNDOR
Table 3
Functional and adjunctive characteristics of hemifacial microsomia
Movement
TMJ
Mandibular
Kaban Condylar deviation on
type Hinge rotation translation opening
I, IIA Normal with Reduced Toward
unrestricted (type I), ipsilateral
movement absent side
(type IIA)
IIB, III Absent but Absent Toward
movement ipsilateral
unrestricted side
ramus/condyle unit (Fig. 7B–J). As with HFM
type I/IIA, isolated mandibular osteotomies to
gain vertical length and correct rotation pur-
posely incorporate the placement of an ipsilat-
eral posterior open bite. This occlusion is
slowly reduced at regular intervals over a 1- to
2-year time frame to allow for occlusal leveling
as unrestricted maxillary growth occurs. Older,
nongrowing patients who have HFM-type IIB
still require reconstruction of the nonfunctional
TMJ. This reconstruction is again preferentially
addressed with autogenous bone grafting. Simul-
taneous Le Fort I and contralateral mandibular
osteotomies are mandatory, however, if the sur-
geon is to adequately address not just the occlu-
sal plane but all other 3D asymmetric issues.
Management of hemifacial microsomia type III
Patients who have HFM-type III exhibit the
greatest severity of osseous, muscular, and soft
tissue hypoplasia or aplasia. The use of functional
dentoalveolar orthopedic appliances in these pa-
tients is avoided because the severity of the defects
usually prevents any meaningful correction with
growth. Rather, early treatment of patients who
have HFM-type III consists of TMJ reconstruc-
tion as with HFM-type IIB. The emphasis in
patients who have type III is on early reconstruc-
tion in the primary dentition stage (ages 2–5) as
soon as the midface deformity begins to develop.
The surgical reconstruction of the TMJ, mandib-
ular lengthening osteotomies, and management of
the surgically created open bite are identical to
those described for patients who have HFM-type
IIB. Adult patients who have HFM-type III with
no prior surgical intervention require extensive
osseous and soft tissue reconstruction similar to
et al
Miscellaneous
Facial nerve Soft palatal
function Hearing movement
Varies Decreased on Decreased on
ipsilateral side ipsilateral side
Varies Decreased on Decreased on
ipsilateral side ipsilateral side
the nongrowing patients who have HFM-type
IIB.
Management of hemifacial microsomia types I- III
with distraction osteogenesis
Distraction osteogenesis (DO) is now a well-
known method of forming bone in the craniofacial
skeleton through osteotomy and sequential stretch-
ing of the healing callus. This technique has been
used in syndromic and nonsyndromic patients in
whom the magnitude of planned movements re-
quired for elimination of existing hard tissue
discrepancies would be unattainable with conven-
tional orthognathic osteotomies because of soft
tissue limitations, instability, and relapse (Fig. 9A).
Moreover, inductive plastic effects on the hard and
soft tissues and the possibility of molding the results
have led to DO gaining increasing popularity in the
treatment of congenital and acquired deformities
[69]. Although the use of DO for the reconstruction
of severe mandibular deformities in patients who
have HFM-type III has been described [70], it has
been applied with increasing frequency to patients
who have less severe forms of HFM (Fig. 9B, C)
[71] and has even been used to simultaneously ad-
dress maxillary and mandibular defects [72,73].
Early problems with a lack of rotational control en-
countered with unidirectional distractors are now
being addressed with multiplanar mandibular
(Fig. 10) and maxillary distractors [74]. DO still
has the disadvantages of increased treatment
time, increased hardware costs, the possibility of
external fistulae, and an increased incidence of iat-
rogenic apertognathia requiring compensatory or
staged Le Fort I osteotomy [75]. Although aesthetic
and psychologic advantages of DO are well ac-
cepted, it should be applied in the treatment of
 MANAGEMENT OF FACIAL ASYMMETRY 409

Fig. 7. (A) Canted occlusal plane in this 6-year-old girl who has a right-sided type IIB hemifacial microsomia is accen-
tuated by the use of a tongue blade placed between the teeth in occlusion when compared with the plane of the inter-
pupillary line. (B) Asymmetry of the lower third of the face with canting of the occlusal plane upward to the right in
a 6-year-old girl who has right-sided type IIB hemifacial microsomia. (C) Note the canted occlusal plane of the dentition
and shift of the mandibular dental midline to the left. (D) Preoperative panoramic radiograph showing type IIB hemi-
facial microsomia deformity. (E) Costochondral graft harvested to reconstruct right temporomandibular articulation.
(F) Costochondral graft secured with rigid fixation screws. Note the occlusal wafer is wired in to begin treatment of
the canted occlusal plane with selected grinding of the functional appliances. (G) Costochondral graft evident on the
postoperative panoramic radiograph. (H) Tracing of the canted occlusal plane preoperatively. (I) Tracing of the leveled
occlusal plane following treatment with functional appliances. (J) Functional appliance with adjustable occlusal plane.

