Cleft lip and palate

 Cleft lip and palate are considered one of the
most common birth defects that possess
significant medical, psychological, social, and
financial implications on the affected individuals
and families.
Clefts have a complex etiology with both
genetics and environment playing a role.
Risk factors such as folic acid deficiency,
maternal age and maternal smoking have been 2

Orofacial clefts (OFCs) describe a range
of neonatal anomalies that involve
structures around the oral cavity and may
extend to the surrounding facial structures
resulting in extensive craniofacial
deformity.
The main categories are
•ISOLATED CLEFT PALATE (CP)
•CLEFT LIP WITH OR WITHOUT
CLEFT PALATE (CL/P).
Both types may present either isolated or
as part of a syndrome or other associated
abnormalities.

In addition to the aesthetic disfigurement, a child with cleft lip and/or
palate suffers substantial functional morbidity such as restricted
maxillofacial growth, speech anomalies, swallowing and feeding
difficulties, hearing loss and/or recurrent ear infections.
 Although not generally life-threatening, living with a cleft elicits a
significant health burden

patient
Pediat
-rician
Pedo
-dontist
Orthodontist
Oral
surgeon
Prostho
-dontist
Social
worker
ENT
Plastic
surgeon
Psychia
-trist
Speech
pathologist
Genetic
scientist

The orthodontist plays an important role in cleft lip and
palate care by providing necessary and timely dental and
orthopedic corrections.
Timing and sequencing of orthodontic care for cleft patients
can be divided into developmental periods, which were defined by
age and dental development should be considered as time frames to
accomplish specific objectives.

South Africa: 2006 study:
participants included 35 cleft patients and their families
Beliefs about the cause:
•God
•Ancestors punishing the mother
•Fate
•Genetics and family history of the condition
Beliefs of African Americans in US are similar (punishment for
something the mother has done, evil spirits, or displeasing a god)

Nigeria 2007 study regarding the beliefs of mothers
in Nigeria who had a child with a cleft lip or palate
Identified as (Muslim)= believed cleft was an act of God
Other beliefs included the mother going outside during an
eclipse while pregnant or laughing at someone with a cleft lip
Identified as (Christian)= believed cleft was due to evil spirits
or punishment from ancestors
Other beliefs included curses, not having enough food during
pregnancy or hereditary/environment factors

Asia:1990
paper discussing the beliefs of people of Asian/Pacific Island
descent living in the United States:
•Some view a cleft as a gift from God, while others view it as a
curse
•Many beliefs exist about the role different foods play in causing
or healing physical problems
Ex/ eating hare while pregnant could cause a cleft lip
•Members of some religions, such as Buddhism, may view a
cleft as part of a person's karma and not treat it at all.
•Beliefs regarding the cause include spirits, negative forces,
punishment for the actions of ancestors and eating certain foods

It is difficult to trace the etymologic history of CL/P. The condition is
as old as mankind itself, and it has been described in different ways by
the people of every era.
Hippocrates (400 BC) and Galen (150 AD) mentioned cleft lip, but
not cleft palate in their writings.
 Cleft palate – Fanco (1556)
 Repair of cleft lip – as early as 255-206 BC in China.
 Parea (1561), a French dentist was the first to put an obturator to fill
the cavity of cleft in order to facilitate eating and speech.
1
0

Le Monnier (1764), a French surgeon tried to repair cleft palate
surgically.
In following years, many attempts were made to close cleft palate
surgically but failed due to tension developed at median suture.
Fergusson (1844) and Van Langenback (1862) greatly improved
surgical techniques for repairing clefts.
1
1
H.K.Cooper(1930’s)
Introduced the integrated team concept and formed the Lanchester cleft
palate clinic

 Acc.to Fog- Anderson(1964),earliest records of
incidence of CL & CP were published by a
Russian, Frobelius in 1864.
 He found 118 cases among 180,000 children in a
hospital in St. Petersburg;an incidence of 1:1525
or 0.65 per 1000 births.
12

 Another study was done by Murray in 1904.
 He commented that it occurs with varing frequency
throughout the world .
 Among the uncivilized natives it depends upon their
religious beliefs which determines whether such child
will be put to death or allowed to live.
 Tunte in 1969 found a rise of 50% in cleft incidence
between 1901 and 1961 in Germany.
13

14
Incidences of the deformity in various countries were
tabulated by Fog-Andersen .

 An increase in the incidence is seen over a period
of time.
 This was due to decrease in operation mortality
because of improved anaesthetic techniques
16

Isolated cleft palate 30 -45%
Isolated cleft lip 20-30%
Cleft lip with cleft
palate
35-55%
17

Race Incidence per
1000
Sex variation
Negroes 0.5 > In females
Caucasian 1.0 > In males
Japanese 2.34 Cl > in females
&cl with cp more
in males
American 2.91
Indian 3.63 19

 According to Edwards (1961),Wehrung & Hey in
(1970),it appears that affected births are more in
early part of the year.
21

 No association is found between social class and
incidence of cl &cp.
 There is no implication of social and geographic
factors, though increased maternal age was held by
some to be significant.
22

 In order to address the challenge of both aetiology and
quality of cleft care, a co-ordinated multi-center
approach is being planned to address this through a
project entitled the “Indian collaboration on
craniofacial anomalies” with the acronym
“INDIACRAN”.
 This aims to adopt a comprehensive multi-disciplinary
approach and address (a) quality of care through inter-
center comparisons, and (b) aetiology through a gene-
environment interaction approach.
Mossey, P. and Little, J., 2009. Addressing the challenges of cleft lip and palate research in India. Indian journal of plastic surgery: official
publication of the Association of Plastic Surgeons of India, 42(Suppl), p.S9.

Cleft of lip is denoted as CL.
 Cleft of lip along with alveolus is denoted as CLA.
 complete cleft extending from a unilateral cleft lip
and primary palate passing through the mid-palatal
suture to the soft tissue uvula is denoted as UCLP(
unilateral cleft lip and palate).
Bilateral cleft of lip and premaxilla which extends
down to the bifid uvula is denoted as bilateral
complete cleft of the lip and palate (BCLP).
Isolated cleft of palate can be abbreviated as CPO.

