357

CLINICS IN
PLASTIC
SURGERY
Clin Plastic Surg 34 (2007) 357367

Facial Skeletal Growth and Timing

of Surgical Intervention
Russell R. Reid,
-

MD, PhD

Embryology of the craniofacial region

Facial growth of skeletal structures
The upper face
The midface
The lower face

Various forces and factors influence the development and maturation of the craniofacial skeleton.
These encompass genetic and micro- and macroenvironmental factors whose intricacies and interplay must be understood, recognized, and
respected in the surgical planning and treatment
of maxillofacial deformities. The theories of and
experimentation with such factors, which dictate
the timing of surgical intervention, are the focus
of this article. The common procedures that
make up the surgical armamentarium of the maxillofacial surgeon are cataloged in the setting of
this developmental timeline.Various forces and factors influence the development and maturation of
the craniofacial skeleton. These encompass genetic
and micro- and macro-environmental factors
whose intricacies and interplay must be understood, recognized, and respected in the surgical
planning and treatment of maxillofacial deformities. The theories of and experimentation with
such factors, which dictate the timing of surgical
intervention, are the focus of this article. The common procedures that make up the surgical armamentarium of the maxillofacial surgeon are
cataloged in the setting of this developmental
timeline.

Clinical implications: the timing of surgical

intervention
Summary
References

Embryology of the craniofacial region

Two main types of bone development are wellknown to play an integral role in the development
of the facial skeleton: intramembranous ossification
and endochondral ossification. The former process
stems from neural crest cell templates that differentiate into osteoblasts, which form a center of ossification during the 7th week postconception. The latter
process entails the condensation of mesenchymal
precursor cells into a cartilaginous matrix, which
provides an anatomical model (or prototype) for
the incumbent bone. Interestingly, the facial structure is a hybrid of osteogenic mechanismsthe cranial vault, upper face, midface, and majority of the
mandible arising from intramembranous ossification, and the cranial base arising from endochondral
sources. Once thought to be critical in terms of bony
replacement [1,2] (eg, autogenous bone graft augmentation or reconstruction of the face), this embryologic distinction has no bearing on the fate or
survival of the donor bone used. Rather, the cortical-cancellous composition of the bone, the mechanical forces the bone graft is subjected to, and
the recipient site determine bone graft survival,
and the maintenance of bone volume [3,4].

Section of Plastic and Reconstructive Surgery, University of Chicago Medical Center, 5841 South Maryland
Avenue, MC 6035, Chicago, IL 60637, USA
E-mail address: rreid@surgery.bsd.uchicago.edu
0094-1298/07/$ see front matter 2007 Elsevier Inc. All rights reserved.

plasticsurgery.theclinics.com

doi:10.1016/j.cps.2007.04.002

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Developing bone therefore receives signals,

whether genetic, chemical, or mechanical, that
not only induce proliferation and differentiation,
but also impact the contour, shape, and volume
of bone in any given area. Whitaker described
this genetic framework most aptly in his theory of
biologic boundaries: The body has a predetermined, genetically controlled, physical self-identity
defining its physical boundaries . . [5]. In other
words, the program for the basic shape of the facial
skeleton is genetic, and this program is supplemented by mechanical and chemical signals
received by surrounding tissues. Such a developmental process is summarized by two principal, coexisting theories: Wolffs law of mechanical stress
(1870) [6], and Mosss functional matrix theory
(1960s) [7,8]. Bone responds not only to mechanical alterations induced by loading forces (Wolff),
but also specifically to mechanical and paracrine
communication from locoregional functional soft
tissue (eg, muscle) (Moss). On a molecular level,
signal transduction by core-binding factor alpha-1
(cbfa-1) [9], Indian hedgehog (IHH) [10,11], and
Wnt [10,11] incite osteoblastic differentiation,
whereas pleiotropic factors such as fibroblast
growth factors (FGFs) [12], bone morphogenetic
proteins (BMPs)1 9 [13], and transforming
growth factor-b variants (TGFb13) [14,15] and
their corresponding receptors are a few of the biological signals that induce osteogenesis at the sutural level (see below). Recently, Rhee and
colleagues [16] have characterized a mechanotransduction system based upon extracellular signal-related kinase (ERK) type 1 and 2 and BMP2/4,
thereby linking mechanical and chemical signals
for the modification of bone. Although these findings are based on distracted bone, it is believed that
this system can also be extrapolated to nonmanipulated, developing bone.