HFM after careful patient selection with a realiza-
tion of the short- and long-term limitations.
Soft tissue correction in hemifacial microsomia
types I–III
Many other deformities associated with HFM
must also be addressed in addition to the osseous
defects. For instance, as many as three [65] to six
[54] staged surgical reconstructions for the
treatment of auricular deformities may be re-
quired. External ear anomalies range from skin
tags to complete absence of the pinna.
Secondary treatment of other osseous contour
defects of the mandible, zygoma and temporal
bone may be corrected with autogenous rib,
calvarial, or iliac onlay grafts or with custom
fabricated alloplasts. Rhinoplasty and revision
genioplasty may also be entertained at this stage
410 SÁNDOR
Fig. 7 (continued)
[65]. Remaining soft tissue anomalies and volume
defects should only be addressed after all hard tis-
sue defects have been reconstructed and facial
growth has terminated. Although the severity of
a given soft tissue defect most often parallels
that of the underlying skeletal deformity [62],
imaging studies serve to remind clinicians that
the extent of skeletal hypoplasia of involved facial
bones does not necessarily always predict the full
extent of volume loss or hypoplasia in the
attached musculature [76]. Nevertheless, the treat-
ment of soft tissue hypoplasia in HFM follows
two major paths. Minor volume defects may be
successfully addressed using injectable fillers,
such as autologous fat grafts [77,78]. Larger,
more severe defects are often best addressed using
fasciocutaneous microvascular flaps because they
are capable of providing a greater amount of
augmentation [78,79].
Costochondral graft overgrowth
Costochondral graft overgrowth is a rare compli-
cation of costochondral grafting for the reconstruc-
tion of the ramus/condylar unit. Such overgrowth
threatens to undo the reconstruction or correction of
a mandibular asymmetry. Perrot and colleagues [80]
et al
have followed 26 patients who had 33 costochondral
grafts for an average of 48 months. There were no
signs of linear overgrowth of the costochondral grafts
in 7 growing patients who had 8 reconstructed joints.
They reported 2 cases of what they termed lateral con-
tour overgrowth with an abnormal increase of the
mass of the graft in the region of the costochondral
junction [80]. Four mandibular asymmetries devel-
oped in the 19 nongrowing patients who were treated
with costochondral grafts. Two were the result of con-
tralateral resorption of the unoperated condyles and
two were the result of remodeling with decrease in
the lengths of the reconstructed ramus condylar units
[80].
We present a case of costochondral graft
overgrowth that involves a patient who was
treated for apparent trismus at the age of 8 years
with a left-sided costochondral graft (Fig. 11A–
C). She was lost to follow-up for 12 years and
returned with massive costochondral graft over-
growth (Fig. 11D–J). Although such cases are
rare, they do alert the clinician to the possibility
of late costochondral graft overgrowth.
Condylar and hemimandibular hyperplasia
Significant facial asymmetry can occur with
unchecked unilateral growth of the mandible.
 MANAGEMENT OF FACIAL ASYMMETRY 411

Fig. 8. (A) Severe medial ward displacement of residual ramus and angle of mandible seen on the frontal view of this 3D
stereolithic skull. (B) Lateral view of stereolithic skull of severe type IIB hemifacial microsomia. Some clinicians believed
this could be classified as a type III but there seemed to be some condylar vestige.

