Cleft palate

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1. CLEFT PALATE
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2. INTRODUCTION
Cleft - fissure, split or gap
Congenital abnormality that occurs in the
secondary palate (soft and hard palate). Its
occurrence may be unilateral, bilateral,
complete or incomplete.
Cleft Palate can be non-syndromic or it can
appear as a part of a syndrome or recurrence
pattern.
Cleft of hard palate - deficiency of mucosa and
bone.
Cleft of soft palate - deficiency of mucosa and
hypoplasia of muscles.
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3. INCIDENCE
Most common congenital deformities of the head and neck.
The incidence varies widely depending on geographic origin, racial and
ethnic group, environmental exposures, and socioeconomic status.
1 in 1,000 births in whites, 1 in 500 births in Asians and Native Americans,
and approximately 1 in 2,400 to 2,500 births in people of African descent
Results from the lack of fusion of the frontonasal and maxillary processes
during the development
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4. HISTORY
1552 - Dr. Houlier proposed suturing of the palatal clefts.
1564 - Dr. Ambroise Pare used obturators for palatal perforations.
1764 - Le Monnier, a French dentist, attempted the first palate closure.
1816- Dr. Carl Von Graefe was the person to perform the velar repair of
the cleft.
1828 - Dr. Dieffenbach first to close a cleft in the hard palate.
1859 – Dr. Bernhard von Langenbeck, the father of modern-day
palatoplasty performed the bipedicled mucoperiosteal flap for the repair
of a cleft palate.
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5. Veau (1931), Wardill (1937) and Kilner (1937) described the uni-pedicle
mucoperiosteal flap based on the greater palatine artery.
1944 - Dr. Schweckendiek advocated the use of a 2-stage cleft palate
closure.
The soft palate was closed early (4-6 months), with the closure of the hard
palate delayed until 4-5 years.
Done to improve velopharyngeal function during the initial speech
development
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6. Embryology
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7. Maxillary process fuse with medial and lateral nasal processes to form upper lip and primary
palate respectively
DEVELOPMENT OF PALATE
Development begins in 6th week
Palate is formed by contribution of
1. Maxillary process
2.Palatal shelves given off by maxillary process
3.Fronto-nasal process
Develops from-
1.Primary palate(from medial nasal process)
2.Secondary palate(from maxillary process)

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8. Cleft of palate occurs in number of ways:
 Defective growth of palatal shelves
Delayed or total failure of shelves to elevate
and attain a horizontal position
Post fusion rupture of shelves
Failure of mesenchyme consolidation
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9. ETIOLOGY
ENVIRONMENTAL FACTORS:
Advanced parental age,
Maternal smoking and alcohol consumption,
Intake of drugs [anticonvulsant (phenobarbital and phenytoin), retinoic
acid) Cortisone/ steroids, Mercaptopurine, Methotrexate, Valium during
pregnancy.
Intrauterine exposure to rubella.
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10. Genes

Transforming growth factors alpha and beta
(TGF alpha, TGF beta 2, TGF beta 3).
Retinoic acid receptor (RAR), the methylene
tetrahydrofolate reductase receptor (MTHFR)
and the folic acid receptor (FOLR1).
MSX-1 and MSX-2.
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11. ASSOCIATED SYNDROMES
Velo-cardio-facial syndrome,
Treacher Collins syndrome,
 Apert syndrome
Di George syndrome
Van der Woude (AD)
Pierre Robin Syndrome
Goldenhar syndrome
Fetal alcohol syndrome
 Fetal phenytoin syndrome
Fetal valproate syndrome
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12. CLINICAL MANIFESTATION
Feeding and nutritional problems
Speech problem
Hearing problem and ear infection
Cosmetic problems
Dental problems
Psychological problems
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13. DENTAL PROBLEMS
Congenitally missing teeth( mostly upper lateral incisors)
 Presence of supernumerary, neonatal and natal teeth
 Ectopically erupted tooth
Enamel hypoplasia
Microdontia, macrodontia
Fused teeth
Gemination, dilaceration
Tendency towards class III skeletal pattern
Posterior and anterior cross bite
Deep bite
Spacing/ crowding
Protruding premaxilla
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14. ESTHETIC PROBLEMS

 Facial disfigurement
Orofacial structures
can be malformed
and congenitally
missing
Nasal deformity

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15. CLASSIFICATION
DAVIS AND RITCHIE CLASSIFICATION
Group I- Prealveolar clefts involving only lips.
Unilateral
 bilateral
Median
Group II- Post alveolar clefts that comprises hard and soft palate
clefts upto the alveolar ridge
Group III- Alveolar clefts. Complete clefts involving the palate,
alveolar ridge and lips.
Unilateral
Bilateral
Median
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16. Kernahan’s stripped ‘Y’ classification
Block 1 and 4 – Lip
 Block 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
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17. Asok kumar RS OMFS