1.) Heredity:
 Transmitted through a male as sex linked recessive gene.
 Predisposition for cleft lip is 40% while only 18-20% for cleft
palate.
 Much evidence supports the view that genetic factors are
associated with orofacial clefting.
 In twins with cleft lip-palate, concordance is far greater for
monozygotic twins (40%) than for dizygotic twins (4.2%).
(Wyszynski and Beaty 1996)

26
Bixler has divided oral clefts into 3 groups:
I. Syndromic- single gene disorders,chromosomal and
environmental factors.1% cl or cp & 85% cp.
II. Familial : includes 2 or more affected individuals in 1st ,2nd or
3rd degree relatives.25% cl/cp &12% of cp
III. Isolated or non familial: includes all kinds with only 1st person
affected in all relatives.

According to Bhatia, the two possible modes of transmission are—by
a single mutant gene producing a large effect, or by a number of genes
(polygenic
inheritance) each producing a small effect together creating this
condition.
More recently, researchers have expanded upon this concept and
reiterated that there are two forms of cleft.
The most common is hereditary, its nature being most probably
polygenic
(determined by several different genes acting together). In other
words, when the total genetic liability of an individual reaches a
certain minimum level, the threshold for expression is reached and
cleft occurs.
The second form of cleft is monogenic or syndromic and is
associated with a variety of other congenital anomalies. Since these
are monogenic, they are the

Multifactorial Threshold Hypothesis
Multifactorial inheritance theory implies that many
contributory risk genes interact with one another and
the environment and collectively determine whether
the threshold of abnormalities is breached, resulting
in a defect in the developing fetus. This theory
explains
the transmission of isolated cleft lip or palate, and it
is
extremely useful in predicting occurrence risks of
this
anomaly among family members of an affected
individual.

29
 University of Iowa researchers
have discovered that mutations
in FGF signaling pathway genes
contribute to cleft lip and palate.
The top figure shows the normal
sequence for a region of the
FGFR1 gene
 The bottom figure shows a
mutation in the same region for a
person with cleft lip and palate.
(Credit: University of Iowa, Jeff Murray
Lab/Bridget Riley)

Syndrome delineation involving orofacial clefting has been discussed and
reviewed by Cohen and Bankier (1991
 Van der woude Syndrome
 Treacher Collins Syndrome Autosomal Dominant
 Cleidocranial Syndrome
 Ectodermal Dysplasia
 Stickler’s Syndrome
 Roberts Syndrome
 Appelt Stndrome
 Christian Syndrome Autosomal Recessive
 Meckel Syndrome

Van der Woude syndrome (VDWS) is a genetic disorder characterized by the
combination of lower lip pits, cleft lip with or without cleft palate, and cleft palate
alone (CP).

Treacher Collins syndrome (TCS) is
a genetic disorder characterized by deformities
of the ears, eyes, cheekbones, and chin.
Complications may include breathing
problems, problems in seeing, cleft palate,
and hearing loss.

These patients have flexion
contractures of various joints,
micrognathia, scanty hair,
delayed growth, microcephaly
with or without mental
retardation, haemangiomas
especially in the head and neck
region, corneal opacity, ear
anomalies, and may have cleft
lip and palate.

Meckel syndrome (MKS) is a rare, lethal, genetic, multiple congenital anomaly
disorder characterized by the triad of brain malformation (mainly occipital
encephalocele), large polycystic kidneys and polydactyly, as well as associated
abnormalities that may include cleft lip/palate, cardiac and genital anomalies, central
nervous system (CNS) malformations, liver fibrosis, and bone dysplasia.

2.) Environmental Factors:
Usually occurs due to various influences during Ist trimester.
Teratogens responsible for birth defects have been reviewed by
Cohen (1997).
- Ethyl Alcohol- causes FAS (fetal alcohol Syndrome).
- Cigarette smoking appears to be correlated with clefting and
may act alone or synergistically with TGFa (Shaw et al 1996,
Kallen 1997)
- Anti seizure drugs.eg: diphenyl hydantion and

Malnutrition:
 Hypervitaminosis A: acute maternal exposure to 13-cis retinoic
acid during first trimester causes cell death in the pharygeal arch
leading to facial clefting. Vit A analogue used as an anti-acne
drug. Also proved by animal experiments.
 Folic Acid: Deficiency of folic acid affects virtually every organ
system. It affect the neural tube- neural crest cell migration and
differentiation. Tolarova and Harris (1995) .
 Wills et al (1999) studied the folate metabolism in cleft palate
and general population. Their results strongly suggested that
impairment of folate
 Anaemia and anorexia

Infection During Pregnancy:
Rubella infection during the first 3 months associated
with clefting.
Parental Age:
Shaw et al presented evidence that women above the
age of 35 had a doubled risk of having a child with
CL/CP above 39- tripled risk.
Consanguineous marriages- increased risk of CLCP in
child

•Most facial processes begin as two separate swellings separated
by a groove.
• Merging is the process by which the groove between two facial
processes is eliminated.
•The tissues in the groove “catch up” by proliferating more
rapidly than the surrounding tissues, causing the groove to
become progressively shallower until it smoothes out.
•Examples of merging are: merging of the 2 mandibular
processes (the former mandibular arch) in the midline, merging
of the 2 medial nasal processes in the midline, merging of lateral
nasal and maxillary processes, and the merging of mandibular
and maxillary processes.

