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2
1 Orofacial Clefting
150seconds an infant is born with an orofacial
cleft which amounts to about 210,000 children
per year [13].
Cleft lip accounts for about 25% of all clefts,
and combined CL/P constitutes about 45%. The
occurrence of cleft lip seems to be more frequent
and more severe in boys than in girls. Unilateral
clefts tend to be more common than bilateral
clefts, with a ratio of 4:1. About 70% of unilateral
cleft occurs on the left side of the face. Syndromic
clefts account for about 50% of the total cases,
and more than about 300 syndromes have been
described [6].
1.3 Clinical Implications
CLP is one of the most common birth defects that
pose signicant medical, psychological, social,
and nancial implications on the affected families. Signicant functional morbidity is associated with CLP in addition to cosmetic
disgurement. Difculty in speech, swallowing,
and feeding difculties, hearing loss and recurrent ear infections are a few to mention [12, 14].
In underdeveloped countries, CLP can be
associated with signicant morbidity due to a
lack of health care facilities. Spoon-feeding was
unheard of, and there were no visiting doctors or
health care workers to educate parents on how to
feed the infants [15–17]. Hence babies born with
cleft deformities in rural areas mostly died within
a few days after birth due to starvation.
1.4 Impact ofOrofacial Cleft
inPerinatology
Children born with orofacial cleft have signicantly higher mortality in the rst 2 years of life.
A multidisciplinary approach to orofacial clefting is accepted all over the world. The team consists of plastic surgeons, maxillofacial surgeons,
otolaryngologists, speech therapists, audiologists, orthodontists, psychologists, health care
workers, and specialist nurses. The plan for treatment includes primary surgery for defect closure,
speech therapy and an orthodontic plan. Later,
secondary and tertiary surgeries to rene the initial surgical results may be planned.
1.5 Global Burden ofDiseases
Fortunately, children who have access to timely
cleft care rarely suffer lasting disabilities due to
orofacial cleft [4]. However, access to timely
cleft care varies considerably worldwide, resulting in disparate rates of death and disability
between children in high-income and low- and
middle-income countries [12, 18]. In developing
parts of the world, there is a lot of health disparities and inequality in the management of OFC
patients as there is a high number of affected
cases.
Majority of children born each year with an
orofacial cleft are from developing countries.
Most of the affected children are born in rural
areas where medical care is usually substandard,
and in the absence of any intervention, the mortality due to orofacial cleft is very high. In parts
of the world where there are ample poverty and
deprivation levels, the infant with an orofacial
cleft tends to be neglected [15–17].
Children born with an oral cleft in a community where clefts carry a signicant stigma or in a
community without access to cleft care are prone
to abandonment [5]. The global burden incurred
from OFCs in terms of physical morbidity, health
care expenses, emotional distress, and social dysfunction are signicant for affected individuals,
their families and overall society [6].
In this era, good prenatal ultrasound standards
include screening for cleft lip and in the future,
we might achieve a detection rate as close to
100%. Increased detection rates are possible
with the help of newer techniques, constant
innovation in ultrasound technology and a regular process of teaching and research in this
area.
If the majority of these clefts are detected
prenatally, then they can be referred to multidisciplinary counseling teams, which would lead to
a real improvement in the follow-up of affected
families [19]. Nutritional, environmental, and
familial aspects can be taken into account for
References
3
pregnancy planning which has been shown to
have a protective effect for prevention [18].
References
1. Pereira AV, Fradinho N, Carmo S, de Sousa JM,
Rasteiro D, Duarte R, Leal MJ. Associated malformations in children with orofacial clefts in Portugal:
a 31-year study. Plast Reconstr Surg Glob Open.
2018;6(2):e1635.
2. Wong FW, King NM. The oral health of children
with clefts-a review. Cleft Palate Craniofac J. 1998
May;35(3):248–54.
3. Hunt O, Burden D, Hepper P, Johnston C.The psychosocial effects of cleft lip and palate: a systematic
review. Eur J Orthod. 2005 Jun 1;27(3):274–85.
4. Carlson LC, Hatcher KW, Vanderburg R, Ayala RE,
Kabetu CE, Magee WP III, Magee WP Jr. A health
systems perspective on the mission model for cleft lip
and palate surgery: a matter of sustainability or responsibility? J Craniofac Surg. 2015 Jun 1;26(4):1079–83.