18. Veau’s classification

Group 1 – Cleft involving soft palate only
Group 2 - Cleft of hard and soft palate
extending upto incisive foramen
Group 3 – Complete unilateral clefts
involving soft palate, hard palate, lips
and alveolar ridge
Group 4 - Complete bilateral clefts
affecting the soft palate, hard palate, lips
and alveolar ridge

a
b
d c
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19. DIAGNOSIS
Prenatal ultrasound – 2D or 3D
Color Doppler ultrasonography
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20. ANATOMICAL CONSIDERATIONS
Based on the embryonic origin, the bony portion of the palate is divided into primary and
secondary palates.
The primary palate consists of premaxilla, alveolus, and lip, which are anterior to the incisive
foramen.
The secondary palate includes structures posterior to the incisive foramen, and these are
paired maxilla, palatine bones and pterygoid plates.
The following six muscles have attachment to the palate.
1.Levator veli palatini,
2.Superior constrictor pharyngeus,
3. Musculus uvulus,
4.Palatopharyngeus,
5.Palatoglossus and
6.Tensor veli palatini.
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21. Among these muscles, three muscles that appear to have the greatest contribution to
the velopharyngeal function are levator veli palatini, superior constrictor
pharyngeus and musculus uvulus.
 The levator veli palatini pulls the velum superiorly and posteriorly to oppose the
velum against the posterior pharyngeal wall.

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22. The medial movement of the
pharyngeal wall, attributed to superior
constrictor pharyngeus, adds in the
opposition against the posterior
pharyngeal wall to form the competent
sphincter

This abnormal insertion contributes to
the overall shortness of the palate and
levator sling cannot be created, may
result in inability of the palate to reach
the posterior pharyngeal wall and
achieve velopharyngeal competence.
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23. PREOPERATIVE CONSIDERATIONS
TIMING OF PALATAL CLOSURE
Timing of the surgical repair of lip and palate has been controversial among cleft
surgeons.
 In 1921, Sir Harold Gillies wrote, ‘CLOSE THE LIP EARLY AND REPAIR THE
PALATE PRIOR TO SPEECH’
The ultimate outcome to be aimed for the repair of a cleft palate is the development of
normal speech.
The speech outcome depends on the surgical technique and the timing of the palate
repair.
Performed between 12-18 months.
Ideally, one should consider the development of babbling as an indicator of the time to
reconstruct the palate.
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24. PRENATAL MEDICAL HISTORY

Familial history with clefts
Evaluation of family members should be undertaken to
assess any genetic factors.
Examination of child for congenital heart disease , limb
and ocular abnormalities
Diagnosis of cleft both syndromic and non syndromic.
PREOPERATIVE CONSIDERATIONS
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25. CONTRAINDICATIONS FOR CLEFT PALATE REPAIR:

Hemoglobin < 10 gm/dl
Asymptomatic, untreated malaria.
Malnourished children
Central neurologic disorder that prevents speech.
Upper respiratory infections.
Medical comorbidities conferring prohibitive risk as in valvular heart
disease

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26. GOALS OF CLEFT PALATE REPAIR
Reconstruct velopharyngeal competence.
Restore separation of oral and nasal cavities for improved feeding.
Restore Eustachian tube function
Produce anatomical closure of the defect.
Create an environment favorable for development of normal speech.
Minimize the maxillary growth disturbances and dento-alveolar
deformities.

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27. SURGICAL TECHNIQUES
Von Langenbeck’s bipedicle flap technique
Veau-Wardill-Kilner Pushback technique
Bardach’s two-flap technique
Furlow Double opposing Z-Plasty
Intravelar veloplasty
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28. Position of the patient
Supine with neck extended either
by keeping a pillow or a rolled
towel under the shoulder
 A head ring under the occiput
helps in stabilizing the head.
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29. Armamentarium
Cushing forceps
Palate dissector
Cronin Cleft palate elevator
Dingman mouth gag
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30. Blair periosteal elevator
No.1 Woodson periosteal elevator
Reynolds scissors Kilner scissors
Jeter-Woodson hard palate elevator
Cleft Palate Hook
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31. von Langenbeck procedure

Bipedicle mucoperiosteal flaps
Incising along the oral side of the cleft
edges and along the posterior alveolar
ridge.
 Mobilize the flaps medially with
preservation of the greater palatine
arteries and close in layers.
Disadvantage: Speech outcome is poor
because of inadequate retroposition
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32. PALATAL LENGTHENING-V-Y PUSHBACK-VEAU-WARDILL-
KILNER TECHNIQUE

Placing a V to Y incision and closure on the hard
palate.
The muscle closure is done as a separate layer.
 The velopharyngeal function is improved since
there is an increased palatal length.
DISADVANTAGE:
Creates a larger area of denuded palatal bone
anterolaterally and also associated with a higher
incidence of fistula formation
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33. Asok kumar RS OMFS

34. INTRAVELAR VELOPLASTY

In 1968 Braithwaite first described the dissection of the Levator Palatini muscle from the
posterior border of the hard palate, nasal and oral mucosa and posterior repositioning
Dissection and freeing of the abnormal attachment of levator palatini muscles and re-
approximation as a midline layer.
Excellent speech outcomes.
Lengthens the palate and
Restores the normal muscular
sling of the levator veli palatini.
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35. Double-opposing Z-plasties-Furlow’s
technique

