Download Review Article Bilateral Cleft Lip and Palate: An Overview and

Balkan Military Medical Review
Oct - Dec 2012; 15(4): 305 -316
Review Article
Bilateral Cleft Lip and Palate: An Overview and Discussion of the
Literature
Dimitrios STAVROPOULOS1, Chryssoula KALAPODA2*
Affiliation of the authors:
1. DDS, Dipl.Ortho, PhD, Department of Orthodontics, Naval Hospital of Athens, Greece
2. MD, MSc, Ophthalmologist, Department of Ophthalmology, Attikon General Hospital,
Athens, Greece
Corresponding author:
Lt Commander Dimitrios STAVROPOULOS, (Navy), DDS, Dipl.Ortho, PhD
Department of Orthodontics
Athens Naval Hospital
70, Deinokratous Street
GR 115 25, Athens, GREECE
Tel: +30 210 7261297
Fax: +30 210 7294132
E-mail: [email protected]
Stavropoulos D. et al: Bilateral Cleft Lip and Palate
Abstract
The most severe expression of the
congenital clefts of the lip and palate
(CLP) is the bilateral cleft lip and palate
(BCLP), which runs through the lip, the
hard, as well as the soft palate. At birth,
the maxilla of a child with BCLP is
divided into three parts: the premaxilla,
which is usually protruded, and the two
lateral maxillary segments. It seems that
the reasons for the abnormal facial
morphology in patients with CLP
involve three groups of factors: intrinsic
developmental deficiencies, functional
distortions affecting the position and
growth of both normal and abnormal
parts, and iatrogenic (mainly surgical)
factors. The iatrogenic factors are
implicated as the major source of the
midface deficiency reported in patients
with CLP. Hypodontia is a very common
dental trait in individuals with BCLP,
most frequently involving the upper
lateral incisors and the second
premolars. Posterior and anterior dental
crossbites
and
maxillary
incisor
rotations are also very common.
Although no consensus has been reached
on the efficacy and the effectiveness of
the different treatment modalities
applied, it is evident how tremendously
important it becomes to offer centralized
treatment to these suffering patients,
based on team work of closely
cooperating
medical
and
dental
specialties.
306
these defects still presents a major clinical
problem, but also because they interfere
with two of the most important human
means of communication: facial expression
and speech.
The most severe expression of the
common orofacial clefts is the bilateral
cleft lip and palate (BCLP), which runs
through the lip, the hard, as well as the soft
palate (Figures 1, 2). It appears when the
embryonic medial nasal and maxillary
processes fail to unite on both sides. At
birth, the maxilla of a child with BCLP is
divided into three parts: the premaxilla,
which is usually protruded, and the two
lateral maxillary segments, which may also
deviate in size and position (Figure 2).
The nose is wide and flat, due to flared alar
bases and short columella [1].
Figure 1: A picture of a neonate with BCLP
Keywords: Bilateral cleft lip and palate,
treatment, surgery, growth
Introduction
Congenital clefts of the lip and
palate (CLP) constantly raise high research
interest not only because the treatment of
Figure 2: Maxillary stone model of a neonate with
BCLP
307
Hagberg et al. [2] found an
incidence of newborns with BCLP of
0.3/1000 live births in the county of
Stockholm in Sweden. Bilateral clefts
appeared at about 1/3 in frequency
comparing to unilateral ones. Generally
speaking about all types of CLP, it seems
that the highest incidence rate is
encountered in Orientals (2-3/1000 live
births), then in Caucasians (about 1/1000
live births) and finally in Black population
(about 0.4/1000 live births) [1].
Nevertheless, it has to be pointed out that
the CLP incidence reported in the
literature is strongly influenced by the
geographical area where the scientific
study is performed and the time spans. For
instance, in South European countries the
CLP incidence is reported to be around
1/1000 live births, whilst in Northern
European countries the incidence is
reported to be around 2/1000 live births
[3].
It seems that there is a clear gender
difference in patients with BCLP. It has
been observed that the incidence in males
has been double that of the females [4].
In a study by Milerad et al. [5], an
association between severe clefts and
additional malformations was found. A
BCLP was associated with other
malformations, such as cardiovascular
defects, malformations of the vertebral
column and the limbs, in 35% of the cases.
The authors concluded that although many
associated congenital defects can be
detected in a physical examination, the
high prevalence of congenital heart disease
(16 times more than that reported for the
general population) may justify a routine
echocardiographic screening in extensive
cleft cases.