Perhaps the two best-documented conditions Classification

exemplifying these types of mandibular asymme-
try are those of condylar hyperplasia (CH) and
hemimandibular hyperplasia (HH). CH, as the
name implies, produces excessive unilateral
growth of the condyle resulting in associated
facial asymmetric deformities [81]. HH is similarly
characterized by a diffuse enlargement of the con-
dyle, the condylar neck, and the mandibular ra-
mus and body [82]. Although both are
recognized to be self-limiting, non-neoplastic
pathologic processes, much debate concerning
their cause, pathogenesis, and true relationship
still exists.
In considering their underlying causes, both
conditions have been documented in patients
following previous trauma [83–86]. Conversely,
they have also been shown capable of idiopathic
development [87,88]. They can arise in patients
of varying age and growth states and hence can
exist as either developmental or acquired
processes. The exact cause and pathogenesis for
each condition is thus unknown. Suggestions
and theories put forth to explain their existence
vary from neurotrophic, circulatory, and hor-
monal disturbances [84] to intrauterine influences
[81]. Despite these unknowns, both disorders
have been shown to have at their basis persistent
or resumed activity of the cartilaginous
growth center of the mandibular condyle
[81,82,85,89,90].
The morphologic configuration of the unilat-
eral hyperplastic condyle and mandible lies at the
heart of controversy when it comes to the
classification of these two types of facial asym-
metry. In 1985 Toller [91] classified CH into two
types based on the manifestation of the facial
asymmetry. According to Toller [91], type I CH
is the more common of the two subtypes, with
the classic presentation of excessive vertical
growth of the condylar neck leading to a contra-
lateral deviation of the chin and a concomitant
posterior dental cross-bite. The less common
type II deformity described by Toller [91] mani-
fests a downward vertical enlargement and bow-
ing of the mandibular ramus and body on the
ipsilateral side with the presence of a more severe
posterior occlusal open bite and crossbite. The
condylar head is usually normally shaped in
type I CH and may be normal or hyperplastic
in type II.
In 1986 Obwegeser and Makek [85] attempted
to reclassify type I and type II CH into hemiman-
dibular elongation (HE) and HH, respectively.
They believed that the term ‘‘condylar hyperpla-
sia’’ referred to hyperplasia of the condyle alone
and that it should not be used to describe the
two hemimandibular anomalies as suggested by
Toller [91]. Rather, they indicated that these two
types of mandibular hyperplasia existed in pure
412 SÁNDOR et al

Fig. 9. (A) Stereolithic skulls are particularly helpful in planning distraction osteogenesis procedure not only to ensure
the correct vectors of distraction but also to ensure that the required hardware will fit on the unpredictably hypoplastic
ramus of the mandible. (B) External distractor that can be adjusted in three planes of space to permit more accurate
guidance of the distracted mandible. (C) Successful distraction of the mandibular segments bilaterally shown on this
postoperative panoramic radiograph.

and mixed forms based on the clinical, radio- Patient evaluation

graphic, and histologic findings they had noted
in several patients.
In 1996 Chen and colleagues [92] proposed
that all cases of HH and HE actually repre-
sented variations of condylar overgrowth. They
believed that unchecked condylar overgrowth
progresses into HH and HE. Despite these
differences in nomenclature, clinicians should
recognize that two forms of mandibular hyper-
plasia exist. They should also appreciate that
the overall severity of the facial asymmetry
and degree of underlying skeletal and dental
compensation with each form is highly variable
and ultimately depends on the age of the patient
and the rate and length of time hyperplasia has
been active [91,93].
The clinical picture varies widely, depending
on the onset of the growth disturbance relative to
the age of the patient, the rate of growth, and the
extent of mandibular involvement. The most
typical clinical history and presentation is one
in which the patient or the patient’s parents have
been aware for some time of a progressive
deviation of the lower jaw to the contralateral
side (Fig. 12A). This deviation may or may not
be associated with skeletal and dental progna-
thism and is rarely associated with pain or mal-
function of either the affected or unaffected
TMJ. Compensatory skeletal adjustments, in-
cluding occlusal canting (Fig. 12B), may exist
despite the absence of an ipsilateral posterior
 MANAGEMENT OF FACIAL ASYMMETRY
Fig. 10. A multiplanar internal distractor to help guide
the mandible downward and forward.
open bite (Fig. 12C). This manifestation is plau-
sible, of course, in the actively growing patient in
whom the hyperplastic growth rate on the
affected side is slow enough that it still allows
for compensatory ipsilateral maxillary vertical
growth, thereby maintaining a functional, yet
canted, occlusion.
Conventional radiographic examination of CH
or HH performed in a growing child may addi-
tionally demonstrate the typical enlargement of
the affected condyle, elongation/enlargement of
the ipsilateral ascending ramus and mandibular
body, and tilted occlusal plane (Fig. 12D, E).
Although previously serial clinical and plain film
radiographic views alone were used for diagnosis
and treatment planning, the condylar growth
activity, which often dictates surgical treatment
strategies, cannot be assessed by conventional
radiologic procedures [94].
Serial radionuclide skeletal scintigraphy or
isotope bone scanning has been successfully used
for years in the assessment of CH and HH causing
mandibular asymmetry [94,95]. Conventional
bone scans are planar or two-dimensional nuclear
medicine imaging techniques that make use of
comparative ratios of radioisotope uptake by cells
exhibiting increased metabolism and turnover,
413
most often using technitium-99 (tech-99). They
are thus commonly used to identify the presence
of active growth in several tissues, including oste-
oblasts potentially located within the condylar
and mandibular regions (Fig. 12F). More recent
advances in nuclear imaging for use in CH and
HH include the use of single photon emission
computed tomography (SPECT). Compared
with planar scintigraphy, SPECT increases image
contrast and improves lesion detection and
localization [96]. This technique has already been
shown to demonstrate enhanced diagnostic accu-
racy for CH and HH compared with conventional
planar tech-99 scanning [97–99]. There are,
however, limitations in sensitivity and specificity
with false positive results most often occurring
in patients who have associated TMJ infection,
dysfunction, or neoplasia [95,100–102]. Neverthe-
less, as access to this technique becomes available,
its enhanced ability to visualize hard and soft tis-
sue in 3D combined with its potential for assessing
structures in real time [101] will undoubtedly lead
to the replacement of standard tech-99 scans for
use in craniofacial imaging.
Treatment
Treatment modalities and philosophies of care
for patients afflicted with these conditions vary
greatly. This difference is because of the variabil-
ity in age, overall skeletal growth, presence or
absence of active hyperplasia, and degree of facial
asymmetry with which patients may present.
These variables are further compounded in com-
plexity by other issues affecting the final treatment
path, including the aggressivity or extent, timing,
and potential number of procedures that may be
required to restore proper form and function.
Many practitioners believe strongly that early
diagnosis is paramount with the primary principle
of treatment being the elimination of the patho-
logic condylar growth site as soon as possible to
mitigate the extent of the developing facial
asymmetry that so often follows [89,93,103,104].
Proponents of this treatment strategy have there-
fore successfully used a wide array of surgical
techniques ranging from isolated high condylar
shave to staged and simultaneous TMJ and
orthognathic surgery [103,104]. CH and HH are
self-limiting pathologic processes by virtue of their
nonneoplastic natures [81,82]. Additionally, the
function of the TMJ, regardless of the severity
of the facial asymmetry, is usually normal. The
attempted elimination of the hyperplastic tissue
414 SÁNDOR et al