•Fusion is the process by which two facial
processes, that were initially separated by a space,
grow together .
• An example of fusion is the formation of the
secondary palate where two facial processes grow
toward each other, touch each other and then fuse in
the midline. In fusion, unlike merging, the

• Development of facial
structures starts at the end
of 4th week
• 5 facial prominences
around stomatodeum
1. Unpaired frontonasal process
2. Paired maxillary
prominences
3. Paired
mandibularprominences
1
2

In following 2 weeks –
• The 2 medial nasal processes fuse in midline – upper lip
• Mandibular processes fuse in midline – lower lip
43
Thronton JB, Nimer S and Howrd P.The incidence, classification, etiology and embryology of oral clefts. SeminOrthod 1996;2:162-168

• The maxillary and lateral nasal process separated by nasolacrimal
groove/duct
• Frontonasal process – bridge of the nose
• Medial nasal process – tip of nose and philtrum of upper lip
• Lateral nasal process – ala of the nose
44
Thronton JB, Nimer S and Howrd P.The incidence, classification, etiology and embryology of oral clefts. Semin Orthod 1996;2:162-168

 As the medial nasal prominences merge with the maxillary
prominence, they form an intermaxillary segment.

The intermaxillary segment gives rise to :-
1. philtrum of the upper lip.
2. The premaxillary part of the maxilla
3. The primary palate.

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
A diagram of the hard and soft palates, as
they appear viewed from below. The area of the
front teeth corresponds with the primitive
palate, formed largely by the two medial nasal
processes. The shaded part of the palate (part
of the hard palate in front, and the soft palate in
the back) is formed by the two palatal
processes, which come together and fuse in
the midline. Clefts are possible at all “seams”
between the medial nasal processes and the
palatal processes and in the midline between
the two palatal processes.

• Secondary palate – formed from 2 outgrowths from maxillary
prominences – palatine shelves
• Fuse in midline at 7th week
• Incisive foramen – midline landmark between primary and secondary
palate
53
Thronton JB, Nimer S and Howrd P.The incidence, classification, etiology and embryology of oral clefts.

View of right half of a 6
week-old human embryo
showing early vertical palatal
shelf and lip forming
from the maxillary
( b ) Palatal shelves of a
7-week-old
human embryo showing
( c ) Palatal shelves of an
8-week-old
human embryo showing the
horizontal shelves approaching
each other and the
anterior primary
( d ) The nearly fused
palatal shelves of a
9-week-old human fetus.
site of primary palate
posterior edge of secondary
palate
anterior end of right shelf
The soft palate region
is still unfused

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.

When amniotic bands or strands of
connective tissue detach in utero from
the amniotic sac, which the fetus then
swallows, tethering the fetal face to
the amnion and tearing through the
face to form congenital disruption
clefts that are unrelated to embryonic
fusion lines.

( a ) unilateral cleft lip; b ) bilateral cleft lip
( c ) oblique facial cleft and unilateral cleft lip
( d )median cleft lip; ( f ) unilateral macrostomia

63
Allori AC et al. Classification of Cleft Lip/Palate: Then and Now. Cleft Palate–Craniofacial Journal 2016;53(1)
Group I: Prealveolar process cleft (clefts affecting the lip)
1. Unilateral (right/left: complete/incomplete)
2. Bilateral (right: complete/incomplete; left: complete/incomplete)
3. Median (complete/incomplete)
Group II: Postalveolar process cleft (clefts affecting the palate)
1. Soft palate
2. Hard palate

64
1. Unilateral (right/left:
complete/incomplete)
2. Bilateral (right:
complete/incomplete; left:
complete/incomplete)
3. Median (complete/incomplete)

65
A] Cleft lip
Class I : U/L notching of vermillion border,
not extending into the lip.
Class II : cleft extending into the lip,
but not including the floor of the nose.
Allori AC et al. Classification of Cleft Lip/Palate: Then and Now. Cleft Palate–Craniofacial

 Class III: extending into the floor of the nose.
 Class IV: any b/l cleft of the lip, whether
incomplete or complete.

B] Cleft palate
Class I : soft palate
Class II : soft/hard palate extending no further than incisive
foramen.
Class III: complete unilateral cleft, extending from uvula
to incisive foramen, then deviating to one side
Class IV: two clefts extending forward from the incisive
foramen into the alveolus.
67

68
1. Harelip (single or double)
2. Harelip with cleft palate
3. Isolated cleft palate
4. Rare atypical clefts, e.g., median cleft lip

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

70
A. Clefts of primary palate only
• Unilateral
— Complete
— Incomplete.
• Median
— Complete (premaxilla absent)
— Incomplete (premaxilla rudimentary)
• Bilateral
— Complete
— Incomplete
This is an embryological classification. The primary
palate denotes the lip, alveolar ridge and the premaxilla
and the secondary palate refers to the hard and the soft
palate which evolves from the maxillary shelves.

B. Clefts of secondary palate only
• Complete
• Incomplete, or
• Submucosal
C. Clefts of primary and secondary palate
• Unilateral (right or left)
— Complete or incomplete.
• Median
• Bilateral

72
1. Clefts of the prepalate (cleft of lip and embryologic
primary palate)
a. Cleft lip (cheiloschisis)
b. Cleft alveolus (alveoloschisis)
c. Cleft lip, alveolus, and primary palate
(cheiloalveoloschisis)
2. Clefts of the palate (cleft of the embryologic
secondary palate)
a. Cleft of the hard palate (uranoschisis)
b. Cleft of the soft palate (staphyloschisis or veloschisis)
c. Cleft of the hard and soft palate (uranostaphyloschisis)

73
4. Facial clefts other than prepalatal and palatal
a. Cleft of the mandibular process
b. Naso-ocular clefts
c. Oro-ocular clefts
d. Oroaural clefts

The LAHSHAL code splits the relevant parts of the
mouth into six parts:
 L – lip
 A – alveolus
 H - hard palate
 S - soft palate
 H - hard palate
 A – alveolus
 L - lip

 It is a symbolic classification representing the
most severe & extensive forms of CL &CP
deformity.
 By assigning numbers,classification and
retrieval of numbers can be achieved with
ease.
75

 The K and S system is the best available
system today.
 Future developments in classification will
probably include standardised terminology
and a universal coading system so that
computer storage and retrieval is possible.
76

77Allori AC et al. Classification of Cleft Lip/Palate: Then and Now. Cleft Palate–Craniofacial

MILLARD’S MODIFICATION OF THE
KERNAHAN’S
STRIPED “Y” CLASSIFICATION
Millard added two triangles over the tip of the ”Y” to
denote the nasal floor .
This increased the number of boxes to 11 as:
• Block 1 and 5—Nasal floor
• Block 2 and 6—Lip
• Block 3 and 7—Alveolus
• Block 4 and 8—Hard palate anterior to the incisive
foramen
• Block 9 and 10—Hard palate posterior to the
incisive foramen
• Block 11—Soft palate.
The unaffected areas were not shaded and the
shading of the triangles denoted the distortion of the
nose.

