Cleft lip and cleft palate

Contents
DEFINITION
HISTORY
INTRODUCTION
EMBRYOLOGY
ETIOLOGIC INSIGHTS FROM EMBRYOLOGY
www.indiandentalacademy.com

Contents
CHROMOSOMAL ANAMALIES
THRESHOLD MODEL
CLASSIFICATION
INCIDENCE
PRENATAL DIAGNOSIS

Contents
PHOTOGRAPHY
PROBLEMS IN CLEFT LIP AND PALATE
SPECIAL GROWTH PROBLEMS
ROLE OF SOFT PALATE
ETIOPATHOGENESIS

Contents
EURO CLEFT STUDY
GOSLON YARD STICK
INTERDISCIPLINARY APPROACH
PHILOSOPHY OF ORTHODONTIC MANAGEMENT
3D TECHNOLOGY IN DOCUMENTATION

Contents
NASO ALVEOLAR MOULDING
IMPRESSION PROCEDURE
TIMING OF ORTHODONTIC TREATMENT
PHASE I AND II ORTHODONTIC TREATMENT
SECONDARY ALVEOLAR BONE GRAFTING

Contents
ORTHOGNATHIC SURGERIES
DISTRCTION OSTEOGENESIS
FINAL DETAILING
SPEECH CONSIDERATIONS
CONCLUSION AND BIBLIGRAPHY

DEFINITION
The most common craniofacial anomaly
(approximately 1 in 600 to 1 in 700 live births
higher in some populations), characterized by
failure of fusion between certain embryological
processes (swellings) during facial
morphogenesis.

Failure of fusion between the medial and lateral
nasal and the maxillary swellings results in a cleft of
the lip and/or alveolar process.
Failure of fusion between the lateral palatine
swellings results in a cleft of the palate.

HISTORY
Speech disorders in CLCP are noted in wririmgs
of ancient EGYPT
First hare lip is recorded in 1000AD
Parea, French surgeon – designed obturator to
fill cavity in 1561
Le Monnier(1844), Von Langenbeck (1862) gave
various methods of surgical closure of the clefts

INTRODUCTION
Clefts of the lip and palate (CL/P) are the most
common craniofacial birth defects
Prevalence ranging from 1 in 500 to 1 in 2000
depending on the population.

Severity of orofacialcleft anomalies varies,
multidisciplinary treatment is often
necessary and may include craniofacial
surgery
Multidisciplinary nature of cleft care was
realized even in the first recorded surgical
repair of a cleft lip (in the annals of the
Chin dynasty in China, about A.D. 390

EMBRYOLOGY
 Early gene expression and signaling
molecules in development
 Germ layer differentiation, neurulation, and
midline malformations
 Neural crest cell formation, migration, and
differentiation
 Craniofacial development
 Primary palatogenesis

Genes control early embryonic
development through the production of
transcription factors that can be translated
into structural, regulatory, or enzymatic
proteins

Growth factors and morphogens then
target specific embryonic cell populations
and their signal transduction pathways
 Progressive differentiation,
 Migration,
 Shape changes (morphogenetic movements),
and
 Programmed cell death (apoptosis)

The molecular regulation of such
interactions and the mechanisms by which
‘‘pattern’’ development occurs within a
population of cells gives rise to different
tissue types and individual structures,
such as bones, muscles, and teeth

Mechanism of gene expression
Different mechanisms are involved
 Certain growth factors (eg, steroids, retinoic
acid, and thyroxin) passing through the
plasma cell membrane, binding with specific
receptors, and acting directly on the genes to
alter their function

BINDING TO SPECIFIC
RECEPTORS

 Involves certain other growth factors (eg,
• fibroblast growth factors [FGFs],
• transforming growth factor-beta superfamily [TGF-
bs],
• epidermal growth factor [EGF])
 Binds with specific cell surface receptors,
activating intracellular signaling path-ways
and eventually causing gene activation by
paracrine activation

Gene-controlled, growth factor-induced
cell migrations and cell fusions
(fusomorphogenesis) are essential to
organogenesis and normal embryonic
growth
Interruptions in these processes typically
produce embryonic death or congenital
malformations

PROTEIN FORMATION

GERM LAYER DIFFERENTIATION, NEURULATION, AND MIDLINE
MALFORMATIONS
HAPLOID STATE
ZYGOTE
Bilaminar disc 2
layered under control
of homeobox genes
BLASTOCYST
HOMEOBOX GENES 1-2 weeks post
conception
EMBRYO

INITIAL CELL DIVISION

BLASTOCYST

BLASTOCYST
GASTRULATION 3
week
GASTROCYST
3 layered disc
ectoderm, endoderm
& mesoderm
HOMEOBOX GENES
Hall BK. The neural crest in development and evolution.New York: Springer-
Verlag; 1999.
neural crest cells are
fourth germ layer in
vertebrates
The neural plate is
derived from the
neuroectoderm
NEURULATION
PAX6, Sonic Hedge-
Hog (SHH), and
FGF

GASTROCYST

Problems in development during
neurulation may result in midline
neurologic and craniofacial malformations
such as
 holoprosencephaly (single cavity forebrain),
 cycloplegias,
 neural tube defects, and
 midline orofacial clefts
Carstens MH. Development of the facial midline. J Craniofac
Surg 2002;13:129– 87.www.indiandentalacademy.com