Fig. 11. (A) Preoperative lateral cephalogram of this 6-year-old child who has apparent trismus. (B) Left costochondral
graft placed at the age of 6 years shown on the panoramic radiograph. (C) Postoperative lateral cephalogram showing
fixated costochondral graft. (D) Frontal photograph of same patient as in Fig. 10A now 17 years old with severe over-
growth of left costochondral graft. (E) Left lateral oblique view photograph of patient who has left costochondral graft
overgrowth. (F) Right lateral profile photograph of patient who has left costochondral graft overgrowth. (G) Submental
view showing extreme deviation of chin point to the right. (H) Severely displaced dentition in anterior and right direc-
tions. (I) Panoramic radiograph demonstrating severe overgrowth of left-sided costochondral graft to ramus of mandi-
ble. (J) Chin point deviation to the right demonstrated on PA cephalogram in patient who has overgrown left
costochondral graft.
 MANAGEMENT OF FACIAL ASYMMETRY
Fig. 11 (continued)
does not necessarily mean that further surgery will
be avoided at the completion of growth [105].
Consequently our centers, along with others, be-
lieve that strong consideration should be given
to: (1) refraining from any surgery until growth
activity has ceased [82], and (2) the avoidance of
open joint surgery in most patients unless abso-
lutely indicated [106].
Condylar hypoplasia
CH may be developmental, seemingly without
an apparent underlying cause, in which case it is
called idiopathic CH. The most common cause of
CH is acquired, secondary to trauma of the
mandible. It is also possible that at least some
cases of idiopathic CH are caused by occult
trauma that neither the parents nor the practi-
tioner may be aware of. Unilateral CH may also
rarely occur as a result of avascular necrosis of the
mandibular condyle or unilateral involvement of
the temporomandibular joint by rheumatoid
arthritis.
415
Traumatic injuries of the mandibular condyle
can cause a hemarthrosis, particularly with intra-
capsular fractures of the mandibular condyle.
Such an injury may predispose the patient to
frank bony ankylosis of the TMJ, particularly if
the mandible is immobilized for a prolonged
period of time. At the very least, trauma to the
mandible can lead to scarring and restricted
translation of the mandibular condyle. Proffit
and colleagues [107] have termed this functional
ankylosis or soft tissue extracapsular ankylosis.
Waite and Urban [108] believe the greater the
degree of translational restriction, the greater the
facial deformity.
Fig. 13A displays a coronal CT image of the
right condyle of an 8-year-old girl who sustained
comminution and concomitant intracranial dis-
placement of her right condylar head into the
middle cranial fossa following a fall from a bicy-
cle. The results attained with closed reduction
attained and gradual traction can be seen in
Fig. 13B. The patient was also placed on a pro-
gram consisting of early vigorous mobilization.
416 SÁNDOR et al
 MANAGEMENT OF FACIAL ASYMMETRY 417

