Management of cleft lip and palate 1. /certified fixed orthodontic courses by Indian dental academy

MANAGEMENT OF CLEFT
LIP AND PALATE

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

Introduction
Etiology

and Pathogenesis of Clefting
Epidemiology of Cleft lip and Palate
Classification of Cleft Lip and Palate
Prenatal Diagnosis of Cleft Lip and
Palate.
Neonatal Care and Guidelines for
Feeding.
Maxillary Orthopedics

Introduction
 Clefts

of the lip and palate are the most
common craniofacial birth defects and are
among the most common of all birth
defects.
 Although the severity of the defect varies,
multidisciplinary treatment is often
required.
 Recognized way back in Ancient China
(A.D. 390), where the annals of the Chin
dynasty recorded the surgical repair of cleft
lip, along with detailed post-operative
instructions for optimal results.

 In

many countries, craniofacial teams have
been established in order to provide
comprehensive care to the cleft patient.
 The orthodontist is required to work
collaboratively with the team in order to
determine the appropriate timing and
sequencing of treatment, in the context of
the patient’s other health care needs.


Etiology and Pathogenesis of Orofacial
clefting
I. Genetics:
 There

is much evidence to support the view that
genetic factors are associated with oro-facial
clefting.
 In twins with cleft lip-palate, concordance is far
greater for monozygotic twins (40%) than for
dizygotic twins.(4.2%)
 In twins with isolated cleft palate, concordance is
also higher for MZ twins(355) than for DZ twins
(7.8%)
 Though clefts occur sporadically, some families
have more than one individual affected with clefts.

 A.

Single gene etiologies:
 There are almost 300 syndromes which have a
cleft of the lip and palate as a feature.
 Out of these, about 150 syndromes are due to
Mendelian inheritance of alleles at a single genetic
locus.
 Great strides have been made in the past few years
in mapping genes for such Mendelian disorders.
 About 50% : Autosomal recessive.
 40% : Autosomal dominant
 10% : X linked inheritance.
 Out of 150 Mendelian clefting syndromes, about
30 genes have been cloned.

 GL13
 7p13
 PAX3
 2q35
 SIX3
 2p21
 SOX9
 COL2A1

etc……


 B.

Chromosomal anomalies:
 Orofacial clefting is seen as part of phenotype in
wide variety of chromosomal rearrangements,
including trisomies, deletions, duplications, microdeletions or cryptic rearrangements.
 E.g. deletion of 4p (Wolf-Hirschhorn Syndrome),
4q or 5p (Cri-du Chat syndrome) trisomy of 13 or
18, etc.
 Role of small rearrangements such as
microdeletions, cryptic rearrangements in cleft
etiology is important as they are often transmitted
within families.

 Micro-deletion

of 2q11.2 is now known to be the
common etiology for three different syndromes
with cleft of secondary palate as a frequent
feature.
 DiGeorge Syndrome
 Velocardiofacial syndrome
 Conotruncal anomaly face syndrome.
One reason for mapping and cloning genes for
syndromic forms of clefting is to help develop
strategies for delineating the etiology of nonsyndromic form of clefting, which is by far much
more common.

C. Non-syndromic orofacial clefts:
 Early estimates of genetic contribution to
nonsyndromic orofacial clefts ranged from
12-20%, with remainder attributed to
environmental factors.
 Recent studies estimate the genetic
component to be much higher: 20-50%.
 Two general approaches: Large scale family
studies and Linkage studies with specific
genetic markers have been carried out.

 Though

there is consistent evidence from family
studies, of inheritance at a single major locus, the
hypotheses of multiple interacting loci or genetic
hererogeneity cannot be ruled out.
 Until recently, non syndromic clefting was
thought to follow the Multifactorial threshold
model, in which environment played an important
role.
 Recently, linkage analyses have shown candidate
loci on seven chromosomes (1, 2, 4, 6, 14, 17, 19)
to have positive linkage with CL/P, CP or both.
 In addition, genome-wide scans suggest that 3-14
genetic loci may be involved in non-syndromic
clefts of primary and secondary palate.

II. Teratogens:


 Cigarette

smoking appears to be correlated with
clefting and may act alone or synergistically with
TGF-α.
 Dietary supplements of folic acid are known to
reduce the frequency of neural tube defects;
possibly folic acid supplements may also reduce
the frequency of orofacial clefting.
 Mills et al found that prevalence of mutation of
methylene tetrahydrofoliate reductase was higher
in cleft populations than in the general population.
 Thus, impairment of folate metabolism may play a
role in the etiology of orofacial clefting.