5. Stewart BT, Hatcher KW, Sengupta A, Burg RV.Cleftrelated infanticide and abandonment: a systematic
review of the academic and lay literature. Cleft Palate
Craniofac J. 2018 Jan;55(1):98–104.
6. Allam E, Windsor L, Stone C.Cleft lip and palate:
etiology, epidemiology, preventive and intervention
strategies. Anat Physiol. 2014 Jul;4(3):1–6.
7. Murthy J, Bhaskar LV. Current concepts in genetics
of nonsyndromic clefts. Indian J Plast Surg. 2009
Jan;42(1):68.
8. Rittler M, Liascovich R, López-Camelo J, Castilla
EE. Parental consanguinity in specic types of
congenital anomalies. Am J Med Genet. 2001 Jul
22;102(1):36–43.
9. Dixon MJ, Marazita ML, Beaty TH, Murray
JC. Cleft lip and palate: understanding genetic and
environmental inuences. Nat Rev Genet. 2011
Mar;12(3):167–78.
10. Antonarakis GS, Patel RN, Tompson B.Oral healthrelated quality of life in non-syndromic cleft lip and/
or palate patients: a systematic review. Community
Dent Health. 2013 Sep 1;30(3):189–95.
11. Van den Boogaard MJ, Dorland M, Beemer FA, van
Amstel HK.MSX1 mutation is associated with orofacial clefting and tooth agenesis in humans. Nat Genet.
2000 Apr;24(4):342–3.
12. Mossey PA, Little J, Munger RG, Dixon MJ,
Shaw WC. Cleft lip and palate. Lancet. 2009 Nov
21;374(9703):1773–85.
13. Shaw W.Global strategies to reduce the health care
burden of craniofacial anomalies: report of WHO
meetings on international collaborative research on
craniofacial anomalies. Cleft Palate Craniofac J. 2004
May;41(3):238–43.
14. Sinno H, Tahiri Y, Thibaudeau S, Izadpanah A,
Christodoulou G, Lin SJ, Gilardino M.Cleft lip and
palate: an objective measure outcome study. Plast
Reconstr Surg. 2012 Aug 1;130(2):408–14.
15. Petersen PE, Bourgeois D, Ogawa H, EstupinanDay S, Ndiaye C.The global burden of oral diseases
and risks to oral health. Bull World Health Organ.
2005;83:661–9.
16. Murthy J. Management of cleft lip and palate in
adults. Indian J Plast Surg. 2009 Oct;42(Suppl):S116.
17. Higashi H, Barendregt JJ, Kassebaum NJ, Weiser TG,
Bickler SW, Vos T.The burden of selected congenital
anomalies amenable to surgery in low and middleincome regions: cleft lip and palate, congenital heart
anomalies and neural tube defects. Arch Dis Child.
2015 Mar 1;100(3):233–8.
18. Bäumler M, Bigorre M, Mitrofanoff M, Faure JM,
Captier G, Picard A.Prenatal diagnosis of cleft lip and
palate-state of the art. In: Jaso N, d’Cruz AM, editors.
Cleft lip and palate: etiology, surgery & repair, and
sociopsychological consequences. New York: Nova
Biomedical; 2013.
19. Witt PD, Marsh JL.Advances in assessing outcome
of surgical repair of cleft lip and cleft palate. Plast
Reconstr Surg. 1997 Dec 1;100(7):1907–17.
Embryology andAnatomy
ofPalate
2
2.1 Development ofFace
Development of the human face begins from the
fourth week, and the external face is completed
by the sixth week of gestation. The development
of the palate occurs between the sixth to tenth
week of gestation followed by ossication of the
palate and completion of the soft palate by the
twelfth week. The palate subdivides the nasal and
oral cavities by the eighth week of gestation [1].
The oropharyngeal membrane is composed of
ectoderm externally and endoderm internally and
develops during the third week of gestation. This
membrane is seen at the site of the future face
between the primordium of the heart and the primordium of the brain.
The face develops from ve primordia that
appear in the fourth week of gestation, namely
Fig. 2.1 Embryology of
face and mouth:
Disintegrating
buccopharyngeal
membrane in the human
embryo at 4 weeks of
gestation
the frontonasal prominence, the two maxillary
swellings and the two mandibular swellings.
The disintegration of this membrane occurs during the fourth week of gestation to form the opening of the future oral cavity and the foregut
(Fig.2.1) [1].