Clinically, when CLP appears with
other (usually two or more) malformations
in recognizable patterns, it is classified as
syndromic. If it appears as an isolated
defect, or if syndromes cannot be
identified, the term non-syndromic CLP is
Balkan Military Medical Review
Vol. 15, No 4, Oct –Dec 2012
used [6]. Although CLP can be associated
with more than 300 syndromes [7], the
majority of these clefts occur as a nonsyndromic form [8].
More than 250 genes have been
associated with the development of
orofacial clefts in humans [9]. Fraser [10]
suggested that the best fitting model of
CLP inheritance should be a multifactorial
threshold model. Such model describes
diseases with complex etiologies involving
genetic, epigenetic and environmental
components. According to this model,
susceptibility to CLP is contributed by
multiple factors (genetic, epigenetic and
environmental). When these factors
accumulate up to a certain threshold value
in an individual, cleft occurs. Whether the
genetic factors are best explained by a
major locus (a unique chromosomal
location defining the position of an
individual gene or DNA sequence) with
reduced penetration [11] or a model of
multiple interacting loci [12] is still under
scientific debate.
Among the environmental factors
that predispose for CLP, hypervitaminosis
A, folic acid deficiency, smoking habits,
maternal
periconceptional
alcohol
consumption and medications such as the
anti-acne drug isotretinoin, corticosteroids,
and anticonvulsants including phenytoin,
valproic acid and oxazolidinediones have
been reported in the literature [13-16].
Growth of patients with BCLP
Ross [17] postulates that the
reasons
for
the
abnormal
facial
morphology in individuals with CLP
involve three groups of factors: (i) intrinsic
developmental deficiencies, (ii) functional
distortions affecting the position and
growth of both normal and abnormal parts
and (iii) iatrogenic factors. The only
apparent significant intrinsic abnormality
is in the maxillary complex with a
possibility of a slight mandibular
Stavropoulos D. et al: Bilateral Cleft Lip and Palate
deficiency. These intrinsic deficiencies are
assumed
to
be
invariably
mild.
Superimposed on the intrinsic factors are
functional growth factors, mainly from
muscle activity, which cause distortion of
both normal and abnormal parts. An
example of such growth factors is the
premaxillary
protrusion
and
the
underdevelopment of the columella seen in
patients with BCLP [18]. The protrusion of
the premaxilla has been well documented
cephalometrically [19] and has been
attributed to the absence of the lip
restraining effect in unoperated patients
with BCLP [20]. When a group of
unoperated patients with BCLP was
compared with a group of patients with
BCLP who had received lip repair only
during childhood, the latter group
exhibited a significant reduction of the
anterior projection of the premaxilla and
lingual tipping of the upper incisors [21].
Functional
distortions
are
usually
reversible by surgical repair of the lip and
palate. The iatrogenic factors (attributed
mainly to the surgical management) are,
therefore, implicated as the major source of
the midface deficiency reported in patients
with CLP. The specific maxillofacial
growth pattern of the treated cleft face is
assumed to be superimposed on the
intrinsic deficiency present, as well as on
the craniofacial type that is characteristic
for the non-cleft population to which the
patient with CLP belongs.
Will [22] in his review on growth
and development in patients with untreated
clefts, states that the skeletal and thus,
dental width of the unoperated cleft
maxilla, is not inherently decreased, but is
rather increased. The slightly higher
incidence in dental posterior crossbites in
unrepaired adult patients might be
attributed to some degree of arch collapse
brought about by muscle function over the
patient’s lifetime. Similarly, although the length of the maxilla seemed to be
somewhat shorter in many patients, sagittal
308
growth did not seem to be significantly
disturbed. Finally, the mandible was found
in many cases retrusive with a quite steep
mandibular plane.
Friede [23] discusses the growth
sites and growth mechanisms at risk in the
CLP patient management. The importance
of the vomero-premaxillary suture, the
intermaxillary suture and the transverse
palatine suture for the appositional growth
and displacement of the maxillary bony
structures is stressed. Strains from lip
repair, but most importantly, from the
developing scar tissue on the denuded
palatal bones, due to the raising of the
mucoperiosteal flaps for palatal repair,
interfere
adversely
with
the
aforementioned
sensitive
structures.
Abnormal tongue posture due to collapsed
maxillary segments deteriorates the
maxillary dental arch development, both
horizontally and vertically [1].
Long et al. [24] depict the main
characteristics of treated patients with
CLP. They exhibit varying degrees of
maxillary sagittal deficiency, which
increases with age, although in individuals
with BCLP the appearance of the
deficiency may be delayed slightly,
because of the initial prominence of the
premaxilla. Transversally, the maxilla
develops varying degrees of medial
rotation and collapse of the skeletal and
dentoalveolar elements. The predictability
of this collapse and its relationship to the
development of future posterior crossbite is
uncertain.