III. Embryonic basis of orofacial clefting:
Parent sex cells unite
Zygote
formation
2 weeks of rapid proliferation directed
partly by Homeobox genes.
Bilaminar disc (2 distinct germ layers)
Gastrulation (during 3rd week)
Trilaminar disc ( 3 germ layers)
Neurulation (during 3rd week). PAX6, SHH,
FGF signaling
Neural plate is derived from ectoderm and
extends along long axis of the disc

 Problems

in development at this time may result in
midline neurologic and craniofacial malformations
such as holoprosencephaly, cycloplegis, neural
tube defects, midline orofacial clefts.

Neural crest cell formation, migration and
differenciation:
 The ectodermal-derived cells that are found in the
margins of the bilateral neural folds and the
transition zone between neuro-ectoderm and
epidermis.
 They migrate as mesenchyme into the embryonic
processes of the developing head and neck region,
giving rise to diverse neural, skeletal, connective
tissue, dental, cardiac, pigment cells.

 Their

migration is predetermined in part by
interactions with hindbrain neuromeric segments
called rhombomeres and paraxial mesoderm
segments called somatomeres.
 Timing and extent of NCC migration is dependent
on a complex patterning of inductive homeobox
gene (HOX, MSX) signaling.
 Deficiencies in NCC migration or proliferation
produce a variety of craniofacial malformations:
von Recklinghausen’s Neurofibromatosis,
Hemifacial microsomia, Orofacial Clefts,
DiGeorge and Treacher Collins syndromes.

Craniofacial development:
 Primitive craniofacial complex forms during week
4 post conception.
 A series of inductive events between
prosencephalon, mesencephalon,
rhombencephalon and migrating NCC’s helps to
form the five facial prominences (the frontonasal
and bilateral maxillary and mandibular
prominences)
 Movement and destination of NCCs into facial
primordia are controlled by a number of gene
familes including HOXa1, HOXa2, HOXb1,
HOXb3, HOXb4, SHH gene, OTX gene, GSC,
DLX, MSX, LHX, PRRX genes.

Fusion of facial processes


 Clefting

of upper lip and primary palate:
 The upper lip is formed mainly by contributions
from the medial nasal process and the maxillary
processes, and from lateral nasal process during 6th
week of development
 The lateral nasal processes contribute mainly to
the outer parts of the nose.
 Fusion of these processes requires critically timed
co-ordination of growth between the processes,
exact spatial localization, and apoptosis of the
epithelium that forms the transient nasal fin.

 Since

fusion of these processes also creates the
area of alveolar ridge containing central and
lateral incisors, abnormal development of the
nasal fin may be involved with clefts of the
primary palate.
 Primary palatal clefting occurs most commonly at
the incisive fissure that separates the lateral
incisors and the canine teeth. They may present
with dental displacement or dental agenesis, as
well as delayed ossification and decreased volume
of premaxilla and anterior basal bone of maxilla.

 Clefting

of secondary palate:
 The secondary palate is formed by the
fusion of the two lateral palatal processes
projecting medially from the maxillary
processes.
 Requires a complex interaction of palatal
shelf movements, critically timed growth
co-ordination between the processes, and
apoptosis of epithelium along the medial
margins of the palatal shelves.
 Begins at 8 ½ weeks in utero.

 Defects

of the secondary palate are expressed
as failures of elevation, failures of contact and
adhesion, or failures of fusion resulting in
clefts.
Factors which may limit shelf contact include:
 Delay in shelf movement to horizontal position.
 Reduced palatal shelf size
 Deficient extracellular matrix accumulation
 Delayed achievement of mandibular
prominence
 Head extension
 Abnormal craniofacial morphology

 Abnormal

1st arch development
 Tongue obstruction to shelf movement,
secondary to mandibular retrognathia
 Amniotic sac rupture leading to severely
constricted fetal head and body posture.