Neural crest cell formation, migration, and
differentiation
Ectodermal-derived cells that are found in
the margins of the bilateral neural folds
and the transition zone between the
neuroectoderm and epidermis are referred
to as neural crest cells

differentiation
Neural crest cells migrate as
mesenchyme into the developing
embryonic processes of the head and
neck region during neural tube closure (4
weeks postconception)
(eg, neural, pigment, skeletal, connective
tissue, cardiac, dental, and endocrine
cells) are derived from the neural crest
cells

differentiation

Neural crest cells migrate in a segmental
pattern, predetermined in part by
interactions with hindbrain neuromeric
segments called rhombomeres and
paraxial mesoderm segments called
somatomeres

The timing and extent of neural cell
migration and differentiation is dependent
on a complex patterning of inductive
homeobox gene (HOX, MSX) signaling
between the neural crest and adjacent
neural tube

Deficiencies in neural crest tissue
migration or proliferation produce a varied
and extensive group of craniofacial
malformations referred to as
neurocristopathies
 von Recklingshausen neurofibromatosis
 hemifacial microsomia,
 Orofacial clefts,
 Treacher Collin syndromes

A series of inductive events between the
prosencephalon, mesencephalon, and
rhombencephalon and the neural crest
tissue that migrates into the craniofacial
complex and pharyngeal arch apparatus
form the five facial prominences

J Craniof Genet Dev
Biol 1991;11:192– 213;

Five prominences are
 the frontonasal
 the bilateral maxillary process
 mandibular prominences)
Differentiation, growth, and eventual
fusion of these prominences that forms
the definitive face

FACIAL PROMINENCES

Movement and destination of neural crest
tissues into the facial primordia are controlled in
part by a number of gene families
 homeobox genes (HOXa-1, HOXa-2, HOXb-1, HOXb-
3, and HOXb-4),
 the SSH gene,
 the OTX gene (orthodentical homeobox),
 the GSC gene (goosecoid),
 DLX genes (Drosophila distal-less homeobox),
 MSX genes (muscle segment homeobox),
 LHX genes (LIM homeobox),
 PRRX genes (paired-related homeobox)
M.L. Marazita, M.P. Mooney / Clin Plastic Surg 31 (2004) 125–140

CHROMOSOME STRUCTURE

Primary palatogenesis
Primary palate is defined
 as the portions of the facial primordia that
initially separate the oral and nasal cavities
and include the portions of the medial and
lateral nasal processes of the frontonasal
process and the portion of the maxillary
processes that contribute to the separation of
the cavities

Involves a series of local molecular and
cellular events that are closely timed.
Spatial and biomechanical changes
associated with craniofacial growth must
occur in sequence

Primary palate initially forms around the
developing olfactory placodes with the
rapid proliferation of the lateral epithelium
and underlying mesenchyme
Controlled by
 FGFs (FGF8 and FGFR2),
 Bone morphogenetic proteins (BMP4 and
BMP7),
 SHH
 Retinoic acid
Surg 2002;13:129– 87.

Facial prominences enlarge around the
nasal pits to form the premaxillary region
Forebrain elevates as the cranial base
angle decreases, the medial nasal region
narrows, and the maxilla grows forward

M.L. Marazita, M.P. Mooney / Clin Plastic Surg 31 (2004) 125–140www.indiandentalacademy.com

Fusion requires critically timed
coordination of growth between the
processes, exact spatial localization, and
apoptosis of the epithelium
Abnormal development of this epithelium
may be involved with clefts of the primary
palate.

Additional structures in the primary palate
 Dentition,
 Alveolar and basal bone of the primary palate,
 Labial musculature.
 Four tooth buds

Tooth bud formation is dependent on
 Genes - (PAX9, MSX1, SHH, DLX, WNT)
 Growth factors (nerve growth factor, FGF, and
BMPs)

Ossification of the primary palate begins
around the 8 weeks postconception in the
medial nasal prominence and continues
laterally to the maxillary process
Sperber GH. Formation of the primary palatewww.indiandentalacademy.com

OROFACIAL CLEFTING OF THE PRIMARY
PALATE.
Defects can be classified as
 midline (median facial clefts)
 laterally (lateral facial clefts)
Median facial defects occur early and
probably relate closely to the initial events
directing morphogenesis

Lateral facial clefts are defects resulting
from abnormal events usually occurring
later in development once the facial
primordia are in place
Identifying specific cleft mechanisms has
been difficult.

Additional structures that can be affected
by primary palatal clefting
 Dentition,
 Alveolar
 Basal bone of the primary palate,
 Labial musculature.

Primary palate clefting involves
 primary and secondary palates at the incisive fissure
that separates the lateral incisors and canine teeth
Labial defects typically involve discontinuity of
the circumoral musculature and reduced lip
muscle volume in cleft embryos and fetuses
Mooney MP, Siegel M Plast Reconstruc Surg 1988; 81:336– 45.www.indiandentalacademy.com

Unilateral cleft lip

Bilateral cleft lip

Oblique facial cleft

Median
Cleft Lip And Nasal Defect

Bony morphologies of cleft maxilla may
result from an
 initial mesenchymal deficiency during primary
palatogenesis
 from later bone resorption due to a lack of
functional forces on the primary palate
Siegel MI, Mooney MP Cleft Pal-Craniofac J 1991;28:408– 12www.indiandentalacademy.com

Secondary palatogenesis
Defined as the
 portions of the facial primordia posterior to the
primary palate and includes the two lateral
palatal processes that project medially from
the maxillary processes.