Bones of the cranial vault and face exhibit three

basic mechanisms of growth. First, as described
above, ossification can proceed either via intramembranous or endochondral strategies. Principally,
endochondral systems at the skull base (sphenooccipital posteriorly and sphenoethmoidal anteriorly), the midface (septopreshenoid and nasal
septum), and at the mandibular condyle, contribute
to the three-dimensional expansion of the face
throughout childhood into adulthood [17]. Structurally, facial growth also proceeds through a series
of sutures (synarthroses) that are strategically positioned to contribute to the three-dimensionality
of the face: height, width, and projection. Syndesmoses represent articulations between bony surfaces that consist of fibrous connective tissue. As
bone is deposited incrementally against the suture
ends (butt-end type, eg, midpalatal suture; versus
beveled type, eg, zygomaticomaxillary suture), the
opposing bone at the suture expands, and this
bony expansion and displacement is one critical
form of craniofacial growth (Fig. 1). A third means
of bone growth and development is via surface deposition and resorption, which contributes to
bone volume and thickness [18,19]. Specifically,
Enlow [19] has characterized regions of the facial
skeleton according to their depository or resorptive
qualities, with the cranial, frontal, and lower borders of the mandible being sites of bone deposition,
in contrast to the temporal, orbital, malar, maxillary, and alveolar mandibular surfaces that allow
for bone resorption (Fig. 2). As put forth by Scott
[20], facial skeletal growth appears to be bimodal
in terms of age; that is, driven early by functional
matrices and cartilaginous growth centers via a relatively passive sutural system (03 years of age), and
later by bone remodeling, as the growth of the
skeleton approaches a plateau toward adolescence
(310 years of age).

Fig. 1. Remodeling of the craniofacial skeleton occurs by (A) sutural expansion and by (B)
surface bone deposition and resorption resulting in displacement and reshaping of the
individual elements. (Adapted
from Enlow DH. Craniofacial
growth and development: normal and deviant patterns. In: Posnick JC, editor. Craniofacial and
maxillofacial surgery in children
and young adults, vol. 1. Philadelphia: W.B. Saunders; 2000. p. 27;
with permission.)

Facial Skeletal Growth and Surgical Intervention

Fig. 2. Remodeling of the craniofacial skeleton occurs

by continuous inner and outer surface fields of bone
deposition and resorption that can accommodate intrinsic and extrinsic factors. This allows for the dramatic changes in size and shape that occurs from
the infant to the adult craniofacial skeleton.

Facial growth of skeletal structures

The upper face
The upper facial skeleton is that region of the face
bounded by the frontal bone superiorly, the temporal bone bilaterally, and the superior orbital rim inferiorly. This facial subunit corresponds to the
frontonasal prominence, which is primarily of neurocranial origin [18]. As early as the 8th week postconception, ossification centers appear in the
territory of the superciliary arch. These paired
arches incite intramembranous formation of the
paired frontal bones, which fuse by the 6th to 7th
postconception month with the paired zygomatic
processes, nasal spine, and trochlear fossae. At
birth, the paired frontal bones remain separated
by the metopic suture, which is the first suture to
fuse physiologically. In a large retrospective study
examining three-dimensional craniofacial CT scans
of a variety of pediatric nonsynostotic controls,
Weinzweig and colleagues [21] were able to delineate the spatiotemporal parameters of metopic sutural fusion, identifying a mean age of closure at 6
to 8 months. This physiologic early fusion contradicts the classic teaching that the metopic suture
closes before the second year of life [22]. Certainly,
this suture behaves differently compared with its
counterparts. It is of particular interest to note

