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14
Cleft Palate
Katelyn G. Makar
OVERVIEW
EPIDEMIOLOGY
Isolated cleft palate (CP) must be differentiated from cleft lip
and palate
CP
1 in 700 born with orofacial cleft
6 in 10 000 born with isolated CP
No ethnic variation in isolated CP
Syndromes and major congenital malformations more
common with isolated CP
DiGeorge syndrome
Most common
Cardiac defects
Chromosome 22q deletion
Stickler syndrome
Autosomal dominant
Mutation in type 2 collagen
Cleft lip and palate (see Chapter 13: Cleft Lip for further
information)
The vast majority of cleft lips arise spontaneously and are
not inherited
Ethnic variation in incidence
Asians (1 in 500)
Whites (1 in 1000)
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Blacks (1 in 2000)
Syndromic conditions less common (eg, Van der
Woude syndrome)
Predominantly sporadic
Always involves the primary palate, with variable
involvement of the secondary palate
NORMAL PALATE ANATOMY
Hard Palate (Bony Palate; Fig. 14-1)
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Figure 14-1 Anatomy of the hard palate.
A. Normal palatal anatomy with all soft
tissue removed. B. Palatal anatomy with
anterior (hard) palate soft tissue removed.
C. Palatal anatomy with soft tissue intact,
depicting neurovascular supply to palatal
muscles and to mucosa.
(From Dalley AF II, Agur AMR. Moore’s
Clinically Oriented Anatomy. 9th ed.
Wolters Kluwer; 2023. Figures 8.86 and
8.87B.)
Primary palate
Anterior to incisive foramen
Nasopalatine nerve
Sphenopalatine artery
Forms by fusion of median palatine processes (4-7
weeks’ gestation) and fuses with developing secondary
palate
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Failure of fusion on one side results in unilateral
cleft lip and alveolus
Failure of fusion on both sides results in bilateral
cleft lip and alveolus
Secondary palate
Posterior to incisive foramen
Forms by fusion of lateral palatal shelves of maxillary
prominences (8-12 weeks’ gestation)
Contains the greater palatine foramen
Greater palatine nerve and artery (vascular supply
for mucoperiosteal flaps)
Soft Palate (Velum; Fig. 14-2): mucosa and muscles involved
in velopharyngeal (VP) closure (with corresponding innervation)
Figure 14-2 Normal palate muscle
anatomy. Views of the palatal muscles
and their interaction with the pharyngeal
constrictors as shown from (A) inferior and
(B) posterior views.
(From Dalley AF II, Agur AMR. Moore’s
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Clinically Oriented Anatomy. 9th ed.
Wolters Kluwer; 2023. Figure 8.88.)
Levator veli palatini (LVP, CN X)
Lifts velum against posterior pharynx
Function: key muscle involved in VP closure
Normally oriented transversely across velum to
decussate with contralateral muscle in midline, but in
CP it is oriented longitudinally and inserts on posterior
hard palate
Tensor veli palatini (CN V)
Travels around the hamulus (sphenoid bone)
Tendon often divided in repair to further release LVP
(intravelar veloplasty [IVV])
Function: open eustachian tube
Palatoglossus (CN X)
Originates from the tongue, passes through anterior
tonsillar pillar, and inserts on anterior velum
Function: velar depression and glossal elevation
Palatopharyngeus (CN X)
Originates from posterior pharynx, passes through
posterior tonsillar pillar, and inserts on velum
Function: velar depression and retrodisplacement,
medialization of pharyngeal walls
Used for dynamic sphincter pharyngoplasty
Musculus uvulae (CN X)
Originates from posterior nasal spine
Inserts into the base of the uvula (uvula is mostly
devoid of muscle)
Function: works with LVP to elevate and extend velum
Superior pharyngeal constrictor (CN X)
Broad muscle that encloses naso- and upper
oropharynx
Originates from pterygomandibular ligament and
medial pterygoid plate
Inserts into posterior midline at pharyngeal ligament
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Function: medial/sphincteric movement of lateral
pharyngeal wall