Epidemiology of Cleft Lip and Palate
 CL

+ P is etiologically distinct from isolated cleft
palate, except in cases where genetic isolates are
inbred and in syndromes like van der Woude’s
syndrome.
CL + P prevalence rates vary from population to
population.
 Indians: 1.25 / 1000.
 Manipal: 1.23 / 1000 (Valiathan, Dawoodbhoy I,
Oberoi S (JPFA 1996)
 White Caucasians: 1/ 1000.
 Japanese: 2.1 / 1000
 Blacks: 0.3 / 1000 (Lowest)
 Afghans: 4.9 / 1000

 CL+

P is more common in males
 More severe the defect, greater is the proportion of
males affected. (For CL+ P, the M:F ratio is 2:1,
while for CL alone the M:F ratio is 1.5:1)
 Unilateral cleft lip occurs twice as commonly on
the left side than on the right side.
 10-30 % of cases 10-30% of cases are associated
with skin bridges called Simonart’s bands.
 There is a positive family history in 40% of cases.
 Also there is an increased prevalence associated
with consanguinity and increased maternal age.

Isolated Cleft palate:
 This is less common as compared to CL+ P.
 Prevalence rate in Blacks as well as Whites is 0.4 /
1000.
 In Indians it is 0.46 per 1000 live births.(Valiathan
et al, JPFA 1996)
 Females are affected twice as commonly as males.
 Associated more commonly with congenital
malformations.
 There is a positive family history in 20% of cases.
 Not linked to maternal age.

 Variations

such as bifid uvula occur more
frequently than isolated CP (1 in 80 White
individuals.)
 Submucous cleft palate: 1 in 1200 to 1 in
2000 live births.


Classification of Clefts of Lip and
Palate
1. Davis and Ritchie (1922):
Congenital clefts were divided into 3 groups
according to the position of the cleft in relation to
the alveolar process.
Group I : Pre-alveolar clefts, which could be
unilateral, bilateral or median.
Group II: Post-alveolar clefts involving the soft
palate only, the soft and hard palate, or a
submucous cleft.
Group III: Alveolar clefts, unilateral, bilateral or
median.

2. Veau’s Classification ( 1931):
He suggested a classification divided into 4
groups:
Group 1: Cleft of the soft palate only.
Group 2: Cleft of hard and soft palate extending no
further than the incisive foramen, thus involving
the secondary palate alone.
Group 3: Complete unilateral cleft of soft and hard
palate, alveolar ridge and lip.
Group 4: Complete bilateral alveolar cleft , usually
associated with bilateral clefts of the lip.

3. Kernahan and Stark (1958):
They recognized the need for a classification based
on embryology rather than morphology.
The division between the primary and secondary
palates is the incisive foramen.
They divided clefts as follows:
A. Incomplete cleft of the secondary palate.
B. Complete cleft of secondary palate.
C. Incomplete cleft of primary and secondary
palates.
D. Unilateral complete cleft of primary and
secondary palates.
E. Bilateral complete cleft of the primary and
secondary palates.

 Pic

of kernahan and stark


4. Kernahan’s Striped Y Classification:
The incisive foramen is the reference point.
Stippling of the involved portion of the Y
provides rapid graphic representation of the
original pathologic condition, and lends itself
to computer graphic representation


Blocks 1 and 4: Lip.
Blocks 2 and 5: Alveolus.
Block 3 and 6: Hard palate
anterior to incisive
foramen.
Block 7 and 8: Hard palate
posterior to incisive
foramen.
Block 9: Soft palate.


5. Schuchardt and Pfeiffer’s

symbolic Classification
This classification makes use of
a chart made up of a vertical
block of three pairs of
rectangles with an inverted
triangle at the bottom.
The inverted triangle represents
the soft palate while the
rectangles represent the lip,
alveolus and the hard palate as
we go down.
Areas affected by clefts are
shaded on the chart.

6. Lahshal Classification (Okriens, 1987)
Lahshal is a paraphrase of the anatomic areas
affected by the cleft.
Based on the fact that clefts of the lip, alveolus and
hard palate can be bilateral, while clefts involving
the soft palate are usually unilateral
Areas involved in the cleft are denoted by
specifically indicating the alphabet standing for it.
For example, L - - S - - - stands for cleft of right
lip and the soft palate.
LA - S - - L stands for cleft of the right lip,
alveolus and soft palate together with left cleft lip.

7. American Cleft Lip and Palate Association
Classification (Harkins et al 1982)
1. Clefts of Prepalate: This is further subdivided
into clefts of lip, clefts of alveolar process,
which may be unilateral, bilateral or median.
Includes description of antero-posterior extent of
the defect in thirds.
2. Clefts of Palate: Further subdivided into clefts of
soft palate, hard palate, and includes description
of the extent of the cleft antero posteriorly in
thirds, and width in mm.
3. Clefts of prepalate and palate: Any combination
of clefts described under clefts of prepalate and
clefts of palate.