Primary palatogenesis requires closure
and fusion
Secondary palate requires a complex
interaction of palatal shelf movements,
critically timed coordination of growth
between the processes, and apoptosis (or
further differentiation) of the epithelium
along medial margins of the palatal
shelves
Sperber GH. Palatogenesis: closure of the secondary palatewww.indiandentalacademy.com

During week 8 postconception,
 palatal shelves rotate from a vertical position
surrounding the tongue and elevate into
horizontal approximation

Rapid palatal shelf elevation is thought to
result from a number of mechanisms
 changes in the connective tissue matrix and
associated glycosaminoglycans of the shelves
leading to hydration
 swelling, and rapid elevation
 change in shelf vascularity leading to
increased tissue fluid pressure and turgor
 rapid differential mitotic growth of the shelf
mesenchyme

 Movements of the tongue, facial, and
suprahyoid musculature leading to cranial
flexion
Medial edge of the maxillary prominence
are rich in
 FGF8
 SHH
 TGF-b3
 N-cadherin

Fusion along the medial edges and
apoptosis of the epithelium facilitate
closure
At the time of palatal shelf elevation, the
tongue and mandible extend beneath the
caudal portion of the primary palate
facilitating elevation

Ossification of the palate proceeds from
the lateral palatal shelve during week 8
postconception.

Orofacial clefting of the secondary palate.
Defects of the secondary palate are
expressed morphologically
 failures of elevation,
 failures of contact and adhesion
 failures of fusion resulting in clefts
Surg 2002;13:129– 87.www.indiandentalacademy.com

Major factors shown to limit shelf contact
 Delayed shelf movement to the horizontal position
 Reduction in palatal shelf size,
 Deficient extracellular matrix accumulation,
 Delayed achievement of mandibular prominence,
head extension (thus an increase in facial vertical
dimension),
 Abnormal craniofacial morphology,
 Abnormal first arch development,
 Increased tongue obstruction of shelf movement
 Secondary to mandibular retrognathia

Ratio of left-sided to right-sided clefts is
also about 2:1 (marazita 2004)
Prevalence shows a wide range, from
about 1/500 births to about 1/2000,
depending on population
Asian and Amerindian populations have
the highest frequencies
African-derived populations have the
lowest frequencies

“Orofacial clefts have a familial basis” –
Charles Darwin
‘‘the transmission during a century of
hare-lip with a cleft-palate’’ by Sproule
Multifactorial threshold model was
proposed to explain many of the features
of nonsyndromic orofacial clefts (later
rejected) early 2000s

Segregation analyses and statistical
analyses of familial recurrence risk
patterns are consistent with hypotheses of
major locus involvement or relatively few
loci
Schliekelman P, Slatkin Am J Hum Genet 2002;71:1369–85.www.indiandentalacademy.com

Etiologic insights from embryology
Environmental and genetic factors
implicated in orofacial clefting of the
primary palate
A failure of normal disintegration of the
nasal fin or inadequate mesenchymal
migration between the maxillary and
medial nasal processes

Mouse embryos from strains genetically
predisposed to primary palatal clefting
 had medial nasal prominences that were
more medially convergent
 than normal strain embryos, resulting in
decreased
 contact with the lateral nasal prominences
Juriloff DM, Trasler DG. Teratology 1976;14:35– 42www.indiandentalacademy.com

Strains susceptible to spontaneous clefts
of the primary palate
 Smaller distance between the nasal pits,
 Different orientation of medial nasal
prominences,
 Reduction (or absence) of epithelial activity
throughout the developmental period of
primary-palate fusion,
 Hypoplasia of the lateral nasal prominences

Observed ethnic relation
 (Asian derived > European derived > African
derived)
Tongue-tie (which could inhibit protrusion
of the tongue during shelf elevation) is a
familial form of cleft palate in Iceland
Moore G, Williamson R, J Craniofac Genet Dev Biol 1991;11: 372– 6.www.indiandentalacademy.com

Failure of secondary palatal closure is
thought to occur as a by-product of the
primary palate cleft because of the
resulting alterations in the tongue and
palatomaxillary relationships

Chromosomal anomalies
It is seen as part of the phenotype in a
wide variety of types of chromosomal
rearrangements
 Trisomies
 Duplications
 Deletions
 Micro-deletionsor
 Cryptic rearrangements

CHROMOSOME DELETION

TRANSLOCATION

Deletions of 4p (Wolf-Hirschhorn
syndrome)
4q or 5p (Cri-du-chat syndrome)
Duplications of 3p, 10p, and 11p
Trisomy 13 or 18 (and trisomy 9 mosaic)

Role of micro-deletions and other cryptic
rearrangements in orofacial cleft etiology
has recently been recognized

Microdeletions of 22q11.2
 (DiGeorge syndrome,
 Velocardiofacial syndrome,
 Conotruncal anomaly face syndrome

Single gene etiologies
300 syndromes have been described in
which a cleft of the lip or palate is a
feature
Syndromes are due to Mendelian
inheritance of alleles at a single genetic
locus

GENE LOCATION

50% follow autosomal recessive inheritance,
40% follow autosomal dominant inheritance, and
10% follow X-linked inheritance (recessive or
dominant)

Syndromic Clefts
Of the 150 Mendelian clefting syndromes,
approximately 30 genes have been cloned
GLI3, 7p13; PAX3, 2q35—Waardenburg
syndrome;
SIX3, 2p21— holoprosencephaly 2;
SOX9, 17q24.3-q25.1—Camptomelic
dysplasia,
Schutte BC, Murray JC. The many faces and factors of orofacial clefts.
Hum Mol Genet 1999;8:1853– 9.www.indiandentalacademy.com