In 1967, the International Confederation for Plastic and
Reconstructive Surgery convened the 4th International
Congress in Rome.
Classification of the lip, alveolus, and palate (based on embryologic
principles):
1. Clefts of the anterior (primary) palate
2. Clefts of the anterior (primary) and posterior (secondary) palates
3. Clefts of the posterior (secondary) palate

Classification of rare facial clefts (based on topographical findings):
A. Median clefts of the upper lip, with/without hypoplasia or aplasia of the
premaxilla B. Oblique clefts (oro-orbital)
C. Transverse clefts (oroauricular)
D. Clefts of the lower lip, nose, and other very rare clefts.
Clefts within each of groups 1 to 3 received descriptions of all
involved structures (lip, alveolus, hard palate, and soft palate) by
laterality and severity (using the terms total or partial).

82
In 1973, Victor Spina of sao Paulo suggested a minor
revision of the International Classification’s first tier
with the intent to make the terminology more precise.
Spina argued that the terms anterior and posterior
describing palatal defects in group 1 and group 3,
respectively, raised the question, ‘‘anterior or posterior
to what?’’ (The answer, of course, is the incisive
foramen.) Accordingly, Spina renamed group 1 as preforaminal
clefts, group 2 as trans-foraminal clefts, and
group III as post-foraminal clefts.

 Group I: Preincisive foramen clefts
a. Unilateral
b. Bilateral
c. Medial
 Group II: Transincisive foramen clefts
a. Unilateral
b. Bilateral
 Group III: Post incisive foramen clefts
a. Total
b. Partial
 Group IV: Rare facial clefts

ELSAHY’S MODIFICATION OF
THE KERNAHAN’S STRIPED “Y”
CLASSIFICATION
•Elsahy modified the Striped “Y”
further by double lining the blocks 9
and 10 in the hard palate area and
used arrows to indicate the direction
of deflection in
complete clefts.
• He also placed a circle 12 under
the stem of the “Y” to represent the
pharynx and a dotted line from the Y
to circle 12 reflecting the
velopharyngeal competence.
• Another circle 13 was also added
to represent the premaxilla, and the
amount of its protrusion was
indicated by the dotted line with an
arrow.

90
• Prenatal ultrasound – 2D or 3D
• Prenatal counselling
• 22% to 33% rates for detecting facial
clefts
• 73% - fetal cleft lip
• 1.4% - isolated cleft palate
• Color Doppler ultrasonography can
also be used
Graber Vanarsdall and Vig. Orthodontics: Current Principles and

 Three dimensional sonography is a new
technique with more clarity, and viewing of
face in standard anatomic orientation.
93

94
- Non-invasive diagnostic tool
- Confirm fetal viability
- Determine gestational age
- Establish number of fetuses and their
growth
- Check placental location
- Examine fetal anatomy for detecting
malformations
Graber Vanarsdall and Vig. Orthodontics: Current Principles and Techniques. Elsevier 2012

Transabdominal US
- Not reliable till gestational age of
15 weeks
- Done at 20 or more weeks of
gestation
Transvaginal USG
- Earlier visualization (12 weeks)
- Better image resolution
- Greater specificity and sensitivity
95

Babcock and McGahan
(1997)
- Starts with coronal plane
- Assessment continues in
axial view
- Bilateral clefts: sagittal view
- Isolated clefts: axial view
96

97
- Psychological preparation for parents to have realistic
expectations
- Parent education for cleft management
- Preparation for neonatal care and feeding
- Opportunity to investigate other abnormalities
- Possibility of fetal surgery

98
- Emotional disturbance
- High maternal anxiety and
dysfunction
- Termination of pregnancy

Dental
Skeltal
Nasal
Feeding
Ear problems
Speech
Associated anomalies
100
*Jamal GA et al. Prevalence of Dental Anomalies in a Population of Cleft Lip and Palate Patients. Cleft Palate–Craniofacial
Journal,2010;47(4):413-20

 Congenital missing teeth (usually )
 Neonatal teeth
 Super numerary teeth
 Ectopically erupting teeth
 Peg shaped teeth
 Delayed eruption if teeth
 Enamel hypoplasia
 Microdontia / macrodontia
 Fused teeth
 Spacing / crowding
 Posterior & anterior cross bite

 The clefts involving the lip can result in lot of facial
disfigurement. The oro-facial structures may be
malformed and congenitally missing. Deformities of
nose can also occur thus esthetics greatly affected

Associated with disorders with of the middle ear affect hearing
 Diffeculties in language uptake speech.
 Speech defects CP patients
 Speech defects when sounds UL / BL CL patients are not
approximating
 When upper teeth maloccluded sounds th, F,V,S, ZE, SH.

