Cleft lip and palate /certified fixed orthodontic courses by Indian dental academy

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


CONTENTS:
1. INTRODUCTION
2. EPIDEMIOLOGY
3. ETIOLOGY
4. EMBRYOLOGY
5. CLASIFICATION OF CLEFTS
6. TRRREATMENT OF CLEFT LIP AND PALATE:
- INFANT ORTHOPEDICS
- TREATMENT IN MIXED DENTITION
- TREATMENT IN PERMANENT DENTITION
- SURGICAL ORTHODONTICS
- DISTRACTION OSTEOGENESIS
7. CONCLUSION
8. REFERENCES

INTRODUCTION:
Orofacial clefts are among the most common congenital
anomalies requiring multidisciplinary care. Such anomalies include
several handicaps such as impaired suckling, defective speech,
deafness, malocclusion, gross facial deformity and severe
psychological problems.
Cleft of lip and the palate is one such condition, that occurs at
such a strategic place in the orofacial region and at such a crucial
time that it becomes a complex congenital deformity.
Management of CLCP involves a multi disciplinary approach
requiring the services of an orthodontist, oral surgeon,
prosthodontist, otolaryngologist, audiologist, speech therapist,
paediatrician.

EPIDEMIOLOGY:
Cleft lip and palate is a global problem.(0.28-3.74/1000 live births
globally)
Least incidence in negroids(0.4%) and maximum in afghans(4.9%)
Among Indians it seen maximum in Agrawal community and
Brahmins(1.7%).
The incidence of oral clefts is seen more in males than in females.
Cleft lip alone- more in males than female
Cleft palate- more in females than males


ETIOLOGY:
1.) Heredity:
Transmitted through a male as sex linked recessive gene.
Predisposition for cleft lip is 40% while only 18-20% for cleft palate.
It is transferred as:
a) Monogenic/ single gene disorder-conform to mendelian inheritance
b) Polygenic/ multifactorial inheritance- show familial tendency but not
mendelian inheritance
c) Chromosomal abnormalities:
- Down’s Syndrome
- Edwards Syndrome (trisomy 18)
- Trisomy D and E


SYNDROMES WITH CLEFT LIP AND PALATE
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


2.) Environmental Factors:
Usually occurs due to various influences during Ist trimester.
• Environmental terratogens:
-Ethyl Alcohol- causes FAS (fetal alcohol Syndrome).

-Cigarette smoking- 30% increase in cleft lip and palate and 20%
increase in cleft palate in smoking during pregnancy. Nicotine acts
synergistically with TGF.

-Anti seizure drugs.eg: diphenyl hydantion and trimethadione.also
causes growth retardation, craniofacial dysmorphism, mental deficiency


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 antiacne 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.
Anaemia and anorexia
INFECTION DURING PREGNANCY:
Rubella infection during the first 3 months associated with
clefting.
PARENTAL AGE:
Shaw etal presented evidence that women above the age of 35
had a doubled risk of having a child with CLCP.above 39- tripled
risk.
Consanguineous marriages- increased risk of CLCP in child.






EMBRYOLOGY
The first pharyngeal arch (mandibular arch),
develops two prominences:
The maxillary prominence
The mandibular prominence




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.


Mechanism of palatal shelf elevation
*Intrinsic Force within the shelf
*Accumulation of Glycosaminoglycans
*Accumalation and hydration of Hyaluronic acid.
*Increase in vascularity
*Contraction of elastic fibres or muscle fibres.
*Unequal division in the palatal and the oral epithelium
*Neurotransmitters like Serotonin
*Increase in Vimentin expression
*Master controlling gene is FSP-1,ssh,

Local Factors:
•Failure of the head to elevate and become erect at around the
7-9th week
•Failure of the tongue to descend downwards, thus causing a
mechanical interference to fusion of the palatine shelves.
•Deficiency of Oxygen
•Shift of Blood Supply of Face-During the 6th week, most of the
midface is supplied by the Stapedial artery which is the branch
of the Internal Carotid artery.
At around the 7th week, stapedial artery severs from the
internal carotid and its terminal branches join the external
carotid artery. Delay in this vital step can lead to cleft palate.

DAVIS AND RITCHIE CLASSIFICATION (1922):
They classified congenital clefts based on the
position of the cleft in relation to the alveolar
process.
Group I-Pre alveolar clefts Lip
clefts only with subdivisions for
unilateral, median, bilateral.
Group II-Post alveolar clefts
degrees of involvement of soft and
hard palate to be specified till the
alveolar ridge, submucous clefts
included.
Group III-Alveolar clefts is
complete clefts of palate, alveolus
ridge and lip with subdivisions for
unilateral, median, bilateral.