that the metopic system can be viewed as an extension of the chondrocranium (cranial base), as the
direction of suture fusion proceeds from the cranial
base (as early as 3 months of age) cephalad toward
the anterior fontanelle. Histologically, fusion is accomplished by bridging chondroid tissue, termed
by Manzanares [23] as secondary cartilage, which
is distinct from the primary cartilage of the cranial
base. It is thought that this pattern of synchondrosis
allows the upper facial skeleton to grow under the
influence of the rapidly expanding frontal lobes
(functional matrix) until the age of 12 years, at
which point the upper face yields to the constant,
indolent growth of the midface followed by the
lower face that continues into late adolescence
(Fig. 3). This is represented morphologically by
the dramatic shift in cranium: facial ratio that exists
between infancy (8:1) to adulthood (2:1) (Fig. 4).
Cessation of growth of the upper facial component
by this time makes alloplastic cranioplasty safe for
this portion of the skeleton only after the middle
years of childhood (age >12 years). Similarly, orthognathic surgical procedures after cessation of
growth in late adolescence would be expected to
be stable.
The basicranium itself has a significant influence
on the facial form, because the posterior boundary
of the facial mass coincides with the boundary of
the anterior and middle cranial fossa. Early on,
with expansile growth of the anterior and middle
cranial fossa with brain growth, the nasomaxillary
complex and the mandible are affected. This results
in anterior inferior displacement within the nasomaxillary complex, and with it also vertical displacement of the mandible. By age 5 or 6, the
growth in the frontal lobe and the anterior cranial
fossa nearly ceases; however, there is continued
growth of the middle cranial fossa for several

Fig. 3. Skeletal maturity of the cranial vault, the maxilla, and the mandible from infancy to skeletal maturity (scaled to 100% of the adult size). The cranial
vault reaches maturity long before the midface, followed by the mandible.

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Fig. 4. Comparison of the

craniofacial skeletal proportions between the infant and the adult.

additional years, continuing to add to the forward

displacement of the nasomaxillary complex and
vertical displacement of the mandible [2426].

The midface
Of all facial skeletal units, the midfacial region develops from the most complex and sophisticated interplay between a series of sutures, functional
matrices, and bone remodeling. As opposed to the
cranium and upper facial regions, which grow continuously until elementary school age (circa 7
years), the midface responds in fits and spurts to
locoregional and hormonal messengers.
The nose and maxilla
The paranasal sinus spaces, and particularly the nasal septum, have a significant role in the overall
shape, contour, and form of the midface. Once recognized as one of the key growth centers, the nasal
septum provides the centrofacial region with the
height and projection that characterizes this facial
subunit. From the classic but controversial extirpation experiments of Fick (1857) [27], refined
by Landsberger [28], Scott [20,2932], Sarnat
[3336], and Ohyama [37], the cartilaginous nasal
septum and septovomeral complex have been implicated in the downward growth of the midfacial
vault. Embryologically, a septo-(pre)maxillary ligament has been identified [3840], which forms in

utero along the sides and anteroinferior aspects of

the nasal septum and inserts into the anterior nasal
spine, transmitting a downward and forward force
that is corresponded by secondary expansion at
the frontonasal, frontomaxillary, premaxillary-maxillary, and zygomaticomaxillary suture systems. This
bidirectional pull equates in expansion of the vertical length of the cartilaginous septum sevenfold between the 10th and 40th weeks postconception
[18].
The concepts gleaned from these founding studies have been challenged over time. Stemming
from his theory of functional matrix, Moss questioned the intrinsic growth potential of the cartilaginous septum, ascribing its increase to the passive
stretch of local tissues [7]. Moreover, early surgical
manipulation of the nasal cartilages has been advocated by some surgeons [41], with little impact on
long-term growth. In contrast to this, it is wellestablished that more severe disruption of the
centrofacial region during childhood, as in the
naso-orbital-ethmoid fracture, reliably produces
growth disturbances. To this end, Singh and Bartlett
[42] found that 8 out of the 10 pediatric facial fractures requiring secondary correction in their large
series pertained to those of the midface. These
authors felt that obliteration of the cartilaginous
and bony synarthroses that comprise the median
sagittal sector, a tripartite structure composed of