Vertically,
the
intrinsic
mandibular opening rotation may be
accentuated by additional primary and
secondary surgical procedures. The
resultant
mandibular retrusion
can
occasionally mask a maxillary deficiency,
at the expense of bimaxillary retrognathic
facial profile.
Dental development, alignment and
occlusion of patients with BCLP
309
Cleft of the primary palate may
interfere with normal tooth development,
resulting in varied anomalies of the
dentition. They can all be related to the
initial disturbance and disruption of the
embryonic process of dental lamina
formation, mainly in the area of failed
merging and fusion of the medial nasal,
lateral nasal and maxillary processes [1,
25]. Dental traits such as hypodontia,
supernumerary teeth, peg-shaped teeth,
dental delay, ectopic eruptions of teeth,
dental impactions, dental asymmetry and
enamel defects and abnormalities occur
more frequently in patients with CLP.
Hypodontia is very common and most
frequently involves the upper lateral
incisors and the second premolars in the
upper and lower jaws. The tooth most
commonly affected is the upper lateral
incisor [26]. Its absence appears to be in
the range of 10-20% in the primary
dentition and 30-50% in the permanent
dentition [24]. Bartzela et al. [27]
evaluated serial panoramic radiographs of
240 patients with BCLP and found
agenesis of at least one tooth (excluding
third molars) in 60% of patients. The most
frequently missing teeth were upper
permanent laterals and upper and lower
permanent second premolars. The most
common dental agenesis pattern was the
simultaneous agenesis of upper permanent
lateral incisors and all permanent second
premolars.
In unoperated patients with BCLP,
the maxillary dentoalveolar segments may
be rotated medially [20], resulting in arch
collapse and dental crossbites in the canine
region [28]. Anteroposteriorly, a longer
maxillary dental arch has been observed,
attributed to the premaxillary anterior
projection [29].
In operated patients with BCLP,
posterior and anterior crossbites are
frequent and become worse in the
permanent dentition. Maxillary incisor
rotations, lingual dental inclination and
Balkan Military Medical Review
Vol. 15, No 4, Oct –Dec 2012
anterior crossbites are also common.
Maxillary dental midline deviations and
asymmetric dental arch form can also be
found [30].
Treatment modalities
Different treatment protocols are
followed in different countries. Optimal
habilitation
calls
for
centralized
coordinated efforts of a range of clinical
specialties, including pediatricians, plastic
surgeons, oral and maxillofacial surgeons,
otorhinolaryngologists, dentists, orthodo
ntists, speech therapists, psychologists. If
the CLP patient treatment is centralized, 610% of the patients require orthognathic
surgical intervention into the early adult
age; otherwise, this percentage rises to
48% [31].
Surgical treatment
Early surgical manipulation of the
premaxilla
Although the protruded premaxilla
is of great concern for the parents of a
neonate with BCLP and it presents a
clinical challenge for proper lip surgery,
any premaxillary set-back repositioning
has well been abandoned. Damage of the
vomero-premaxillary suture results in a
severe midfacial retrusion in early
adulthood [32].
Nose and lip repair
Cleft lip repair is usually carried
out when the child is 2-3 months of age
[33], one-sided at each time or two-sided at
the same time, according to the surgical
difficulty. A lip adhesion or lip adaptation
is a partial cleft repair that converts a wide
complete cleft into an incomplete one,
without suturing the lip muscular units
[34]. Lip adhesion is usually used as a
primary stage for cleft patients with wide
Stavropoulos D. et al: Bilateral Cleft Lip and Palate
clefts. Definitive lip closure can be done at
a later stage. While the short-term effects
of lip repair in molding the alveolar
segments and narrowing the cleft width are
well documented, the possible long-term
maxillary growth effects are overshadowed
by the subsequent palate repair [35].
According to Mulliken [36], the
established principles for successful nose
and lip repair in BCLP children are: (i)
maintain symmetry, (ii) secure primary
muscular union, (iii) design the prolabial
flap of correct size and configuration, (iv)
form the median tubercle and vermillioncutaneous ridge from lateral labial tissue,
(v) construct the nasal tip and columella by
anatomic placement of the alar cartilages.
Primary nose surgery aims are usually the
primary columellar lengthening and nose
tip projection gain. However, even with
many of surgical protocols available, the
primary lip and nose repair show quite
often poor aesthetic results, therefore,
making plenty of subsequent revision
procedures necessary.