Fig. 13. (A) Right mandibular condyle displaced into the middle cranial fossa of this 8-year-old girl who fractured her
mandible and temporal bone falling from a bicycle. (B) Dislocated fracture of right mandibular condyle retrieved from
right middle cranial fossa by slow sustained traction. (C) Disorganized healing of comminuted intracapsular fracture of
right mandibular condyle treated with aggressive mobilization from 2 weeks after the injury. (D) Panoramic radiograph
2 years after injury showing healed condylar mass with shortening of the right ramus of the mandible. (E) Deviation of
the mandibular dental midline toward the affected right side 2 years after the injury. (F) Frontal photograph showing
deviation of chin point toward the hypoplastic right mandibular condyle 4 years following the injury. (G) Submental
view showing deviation of the chin to the right side. (H) Progressive right-sided deviation of the mandibular dental mid-
line in keeping with the now apparent deviation of the skeletal midlines 4 years following the injury. (I) Skeletal deviation
with posttraumatic condylar hypoplasia despite aggressive mobilization and maintenance of a satisfactory range of
motion.

At the end of treatment a deformed but func-
tional right TMJ existed (Fig. 13C, D). Two
years following the injury the patient developed
a shift of her mandibular dental and skeletal
midline to the right (Fig. 13E). Despite ongoing
active TMJ mobilization therapy and simulta-
neous orthodontic intervention, her midlines
progressively worsened over the ensuing 2 years,
:
leading to a clinically obvious mandibular asym-
metry (Fig. 13F, H, I). The authors believe that
in addition to translational restriction, damage
of this nature sustained by the mandibular
condyle and the surrounding tissues leads to re-
stricted growth, which in this particular case
was beyond the compensatory capacity of the
functional matrix.

Fig. 12. (A) Frontal photograph of 11-year-old girl who has left-sided hemimandibular hyperplasia. Note the deviation
of the chin to the right and the occlusal plane cant upward to the right. Note also the position of the left inferior border
of the mandible compared with the right. (B) Further demonstration of the occlusal cant using a tongue blade. (C) Left
profile photograph of patient who has left hemimandibular hyperplasia. (D) Left-sided hemimandibular hyperplasia
shown in this PA cephalogram. (E) Note the left hemimandibular overgrowth in this 11-year-old girl who has enlarge-
ment of the condylar head and neck, ramus, angle, and body of the mandible on the left side. (F) Note the increased
scintillographic activity on these scans in the left condylar area consistently through all views of the scans.
418 SÁNDOR
Fig. 13 (continued)
The management of facial asymmetry resulting
from CH depends on the degree of hypoplasia. In
the traumatic case described above, interceptive
orthodontics should prevent canting of the max-
illary occlusal plane, thereby potentially limiting
Fig. 14. Skeletal relapse in a 28-year-old woman 2 years
after bimaxillary correction of an asymmetric progna-
thism despite negative condylar technetium scans
preoperatively.
et al
the surgical treatment to the lower jaw only. In
such instances a derotational osteotomy of the
mandible after growth cessation could be acc-
omplished either by using either bilateral sagittal
split osteotomies or a right sagittal split osteot-
omy and left intraoral vertical ramus osteotomy.
If the condyle becomes grossly hypoplastic and
severe trismus develops, then a costochondral
graft to reconstruct the ramus/condyle unit may
be necessary.
Summary
The preceding cases and corresponding
descriptions are designed to highlight some of
the more common causes of facial asymmetry.
Successful surgical outcomes are predicated on
a sound knowledge base that allows for accurate
diagnostic evaluation, growth monitoring, and
well-planned adaptable single or serial treatments
aimed at the correction of such deformities.
Long-term monitoring of patients who have facial
 MANAGEMENT OF FACIAL ASYMMETRY
asymmetry is important to ensure that complica-
tions caused by delayed growth are also managed
(Fig. 14).
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