The external face is formed from the frontonasal process and the mandibular pharyngeal arch
that is separated by the oropharyngeal membrane.
The tissues of the frontonasal process that cover
the forebrain are predominantly of neural crest
origin, and this gives rise to a pair of medial nasal
process. The tissues of the mandibular pharyngeal arch are of mixed mesoderm and neural crest
origin.
The medial nasal process contributes to form a
globular intermaxillary process and a pair of lateral nasal process. The rst pharyngeal arch gives
Frontonasal prominence
Nasal placode
Maxillary swelling
Disintegrating buccopharyngeal membrane
Mandibular swelling
nd
pharyngeal arch
2
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021
L. R. Selvaraj, T. Ziyaullah, First and Mid Trimester Ultrasound Diagnosis of Orofacial Clefts,
https://doi.org/10.1007/978-981-16-4613-3_2
5
6
y process
2 Embryology andAnatomy ofPalate
rise to a pair of mandibular processes and a pair
of outgrowths of the arch, which are the maxillary processes. This later gives rise to a pair of
palatal processes.
Paired maxillary processes develop simultaneously at the base of the rst pharyngeal arch,
which grows both ventrally and medially to surround the future oral cavity. The maxillary processes grow rapidly to meet the lateral nasal
processes and then fuses with the lower extension
of the medial nasal processes. The lower exten-
sion is also known as the globular or intermaxillary process, and that later forms the philtrum
of the upper lip (Fig.2.2) [1].
The groove between two facial processes is
eliminated through a process of merging. For
example, in the process of merging of the two
medial nasal processes in the midline, the tissues
in the groove proliferate more rapidly than the
a
surrounding tissues causing the groove to become
shallow and then the groove disappears. Absence
of merging leads to the formation of facial cleft
which is a deep depression between the facial
processes.
2.2 Palate Formation
The development of the mammalian secondary
palate is a complex and critical event. Palate
embryogenesis has been the target of much research
with the long-term aim of rational prevention for
cleft palate. The palate anterior to the incisive
foramen is the premaxilla or the primary (primitive) palate and posterior to it is the secondary palate, which is formed by the palatal shelves.
Phylogenetically cleft palate is ancestral to the
intact palate, and secondary palate development
b
Medial Nasal process
Lateral Nasal process
Maxillary swelling
Mandibular swelling
c
Philtrum
Fig. 2.2 Development of the face. (a) Formation of
medial and lateral nasal processes from the frontonasal
prominence at 6 weeks. (b) The medial nasal processes
Intermaxillar
fuse at the midline to form the intermaxillary process at
7 weeks. (c) The intermaxillary process forms the philtrum of the upper lip at 10weeks
2.2 Palate Formation
7
appears to be absent in lower vertebrates. Vertical
growth of the palatal shelves is peculiar to mammals, and certain amphibians and birds have a
natural cleft palate [2]. True to the hypothesis
that “Ontogeny recapitulates Phylogeny,” the
secondary palate develops later in gestation following the formation of the primary palate.
2.2.1 Development ofthePrimary
Palate
The primary palate or the premaxilla develops at
the same time as the external face. After the contact of the medial and lateral nasal processes, the
medial nasal and maxillary processes come
together and pinch some epithelium between
them. This sheet of epithelium is composed superiorly by the future nasal epithelium and inferiorly by the future oral epithelium. The core of the
primary palate is formed by the continuous mesenchyme between the medial nasal and maxillary
processes.
The medial processes continue to grow and
fuse to form the intermaxillary process, which
will ultimately give rise to the philtrum and primary palate. As the upper lip and palate com-
plete their formation before initiation of
secondary palatogenesis, the nasal epithelium
continues to touch the oral epithelium behind the
primary palate. As there is anteroposterior
growth in the face, the primary palate soon
becomes too short to provide adequate separation between the oral and nasal cavity. Hence the
secondary palate now develops to separate these
cavities further [2–4].
2.2.2 Development ofSecondary
Palate
The four steps in secondary palate formation are
as follows
1. Initiation of palatal shelf formation
2. Palatal shelf elevation
3. Palatal shelf adhesion
4. Fusion of palatal shelf
By 7–8 weeks of gestation, the medial walls
of the maxillary processes produce a pair of thin
medial extensions called the palatal processes
or palatal shelves. The palatal shelves grow ver-
tically downwards and parallel to the lateral surface of the tongue before 8weeks (Fig.2.3a). The
growth in the stomodeum and the occurrence of
mouth opening reexes lead to the tongue being
withdrawn from between the vertical shelves.