Palatal repair
Posnick [33] states that the main
objectives in cleft palatal repair include the
achievement of an intact hard and soft
palate. The latter should be able to achieve
velopharyngeal closure during normal
phonation. Berkowitz [37] outlines four
common protocols for timing the palatal
surgery: early complete palatal repair (3-9
months), delayed complete palatal repair
(12-24 months), late complete palatal
repair (2-5 years) and two-stage palatal
repair with early velar closure (3-9
months) and delayed hard palatal closure
(2-9 years). With the assumption that all
palatal repairs have the potential to disturb
maxillary growth and that the unoperated
cleft maxilla exhibits near-normal growth
potential, it seems logical to conclude that
delaying the procedure until the maxilla
has completed more of its growth is a
310
desirable approach. However, with the
possibility of worse speech performance in
individuals with delayed palatal repair
[38], the growth improvements that may be
possible can equally be negated in value,
because of these concerns [35]. Ross [17]
suggests the possibility that the growth
effects of a given procedure may be more
related to the skill of the surgeon rather
than to the particular technique used.
The old use of hard tissue for
palatal closure has been well discontinued,
due to the severe midfacial deficiency it
caused [39], therefore only soft tissue
closure of the palate with mobilization of
mucoperiosteal flaps is currently a standard
procedure. Nevertheless, care should be
paid not to leave areas of denuded palatal
bone, especially adjacent to the alveolar
process, as it leads to scar tissue formation
with all its adverse contractile effects on
maxillary and dentoalveolar growth and
development [23]. In an effort to achieve
significant reduction in scar tissue
formation the attempt to use split-thickness
supraperiosteal flaps [40] has been
reintroduced.
Surgical
management
Velopharyngeal Insufficiency (VPI)
of
VPI occurs in 20-30% of children
born with palatal clefts after primary
palatal repair [41]. VPI results from an
inability
to
accomplish
adequate
velopharyngeal closure due to a structural
or functional deficit in the nasopharynx
(i.e., short or poorly mobile velum). The
aim of any surgical procedure is to reduce
the nasal airflow during speech, which
produces phonetic aberrations. The most
widely used techniques today are the
pharyngeal flap and the pharyngoplasty
[42]. The pharyngeal flap remains attached
to the posterior pharyngeal wall, while the
other end is sutured to various locations in
the soft palate to diminish the size of the
velopharyngeal port. From the existing
311
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Vol. 15, No 4, Oct –Dec 2012
literature it is difficult to conclude whether
the pharyngeal flap has a mechanical or
functional influence on maxillofacial
growth [35]. The sphincter pharyngoplasty
creates a soft tissue diaphragm, narrowing
the nasopharynx and allowing for
velopharyngeal closure [43].
Periosteoplasty – gingivoplasty
Skoog [44] introduced a surgical
approach for primary repair of complete
alveolar clefts utilizing periosteal flaps.
The rationale for this method was to induce
subperiosteal bone formation for creating
bony continuity for bridging the alveolar
process, even from infancy [45]. However,
longitudinal data failed to show
satisfactory maxillary growth and ability to
produce bone in wide clefts [46]. At the
Institute of Reconstructive Plastic Surgery
of New York University Medical Center,
following a course of maxillary alveolar
segment approximation in patients with
clefts with the use of intraoral acrylic
plates, a gingivoperiosteoplasty (gingivo
plasty) is performed [47]. However, no
current credible long-term data have been
presented so far supporting this technique.
Early or primary alveolar bone
grafting, introduced in the late 1950s, has
now been abandoned in the light of studies
showing association with later maxillary
retrusion [48]. Late or secondary alveolar
bone grafting (i.e., during the mixed
dentition) is currently carried out [49].
Midfacial growth disturbance is considered
minimal, as by the age of 8 years growth in
width and length of the anterior maxilla
has almost ceased [50, 51]. Furthermore,
the adjacent to the grafted area developing
tooth (permanent lateral incisor or canine)
can erupt through the graft to its final
position in the dental arch. KuijpersJagtman and Long [35] suggest that it may
be possible in the future that varied time of
secondary bone grafting might be optimal:
earlier in patients with healthy lateral
incisors or central incisors with marginal
bone support requiring an intact alveolar
ridge at a younger age, but risking some
growth interference if done too early; later
in patients with adequate support for cleftadjacent teeth, in which the risk of
maxillary growth problems exceeds the
benefits of additional surgery at a much
younger age.