 Maxillary
deficiency
 Mandibular
prognathism
 Class III
malocclusion
 Concave profile
57
*Ana Paula Ramos Bernardes da Silva, Beatriz Costa, Cleide Felício de Carvalho Carrara, Dental Anomalies of Number in The
Permanent Dentition ofPatients

5
8
 Oronasal fistulas
 Draining of oral fluids in nasal cavity and
vice versa
 Bottle, cup and spoon, tube feeding
 Infant held at 30-450 angle to aid
swallowing

Psychological stress due to their abnormal facial
appearance they have to put up with staring,
curiosity, pity et

TREATMENT SEQUENCE IN
CLEFT LIP AND PALATE
PATIENTS

Pre surgical
Orthopedics
1-4 weeks Repositioning palatal segment
facilitates lip repair
done less frequently now
Lip closure 8 to 12 weeks May be preceded by preliminary
lip adhesion as an alternative to
presurgical orthopedics
Palate closure 18 to 24 months Closing only the soft palate
initially an alternative, but one
stage closure of the hard and soft
palate is the usual procedure
Speech therapy 6 to 11 years Articulation errors often develop
as child tries to compensate for
cleft
Early orthodontics 7 to 8 years Usually incisor alignment and
maxillary transverse expansion
Alveolar grafting 6 to 10 years Needed before permanent canines
erupt; timing determined by stage
and sequence of dental
development

Comprehensive
orthodontics
11 to 14 years Class III elastics often very
helpful
Pharyngeal flap
surgery
9 to 19 years Only if required to overcome nasal
air leakage during speech
sometimes needed after loss of
lymphoid tissue in the
nasopharynx at adolescence or
following maxillary advancement
Orthognathic
surgery
17 to 19 years
Maxillary advancement, perhaps
combined with mandibular set-
back; not done until growth
completed except in rare instances
of severe psychosocial impact;
needed infrequently
Fixed
prosthodontics
17 to 19 years
Replacement of missing lateral
incisors: comprehensive treatment
only after growth completed

Goals and objectives of treatment are to :
1. Close vestibular and palatal oronasal fistula.
2. Restore physiologic continuity of the dental arch to enable
oral and dental health to be maintained
3. Provide bone for stability and continuity of the dental arch
(bone grafting)
4. Allow eruption of the permanent teeth or placement of dental
implants through bone graft.
5. Provide support for the lateral ala of the nose
6. Orthodontic alignment of teeth
7. Facilitate nasolabial muscle and soft tissue reconstruction
8. Establish functional nasal airway
9. Provide support for the lip
10. Prevent tooth loss caused by lack of periodontal bone
support

Divided the treatment into 8 phases:
• First stage – Prenatal phase
Complete history of gestation and maternal health,
counseling of the parents
Genetisist and other Social workers
6
7

• Second stage – at birth
Pediatrician discusses the condition with the parents,
Surgeon advises about the operative plan,
Dental specialists appraises the arch relationships
• Third stage – birth to 1 year
Pediatrican - advises about the feeding
Surgeon - carries out the lip closure (rule of 10)
Dental specialist - secures the models and radiographs
Speech therapist - discusses about the insufficiency and
incompetence of the pharyngeal seal 6
8

• Fourth stage – 1-2yrs
Pediatrican - takes care of the health and nutrition.
Surgeon carries out the closure of the hard palate 1:2
soft palate 1:6
Speech therapist - monitors the vocabulary and option
of a prosthetic replacement
ENT - monitors the ear condition.
• Fifth stage – 2-6 years
Orthodontist – arch relations, crossbites, developing
malocclusion
113

• Sixth stage – 6-12 years
Surgical corrections - secondary closure /repair of palate,
lip and the nose
• Seventh stage – 12-18 years
Surgical follow up on the lip and nose correction,
orthodontic
treatment
is
continued
• Eighth stage – 12 years onwards
Regular patient follow-up
114

1. No preoperative orthopedics.
2. Closure of Cleft lip in infancy – Millard procedure -3
months
3. Closure of the remaining isolated cleft – Von Langenbeck
-18 months.
4. Secondary operations 18-30 yrs of age.
115

1. Pre dental treatment-1-18 months of age.
2. Deciduous dentition 3-6 yrs of age-full eruption of
primary dentition.
3. Early mixed dentition 7-9 yrs- after or during
the eruption of permanent maxillary incisors.
4. Late mixed and early permanent dentition 9 ½ yrs
onwards
116

1. Infancy – before the initial surgical repair of the lips.
2. During late primary and early mixed dentition.
3. Late mixed and early permanent dentition.
4. Late teens (after completion of facial growth in conjunction
with orthognathic surgery).
117

• Birth to 1
year
Deciduo
us
dentitio
n
• 1 to 6
years
Mixed
dentitio
n
• 6 to 12
years
Permane
nt
dentitio
• 12
years
and adult
75

Orthodontic care is provided at 3 stages of childs
development:
 Presurgical orthopaedics for lip repair and palatal
surgery.
 Early mixed dentition orthodontics for correction
of gross irregularities causing functional
disturbances of occlusion.
 Orthodontic treatment of permanent dentition for
final correction and detailing of any malocclusion.
119

It is the active movement of maxillary
fragments prior to the surgical repair of cleft lip
in infants with complete clefts of lip & palate.
120

Secondarily it is the passive obturation of a
palatal cleft in infants ,which encourages the
normal growth of palatal shelves at a later
stage than usual thus resulting in narrowing of
cleft.
121

It is one of the most controversial area dealing
with treatment by applying PSOT.
122

Feeding obturator
 The feeding obturator is a prosthetic aid that is designed to obturate the cleft
and restore the separation between the oral and nasal cavities.
 It creates a rigid platform
 The obturator also prevents the tongue from entering the defect and
interfering with spontaneous growth of the palatal shelves.
 reduces nasal regurgitation,
 reduces the incidence of choking,
 also helps in the development of the jaws and
contributes to speech

INFANT ORTHOPEDICS
Infant orthopedics was pioneered by Burstone at Liverpool in 1950s.
Two movements were carried out- expansion of the collapsed segments and pressure
against premaxilla to reposition it posteriorly to its correct position.
Done by placing light elastic strap across the anterior segment that applies a contraction
force. In severe cases pin retained appliances may be required.
Also consists of a feeder plate with steel wires bent in
to hooks incorporated into the acrylic.
After active treatment for 3-6weeks,it is used a retainer.
Berkowitz reported the present consensus is that these
procedures offer less long term benefit than expected.
Hence now used in severely displaced premaxilla
cases.