Works with palatopharyngeus to form Passavant ridge
Vascular Supply
Greater palatine arteries are primary blood supply for
palatal mucosa
Pedicle for most mucoperiosteal flaps for hard palate
closure
Located in posterolateral hard palate
Lesser palatine arteries: supplies soft palate
Sphenopalatine artery
Ascending pharyngeal artery of external carotid
Ascending palatine branch of facial artery
Innervation
Hard palate: greater palatine (CN V) and nasopalatine
nerves (CN V)
Soft palate: lesser palatine nerve (CN V)
CP ANATOMY AND CLASSIFICATION
Variable Severity
Bifid uvula only
Submucous CP: intact mucosa with aberrant musculature,
only requires repair if patient demonstrates velopharyngeal
insufficiency (VPI)
Bifid uvula
Hard palate notch (palpable on exam)
Zona pellucida: pale midline mucosa
Soft palate cleft only (Veau type I)
Cleft of soft palate and bony palate up to incisive
foramen (soft and hard palate, Veau type II)
Complete cleft (a component of cleft lip and CP)
Primary and secondary palate
If unilateral complete, Veau III
If bilateral complete, Veau IV
Anomalous Insertion of Tensor and LVP
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Eustachian tube dysfunction and decreased middle ear
drainage
Recurrent otitis media leading to hearing loss
Myringotomy tubes
Placed in 95% of CP patients
Often at time of CP repair
*LVP muscles abnormally oriented in anteroposterior
direction instead of transverse direction, inserting onto
posterior margin of hard palate
PALATAL EMBRYOLOGY
Primary Palate (4-7 Weeks)
Lip, alveolus, nostril sill, and hard palate anterior to incisive
foramen.
Medial and lateral nasal prominences of frontonasal
process migrate and fuse to form median palatine process.
Median palatine process forms from fusion of bilateral
median nasal prominences and becomes premaxilla.
Secondary Palate (8-12 Weeks)
Includes hard palate posterior to incisive foramen and soft
palate.
Bilateral palatine shelves develop from medial maxillary
process.
Lateral palatine shelves hang vertically then lift horizontally.
Right lateral palatal process becomes horizontal before
left, which may explain higher incidence of left-sided
clefts.
Fusion takes 1 week longer in females, which may
explain increased incidence in females.
Fusion starts at incisive foramen and moves posteriorly.
When interrupted, CP results.
ETIOLOGY
Genetics
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CP: usually sporadic unless associated with a syndrome
CLP: polygenic, usually sporadic
Environment
Smoking: inconclusive but many studies have implicated its
role
Teratogens: alcohol, isotretinoin, topiramate increase risk
Obesity
Folic acid supplementation may be protective
Robin Sequence
Micrognathia leads to glossoptosis, which may cause CP
Lateral palatine processes may be unable to fuse due
to glossoptosis, causing CP
Clinical triad of micrognathia, glossoptosis, and airway
obstruction (do not have to have a CP to be diagnosed
with Robin sequence)
Conservative measures: prone positioning and
nasopharyngeal airway
Sleep study
Laryngoscopy to assess if other levels of airway
obstruction exist (tracheomalacia, bronchomalacia)
Consider mandibular distraction if single-level
obstruction at tongue base
INITIAL EVALUATION
Feeding and Weight Gain
Haberman or cross-cut nipple required due to poor oral
suction.
Palate repair is often performed at age 1 year but may be
delayed if the patient has multiple comorbidities or if
language is delayed.
Examination
Use penlight and tongue depressor.
Crying infant is easier to examine.
Place child supine and upside-down on parent’s lap.
Look for bifid uvula.
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Vomer will be visible above palate in cases of bilateral
CLP (Fig. 14-3A).
Figure 14-3 Von Langenbeck
palatoplasty. A. Preoperative
appearance of bilateral cleft palate,
surgeons view. Incisions are
planned along the cleft margins and
in the vomerine mucosa (midline).
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