Orthognathic surgery
Bone grafting
Despite the primary lip and palate
repairs, a residual perialveolar oronasal
bony defect through the alveolar ridge,
anterior part of the hard palate and the
floor of the nose will remain to be
addressed at a later stage. The best way to
bridge this residual defect is by alveolar
bone grafting [33], which produces support
of cleft adjacent teeth, stabilization of the
cleft maxillary segments, support of the
alar bases and ability to expand the
interpremaxillary suture [24]. In patients
with BCLP alveolar bone grafting is often
performed in two stages (each cleft side at
a time).
The primary lip and palate repair
performed during infancy and early
childhood provides the foundation for
normal
speech,
occlusion,
facial
appearance and self esteem at the expense
of varying maxillary growth restriction due
to scar tissue formation. Restriction of
maxillary development may continue
throughout the growing period and, thus,
the situation may worsen with age [1]. The
basic orthognathic procedure usually
performed for correcting maxillary
hypoplasia is a Le Fort I osteotomy [52],
sometimes in combination with mandibular
set-back [53], applied after completion of
facial growth. The use of stabilizing miniplates and autogenous bone grafts to
Stavropoulos D. et al: Bilateral Cleft Lip and Palate
enhance healing will usually result in
acceptable postoperative stability after the
maxillary surgery. Nevertheless, in
anticipation of a degree of postoperative
skeletal relapse, surgical overcorrection of
several millimeters is planned, both in the
horizontal and transverse dimensions [54].
The application of distraction osteogenesis
techniques to cleft-related maxillary
deficiencies has broadened treatment
versatility and expectations [55]. These are
gradual bone lengthening techniques by the
employment of distraction devices that
separate the bony segments at the
osteotomies sites [56, 57].
Orthodontic treatment
Presurgical orthopaedics or infant
orthopaedics
Infant orthopaedics, originated in
the 1950’s, is widely used today in many forms, varying in duration and combined
with various surgical protocols [23]. This
treatment modality aims primarily at active
molding and repositioning of the deformed
nasal cartilages and alveolar processes, as
well as the lengthening of the deficient
columella and retraction of the protruded
premaxilla of neonates with BCLP into the
keystone position between the lateral
alveolar segments [47, 58]. The main
objective is to reduce the severity of the
original cleft deformity, therefore enabling
the surgeon to achieve better and more
predictable repair of the alveolus, lip and
nose. Active or passive molding plates
have been used, as well as extraoral
traction to set back the premaxilla in
patients with BCLP, and nasal stents to
form the alar cartilages. This technique has
been termed as "nasoalveolar molding"
(NAM). A typical NAM appliance consists
of an intraoral molding plate with nasal
stents to mold the alveolar ridge and nasal
cartilage simultaneously [59]. To date, the
only prospective randomized clinical trial
312
of infant orthopaedics published, revealed
no benefits of this procedure [60].
Deciduous dentition treatment
Long et al. [24], in their extensive
review paper on orthodontic treatment on
children with complete CLP, suggest that
most orthodontists either deliver treatment
only for severe functional problems or
others see no benefit to primary dentition
intervention at all. They conclude that the
strongest argument against deciduous
dentition treatment is that it does not pass
the "burden of the patient versus benefit of
the treatment" test. Usually, no orthodontic
treatment is performed during the
deciduous dentition.
Mixed dentition treatment
The most frequent procedure is the
correction of posterior dental crossbites,
usually before the alveolar bone grafting of
the residual cleft (in case a surgical
treatment protocol has been employed
from the first years of life of a child with
BCLP). The orthodontic appliances of
choice are intraoral expansion appliances,
such as a quad-helix or removable intraoral
plates with expansion screws.
Other procedures carried out may
include incisor alignment and proclination
to remove crowding, rotations and anterior
crossbites, and maxillary protraction to
reduce maxillary retrusion [1, 23, 24].
Permanent dentition treatment
The
definitive
orthodontic
treatment starts after the eruption of the
permanent teeth. It involves the application
of orthodontic fixed appliances and may be
carried out in cooperation with a
maxillofacial surgeon, if orthognathic
surgery (usually when craniofacial growth
has ceased) is part of the overall treatment
plan.
313
From the initial statement that an
orthodontist, especially in children with
BCLP, should not be trapped in ideal goals
[1], nowadays with a centralized team care
for children with CLP, more and more
patients
receive
normal,
everyday
orthodontic treatment procedures during
the permanent dentition [24]. The use of
fixed appliances and the proper
cooperation of the patient can usually solve
dentoalveolar problems and compensate
for adverse dental relationships, if not too
severe.
In case of missing teeth, decisions
have to be made whether a fitting of
conventional bridgework or an implantborne prosthesis will be used, or if possible
orthodontic space closure will be done.