The use of an external elastic force to reduce
premaxillary protrusion.
Head bonnet with attached elastic placed
against the protruding premaxilla causes it to
ventro flex with the fulcrum at the
premaxillary vomerine suture

• Hoffman (1678) – extraoral devices to retract
protruding premaxilla
• McNeil (1950s) – presurgical orthopaedic
• Hotz – premaxilla is normally placed, by age 10, face
grows downward and forward into balance with
premaxilla
126
*Samuel Berkowitz. Celft Lip and Palate. 2006. 2nd edition Page

• Grayson (1993) – first technique to correct the
alveolus, lip and nose in cleft infants
• Matsuo (1988)
- Research for cartilage moulding
- high maternal level of estrogen at the time of birth
correlates with an increase in hyaluronic acid, which
inhibits the linking of the cartilage intercellular matrix
7
7

• Matsuo used a stent, silicone tubes to shape the
nostrils
Grayson (1999) adapted his nasal stent to extend from
the anterior flange of an intraoral molding plate.
This new technique was named – “ Nasoalveolar
molding”
7
8

• Reduce severity of initial cleft deformity
• Columella – Nonsurgical lengthening (in bilateral clefts) and
uprighting (in unilateral clefts)
• Reduction in the width of the alveolar cleft segments until
passive contact of the gingival tissues is achieved.
7
9

8
0
• A heavy-bodied impression material is used to take the
initial impression as soon after birth as possible.
• Grayson and Maull(1999) held infant in upside down position to
keep the tongue forward which permitted fluids to draw off the
oral cavity when impression tray is placed
• Yang (2003) took the impression using a pre-trimmed customized
pediatric tray with the baby being held in the erect position,
by one of the parents

• Prashanth (2013), Mishra (2010) obtained impression
when the infant was awake in a proneposition on the
dental chair, the child is held on the lap of their parents
with no anesthesia.
• Dubey (2011) made impression of the cleft region upper
arch using
ice cream stick and impression compound.
131

• Plate – clear self-cure acrylic, trimmed with a denture
soft material
• 2–3 mm in thickness
• The retention arm – 40 degrees to get appropriate
activation and to avoid dislodgement of the NAM
plate from palate
132

• The nasal stent is added to the intraoral molding
plate when the cleft alveolar gap is reduced to
5mm or less
• Stent – 0.036-in gauge round stainless steel wire
• The intranasal portion is formed from hard acrylic,
covered with a thin layer of soft spongy acrylic
denture liner
133

• Elastics used are 0.25 inch and it should be
stretched about two times the diameter for
activation force of about 2 Oz
134

135

136
• Irritation of the oral mucosal or gingival tissue
• Ulceration of intraoral tissues
• The intranasal lining of the nasal tip can
become inflamed
• Skin irritation due to tape usage
• Parent compliance required
• Moulding plate may get dislodged and
obstruct the airway

137
• Short-term: the tissues are well aligned prior to
primary lip and nose repair
• Long-term:
• change in nasal shape is stable
• Reduced number of surgical revisions
• Reduction of treatment cost
• Shetty V et al (2017) - improves arch symmetry and
stability, and thus may prevent arch collapse in the long
term

8
8
• Goal: improve facial aesthetics by restoring nasal
and lip contour
• Timing: 3 to 6 months
• Millards “RULE OF TEN”
[term coined by Wilhelmmesen and Musgrave in
1969]
• 10 weeks (age)
• 10 pounds (weight)
• 10 gm/dl (Hb)

8
9
1. Tennison – Randall (Z Plasty)
2. Millards rotation advancement repair
3. Rose – Thompson straight line repair

 1920s -1930s – repair the defect by establishing
an anatomical continuity
 Priority of
treatment
- Improve speech
ability
- Dental function
- Facial aesthetics
 Importance of growth not
recognized140
*Berkowitz S. A Comparison of Treatment Results in Complete Bilateral Cleft Lip and Palate Using a Conservative Approach Versus Millard-Latham PSOT

 1950s – Two schools of
thoughts
9
2
• McNeil and Burston
• Align palatal segments
• Delay palatal closure till 5-
9 years of age
Presurgical
Orthopedics
• Led by Pruzansky
• Did not favour PSOT
• Palatal closure at 2-4 years
of age
Immediate
surgery

9
3
 Latham manipulated the palatally pinned
presurgical orthopaedic appliance –
mechanical expansion of the lateral palatal
segments is followed by the retraction of the
protruding premaxilla into position within the
arch
 Floor of nose is surgically closed
 Gingivoperiosteoplasty – migration of alveolar
bone cells –close alveolar gap

9
4
 Modified appliance – a premaxillary
stainless steel pin 7/10 mm in diameter
is inserted through the posterior stem of
the premaxilla.
 3 Oz force per side for premaxilla
retraction
 Premaxilla retraction and expansion
 8-14 days – premaxilla is positioned
within the palatal segments

14
4
• Graber (1950s) – surgery performed early, caused
severe midfacial deformity later
• Brophy, first proponent of surgical technique –
steel-clamp and silver-wire bony closure
technique
• von Langenback soft tissue procedure alone to
approximate lateral
halves of maxilla and reduce intermaxillary width

• Graber, Slaughter and Brodie (1950s-1960s) –
negative reports on surgical procedure done at an
early age
• “No palatal surgery at an early age” (before 12
months)
14
5
• James Scott (1956) – Sutural growth theory
• McNeil and Burston – adopted his theory –
functional paediatric prosthesis – palatal closure
between 5 to 9 years of age

• Melvin Moss (1968) – functional matric theory –
septal cartilage grows as a secondary response
• McNeil – Father of presurgical orthopaedics –
supported Scott’s theory
• Burston – premaxilla was normal and lateral palatal
segments were
retruded in face
• Presurgical orthopaedics + primary bone grafting
within first year of life
• Prusanky – opposed the same 14
6

14
7
• Control and modify postnatal development of maxilla
• Early alignment for better occlusion and function –
swallowing and speech
• Reduce middle ear infections

• Berkowitz (1978) – “State of art”
• Primary bone grafting – deleterious effects on
midface
• No evidence that PSOT normalize feeding,
tongue posture, swallowing or growth
14
8

14
9
• Same surgery performed can cause in different
results at different ages:
1. The cleft defect
2. The facial growth pattern
3. The surgical procedure