COL2A1,12q13.1-q 13.2—Stickler syndrome
type I; COL11A2, 1p21— Stickler syndrome type
II,
GPC3, Xp22—Simpson- Golabi-Behmel
syndrome),
cell signaling molecules (FGFR2, 10q26, Apert-
Crouzon syndrome;
PTCH, 9q22.3—basal cell nevus syndrome;
SHH, 7q36, holoprosencephaly

Genetic etiologies of nonsyndromic
orofacial clefts
Contribution to nonsyndromic orofacial
clefts ranged from about 12% to 20%
Statistical analyses of recurrence risk
patterns have been consistent with
experimental models with 3 to 14
interacting loci.

HUMAN CHROMOSOMES

Linkage and association studies
Linkage analyses assess the co-
segregation of alleles at a genetic locus of
known chromosomal location (marker)
and a disease locus.

THRESHOLD MODEL

THRESHOLD MODEL
 Although the disorder is obviously familial, there is no
distinctive pattern of inheritance within a single family.
 The risk to first-degree relatives, determined from family
studies, is approximately the square root of the
population risk.
 The risk is sharply lower for second-degree than for first-
degree relatives, but it declines less rapidly for more
remote relatives.

THRESHOLD MODEL
The recurrence risk is higher when more
than one family member is affected.
The more severe the malformation, the
greater the recurrence risk.
If a multifactorial trait is more frequent in
one sex than in the other, the risk is higher
for relatives of patients of the less
susceptible sex.

THRESHOLD MODEL
If the concordance rate in DZ twins is less than
half the rate in MZ twins, the trait cannot be
autosomal dominant, and if it is less than a
quarter of the MZ rate, it cannot be autosomal
recessive.
An increased recurrence risk when the parents
are consanguineous suggests that multiple
factors with additive effects may be involved

Candidate loci or regions on seven
chromosomes
 Chromosomes 1, 2, 4, 6, 14, 17, and 19) have
positive linkage or association results in CL/P,
CP, or both;

Genome-wide scans

Genome-wide scans
Analyses of recurrence risk patterns
suggest that there may be about 3 to 14
genetic loci involved in nonsyndromic
clefts of the primary palate (with or without
the secondary palate)
Schliekelman P, Slatkin M. Am J Hum Genet 2002;71:1369–85.www.indiandentalacademy.com

Contradictory results from candidate locus
approaches and the availability of dense
maps of markers, studies of orofacial
clefting are now turning to genome wide
scans

CLASSIFICATION

Davis And Richie Classification
Morphological classification based on
location of the cleft relative to the alveolar
process
 Group I
 Group II
 Group III

Davis And Richie Classification(1922)
Group I: Prealveolar Clefts
 Clefts involving only lip are classified as
• Unilateral
• Bilateral
• Median
Group II : post alveolar clefts :
 Comprises different degrees of hard and soft
palate clefts extending upto the alveolar ridge

Complete unilateral cleft lip and
palate on right side

Davis And Richie Classification
Group III: alveolar clefts:
 Complete clefts involving palate, alveolar
ridge & lip; subdivided into
• Unilateral
• Bilateral
• Median

Complete bilateral cleft of lip and
primary palate

VEAU’S CLASSIFICATION (1931)
Classified into four groups
Group 1: clefts involving soft palate only
Group 2: clefts involving hard & soft palate
extending upto incisive foramen

VEAU’S CLASSIFICATION (1931)
Group 3: complete unilateral clefts
involving the soft palate hard palate, lip
and alveolar ridge
Group 4: complete bilateral clefts affecting
soft palate, hard palate, lip and alveolar
ridge

Fogh Anderson Classification
Group 1: they are clefts of lip. It can be
subdivided into
 Single – unilateral or median clefts
 Double – bilateral clefts
Group 2: clefts of lip and palate. Sub
classified into
 Single – unilateral clefts
 Double – bilateral clefts

Fogh Anderson Classification
Group 3: clefts of palate extending upto
the incisive foramen

Schuchardt & Pfeifer’s Symbolic
classification
Chart is made up of vertical blocks and a
triangle
Rectangles represent lip, alveolus and
hard palate.
Triangle indicates soft palate
Disadvantages are difficulty in typing,
writing & communication

Schuchardt & Pfeifer’s Symbolic
classification
Left Right
Lip
Alveolus
Hard palate
Soft palate
Total Cleft Partial Cleft

Kernahan’s stripped ‘y’
Classification
Symbolic classification put forward by
Kernahan and stark
Uses a stripped ‘Y’having number blocks
representing specific area of oral cavity
Block 1and 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

Kernahan’s stripped ‘y’
Classification
Right Left
1
2
6
3
5
4
7
8
9

MILLARD’s MODIFICATION
1
2
6
3
5
4
7
8
9
R L

MILLARD’s MODIFICATION
Inverted triangles are nasal floor and
shaded when they are involved

ELASAHY’s MODIFICATION
Double lining of 9, 10 in hard palate area
used to indicate the direction of
thedeflection in complete clefts
11- soft palate
Circle 12 – pharynx, dotted line represents
velopharyngeal incompetence
Circle 13- premaxilla if protruding