Chetpakdeechit et al. [61] evaluated 35
persons with total BCLP, treated by the
Gothenburg CLP team. A good symmetry
and a straight midline between jaws were
found after treatment for 60% of the young
adults. It was more common to have
canines positioned in the region of a
missing or extracted lateral incisor
compared to having the lateral incisor
replaced with an implant or other
prosthodontic treatment.
Finally, when the orthodontic result
has been attained, permanent retention is
advisable in individuals with BCLP [62].
Conclusion
In conclusion, habilitation of
patients with BCLP proves to be a very
controversial area and demanding process,
as seen both from a treatment as well as
from a scientific point of view. Although
no consensus has been reached on the
efficacy and the effectiveness of the
different treatment modalities applied, it is
evident how tremendously important it
becomes to offer centralized treatment to
these suffering patients, based on team
work of closely cooperating medical and
dental specialties.
Balkan Military Medical Review
Vol. 15, No 4, Oct –Dec 2012
References
1.
Ross R, Johnston M: Cleft
Lip and Palate. Baltimore, Williams &
Wilkins, 1972, pp. 17-46, 114-120, 158205, 227-289.
2.
Hagberg C, Larson O,
Milerad J. Incidence of cleft lip and palate
and risks of additional malformations.
Cleft Palate Craniofac J 35:40-45, 1998.
3.
Gundlach KK, Maus C.
Epidemiological studies on the frequency
of clefts in Europe and world-wide. J
Craniomaxillofac Surg 34 Suppl 2, 2006.
4.
Pannbacker M. Congenital
malformations and cleft lip and palate.
Cleft Palate J 5:334-339, 1968.
5.
Milerad J, Larson O, Ph
DD, Hagberg C, Ideberg M. Associated
malformations in infants with cleft lip and
palate: a prospective, population-based
study. Pediatrics 100:180-186, 1997.
6.
Wong FK, Hagg U. An
update on the aetiology of orofacial clefts.
Hong Kong Med J 10:331-336, 2004.
7.
Gorlin R, Cohen A, Michael
M, Hennekam R, eds. Syndromes of the
Head and Neck, New York, Oxford
University Press, 2001.
8.
Wong F. Application of
genetic analyses in studies of syndromic
and non syndromic cleft lip and palate.
Doctoral thesis. Stockholm, Karolinska
Institute, 2000.
9.
Gene
Cards.
http://www.genecards.org.
Last
date
accessed 31 May 2012.
10.
Fraser FC. The genetics of
cleft lip and cleft palate. Am J Hum Genet
22:336-352, 1970.
11.
Hecht JT, Yang P, Michels
VV, Buetow KH. Complex segregation
analysis of non-syndromic cleft lip and
palate. Am J Hum Genet 49:674-681,
1991.
12.
Mitchell LE, Risch N. Mode
of inheritance of non-syndromic cleft lip
Stavropoulos D. et al: Bilateral Cleft Lip and Palate
with or without cleft palate: a reanalysis.
Am J Hum Genet 51:323-332, 1992.
13.
Bille C, Olsen J, Vach W, et
al.: Oral clefts and life style factors-a
case-cohort study based on prospective
Danish data. Eur J Epidemiol 22:173-181,
2007.
14.
Eppley BL, van Aalst JA,
Robey A, Havlik RJ, Sadove AM. The
spectrum of orofacial clefting. Plast
Reconstr Surg 115:101e-114e, 2005.
15.
Fawcett LB, Buck SJ,
Beckman DA, Brent RL. Is there a no-effect
dose for corticosteroid-induced cleft
palate? The contribution of endogenous
corticosterone to the incidence of cleft
palate in mice. Pediatr Res 39:856-861,
1996.
16.
Webster WS, Johnston MC,
Lammer EJ, Sulik KK. Isotretinoin
embryopathy and the cranial neural crest:
an in vivo and in vitro study. J Craniofac
Genet Dev Biol 6:211-222, 1986.
17.
Ross
RB.
Treatment
variables affecting facial growth in
complete unilateral cleft lip and palate.
Cleft Palate J 24:5-77, 1987.
18.
King BF, 3rd, Workman
CH, 3rd, Latham RA. An anatomical study
of the columella and the protruding
premaxillae in a bilateral cleft lip and
palate infant. Cleft Palate J 16:223-229,
1979.
19.
Ortiz-Monasterio F, Rebeil
AS, Valderrama M, Cruz R. Cephalometric
measurements on adult patients with nonoperated cleft palates. Plast Reconstr Surg
Transplant Bull 24:53-61, 1959.