15
0
*Peterson S. The Relationship Between Timing of Cleft Palate Surgery and Speech Outcome: What Have We Learned, and Where Do WeStand in the
1970s
• Mid to late 1970’s – 18 to 24 months surgical palate
repair
• General trend of better speech results with earlier
ages at surgery
• Jolleys (1954) – approximately 90% of children
who underwent surgery before the age of 2 years
had good or excellent speech
• General age range for surgery – 6-9 months,

1980 – 1990s
• Kaplan (1981) – palatal closure between age of 3 to 6
months
• Dorf and Curtin (1982,1990) – importance
for phonemic development or articulation
age
• Greater discrepancy in speech performance
between the "12 months and younger group" and
the children operated on over the age of 12 months
• Ross (1987) – slightly better facial growth if surgery
done in the first year of life
15
1
*Peterson S. The Relationship Between Timing of Cleft Palate Surgery and Speech Outcome: What Have We Learned, and Where Do WeStand in the

1. Von Langenback
2. V-Y palatoplasty by
Veau
3. Furlow’s technique
4. Wardill Kilner’s push
back
10
3

 Velopharyngeal insufficiency is a disorder resulting in the improper closing
of the velopharyngeal sphincter (soft palate muscle in the mouth) during
speech, allowing air to escape through the nose instead of the mouth.
 During speech, the velopharyngeal sphincter must close off the nose to
properly pronounce strong consonants such as "p," "b," "g," "t" and "d."
 The two main speech symptoms of velopharyngeal insufficiency are:
 hypernasality and
 nasal air emission.

 Speech Therapy
 Some speech problems linked with VPI, such as mispronouncing words,
can be treated by speech therapy. Treatment focuses on teaching the
child the correct manner and place of articulation
 Sometimes an obturator is recommended to treat VPI.
 An obturator is like a modified dental retainer with a speech bulb or palatal
lift attached to the back. Each obturator is shaped uniquely to fit the
patient’s muscle movements.
 Speech Surgery: Palatoplasty
Sphincter pharyngeoplasty

 PRIMARY DENTITION STAGE :
 Treatment priorities is to correct crossbite by using removal plates or
lingual arch.
 To control or eliminate oral habits, functional shift or space loss after
premature loss of primary teeth
 Afetr the first phase, a removable retainer (atleast night time) is worn till
the next phase is begun.

 MIXED DENTITION
 A tentative decision on extraction of supernumerary teeth and overretained
teeth.
 Correction of cross bite- jack screw, RME, quad helix, Niti expanders
 Maintain space for proper eruption of teeth.
 Expand collapsed segment to improve surgical access to the graft site.
 Traumatic occlusion is eliminated in preparation of alveolar graft. (By
aligning offending tooth)
 Correction of jaw relationship- Face mask Therapy

 FACE MASK THERAPY
 Used in mild maxillary deficient cleft patient
 Orthopaedic forces for maxillary protraction
 Orthopaedic force 350-500 gm per side over 10-12 hr
/ day for an average of 12-15 months.
 Stability IS Questionable)
 Because of two reasons
 Counter pressure of a tight lip on the maxilla. Which inhibits its
growth
 Scarring in pterygo maxillary region after extensive tissue
mobilization for palatal closure

Rationale for bone grafting
 To restore physiologic continuity of arch for esthetic and hygenic replacement
 To provide bone for stability of dental arch and the premaxillary segment
 Bone is provided into which unerupted teeth may erupt.
 At the time of placement of graft, patent oronasal fistulas can be closed
 To allow orthodontic alignment of teeth
 To provide support for the lip and the alar base and the nasal tip.

Alveolar bone grafting divided in two types:
1) Primary alveolar bone grafting: done at the time of lip closure at around 10-12 weeks.
Common in 1950s. Causes hinderance in maxillary growth.
2) Secondary alveolar bone grafting: done after lip closure at later stage. This is can be
dived into three:
Early (2-5 years): performed in primary dentition. Rationale is to allow eruption of the
lateral incisor if present. Can affect growth of midface.
Intermediate (6-15years): performed in late mixed dentition time to allow the eruption of
the permanent canine in the graft. There is minimal interference in growth.
Late secondary alveolar bone grafting (adolescence to adulthood):
Aids in replacement of missing teeth with implants.

CURRENT CONTROVERSIES
THREE CONTEMPORARY CONTROVERSIES ARE:
1) Timing of grafting
2) The type of bone for alveolar grafting and donor site
3) Sequencing of orthodontic expansion.
Favor of 8-10 year of age (when canines about to erupt-one quarter to two
thirds of root complete)- Bergland etal
 Erupting tooth is a potent stimulus for bone formation.
 After tooth eruption is complete, it can be very difficult to induce the
formation of new bone.
 Prevents eruption into cleft-periodontal defect
 If placed after eruption of permanent teeth then chances of damaging
roots and resorption

EXPANSION:
If Expansion done before grafting, as after the graft mature and sutures fuse it is difficult
to expand maxilla later. Also Expanding the arch before grafting increases the size of
cleft and thus more area for placement of bone. But increased amount of bone required
and requires more soft tissue dissection for closure.
Expansion can also be done 6wks after grafting. It has a potential of stimulating
immature bone which may enhance graft survival

GRAFTING MATERIAL
Autogeous Advantages
 Iliac crest adequate quantity easily
condensed & placed
little donor site morbidity
 Tibia adequate volume
quality similar to iliac crest
 Rib for infants.
 Cranial bone inadequate quantity
less resorption
rapid vascularization
predictable quality
Allogenic grafts: it acts a scaffold into which new bone develops. Freeze dried
bone( increased chances of immune reaction, HIV infection, longer post operative
phase)
REVASCULARISATION OF GRAFT IS SLOW.