ELASAHY’s MODIFICATION
2
3
6
4
7
8
9
10
5
11
12
1
13

LASHAL CLASSIFICATION
Presented by Okreins in 1987
L – Lip
A – Alveolus
H – hard palate
S – Soft palate
H – Hard palate
A – Alveolus
L – Lip

TESSIER’S CLASSIFICATION OF
ATYPICAL CLEFTS

Incidence of the Cleft lip & Palate
Incidence Globally
 Cleft showed highest incidence in Japan,
Indonesia followed by India & Australia
Incidence in INDIA
 1 in 800 with 30,000 cleft births per year

Incidence regionwise
 1 in 900 births in AP
 1 in 760 births in Assam
 1 in 643 in Rajasthan
 1 in 867 in Maharashtra
National sensus for the physically challenged – Tata Institute 2007www.indiandentalacademy.com

Prenatal Diagnosis of Oral Clefts
Antenatal diagnosis of facial clefts allows
for adequate counseling and planning for
prenatal care and delivery.
Antenatal diagnosis as early as 12 weeks
of gestation by transvaginal ultrasound

12 weeks of gestation
Nyberg DA,Radiology 1995; 195:677–684.www.indiandentalacademy.com

Ultrasound features
In the frontal plane, disruption of the
normal midfacial architecture,with absence
of the maxillary ridge
Broadening of the nasal cavity
In the coronal a soft tissue mass
projecting anteriorly from the midline nasal
septum below the nose

Ultrasound Classification
Type 1
 an isolated cleft lip
without palate
Type 2
 unilateral cleft lip and
palate.
Nyberg DA,Radiology 1995; 195:677–684.www.indiandentalacademy.com

Type 3 is bilateral
cleft lip and palate

Type 4 is the median cleft.
Type 5 refers to clefts associated with
amniotic bands or limb-body-wall complex.

Examination of the fetal face in not
currently included in the guidelines for
performance of the antepartum obstetrical
ultrasonographic evaluation published by
the American Institute of Ultrasound in
Medicine
J Ultrasound Med 1996; 15:185–187.www.indiandentalacademy.com

COLOR DOPPLER
ULTRASONOGRAPHY
Used to visualise the flow of the amniotic
fluid from the mouth to the nasal cavity

3D Ultra sonography
Views fetal face with greater clarity
Sensitivtiy is greatly increased

ADVANTAGES OF PRENATAL
DIAGNOSIS
Psychological preperation
Education of parents
Preparation for neonate care
Chromosomal abnormalities
Possibility of fetal surgery

DISADVANTAGES OF PRENATAL
DIAGNOSIS
Increased maternal anxiety
Emotional disturbance
Ethical concerns

PHOTOGRAPHY
Objective results of craniofacial surgery
are usually evaluated by comparing pre-
and postoperative photographs.
Healthy individuals with no gross facial
asymmetry, grids and cephalostats may
lead to inter-individually comparable and
reproducible photographs.

Applied to cleft patients or subjects in need of
corrective surgery, the protocols will not
standardize the photographs
Certain amount of asymmetry is considered to
be normal
Cleft Palate–Craniofacial Journal, September 2000, Vol. 37 No. 5www.indiandentalacademy.com

Asymmetry of tragus leads to asymmetry of the
bilateral Frankfurt horizontal lines, the facial
inclination measured in the left lateral view
differs from that in the right lateral view

Underdevelopment of the lower half of the
face and a flat nasal bridge
 The head is kept too far inclined if the
Frankfurt horizontal is kept to align the
horizontal indicator of a grid
 In the frontal view, the subject would be
forced to look at the photographer from under
his eyebrows

Nine photographs are taken for a standard
facial series
 Three frontal,
 Three right-sided,
 Three leftsided lateral photographs
 Nasal series - an extra basal view of the nose
is made

For each of the three frontal photographs,
the position of the camera is varied a few
millimeters to the left and the right side
Lateral photographs,
 the camera is installed lateral to the outer
corner of the eye, and a constant marker on
the wall in front of the chair is used for the
patient to fix on

Problems associated with cleft lip &
palate
Psychological problems
Dental problems
Speech and hearing problems
Esthetics

Psychological problems
Disfigurement causes Psychological
stress for the patient & family
Child performs bad in acdemics due to
hearing &speech problems

Dental
Under developed maxilla
Some problems are
 Multiple missing teeth
 Mobile premaxilla
 Anterior or posterior cross bite
 Ectopically erupting teeth
 Impacted teeth
 Supernumeraries
 Poor alignment of arches
 Multiple decayed teeth & periodontal complications

Esthetics
Un-repaired cleft lip & palate causes
disfigurement
Maxilla remains under developed
Skeletal Class III profile
Lip & nose abnormalities

Speech and hearing problems
Definitive speech problems
Middle ear infections
Oro nasal Communications

Special Growth Problems In Cleft
Cases
Incomplete labiomaxillary arch cleft ,
muscles of nasal floor cannot bridge the
gap
3 muscles of the ring
 Superior nasal ring
• Transverse nasal muscle, levators of upper lip
 Middle nasal ring
• Orbicularis oris muscle of both upper & lower lip
 Lower labiomental ring

Transverse nasal muscle
 Important element of the nasolabial ring
 Passes from the anterior border of nasal bone to the
incisive crest and to the nasal septal perichondrium
 Actions - nostril constriction; along with the fibers of
orbicularis oris provides support to upper lip