II VEAU’S CLASSIFICATION
(1931):


Group I Cleft of
soft palate only



Group II - Cleft of hard and
soft palate, extending no
further than the incisive
foramen thus involving the
secondary palate alone.





Group III - Complete
unilateral cleft of soft and
hard palate, lip and
alveolar ridge

Group IV - Complete
bilateral cleft of soft and
hard palate, lip and
alveolar ridge on both
sides.

III KERNAHAN’S STRIPED “Y”
CLASSIFICATION (1971):




In this classification the incisive
foramen is taken as the reference
point
“Y” logo are each divided into three
sections, representing the lip, the
alveolus and the hard palate as far
back as the incisive foramen. The
stem of the “Y” is also divided into
three parts, representing varying
degrees of clefting of the hard and
soft palates.


V MILLARD’S CLASSIFICATION
(1977):




A modification of
Kernahan’s striped “Y”
classification.
. The inverted triangles
represent the nasal arch the
upright triangles represent
the nasal floor.

LAHSHAL CLASSIFICATION:
L- lip
A- Alveolus
H- hard palate
S– soft palate

Treatment of CLCP: A brief Overview


FEEDING TECHNIQUES


When a cleft lip is present, it may be difficult for the baby
to make a good seal around the nipple.



Babies with cleft palate usually need special bottles and
techniques to feed properly.



There are three types of bottles for feeding babies with
clefts –



the Mead-Johnson Cleft Palate Nurser,
the Haberman Feeder and
the Pigeon Nipple:





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.



Displacement of segment make lip
repair more difficult



Orthopaedic appliances are used to
resposition the segment in early
infancy, before lip closure



These appliances also act as
“feeding plate” for infants

Two types of orthopaedic appliances
 Active: pin retained,controlled forces
 Passive:


Naso Alveolar Moulding

Nasoalveolar molding is a nonsurgical method of reshaping the
gums, lip and nostrils before cleft lip and palate surgery,
reducing the severity of the cleft. Surgery is performed after
the molding is complete, approximately three to six months
after birth.



PRESURGICAL NASO ALVEOLAR MOLDING

(Grayson etal, 1999)
Actively mold and reposition the deformed nasal cartilages and
alveolar processes and lengthen the deficient collumella.


LIP CLOSURE


Surgical closure of a cleft lip is done as early in infancy as
is compatible with a good long-term result.



at 10 to 12 weeks of age. Therefore PNAM should be
completed by then.

Techniques
 Rotation-advancement technique of Millard
 Delaire philosophy


PALATE CLOSURE
Objective:
•
Join the cleft palatal edges,
•
Lengthen the soft palate,
The timing of closure is controversial. Can be done early at 824 months or at 9-12year
At 18-24 month Development of normal speech
 Tendency towards maxillary underdevelopment
At 9-12year Normal growth of maxilla with unrepaired cleft
 Reduces surgical morbidity and infection

Latest suggestion




Closure of soft palate –age of 12 month
Help in development of Speech
No growth retardation with early soft palate closure
Closure of hard palatewww.indiandentalacademy.com
–age of 5-6year

Velopharyngeal Insufficiency


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.




VPD is of 3 types:
a) Velopharyngeal Mislearning: due to articulation difficulties
b) Velopharyngeal Incompetence: Due to functional abnormalities.
(paresis, dysarthia)
c) Velopharyngeal Insufficiency: Structural problems like cleft or bifid
uvula etc

Diagnostic Procedures




Measurement of nasal airflow
McKay-Krummer instrument
Aerophonoscope
Fiberoptic naso-endoscopy
Videofluoroscopy
Voice resonation Evaluation
Articualtion assessment
Oral motor assessment


Treatment of VPI








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


AIM OF TREATMENT IN CLCP PATIENTS:










To get optimum alignment.
Harmonize relationship of the dental arches for speech,
mastication, oral health and facial appearance.

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 1215 months.
Stability…….(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


Iliac crest



Tibia



Rib



Cranial bone

Advantages

adequate quantity easily
condensed & placed
little donor site morbidity
adequate volume
quality similar to iliac crest
for infants.
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 OFwww.indiandentalacademy.com
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.

Orthognathic Surgery combined with
Orthodontics
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.

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.



TIMING
 Never indicated in active facial growth
 Ideal time : age 18-19


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.


REFERENCES:
• CRANIOFACIAL DEVELOPMENT- Sperber
•Surgical orthodontic treatment- Proffit and White
•Grayson etal, Pre surgical naso alveolar molding, cleftliip- craniofacial
journal 1999:35
•Advances in management of cleft palate: Edwards and Watson
•Cleft lip and palate, Seminars in Orthodontics
•Baik et al. surgical orthodontic treatment in patients with clcp:
conventional surgery vs maxillary distraction, world J Orthod;2:331-40


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