Facial Skeletal Growth and Surgical Intervention

chondrocranial spheno-ethmoidonasal, vomeropremaxillary, and pterygo-palatomaxillary portions

[43], contributes to the midfacial retardation of
growth seen in severe facial trauma.
Above all other facial subunits, the midface relies
heavily on sutural expansion to reach adult dimensions. The orientation of the major sutures of the
face were once thought to be arranged parallel to
the direction of growth. Parallelism of the principal
external sutures, (frontomaxillary, temporozygomatic, zygomaticomaxillary, and pterygopalatomaxillary) has since been disproved. Several
studies instead point to the multidirectionality of
sutural growth, varying from 0 to 82 degrees in relation to the sella-nasion line [44,45]. This directionality not only varies from suture to suture, but
also changes for each suture with age [46]. Overall,
the frontomaxillary, zygomaticofrontal, ethmoidomaxillary, and frontoethmoidal sutures respond to
nasal septal and ocular globe expansion by bone
deposition and growth in a vertical direction,
thereby contributing to midfacial height. [47,48].
In terms of downward and forward midfacial
growth, the median sagittal sector (see above)
largely contributes to growth in an anteroposterior
direction (midfacial projection) (Fig. 5). Finally,
the last dimension of midfacial growth (midfacial

Fig. 5. Suture-directed growth at various sites, resulting in an overall downward and forward transposition of the midface relative to the cranial base.
Vertical (blue arrows): Frontozygomatic suture, Frontonasal suture, Frontomaxillary suture, Alveolar bone
deposition; Sagittal (green arrows): Nasomaxillary suture, Temporozygomatic suture, Maxillary tubersosity
bone deposition; Transverse (red arrows): Zygomaticomaxillary suture, Midpalatal suture.

width) is controlled by transverse maxillary expansion (age 02) at the intermaxillary suture, midpalatal suture, and the zygomaticomaxillary suture,
the last of these induced by ocular globe enlargement. The signals, which drive the spatiotemporal
sequence of growth, remain unclear.
Simultaneously within the facial mass itself, bone
deposition occurs at the various facial sutures and
surfaces to allow volumetric enlargement while undergoing resorption along opposing surfaces. The
sagittal lengthening of the maxillary arch occurs
by progressive bone deposition along the posterior
surface of the maxillary tuberosity. Simultaneously,
bone deposition along the lateral surface at the tuberosity increases the transverse width of the arch.
With this posterior growth, the whole maxilla undergoes a forward displacement in the anterior direction. Similarly, with the malar complex, growth
(bone deposition) occurs along the posterior surface and the lateral surface, while simultaneously
the anterior and medial surfaces undergo resorption. The malar complex maintains its continuity
with the maxilla, and also undergoes a forward displacement with posterior growth [2426].
One definite stimulus for development of the
midface (and the lower face) is derived from the
budding deciduous and permanent dentition
(Fig. 6). This functional matrix provides the necessary signals for the alveolar subunit of the maxilla,
which responds by bony deposition along the alveolar surfaces and resorption anteriorly at the arbitrary cephalometric point A. The timing of this
growth coincides with mandibular growth and intercuspation of the maxillary arch with the mandibular arch (age 812). Dental eruption at the
maxillary level is also sequenced with the development and pneumatization of the maxillary sinus
(see below).
The palate
The growth and development of the hard and soft
palate are also critical for the establishment of
three-dimensionality of the midface. Critical landmarks of palatal embryogenesis have been well-reviewed by Sperber [49] and others, and include
development of the three primordia of the palate
(lateral palatal shelves from the lateral maxillary
prominence and primary palate of the frontonasal
prominence) by postconception week 6, reorientation of the lateral shelves from a vertical to horizontal plane by postconception week 8, and fusion of
the three palatal elements to produce a flat, unarched roof to the mouth by postconception week
8 to 10. Initially biased to grow in an anteroposterior direction, the prenatal palate transitions to
growth in a transverse direction, thereby expanding
bilaterally via bony apposition at the midpalatal