8.Tessier’s Classification of Unusual Craniofacial
Clefts (1976)
 Anatomic and descriptive classification system for
more complex orbitofacial clefts.
 Numbers are assigned to the site of clefting
depending on their relationship to the sagittal
midline.
 Both soft tissue and bony clefts are described.


Diagnosing Cleft Lip and Palate
 Cleft

lip and palate may be diagnosed by
prenatal ultrasound, which has become more
common because refinements of the diagnostic
tool provide images by which congenital and
developmental anomalies may be detected more
clearly.
 It gives the parents the opportunity to be
prepared for the birth of an infant with a facial
anomaly.
 Prenatal counseling provides patients with a
level of awareness and realistic expectations at
time of delivery.www.indiandentalacademy.com

 With

the help of prenatal ultrasonography 2223% of clefting cases can be detected.
 Cleft lip is easier to diagnose sonographically
than cleft palate.
 A recent study showed a 73% detection rate for
fetal cleft lip with ultrasonography.
 Prenatal detection of cleft palate with this
technique is much lower (1.4%)
 Detection rate for fetal cleft lip is improved
greatly if USG is performed after 20 weeks of
gestation.

Limitations of ultrasound technique for
diagnosing orofacial cleft include:
 Unfavorable position of fetus
 Hand or umbilicus overlying the face
 Maternal obesity
 Presence of multiple gestation
 Reduced amniotic fluid
 Prior abdominal surgery
 Additional fetal abnormalities

 Three

dimensional
ultrasonography imaging
is a new technique that
presents views of the
fetal face with greater
clarity than conventional
2D imaging.
 Its sensitivity in
diagnosing cleft lip and
palate is considerably
greater than 2D imaging.
(Johnson et al,
Radiology, 2000)

Advantages of Prenatal Cleft Diagnosis:
 Psychological preparation of patients
 Education of parents on management of cleft
 Preparation for neonatal care and feeding.
 Opportunity to investigate for other structural or
chromosomal abnormalities
 Increased choices for patients on whether to continue
the pregnancy.
 Possibility for fetal surgery
 Ability for the plastic surgeon to prepare a plan of
management, once the sonologist characterizes the
specific type of cleft.

 Disadvantages:
 Higher

maternal anxiety
 Potential for a decision to terminate the
pregnancy even in the absence of other
malformations.


Fetal surgery and Cleft lip and Palate
(From Papadopulos et al, Br J Plastic
Surg 2005)
 Open

fetal surgery has been performed in only a
few centers around the world, for life threatening
conditions of the fetus which were diagnosed by
ultrasound.
 Disadvantages include its invasiveness, induction
of premature labor and fetal death.
 Recent advances in endoscopic surgery may allow
keyhole access to the amniotic sac and reduce
morbidity of fetal surgery.
 As the techniques improve, fetal surgery could
also be applied to non life threatening
malformations. www.indiandentalacademy.com

 This

would be advantageous because wound
healing in the fetus takes place without the
formation of a scar or callus.
 In addition maxillary growth restrictions could be
prevented.
 In the last 2 decades extensive research has been
done on rabbits and sheep, with considerable
success in repair of surgically created clefts in the
fetus.
 However, the authors state that there are still too
many unsolved problems with intra-uterine
surgery, which make it ethically unjustifiable in
humans, at present.

Neonatal Care and Feeding Guidelines
 It

is important to address parental anxiety and
trauma
 Early contact and counseling
 Explanation of normal and altered anatomy and
physiology can guide toward successful feeding.
 The normal process of feeding involves sucking
and swallowing.
 In patients with cleft lip with alveolus, it is not a
problem and can be achieved with slight
adjustments such as placing a finger over the cleft.
This creates negative pressure inside the oral
cavity and results in effective swallowing.

 In

cleft palate patients this pressure cannot be built
up as air is drawn out through the defect to the
nose.
 A variety of nipples and feeding devices are
available which include; Lambs nipple, enlarged
cross cut nipple, Mead Johnson Cleft palate
nursing bottle.
Guidelines during feeding:
 The infant is positioned at 45-60 degrees angle to
decrease nasal regurgitation.
 The nipple is directed to the intact part of the
palate.
 The child is burped frequently because of
excessive air swallow.