This mechanical withdrawal of the tongue is
mediated by the functioning hyoglossus muscle
and neuromuscular jaw joint activity [5–7]. Due
to tongue withdrawal, there is an elevation of
palatal shelves.
Palatal shelf elevation occurs in a conducive
orofacial environment. During the period of shelf
elevation, there is almost no growth in head width
but constant growth in head height [8]. This
allows the palatal shelves to position themselves
above the dorsum of the tongue (Fig.2.3b).
Following elevation, the shelves proliferate
towards midline, eventually making contact with
each other. This contact at the medial edge epithelium initiates a molecular cascade of events
that leads to epithelial-mesenchymal transformation allowing mesenchymal fusion.
Fusion is the process by which two initially
separated facial processes, grow towards each
other, touch each other and then fuse in the
midline, e.g., formation of the secondary palate.
During the process of fusion, the epithelium
breaks down at the point where the two processes
meet [1].
Fusion starts at the incisive foramen and proceeds posteriorly to end at the uvula [8]. After
fusion, the mesenchymal condensation in the
anterior part of the secondary palate undergoes
intramembranous ossication from cranial neural
crest derived osteoblasts [9]. Posteriorly, myogenic differentiation of mesenchymal condensations gives rise to the musculature of the soft
palate.
At the same time as secondary palatogenesis,
the medial nasal processes and frontonasal prominence proliferate to form a midline nasal septum
[3]. The septum further grows caudally from the
roof of the nasal cavity and fuses with the palate
along the midline [1, 10, 11] (Fig.2.3c).
8
Nasal
Septum
alatal
abc
2 Embryology andAnatomy ofPalate
Palatine
Shelf
7th week
Tongue
Nasal Chamber
Palatine
Shelf
8th week
Tongue
10th week
Nasal
Septum
Tongue
Fused Palatal
Shelves
Fused P
Shelves
Fig. 2.3 Formation of the secondary palate and nasal
septum. The palatine shelves initially grow inferiorly on
either side of the tongue (a) but then rapidly rotate upward
Abnormalities in any of the abovementioned
steps of facial development can result in orofacial
clefting. The two most common types of orofacial
clefts are cleft lip and cleft palate. Cleft lip arises
from lack of fusion of the mesenchyme of the maxillary prominence and intermaxillary process. The
resulting cleft may range in severity from a minor
notch in the vermilion border to a complete separation of the lip from the philtrum and nasal cavity
[3]. Each site where merging or fusion occurs
during the development of the face and palate is a
potential site for facial or palatal cleft [1].
2.3 Anatomy ofPalate
The palate separates the nasal cavity from the
oral cavity, and the hard palate forms a rigid oor
of the nasal cavity. The palate is divided into hard
palate in anterior two-thirds and soft palate in
to join in the midline (b) where they fuse with each other
and also with the inferior edge of the nasal septum (c)
posterior one thirds. The hard palate consists of
the anterior most triangular premaxilla in the
midline, palatal processes of the maxilla on
both sides and horizontal plates of the palatine
bone posteriorly. They all fuse at the suture line.
The premaxilla holds the four incisor teeth.
The palatine process of the maxilla is situated
between the maxillary arches comprising most of
the hard palate and meets the palatine bones posteriorly. There are three important foramina in the
hard palate, namely the incisive canal, greater
palatine foramina and lesser palatine foramina for
the passage of the neurovascular bundle. The incisive canal is located at the anterior midline of the
maxilla posterior to incisor teeth. Many research-
ers have used the incisive foramen as a dividing
landmark to classify the types of cleft palate.
Median palatine suture lies between the pala-
tine processes of the maxilla and between the
palatine bones. Incisive suture lies between the
ygoid process medial plate
Pyramidal process
2.4 Anatomy ofVomer
9
palatine process of the maxilla and premaxilla.
Transverse palatine suture lies between the horizontal plates of the palatine bones and the palatine process of the maxilla. The posterior margin
of the hard palate is marked by the posterior nasal
spine in the center. The pterygoid process and
pyramidal process are seen laterally on either
side (Fig.2.4). The posterior margin of the hard
palate is an important anatomical landmark
that is visualized in ultrasound to assess the
integrity of the bony hard palate.