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Fig. 6. Dental eruption pattern from primary dentition to permanent dentition. Volumetrically, the developing
primary and secondary dentition occupy a significant percentage of the maxillary and mandibular mass. Skeletal
surgery in the stage of mixed dentition can injure permanent developing tooth buds. (A) Infancy. (B) Primary
dentition stage. (C) Mixed dentition stage. (D) Permanent dentition stage.

suture and the lateral alveolar borders by 24 weeks

postconception.
Postnatal development of the palate relies heavily
on adjacent functional matrices, which stimulate
appositional growth at the principal sutures, and
bone remodeling at nonsutural surfaces. Growth
in a transverse direction, as stated above, proceeds
via the midpalatal suture, which witnesses its greatest expansion during the first 2 years of life. Despite
interruption of growth at this site by age 2, the midpalatal suture fails to undergo ossification (synostosis) before the age of 30 years[47,48]. This allows
for palatal expansion with pre- or postsurgical orthodontics well into adulthood. Further increase
laterally by appositional forces continues until the
middle years of childhood (age 7). As the permanent dentition erupts through the alveolar process,
the palate becomes more arched. This functional
matrix works synergistically with another, the maxillary antra, which descend fully to meet the nasal
floor/palatal roof by age 12. Thereafter, palatal
and maxillary growth proceeds through apposition
and resorption, as put forth by Enlow [19].
The paranasal sinuses
The maxillofacial skeleton, and in particular, upper
and middle facial thirds, is sculpted not only by
bone deposition/resorption, sutural expansion,
and growth of the related soft tissues (eg, fat pads,
muscles of mastication, orbit), but also by the
growth and maturation of the paranasal sinus system. Derivatives of the ethmoid air cells, the four
principal sinuses (frontal, ethmoidal, sphenoidal,
and maxillary), begin as crude invaginations that
begin to invade their corresponding bony neighbors from 6 months to 2 years of age. Procession
of these cells in secondary pneumatization from
0 to 2 years anteriorly yields the nascent frontal

sinuses, which aerate to radiographic dimensions

by age 7. The ethmoid and sphenoid sinuses also
progress during this period. A keystone to the midface, the maxillary sinus is over 100 cm [3] at birth
[50] and grows 2 mm vertically and 3 mm anteroposteriorly each year. Rapid maxillary antral expansion colocalizes with dental eruption during the
early and mixed dentition phases of growth (ages
612). The maxillary sinus achieves its full dimensions by puberty.

The lower face

Although the last element to skeletally mature, the
mandible is a keystone in the development of the
facial skeleton, providing normo-occlusion and
the maintenance of anteroposterior facial height.
A first pharyngeal arch derivative, the mandible is
formed by a primordium of migrating neural crest
cells that appear as early as the fourth postconception week. Interestingly, as in the upper viscerocranium (forehead, orbits), a key functional matrix for
mandibular development is neural in nature: the
trigeminal nerve, whose mandibular division bifurcates and stimulates the formation of a single ossification center at 6 weeks postconception [51,52].
Meckels cartilage, the endochondral template for
mandibular osteogenesis, coincides with this ossification center. Endochondral ossification proceeds
bidirectionally to contribute to the mandibular parasymphysis, body, and angle portions.
Along with this primordial growth center, the
condylar process is engendered from cartilaginous
condensations, and matures into a joint capsule
during the 11th week postconception [53]. This
highly organized structure on a histological level
[54] matures into both a sophisticated articular surface, and a site for ongoing endochondral ossification. Secondary cartilages that develop also give