 Adjust

the flow of milk to the ability of the child
to swallow.
 Observe the child for choking, cyanosis and
abdominal distension.
 Use feeding appliances if required.
Feeding appliances:
 These should be considered if other methods are
not successful in the first two weeks. They seal the
oro-nasal fistula and enable the child to suck by
negative intra-oral pressure.
 Can be constructed by an orthodontist, pedodontist
or prosthodontist or general dentist.

 Procedure:
 Alginate

impression: the tray should extend from
maxillary frenum at the cleft lip site, posteriorly past
the end of the alveolar ridges into the palate, and
laterally to include the lateral mucobuccal fold.
 In bilateral cleft applainces the finish line is not
placed in the anterior area. The bilateral segments are
supported uniformly from the lateral position which
allows premaxilla to drift posteriorly under lip
pressure.
 The cleft area and superior aspect of nasal passage
should be waxed out during fabrication of the plate.
 A small hole should be placed anteriorly in the plate
to tie a dental floss to the appliance.

Other considerations:
 Airway assessment
 Monitor weight gain
 Complete medical and genetic evaluation to
identify any syndrome
 Audiology and otology evaluation
 Plan surgical repair

Maxillary Orthopedics /
Naso-alveolar molding.
 Cleft

lip and palate can present with considerable
variation in severity and form.
 Generally, the wider more extensive clefts are
associated with more significant nasolabial
deformity.
 These clefts, deficient in hard and soft tissue
elements, present a significant surgical challenge
to achieve a functional and cosmetic outcome.
 From a surgical viewpoint, chances of achieving a
finer surgical scar, good nasal tip projection and
more symmetrical ,well defined nasolabial
complex would be better if the infant presents with
a minor cleft deformity.

A

fine scar forms when a surgical incision heals under
less tension.
 Thus, the principal objective of presurgical nasoalveolar
molding (NAM) is to reduce the severity of the initial
cleft deformity.
 This enables the surgeon and the patient to enjoy the
benefits associated with the repair of a cleft deformity
which is of minimal severity.
 Neonatal maxillary orthopedics is usually initiated during
the first or second week following birth, in absence of
other medical complications, and may be carried out by
the orthodontist, the pedodontist, or the prosthodontist.
 However, there is still a lack of agreement on early
management due to the lack of controlled studies that
show better outcome www.indiandentalacademy.com
with maxillary orthopedics.

Historical perspective:
 Numerous techniques have been documented over
the centuries to improve the position of cleft
alveolar segments.
 In 1686, Hoffman described the use of a head cap
with arms extended to the face to retract the
premaxilla and narrow the cleft.
 The modern concept of an intra-oral device to
reposition the cleft alveolar segments was
introduced by McNeil (Univ. of Glasgow) in
1950. Through a series of acrylic plates, the
segments were actively molded into the desired
position

 In

1969, Rosenstein introduced the concept of
passive control of cleft segments. Through the use
of a passive appliance, the continuous force of the
repaired lip could be used over time to attain a
more normal arch contour, with the cleft segments
coming together to form a butt joint.
 In 1975, Georgiade and Latham introduced a pinretained appliance to simultaneously retract the
maxilla and expand the posterior segments over a
period of days.
 Hotz (1987) described the use of a passive
orthopedic plate to slowly align the cleft segments
without retracting the maxilla. He felt that by the
age of 10, the face would grow forward into
appropriate balance with the premaxilla.

 During

the 1980s, original research for
molding cartilage was performed by Matsuo.
He recognized that the cartilage in the
newborn is soft and lacks elasticity. This was
attributed to high level of estrogen at the
time of birth, which in turn led to increased
hyaluronic acid levels
 Hyaluronic acid inhibits the linking of the
cartilage intercellular matrix, and may be
necessary to relax ligaments, cartilage and
connective tissue enabling the fetus to pass
through the birth canal.

 The

level of estrogen begins to decline
immediately after birth.
 Matsuo used a stent in the form of silicone
tubes to shape the nostrils.
 Grayson (1993) adapted the nasal stent to
extend from the anterior flange of an intraoral molding plate. Advantages of this
method are: Skillful application of force for
nasal molding, and no need for intact nasal
floor.

 The

popularity of maxillary orthopedics
was well accepted in the 1960’s and 1970’s,
to eliminate the need for subsequent
orthodontic treatment.
 Later reports suggested that although the
initial results of lip repair were easier to
attain with cosmetic improvement, there
was no long term benefit on the growth of
the midface and dento-alveolus.