20.
Bishara SE, de Arrendondo
RS, Vales HP, Jakobsen JR. Dentofacial
relationships in persons with unoperated
clefts: comparisons between three cleft
types. Am J Orthod 87:481-507, 1985.
21.
da
Silva
Filho
OG,
Carvalho Lauris RC, Capelozza Filho L,
Semb G. Craniofacial morphology in adult
patients with unoperated complete
314
bilateral cleft lip and palate. Cleft Palate
Craniofac J 35: 111-119, 1998.
22.
Will LA. Growth and
development in patients with untreated
clefts. Cleft Palate Craniofac J 37:523526, 2000.
23.
Friede H, Katsaros C.
Current knowledge in cleft lip and palate
treatment from an orthodontist's point of
view. J Orofac Orthop 59:313-330, 1998.
24.
Long R, Semb G, Shaw W.
Orthodontic treatment of the patient with
complete clefts of lip, alveolus and palate:
lessons of the past 60 years. Cleft Palate
Craniofac J 37: 533, 2000.
25.
Bohn A. Dental anomalies
in hare lip and cleft palate. Acta Odontol
Scand 21(suppl.38): 1-109, 1963.
26.
Ranta R. A review of tooth
formation in children with cleft lip/palate.
Am J Orthod Dentofacial Orthop 90:1118, 1986.
27.
Bartzela TN, Carels CE,
Bronkhorst EM, Ronning E, Rizell S,
Kuijpers-Jagtman AM. Tooth agenesis
patterns in bilateral cleft lip and palate.
Eur J Oral Sci 118:47-52, 2010.
28.
Latief BS, Lekkas C,
Kuijpers MA. Maxillary arch width in
unoperated adult bilateral cleft lip and
alveolus and complete bilateral cleft lip
and palate. Orthod Craniofac Res 13:8288, 2010.
29.
da Silva Filho OG, de
Castro Machado FM, de Andrade AC, de
Souza Freitas JA, Bishara SE. Upper
dental arch morphology of adult
unoperated complete bilateral cleft lip and
palate. Am J Orthod Dentofacial Orthop
114:154-161, 1998.
30.
Semb
G,
Shaw
W.
Orthodontics. Eds: Watson A, Grunwell P,
Sell D: Management of Cleft Lip and
Palate, London, Whurr Publishers Ltd,
2001.
31.
Semb G, Abyholm F,
Tindlund R, Lie R. Cleft lip and palate: an
315
overview. Nor Tannlegeforen Tid 110:800804, 2000.
32.
Friede H, Pruzansky S.
Long-term effects of premaxillary setback
on facial skeletal profile in complete
bilateral cleft lip and palate. Cleft Palate J
22:97-105, 1985.
33.
Posnick J. The staging of
cleft lip and palate reconstruction: infancy
through adolescence. Ed: Posnick J:
Craniofacial and maxillofacial surgery in
children and young adults, Philadelphia,
WB Saunders company, 2000, pp. 785-826.
34.
Randall P. A Lip Adhesion
Operation in Cleft Lip Surgery. Plast
Reconstr Surg 35:371-376, 1965.
35.
Kuijpers-Jagtman A, Long
R. The influence of surgery and orthopedic
treatment on maxillofacial growth and
maxillary arch development in patients
treated for orofacial clefts. Cleft Palate
Craniofac J 37:527, 2000.
36.
Mulliken JB. Repair of
bilateral complete cleft lip and nasal
deformity--state of the art. Cleft Palate
Craniofac J 37: 342-347, 2000.
37.
Berkowitz S. A dissent: cleft
palate closure in the neonate. Cleft Palate
Craniofac J 33: 352-358, 1996.
38.
Peterson-Falzone SJ. The
relationship between timing of cleft palate
surgery and speech outcome: what have
we learned, and where do we stand in the
1990s? Semin Orthod 2:185-191, 1996.
39.
Friede H, Johanson B.
Adolescent facial morphology of early
bone-grafted cleft lip and palate patients.
Scand J Plast Reconstr Surg 16:41-53,
1982.
40.
Perko MA. Primary closure
of the cleft palate using a palatal mucosal
flap: an attempt to prevent growth
impairment. J Maxillofac Surg 2:40-43,
1974.
41.
Riski JE. Articulation skills
and oral-nasal resonance in children with
pharyngeal flaps. Cleft Palate J 16: 421428, 1979.
Balkan Military Medical Review
Vol. 15, No 4, Oct –Dec 2012
42.