The posterior one-third of the palate is formed
by the soft palate, which is exible and mobile. It
consists of muscle bers, connective tissue, secretary glands lined by stratied squamous epithelium. Its anterior third is brous, middle third
muscular, and posterior third glandular. The soft
palate forms the roof of the oropharyngeal isthmus, and elevation of the soft palate effectively
closes the communication between the nasopharynx and oropharynx.
The borders of the soft palate are as follows:
superiorly, the posterior margin of hard palate, laterally it continues with the wall of pharynx, and the
lower border ends in a free conical projection
called the uvula. The uvula serves as the landmark
to evaluate the secondary palate in ultrasound.
2.4 Anatomy ofVomer
The vomer bone is one of the unpaired facial
bones and lies in the midline between the two
nasal cavities forming the posteroinferior parts
of the bony nasal septum. It is a thin at bone
trapezoidal in shape with two surfaces and four
borders (Fig.2.5). The superior border is thick
and articulates with the sphenoid bone. The
inferior border articulates with the medial
nasal crest of the maxilla and the palatine
bones.
The anterior border is the longest one and
articulates with the perpendicular plate of the
ethmoid in the upper half and nasal cartilage in
the lower half. The posterior short concave border does not articulate with any bone but separates the posterior choanae.
The vomer bone ossies by intramembranous
ossication during the ninth week of intrauterine
life. The vomer is visible radiologically at about
11 weeks. The vomer is known to play an
essential role in the anteroposterior development of the palate. The vomer is almost isolated
from the maxilla in cases of a cleft in the secondary palate, which leads to loss of maxillary forward growth.
Fig. 2.4 Hard palate:
Inferior view Line
diagram showing the
bony components of the
palate and suture lines.
Brown shaded portion
indicates the visible
bony posterior edge of
the palate in ultrasound
Incisive fossa
Incisive suture
Median palatine suture
Transverse palatine suture
Posterior nasal spine
Pter
Pterygoid process lateral plate
Vomer
10
2 Embryology andAnatomy ofPalate
Fig. 2.5 Line diagram
illustrating the
anatomical relationship
of vomer bone. FB
Frontal bone, FS Frontal
Sinus, NB Nasal bone,
SC Septal cartilage, MP
Palatine process of
maxilla, LP Lateral
process of palatine bone,
HP Horizontal process
SS
of palatine bone, SB
Sphenoid bone, VB
Vomer bone, EB
Ethmoid bone, SS
Sphenoid sinus, CG
Crista galli
SB
References
1. Moss-Salentijn L, Edwin SR.Larsen’s human embryology. 3rd ed. NewYork: Columbia University; 2002.
p.352; pp.365–371; 398–404
2. Ferguson MW. Palate development. Development.
1988;103(Supplement):41–60.
3. Tarr JT, Lambi AG, Bradley JP, Barbe MF, Popoff
SN.Development of normal and cleft palate: a central role for connective tissue growth factor (CTGF)/
CCN2. J Dev Biol. 2018 Sep;6(3):18.
4. Li C, Lan Y, Jiang R. Molecular and cellular mechanisms of palate development. J Dent Res. 2017
Oct;96(11):1184–91.
5. Wragg LE, Smith JA, Borden CS.Myoneural maturation and function of the foetal rat tongue at the time
of secondary palate closure. Arch Oral Biol. 1972 Apr
1;17(4):673–82.
6. Humphrey T. The development of mouth opening
and related reexes involving the oral area of human
fetuses. Ala J Med Sci. 1968;5:126–57.
FB
FS
CG
NB
EB
SC
VB
HP
LP
MP
7. Humphrey T.The relation between human fetal mouth
opening reexes and closure of the palate. Am J Anat.
1969 Jul;125(3):317–44.
8. Diewert VM.A quantitative coronal plane evaluation
of craniofacial growth and spatial relations during
secondary palate development in the rat. Arch Oral
Biol. 1978 Jan 1;23(8):607–29.
9. Kim S, Lewis AE, Singh V, Ma X, Adelstein R, Bush
JO.Convergence and extrusion are required for normal fusion of the mammalian secondary palate. PLoS
Biol. 2015 Apr 7;13(4):e1002122.