Different lengthening
procedure of the palate due to
change in position of the velar
and pharyngeal tissues.
 Speech development was
excellent in this technique.
In wide clefts, this type of
closure may not be possible
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36. Asok kumar RS OMFS

37. VOMER FLAP
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38. TWO-FLAP PALATOPLASTY - (BARDACH
AND SALYER-1984)
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39. Asok kumar RS OMFS

40. Asok kumar RS OMFS

41. Postoperative management

NPO until 6 post-operative hours or the next day.
Hydration is maintained during this time with intravenous fluid.
Vital signs continuously monitored for 24-48 h.
 Arm splints and Arm restraints were also applied to prevent a child
from disrupting the wound by placing the fingers into mouth.
Oral feeding is initiated by spoon or drinking from cups.
The liquid diet is continued for 7-10 days with solid food to follow

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42. COMPLICATIONS
IMMEDIATE COMPLICATIONS
1.Haemorrhage
2.Respiratory obstruction
3.Hanging Palate
4.Dehiscence of the repair
5.Oronasal fistula formation
LATE COMPLICATIONS
1.Bifid uvula
2.Velopharyngeal Incompetence
3.Abnormal speech
4.Maxillary hypoplasia
5.Dental malpositioning and malalignment
6.Otitis media
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43. SECONDARY CORRECTIONS
Closure of palatal fistulae
Palatal fistulae must be considered functional complications related to the type of
primary repair.
The fistula may be present in front of, through or behind the alveolus or in the main
hard palate.
Symptoms
Increased nasalance in speech.
Regurgitation of fluids to the nose.
Halitosis.
Increased incidence of ear and paranasal sinus infections
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44. Asok kumar RS OMFS

45. CLOSURE BY TONGUE FLAPS

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46. CLOSURE BY TONGUE FLAPS
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47. VELOPHARYNGEAL INCOMPETENCE
Diagnosed as being unable to
raise the velum to meet the
posterior pharyngeal wall to seal
the nasal airway during speech.
Cleft of the soft palate prevent
the muscular action of the palatal
elevators
Presence of a palatal fistula or
fistulae
Submucous cleft palate
Neuromuscular abnormalities
(congenital or acquired)
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48. HYNES PHARYNGOPLASTY

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49. CLOSURE OF ALVEOLAR CLEFT

Alveolar bone grafting
The maxilla with cleft has a bony deficiency at the canine-lateral incisor region.
Lack of bone at the anterior maxilla results in:
Lack of bone for permanent canine eruption ..
Unequal distribution of the growth impetus of the premaxillar vomerine suture which leads
to:
a)Premaxillary protrubance and lateral segments collapse.
b)Midfacial growth retrusion.
c)Poor arch forms.
d)Inadequate alveolar bone.

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50. In order to prevent this ,the bone deficiency can be filled with bone or bone
substitutes. This concept of treatment is called alveolar bone grafting.
Depending upon the timing of this surgery, this treatment has been termed
Primary, Early secondary or Secondary alveolar bone grafting.
a)Primary bone grafting is performed in children younger than 2
years of age.
b)Early secondary bone grafting is performed between 2 and 5 years
of age.
c) Secondary bone grafting is performed greater than 5 years of age.

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51. SECONDARY ALVEOLAR BONE GRAFTING

Stabilisation of maxillary arch
Closure of vestibular and palatal oronasal fistulae
Provision of bone of sufficient quantity and appropriate
quality for the eruption of permanent canine
Provision of support for the soft tissue nasal base and
reconstruction of the hypoplastic piriform aperture
GOALS OF SECONDARY ALVEOLAR BONE GRAFTING

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52. Provision of suitable bony architecture of the premaxilla
and anterior face of the maxilla on the cleft side to support
accurate nasolabial muscles reconstruction
Provision of adequate bone stock for ultimate placement
of osseointegrated implant
To provide better periodontal support for teeth bordering
the cleft
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53. BONE GRAFTING
Bone grafting techniques utilise cancellous bone to promote the formation
of new bone.
Autogenous cancellous bone have an active osteogenic substance that can
produce rapid healing in osseous defects.
Under ideal conditions ,in cancellous bone grafts, early revascularisation is
noted within 1 week and full revascularisation within 3 weeks..
Atraumatic surgical technique, avoidance of heat generation during the
harvesting of the graft and storage of bone particles in a saline soaked
sponge to avoid desiccation are important in maintaining cell viability
before transplantation
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54. HARVESTING THE ILIAC CANCELLOUS BONE GRAFT.
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55. SECONDARY ALVEOLAR BONE GRAFTING FOR ALVEOLAR CLEF REPAIR USING
CANCELLOUS ILIAC BONE GRAFT.
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56. SECONDARY ALVEOLAR BONE GRAFTING FOR ALVEOLAR CLEFT REPAIR USING
rHBMP-2.
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57. Asok kumar RS OMFS