Facial Skeletal Growth and Surgical Intervention

rise to the coronoid process, as well as the symphysis, a specialized synchondrosis that aids in mandibular expansion within the first year of life [55].
Postnatally, mandibular growth relies on two essential forces. First, sutural apposition of bone occurs at the symphysis menti, which contributes
somewhat to increase in bigonial width of the mandible, until it succumbs to endochondral ossification by the first year of life. In succession of this
transverse growth, the chondrogenic layers of the
condyles proliferate, resulting in posterior and superior enlargement of this structure. Appositional
bone growth supplements this chondrogenesis
[56]. Such movement in turn contributes to the
overall increase in vertical ramus length that occurs
somewhere within the preschool years (36 years of
age). This process has been corroborated in gross
and cephalometric analyses of growing nonhuman
primate skulls after unilateral condylectomy [57].
Experimental animals clearly exhibited a decrease
in facial, mandibular, and maxillary height and
length, in addition to ramus length, when compared with control (unoperated) subjects. Interestingly, the same experiments conducted on adult
monkeys demonstrated similar changes in facial
morphology [56,58], suggesting that the condyle itself may not be responsible primarily for mandibular growth at that site, but rather that the
temporomandibular joint and associated mechanical signals from load and muscular forces may be
the critical stimuli for osteogenesis.
In addition to these endochondral forces, the
postnatal mandible responds in a sophisticated
fashion to the local functional matrices (masticatory muscles and budding teeth) via apposition
and resorption. Conjoined with the increase in
bigonial width, the body of the mandible correspondingly necessarily must undergo lengthening
to match the maxillary arch. The anterior surface
of the ramus undergoes remodeling by converting
ramus to corpus. To maintain the width of the ramus, bone is added posteriorly. This backward sagittal growth then results in forward displacement of
the mandible as a whole, because it is with the maxilla. At the posterior region of the ramus, there are
two distinct areas of growth: the posterior edge of
the ramus itself and the condyle. Whereas the posterior edge is a sagittal growth direction, the condyles growth results in an angular vector that is
posterior and superior. The condylar growth results
in anterior inferior displacement of the mandible.
The ramus becomes progressively more upright by
the anterior remodeling that occurs at its base to
lengthen the mandibular body, and simultaneous
bone deposition comparatively on the posterior
ramal surface. Essentially, this results in a rotation
of the ramus and the condylar growth vector

correspondingly more vertical, with a decrease in

the gonial angle. This vertical lengthening then continues long after the horizontal ramal width ceases.
This allows simultaneously accommodating the
vertical growth of the nasomaxillary complex without changing the occlusal relation. Any differential
in this interlocking growth pattern between the
maxilla and the mandible leads to a skeletal sagittal
discrepancy or a rotational imbalance (Fig. 7).
There must also be a corresponding match that
must occur in the transverse width between the
jaws [2426].
The elementary and middle school-age years (712
years) are marked by the transition between deciduous and permanent dentition. Landmark eruption
of the permanent teeth includes the permanent first
molar (67 years), the central incisors (67 years),
and the cuspids (912 years). It is this period of
time before canine eruption (912 years) within
the mixed dentition phase that secondary alveolar
bone grafting (typically with iliac crest corticocancellous substance) is favorable. For further details
on postnatal growth and development of the mandible, Smartt and colleagues [51] have provided a recent and elegant review.

Clinical implications: the timing of surgical

intervention
While growth is present, the orthodontist can guide
the individual teeth into position and alter the direction of growth of the maxilla and mandible regionally, by taking advantage of the active phase
of development through the use of orthodontic
braces, face masks, chin cups, and various appliances (orthodontic growth modification) [5961].
Once skeletal maturity is reached, then surgical intervention is required. Thus timing of intervention
becomes the more critical question that the orthodontist and surgeon ponder [62,63]. In many circumstances, the decision is to postpone surgical
intervention until skeletal maturity in order to
avoid reoperation, because of recurrence of the deformity with continued disproportionate growth.
There are circumstances in which surgery in the immature skeleton is recommended, however, when
whether because of poor self-image or because of
functional reasons, earlier intervention outweighs
the risks of waiting.
Le Fort I osteotomy and advancement, by definition, disrupts and advances the midface at the maxillary level from the cranial base, by dividing the
pterygomaxillary suture. Performed early (before
age 15 in female patients and 17 in male patients),
this form of maxillary advancement can lead not
only to relapse in maxillary retrusion [6466], because the mandible has not reached skeletal