 Additionally,

early or primary bone grafting
associated with maxillary orthopedics at time of
primary lip repair may have compromised the
long-term follow up of treated patients.
 Thus, the use of neonatal orthopedics before
primary surgical lip repair became a matter of
controversy between clinicians.
 The current perspective is that neonatal maxillary
orthopedics, when provided as an adjunctive
procedure to primary definitive lip repair, does
have presurgical benefits.

 In

general, appliances for use in cleft care can be
classified as follows:
 Presurgical and Postsurgical
 Active and passive.
 Extra-oral and intra-oral.
 Huebner

and Liu( Clinics in Plastic Surgery 1993)
advocated the use of passive acrylic appliances to
mold the alveoli under pressure from the repaired
lip.
 In case of unilateral cleft with severely rotated
cleft segment and collapse of arch, they use an
active appliance with a jackscrew prior to lip
closure.

Grayson’s Technique for Naso-alveolar
molding (Clin Plastic Surg 2004)
Objectives:
 Reduce the severity of
initial cleft deformity.
 Lip segments almost in
contact at rest.
 Symmetrical lower lateral
alar cartilages.
 Adequate nasal mucosal
lining.
 Uprighting of inclined
columella.

 In

infants with bilateral
clefts of lip, alveolus and
palate, aims are non-surgical
elongation of the columella,
centering of premaxilla, and
slow gentle retraction of the
premaxilla to achieve
continuity with posterior
cleft segments.
 Additional objectives are
reduction in width of nasal
tip, alar base.

Procedure:
 Heavy bodied silicone impession material is
used to take initial impression as soon after
birth as possible, when cartilage is plastic
and moldable.
 Infant is held upside down by surgeon and
the impression tray inserted into the oral
cavity, seated till impression material just
starts to extrude past posterior border.
 A stone model is poured, and a molding
plate fabricated on it with clear hard acrylic
lined with a thin layer of soft denture
material.

 Care

should be taken to relieve the plate in
area of labial frenum and other areas likely
to ulcerate.
 Parents are instructed to keep the plate in
full time and take it out for cleaning once a
day.
 The appliance is secured extra-orally to the
cheeks and bilaterally by surgical tapes,
with an orthodontic elastic band at one end.


 The

elastics loop over a
retention arm extending from
the anterior flange of the plate
at 45º to the horizontal.
 This prevents unseating of the
appliance; tapes are changed
once a day.
 The retention arm is positioned
at a point on the labial border
of the plate corresponding to
the junction of the cleft lip
segments, when pulled
together. Vertically it should
be at junction of upper and
lower lips at rest.

 Weekly

visits are required to modify the molding

plate.
 Closure of the alveolar gap brings the lip segments
together, reduces the nasal base width, and
introduces laxity of the alar rim.
 Care should be taken not to add the nasal stent
before achieving laxity of the alar rim, else
increase in nostril circumference may result.
 Elastics attached to the retention arm should exert
a force of approximately 2 oz. Retraction of
premaxilla as in bilateral clefts requires higher
force levels.

 Lip

taping: At the 3rd visit, the parents are
instructed to place tapes to approximate the cleft
lip segments. Tape should be applied at the base of
the nose, on the non-cleft side first, then pulled
over and adhered to the cleft side.
 Philtrum and columella should be brought to the
midline.
 Note: Taping too low can cause undesirable
horizontal lengthening of the lip over time.
 Advantage: Lip taping provides some of the
benefits of a surgical lip adhesion without the
associated surgical morbidity, cost, and scarring.

 The

Nasal Stent: When the cleft alveolus is
reduced to 5 mm or less, the nasal stent is
added.
 The stent is made of 0.036 gauge round
stainless steel wire and takes the shape of a
swan neck.
 It is attached to the base of the retention
arm, extends forward and then curves
backward entering 3-4 mm past the nasal
aperture.

 As

the wire extends into
the nostril, it is curved
back on itself to create a
small loop for retention of
the intranasal portion of
the nasal stent.
 This is a hard acrylic
kidney shaped
component, with an added
layer of soft liner

 The

upper lobe enters the nose and gently lifts
the dome till moderate tissue blanching is seen.
 The lower lobe lifts the nostril apex and defines
the top of the columella.
 In the patient with bilateral clefts, there is a need
for two retention arms and two nasal
splints.Fabrication steps are same as described
for a unilateral cleft.
 In addition, a horizontal “prolabial band” of soft
denture material is added to join the lower lobes
of the two stents, spanning the base of the
columella.