Cases
In complete labiomaxillary cleft
 Muscles of the cleft side remain lateral to the
defect and cannot function normally
 Muscles of the upper lip and nasal floor
cannot bridge the gap between cleft
 Muscular integrity of the region is disrupted

Growth on the cleft side is reduced due to
non stimulation from naso labial muscles

Unilateral labiomaxillary cleft
Cleft side
Muscles of the cleft
side remain lateral to
the defect and cannot
function normally
Deprived of the nasal
septum & ANS the
structure collapses
Non cleft side
Nasolabial muscles
inserted into the nasal
septum pull it into the
noncleft nostril
Premaxilla is under
developed as equal
degree of the
interincisive suture

Cases
Alar cartilage of the cleft side is flattened
by the muscular traction
Sagging nasal capsule induces retrusion
of the nasal bone

Role of the palate
To provide barrier between oral and nasal
portions of respiratory tract
Velar actions
Deglutition
Respiration
Phonation (velopharyngeal sphincter)

Soft palate
Blood supply
 Greater palatine artery
 Lesser palatine artery
Nerve supply
 Plexus of maxillary branch of trigeminal
 Facial nerve
 Glossopharyngeal nerve

Muscles of soft palate

Actions of muscles of soft palate
Tensor veli palatini
 Tightens the soft
palate
 Opens the auditory
tube
Levator veli palatini
 Elevates the soft
palate
 Opens the auditory
tube

Musculus uvulae
 Pulls up the uvula
Palatoglossus
 Pulls up the root of the
tongue approximates
palatoglossal arches &
closes oropharyngeal
isthmus

Palatopharyngeus
 Pulls up the wall of the
pharynx and shortens
it during swallowing

Etiopathogenesis of orthodontic
problem
Primary defect caused by the Cleft
Secondary adaptation
Altered facial growth – retrusive maxilla
and normal mandible
68% of the patients treated cleft cases are
mouth breathers

Secondary adaptation
Lowered tongue position
 Lowered mandibular posture
 Increased gonial angle
 Steep mandibular plane
 Retroclined lower incisors

Upper lip tongue seal swallow
 Tongue tries to fill the defect
 Non functional proclined lower lip
 Negative overjet
 Collapsed maxillary arch
 <10mm to 12mm reverse overjet –
orthodontic treatment
 >12-15mm reverse overjet – orthognathic
treatment or distraction osteogenesis

Facial growth with repaired clefts
Cephalometric measurements are smaller
compared to the normal
Smaller stature, head size
Repaired cleft lip
 Maxilla retruded compared to cranial base
 Lower incisors retroclined
 Prominent posterior maxillary height
 Slight decrease in anterior maxillary height
 Increased gonial angle

Relative prominence of maxilla
after primary therapy

Relative prominence
after primary therapy
 By 7 years – normal
proportions
 By 18 years ( growth
completion) – SNA is
reduced by 6°

Effects of post lip repair
Arch collapses due to scar formation
 reduced maxillary arch width
Tight lip (reduced sulcus depth)
Hypodontia & supernumerary teeth in vicinity of
cleft
Poor bony support
High caries & periodontal risk
Maxillo-mandibular dis-cordination
Progressive decline of maxillary prominence

Scar Formation

Decreased Maxillary Width

EURO CLEFT STUDY
Intercenter study of treatment outcome in
patients with complete unilateral cleft lip &
palate
 Part1 : introduction & Nasolabial appearance
 Part 2: cleft form and nasolabial appreance
 Part 3: Dental arch relationships
 Part 4 : patient or parent satisfaction
 Part 5 : discussion & conclusions

Began as a intercenter comparision of
orthodontic records of 9 – 15 years old
children
127 consecutively treated individuals with
repaired cleft cases are considered

Part 1
Introduction & treatment expertise
 Results
 Mean no of operations per center – 3.5 to 6
 Length of orthodontic treatment – 3.3 to 8.5
years
 Attendance per patients – 49 to 94 visits
William Shaw et. Al Cleft Palate–Craniofacial Journal, September 1992,
Vol. 29 No. 5www.indiandentalacademy.com

Part 2
Cleft form and nasolabial appearance
14 angular, 2ratio variables are
considered
4 variables of nasolabial appearance in
127 patients are considered
Results
 At ages 12 & 17 two centers had flatter profile
 One center has retrognathic maxilla

Part 3
Dental relationships
Goslon yard stick
Ranks dental study casts of subjects with
unilateral cleft lip in mate mixed and early
permanent into 5categories:

Goslon yard stick
 Group 1: excellent results (simple or no
orthodontic treatment at all)
 Group 2: good result (simple or no orthodontic
treatment at all)
 Group 3: fair result (complex orthodontic or
orthopedic treatment)
 Group 4: poor result (orthognathic surgery)
 Group 5: very poor result (orthognathic
surgery)
Michael Mars et. Al Cleft Palate–Craniofacial Journal, October 1987,

Goslon Group 1

Goslon Group 2

Goslon Group 3

Goslon Group 4

Goslon Group 5

Goslon yard stick for 17year old
Group 1 : excellent result
 Good horizontal, vertical
 One tooth in lateral segment in crossbite is
acceptable
 Group 2: (good result) positive overjet,
over bite
 Crossbite in 1 lateral segment accepted
Michael Mars et. Al Cleft Palate–Craniofacial Journal, October 1987,

Group 3: (Fair result) edge to edge
anterior occlusion
 Inversion of 1 tooth in frontal region including
canine is accepted
 Unilateral or bilateral cross bite
Group 4: (poor result): negative overjet
with asymmetric upper arch, unilateral,
bilateral crossbite