PERMANENT DENTITION :
Clinical feature of this stage :
 Medial displacement of the maxillary segment giving buccal cross bite
 Relative maxillary retrognathism, giving reversed incisal overjet.
 Deficiency of vertical growth of the upper jaw – REDUCED FACIAL HEIGHT
 rotation, malposition and hypodontia of teeth.
 Supernumerary teeth
 Accentuated curve of spee in maxilla
 Collapsed arch forms
 Poor oral hygiene and caries

ALIGNMENT OF INCISOR TEETH
 Incisors usually rotated and in crossbite. Corrected by means of fixed
orthodontic appliance.
CORRECTION OF LATERAL DIMENSION
 Lack of bony union between two sides of the maxilla, correction in lateral
dimension is relatively straight forward.
 By expansion appliance
Quad Helix Rapid Maxillary Expansion (RME)
Patients with clcp have class III malocclusion bcoz of maxillary deficiency (A-P and
Vertically), coupled with mandibular overclosure. In such cases use of class III elastics
after leveling and aligning will result in upper molar extrusion and favorable downward
and backward rotation of mandible.

Due to severe skeletal discrepancy, there is deterioration of esthetics and occlusion,
psychological implications leading to low self esteem, defective speech, oronasal
fistulas. Such cases require a combined orthodontic and orthognathic approach.
Size and position of maxilla is often a problem, thus maxillary advancement and
occasional down grafting needs to be performed. To correct the transverse problem
multiple segment LeFort I osteotomies may be required. For a bilateral CLCP three-
piece maxillary surgery (allows rotation of segments also) required while for unilateral
CLCP a two piece is sufficient.(Vlachos 1996)

Decompensation:
Usually requires 12 months.
Multiple segment maxillary osteotomies requires segmental treatment. The bracket
positions are altered for teeth adjacent to the osteotomy site.
Dental compensations in the lower arch also should be addressed ie alleviation of
crowding and proclination.
Gaps present in the arches due to the missing teeth must be either closed- stable result
and prevents reopening of oronasal fistula.
Proffit recommends overcorrecting the anterior crossbite in excess of positive overjet-
compensate for post surgical relapse.
In cases with an overjet of more than 8mm mandibular surgery (BSSO) also must be
considered. If not then over advancement of maxilla – unstable and speech defects.

 TIMING
 Never indicated in active facial growth
 Ideal time : age 18-19
Post surgical orthodontics: involves detailing of occlusion, closure of residual
spaces and maintenance of transverse dimension (overlay arches). Lasts for 4-6
months.
Retention: After removal of appliance retainers should be placed immediately.
Temporary vacuum filled retainers to be avoided-transverse control inadequate.
Soldered lingual arch preffered.

DISTRACTION OSTEOGENESIS
1903 . Dr. Gavril of Russia-Bone lengthening of leg.
It is a procedure that moves two segment of bone slowly apart in
such a way that new bone fills the gap.
 In distraction osteogenesis, a surgeon makes an osteotomy in an
bone and attaches a device known as distractor to both sides of
osteotomy.
 The distractor is gradually adjust over a period of days or week to
stretch the osteotomy so new tissue fills it.

Maxillary surgery required in 25-60% of cases with clcp.
(Ross and Subtenly)
Distraction osteogenesis allows soft tissue adaptation, including scar tissue.
Therefore doesn’t cause a problem with vello- pharyngeal insufficiency thus good
results. Distraction Of maxilla first proposed by Molina & Oritz-Monasterio(1998)
EXTERNAL DISTRACTORS
Advantage:
•Direction of force is well controlled
Dis advantage:
•Cranial surgery is required
•Esthetics are compromised

INTERNAL DISTRACTORS
Advantage:
•Esthetics
•Psychological relilef
Disadvantage:
•Difficult to control the direction of force
Prosthodontic Treatment:
It may be required in cases where replacement of missing teeth is essential. Removable or
fixed prosthesis may be given. It allows for improved speech and better esthetics.

CONCLUSION:
 Orofacial clefts have been identified to have a multifactorial etiology and
therefore require an interdisciplinary treatment approach ,comprising a
team effort in which an orthodontist plays a vital role and works hand in
hand with various specialists to provide the best possible line of treatment
with a single minded approach , that is to minimize if not eliminate the
physical, social and the emotional hardship that a person with orofacial
cleft presents.

17
2
1. Graber Vanarsdall and Vig. Orthodontics: Current Principles and
Techniques. Elsevier 2012
2. Jamal GA et al. Prevalence of Dental Anomalies in a Population of Cleft Lip
and Palate Patients. Cleft Palate–Craniofacial Journal, 2010;47(4):413-20
3. Ana Paula Ramos Bernardes da Silva, Beatriz Costa, Cleide Felício de
Carvalho Carrara, Dental Anomalies of Number in The Permanent
Dentition of Patients With Bilateral Cleft Lip: Radiographic Study, The
Cleft Palate-Craniofacial Journal. 2008;45(5):473-476.
4. Sommerland BC. Management of cleft lip and palate. Current Paediatrics
1994
5. Berkowitz S. A Comparison of Treatment Results in Complete Bilateral Cleft
Lip and Palate Using a Conservative Approach Versus Millard-Latham
PSOT Procedure. Semin Orthod 1996;2:169-184
6. Peterson S. 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 1996;2:185-191

7. Samuel Berkowitz. Celft Lip and Palate. 2006. 2nd edition Page number
451-8.
8. Waite P, Waite D. Bone Grafting for the Alveolar Cleft Defect. Semin
Orthod 1996;2:192-
196
9. Vlachos C. Orthodontic Treatment for the Cleft Palate Patient. Semin
Orthod 1996;2:197- 204
10. Posnick J. Orthognathic Surgery for the Cleft Lip and Palate
Patient. Semin Orthod 1996;2:205-14
11. Gardener LK, Parr GR. Prosthetic Rehabilitation of the Cleft Palate
Patient. Semin Orthod 1996;2:215-19
12. Dalston R. Velopharyngeal Impairment in the orthodontic
patients. Semin Orthod 1996;2:220-7.
13. Papadopulos NA. Foetal surgery and cleft lip and palate: current
status and new
perspectives. Br J Plast Surg. 2005 Jul;58(5):593-607
14. Chang J. Fetal plastic surgery: a review and preview. © Chang
www.thefetus.net/
17
3

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