A

vertical tape from the
prolabial band extends
downward to engage
the retention arms with
elastics. This helps to
lengthen the columella
nonsurgically.


Complications associated with Naso-alveolar molding:
 Irritation of oral mucosal or gingival tissue.
 Heavy application of force by upper lobe of nasal stent,
resulting in inflammation of nasal mucosal lining.
 Notching of alar rim due to incorrect position or shape
of lower lobe of nasal stent.
 Irritation of cheeks due to adhesive tape. The tape
should be removed slowly or gently, or warm water may
be used. Else, a skin barrier can be used as a base for the
elastic attachment.
 Taping the arms too horizontally or with inadequate
activation may lead to posterior dislodgement of the
plate.
 A 5 mm hole can be placed in the palatal portion of the
plate to maintain airflow.

Recent studies on maxillary orthopedics:
Long term effects of naso-alveolar molding on
three dimensional nasal shape in unilateral clefts
(Maull et al Cleft Palate and Craniofacial J Sept
1999)
A study done on 10 subjects who underwent
presurgical orthopedics till the age of 4 months
when primary surgery was done. The authors
reported that presurgical naso alveolar molding
significantly increase the symmetry of the nose,
which is maintained long term into childhood.

A

Randomized Prospective Clinical trial of the
Effect of Infant Orthopedics in Unilateral Cleft
Lip and Palate: Prevention of Collapse of Alveolar
segments (Dutchcleft). Prahl et al, Cleft Palate and
Craniofacial J 2003.
 The authors compared two groups of infants
comprising 27 each. One group received infant
orthopedics, while the other did not.
 From the study it was concluded that infant
orthopedics in patients wuth UCLP did not
facilitatate contact between maxillary segments,
nor did it prevent collapse of alveolar segments.

References:
 Marazita

M, Mooney M. Current concepts in the
Embryology and Genetics of Cleft Lip and Cleft
Palate. Clinics in Plastic Surgery 2004; 31(2):
125-140.
 Valiathan A, Dawoodbhoy I, Oberoi S. Incidence
of cleft lip and palate in Manipal.- A live birth
study.Journal of Pierre Fauchard Academy 1996;
10: 15-20.
 Huebner and Liu. Maxillary Orthopedics. Clinics
in Plastic Surgery 1993: 723-741.
 Johnson DD, Pretorius Dh, Budorick NE et al.
Fetal lip and primary palate: 3D versus 2D
ultrasonography. Radiology 2000;21: 236-250.

 Johnson

N, Sandy JR, Prenatal diagnosid of cleft
lip and palate. Cleft Palate and Craniofacial J
2003;40: 186-194.
 Maull D, Grayson B, Cutting C, Brecht B,
Bookstein F. Long term effects of naso-alveolar
molding on three dimensional nasal shape in
unilateral clefts. Cleft Palate and Craniofacial
Journal 1999;36(5): 391-397.
 Prahl C, Kuipers Jagtman A, Vanthoff M, Prahl
Andersen B. A randomized Prospective Clinical
trial of the Effect of Infant Orthopedics in
Unilateral Cleft Lip and Palate: Prevention of
Collapse of Alveolar segments (Dutchcleft). Cleft
Palate and Craniofacial Journal 2003; 40(4): 337342.

 Papadupoulos

N, Papadopulos M, Kovacs H.
Foetal surgery and cleft lip and palate: Current
status and new perspectives. Br J Plast Surg 2005;
58:593-607.
 Grayson B, Maull D. Nasoalveolar molding for
infants born with clefts of the lip, alveolus, and
palate. Clinics in Plastic Surgery 2004;31(2): 149158.
 Emery and Rimoin’s Principles and Pracctice of
Medical Genetics. Rimoin, Connor, Pyeritz, Korf.
4th Edn, Churchill Livingstone, 2002.
 Orthodontics: Current Principles and techniques.
TM Graber, RLVanarsdall Jr, 4rd edn, Mosby,
2005.

 R.E.

Moyers. Handbook of Orthodontics 4 th
edn. Year Book Medical publishers 1988.
 Proffit WR. Contemporary Orthodontics. 3 rd
edition. Mosby, 2000.


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Leader in continuing dental education


Management of cleft lip and palate 1. /certified fixed orthodontic courses by Indian dental academy

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