10. Sadler TW. Langman’s medical embryology. 12th
ed. Philadelphia, PA: Wolters Kluwer/Lippincott
Williams & Wilkins; 2012. p.275–82.
11. Schoenwolf GC, Bleyl SB, Brauer PR, Francis West
PH.Larsen’s human embryology. 4th ed. Philadelphia,
PA: Churchill Livingstone/Elsevier; 2015. p.568–71.
Classication ofOrofacial Clefts
3
Classication of cleft lip and palate is difcult
due to the phenotypic diverse variations in the
form, size, and extent of cleft [1]. There is a need
for a universally accepted classication system
for international communication. Several classications have been proposed, and some have
been based on morphology and others based on
embryology [2–7].
Kernahan and Stark, in the nineteenth century
itself, opined that “If the future is to bring any
increase in our understanding of the cleft lip and
palate problem, a uniform method of classication is essential” [2]. The need for a universal,
simple, and practical classication system
understandable by clinicians and patients is the
need of the hour.
3.1 Classication ofCleft Lip
andPalate
Clefts are classied as either non-syndromic or
syndromic. In non-syndromic conditions, there
are no other physical or developmental anomalies
besides the orofacial cleft [8]. More than 350
Mendelian disorders and uncategorized syndromes are known to be associated with syndromic clefts [9]. Most often, CLP is
non-syndromic, and only 10% of infants born
with cleft lip and palate will have an associated
syndrome. Thirty percent of affected infants with
cleft lip alone will have an identiable associated
syndrome, and 50% of infants with isolated CP
will have associations [10].
Davis and Ritchie proposed a simple system
using the alveolar process as a dividing line for
their categorization: Group I includes cleft
involving the prealveolar process (labial cleft),
Group II includes cleft of the postalveolar process (clefts affecting the palate), and Group III
includes cleft involving the alveolar process [4].
A much detailed classication, including 16
distinct morphological forms of cleft palate with
or without cleft lip, was proposed by Brophy [11]
(Fig.3.1). This was followed by Veau’s greatly
simplied classication of palatal clefts, which
consisted of four morphological forms as quoted
below: “I) Clefts of the soft palate. II) Clefts of
the hard and soft palate, up to the incisive foramen. III) Clefts of the soft and hard palate extending unilaterally through the alveolus. IV) Clefts
of the soft and hard palate extending bilaterally
through the alveolus” [5].
Fogh-Andersen used the incisive foramen as
the embryologically sound dividing line and further rened the denition of an isolated cleft palate [12, 13]. The simplest classication system
for recording cleft lip and palate is ideally to
present a picture of the condition.
Kernahan, in 1971 published his modied
paper “The Striped Y-A Symbolic Classication
For Cleft Lip and Palate” based on his previous
research in 1958 [14]. The advantage of
Kernahan's “striped Y” classication is that it is a
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021
L. R. Selvaraj, T. Ziyaullah, First and Mid Trimester Ultrasound Diagnosis of Orofacial Clefts,
https://doi.org/10.1007/978-981-16-4613-3_3
11
12
1 2 3 4 5
6
11
7 8 9 10
12 13 14 15
3 Classication ofOrofacial Clefts
Fig. 3.1 Illustration of various types of cleft phenotype from Brophy etal. (Reproduced with permission from Elsevier)
visual process and remains the most uncomplicated and useful classication system.
Kernahan’s classication involves numbers from 1–9, depicted as a striped Y with the
affected involved segments shaded in the line diagram (1—Right lip, 2—Right alveolus, 3—Right
maxilla, 4—Left lip, 5—Left alveolus, 6—Left
premaxilla, 7—Hard palate, 8—Soft palate, 9—
Submucous cleft). Kernahan’s striped Y and the
subsequent modications by Elsahy (1973) and
Millard (1976) served to secure the position of
this classication as the predominant system
used in daily clinical practice [14–16].
Nyberg etal. proposed a simple classication
system that has ve categories, namely type 1:
cleft lip, type 2: unilateral CLP, type 3: bilateral
CLP, type 4: midline CLP, type 5: defects associated with amniotic bands or limb body wall complex. Type 1 clefts have a signicantly low rate
of anomalies. Type 2 and 3 clefts have an intermediate prognosis, whereas type 4 and 5 clefts
mostly have associated anomalies and poor
prognosis [17].
Harkins etal., from the American Cleft Palate
Association presented a classication based on
the same embryological principles as described