Pryor LS, Lehman J, Parker
MG, Schmidt A, Fox L, Murthy AS.
Outcomes in pharyngoplasty: a 10-year
experience. Cleft Palate Craniofac J
43:222-225, 2006.
43.
Witt PD, Myckatyn T,
Marsh
JL.
Salvaging
the
failed
pharyngoplasty: intervention outcome.
Cleft Palate Craniofac J 35:447-453,
1998.
44.
Skoog T. The use of
periosteal flaps in the repair of clefts of the
primary palate. Cleft Palate J 2:332-339,
1965.
45.
Millard DR, Jr., Latham RA.
Improved primary surgical and dental
treatment of clefts. Plast Reconstr Surg
86:856-871, 1990.
46.
Hellquist R, Svardstrom L.
Changes in the treatment programme 1964
to 1984 at the Upssala Cleft Palate Centre.
Eds: Hotz M, Gnoinski W, Perko M,
Nussbaumer H, Hof E, Haubensak R:
Early Treatment of Cleft Lip and Palate,
Toronto, Hans Huber Publishers, 1986, pp.
131-134.
47.
Grayson BH, Santiago PE,
Brecht LE, Cutting CB. Presurgical
nasoalveolar molding in infants with cleft
lip and palate. Cleft Palate Craniofac J
36:486-498, 1999.
48.
Brattstrom V, McWilliam J,
Semb G, Larson O. Craniofacial
development in children with unilateral
clefts of the lip, alveolus, and palate
treated according to four different regimes.
II. Mandibular and vertical development.
Scand J Plast Reconstr Surg Hand Surg
26:55-63, 1992.
49.
Bergland O, Semb G,
Abyholm FE. Elimination of the residual
alveolar cleft by secondary bone grafting
and subsequent orthodontic treatment.
Cleft Palate J 23:175-205, 1986.
50.
Bjork A, Skieller V. Growth
in width of the maxilla studied by the
implant method. Scand J Plast Reconstr
Surg 8:26-33, 1974.
Stavropoulos D. et al: Bilateral Cleft Lip and Palate
51.
Bjork A, Skieller V. Growth
of the maxilla in three dimensions as
revealed radiographically by the implant
method. Br J Orthod 4:53-64, 1977.
52.
Bell WH. Le Forte I
osteotomy for correction of maxillary
deformities. J Oral Surg 33:412-426, 1975.
53.
Trauner R, Obwegeser H.
The surgical correction of mandibular
prognathism and retrognathia with
consideration of genioplasty. I. Surgical
procedures
to
correct
mandibular
prognathism and reshaping of the chin.
Oral Surg Oral Med Oral Pathol 10:677689, 1957.
54.
Posnick JC. Orthognathic
surgery for the cleft lip and palate patient.
Semin Orthod 2:205-214, 1996.
55.
Figueroa AA, Polley JW.
Management of severe cleft maxillary
deficiency with distraction osteogenesis:
procedure and results. Am J Orthod
Dentofacial Orthop 115:1-12, 1999.
56.
Ilizarov
GA.
Basic
principles of transosseous compression
and distraction osteosynthesis. Ortop
Travmatol Protez 32:7-15, 1971.
57.
Polley JW, Figueroa AA.
Management
of
severe
maxillary
deficiency in childhood and adolescence
through distraction osteogenesis with an
external, adjustable, rigid distraction
device. J Craniofac Surg 8:181-185, 1997.
58.
Grayson BH, Cutting C,
Wood
R.
Preoperative
columella
lengthening in bilateral cleft lip and
palate. Plast Reconstr Surg 92:1422-1423,
1993.
59.
Grayson BH, Shetye PR.
Presurgical
nasoalveolar
moulding
treatment in cleft lip and palate patients.
Indian J Plast Surg 42 Suppl:56-61, 2009.
60.
Prahl C, Kuijpers-Jagtman
AM, Van't Hof MA, Prahl-Andersen B. A
randomized prospective clinical trial of the
effect of infant orthopedics in unilateral
cleft lip and palate: prevention of collapse
316
of the alveolar segments (Dutchcleft). Cleft
Palate Craniofac J 40:337-342, 2003.
61.
Chetpakdeechit
W,
Stavropoulos D, Hagberg C. Dental
appearance, with focus on the anterior
maxillary dentition, in young adults with
bilateral cleft lip and palate (CLP). A
follow up study. Swed Dent J 34:27-34,
2010.
62.
Melissaratou A. Dental
arches and occlusion in bilateral cleft and
palate patients after two different routines
for palatal surgery. Master’s thesis. Gothenburg, Gothenburg University, 2000.