Group 5: (very poor result) severe
negative overjet with a narrow upper arch,
collapsed cleft side segment

Part 4
80% satisfaction among patients observed
Reliability of the type of questionnaire was
certainly taken into consideration

Integration of services
Orthodontics
Oral surgery
Prosthodontics
Speech therapy
Pediatrics
Psychology
General dentistry
Otolaryngology

Coordinated interdisciplinary team
approach
Surgery
Nursing
SURGERY
PEDIATRICS
SPEECH PATHOLOGIST
OBSTETRICS
ENT, AUDIOLOGY
ORTHODONTICS
NURSING
GENETICS
DENTISTRY
SOCIAL SUPPORT
PSYCHOLOGY
TEAM COORDINATOR

TREATMENT STRATEGIES
Two schools of thought:
 Early closure of lip & palate prioritizing speech
over growth
 Delayed closure of hard palate to optimize
growth

General management overview
Immediately after birth
 Evaluation of geneticist, diagnostic tests
First few weeks – hearing tests
10 to 12 weeks – surgical repair of lip
Before 1 year : team evaluation cleft
palate closure
1½ to 2 years – speech evaluation

2-5 years – medical & behavioral
interventions
5-6 years – monitoring of speech, lip &
nose revision (if necessary)
 7 years – orthopedic & orthodontic
treatment (phase I)
9-11 years – bone grafting of alveolar
defect

12 or later – comprehensive orthodontic
treatment (phase II)
At the end of orthodontic treatment – fixed
appliance bridge
After growth completion – surgical
advancement of maxilla
After end of prosthetic & orthodontic
treatment – final lip revision

Team approach
Coordinated patient centered approach
sensitive to patient & family needs
Overall care for the patient
Should rely on inter disciplinary team
decisions
Orthodontist in a cleft team should
consider the timing & sequence of
treatment in coordination with team
members

Philosophy of Orthodontic
Management
Overview of the problem
Interaction with other team specialists
Evaluation of results
Acquisition of new knowledge
Diagnosis

Overview of the problem
Knowledge of aspects like :
- incidence
- etiology
- embryogenesis
- neonatal anatomy
- physiology
 enhances the ability of the orthodontist to
interact with the team.

Interaction with other team
specialists
Prospective / Retrospective
Prospective :
- proper diagnosis
- treatment planning
- prognosis
Retrospective :
- leads to improvement in rehabilitory
techniques

Evaluation of results
 With regard to :
- The degree to which alignment or normalizing of
underlying hard tissues (dental /skeletal) enhances
surgical repair of overlying soft tissues.
- Facilitate speech therapy measures.
 Prerequisite :
- knowledge of wide variability in craniofacial features
in the cleft population.
- orthodontist willing to compromise

Acquisition of new knowledge
To alter one’s approach
Determination of cost/benefit analysis
Recognition of variability in cleft population
Impractical to attempt to treat all cases alike
Maintenance of good longitudinal records

Diagnosis
A complex undertaking because of the various
complicating factors
Collection of records should begin at birth
- every six months till the age of 2 yrs
- every year after that.
Data base
- patient history
- clinical / radiographic examination
- systemic description of the occlusion and
analysis of the orthodontic records.

A. Patient history
1. Medical – Dental history :
 Primary importance to the accurate description
of the type and extent of cleft present at birth
 Record of the timing and type of surgery
performed to correct the defect
 Well established differences in growth patterns
and dimensions among various types of clefts

Variations in frequency of dental anomalies
depending on cleft type.
( 10-25%)
Potential complicating factors
- Mental retardation.
- Neuromuscular anomalies.
- Skeletal tissue anomalies.
- Frequent upper respiratory infections
- Enlarged tonsils or adenoids
- Other forms of nasal obstruction.

2. Social / Behavioral :
Behavioral characteristics
Lead to extremely poor oral hygiene
Poor prognosis for co-operation
Patient “burn-out”
Orthodontist should be willing to adjust.

3. Somatic growth development and maturation
Includes : - Clinical evaluation
- Serial ht/wt data
- Dental age
- Skeletal age
Infancy / “catch-up” growth

Exhibit lower skeletal ages than normals,
indicating delayed maturation
Aspects like delayed dental development and
retarded eruption to be considered in terms of
possible :
- Serial extractions
- Initiation of active treatment

4. Genetic / Family history :
Family history is significant as cleft
superimposed upon an underlying skeletal
growth pattern may vary from Cl I, Cl II, Cl III
i.e. In class III cases : immediate attention
In class II cases : favourable
5. Habits : - Tongue thrust
- Finger/Thumb sucking
- Prolonged use of pacifiers

B. Clinical and Radiographic
examination
1. Facial esthetics :
 In defects of palate only- facial esthetics are
usually close to normal.
 In case of an extensively scarred palate, there
is a slight maxillary underdevelopment leading
to a straight or mildly concave mid-face profile.
 Also continued growth of the mandible and
nose may worsen the profile.

SCARRED PALATE & MID FACE
DEFICIENCY

Clinical findings
 - Forward rotation/position of pre-maxillary segment
- Tethered nasal tip
- Thin upper lip, protrusive lower lip
- Retrusive soft tissue profile
- Increased lower face height
- Lowered positioning of the tongue due to a constricted,
scarred, obliterated palatal vault
- Mouth breathing
- Enlarged tonsils

CONCAVE PROFILE & DEVIATED
NASAL SEPTUM

2. Intra-oral soft tissue :
 Estimate of the extent , location and severity of
palatal and alveolar scarring provides a clue to :
1. Response of a palate to expansion
2. Degree of retention required.
3. Impediments to tooth movement.
4. Possible cause of altered tongue posture.