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Fig. 7. Growth and development of the midfacial

skeletal development. (A)
Counterclockwise development of the basicranium
displaces the mandible anteriorly. (B) With growth
at the interface, the midface is displaced in the
antero-inferior vector. (C)
With growth at the posterior ramal border and condyle, the mandible is
displaced antero-inferior
vector. The displacement
must match to maintain
the normal maxillary-mandibular occlusal relation.
Any discrepancy leads to
dentofacial skeletal deformity.
(Adapted
from
Enlow DH. Craniofacial
growth and development:
normal and deviant patterns. In: Posnick JC, editor.
Craniofacial and maxillofacial surgery in children and
young adults, vol. 1. Philadelphia: W.B. Saunders;
2000. p. 2729; with
permission.)

maturity (see above), but also can challenge normal

growth patterns and vectors that aid this maturation [66]. Prepubertal interruption of the pterygomaxillary
region,
which
contributes
to
anteroposterior lengthening of the midface, with
osteotomy or bone grafting, may lead to inhibition
of sutural expansion at this region.
In similar fashion, conventional mandibular
osteotomy procedures, when performed before
maturation, can inhibit growth. Moreover, the pediatric mandible houses budding deciduous and

permanent teeth, and the maxillofacial surgeon

must be aware of the subtleties in anatomy
and form of the developing mandible when
considering surgical intervention [51]. Bilateral
sagittal split osteotomy and mandibular repositioning, or anterior horizontal osteotomy of the
mandible (genioplasty), requires a skeletally
mature patient. Cessation of growth of these
structures can be correlated with axial skeletal
growth, by either hand films (to determine
epiphyseal plate closure) or serial cephalometric
Fig. 8. Timeline of possible orthodontic and surgical intervention that can
influence the final form of the facial
skeleton. The diagram is a guide,
and as is discussed in the text, needs
to be placed in the context of the
clinical situation.

Orthodontic Growth Modulation

Distraction Osteogenesis

Orthognathic Surgery
(female)

Orthognathic Surgery
(male)

10

Time (yrs.)

15

20

Facial Skeletal Growth and Surgical Intervention

radiographs (6 months apart) to assess relative

movement of the midface or mandible with respect to the cranial base.
The ability to distract the midface or mandible
has revolutionized treatment of maxillofacial deformities. Such procedures are described in more detail elsewhere in this issue. Our concept of how
distraction affects long-term growth of the facial
skeleton is evolving. Recent studies investigating
long-term relapse of maxillary retrusion following
distraction at the Le Fort I level, for example, demonstrate superior results compared with conventional procedures in terms of length of
advancement and long-term relapse [67]. Distraction osteogenesis appears to be a more physiologic
means of correcting midfacial and mandibular
hypo- and dysplasia, via stimulation of mechanotransduction pathways [16], which in turn recapitulates the bodys normal mechanism for bone
growth and development.

Summary
An awareness of the embryophysiology of craniomaxillofacial growth and development is tantamount in our timing of surgical intervention of
this intricate structure. Although an absolute timeline cannot be constructed, a vague schematic can
be provided (Fig. 8). Future studies at experimental
and clinical levels, targeting particularly the mechanism behind craniofacial distraction osteogenesis,
are critical in advancing our approach to interception of the dysmorphic, yet developing, facial
skeleton. The challenge is to construct an orthodontic-surgical treatment plan staged with the developing facial structures that will favorably alter the
trajectory of the abnormal growth and development, whether as a result of congenital, developmental, or acquired condition.

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