Soft tissues potentially leading to altered
mandibular posture or function.
Abnormal, scarred frenal attachments may affect
the configuration of any appliance.
Monitoring gingival signs of developing
periodontal disease related to poor oral hygiene.

SCARED MAXILLARY FRENUM

3. Muscle balance and function :
The diagnosis and interception of developing
functional problems, from early childhood
through stabilization of the adult dentition is the
most important aspect of clinical evaluation.
Functional alterations due to frequent
occurrence of severely malposed teeth, dental
anomalies and skeletal dysplasia’s.

 Functional alterations :
1. Mandibular closure
2. Tongue function + posture
3. Respiratory patterns
 Effects :
1. Unilateral crossbite in centric occlusion
2. Pseudoprognathism (mixed dentition)
3. Problems of lip tonus + function

4. Dental structures :
 Significant increase in incidence of dental abnormalities
in the cleft population.
1. Supernumerary teeth in the vicinity of the cleft
2. Congenitally missing teeth
3. Hypoplasia
4. Hypocalcification
5. Morphological irregularities
6. Poor oral hygiene leading to caries + pdl disease
 Careful monitoring required as premature loss may
lead to decrease in arch length.

MISSING PERMENENT INCISOR

Malformed Deciduous Anterior
Teeth

Three-dimensional technology for documentation and
record keeping for patients with facial clefts
The guidelines of record keeping for
treatment of cleft lip and palate patients
were first reported by Pruzansky and Lis in
1958
Importance was reinforced by Mazaheri
and Sahni in 1969
Pruzansky S, Lis EF. J Orthod 1958;44:159– 86.

Children over 2 months of age were
referred for radiographic examination
under sedation.
Intraoral and facial impressions were
taken while the infant was awake so that
the infant would maintain his own reflexes.

Impressions were critical procedures that
required at least four assistants and a fair
amount of patience
Mazaheri M, Sahni PP. J Prosthet Dent 1969;21:315– 23

Drawbacks of facial impressions
 difficult to get an infant’s cooperation,
 soft tissue deformation is likely to occur due to
tension and weight of the impression material
 distortion can be increased as the
impressions get filled with plaster and stone
for fabrication of casts
Ma T, Taylor TD, Johnson M. J Prosthet Dent 1990;63:564– 6.

A variety of 3-D acquisition techniques for
soft tissue have been developed in recent
years that can be applied to imaging of the
human body.
Stereophotogrammetry provides an
alternative to overcome the limitations of
facial impressions and 2-D photographs
Burke PH, Hughes-Lawson Am J Orthod Dentofacial Orthop 1989;96:144– 51

Various 3-D techniques are
 Stereophotogrammetry
 3-D noncontact laser surface scanning

3-d Noncontact Laser Surface
Scanning
 Operates on a light-stripe triangulation range-finder
principle.
 Subject’s facial surface is scanned from top to bottom
with a projected class 2 laser light stripe.
 Reliability of this method has been tested and found to
be accurate
Kusnoto B, Evans C. Am J Orthod Dentofacial Orthop 2002;122:342–8

3 D IMAGE

MESH DIAGRAM

Surface laser scanner has great potential
as a method for documentation of cleft
infant due to its accuracy, ease of use,
and convenience.
Images can be stored in the computer for
easy access.
A.C. Da Silveira et al / Clin Plastic Surg 31 (2004) 141–148

C. Description of the occlusion and
analysis of the diagnostic records
 Need to understand the basic D-A and craniofacial
development potential in the cleft population
 According to Graber (1949)
- All children with clefts, if left untreated are capable of
achieving reasonably normal skeletal/dental
relationships.
- Many of the present day orthodontic problems are the
result of the treatment rather than the defect itself.

 The growth potential of the untreated cleft maxilla was
studied in 30 untreated nonsyndromic Indian adults who
had complete unilateral cleft lip and palate
 The observation that the size and position of the cleft
maxilla compared favorably in comparison to a control
group of 30 non-cleft Indian individuals who had a
normal occlusion
Carla A. Evans Clin Plastic Surg 31 (2004) 271– 290www.indiandentalacademy.com

 Various problems encountered :
1. Intra arch alignment and symmetry
2. Profile / esthetics
3. Transverse problems
4. Ant/post sagittal problems
5. Vertical problems

1. Intra arch alignment and symmetry :
 Process of lip repair results in a generalized
reduction in cleft width and max. arch width
dimensions.
 Intra-arch malalignments appear with the
eruption of the permanent dentition.
 Severe rotations/lingual inclination of
permanent incisors in clefts involving the
alveolar ridge.

SEVERE ROTATIONS OF THE
ANTERIOR TEETH

3. Transverse problems :
 Infants : excessive max. width dimensions
(BCLP > UCLP > CP > NORMAL)
 Full deciduous dentition :
(BCLP < UCLP < CP = NORMAL)
 Subsequent skeletal growth might lead to more severe
problems.
 Clinical significance:
Re-expansion will invariably be necessary because
of an incompatibility in growth direction.

4. Antero-posterior sagittal problems :
Variability and uncertainty due to gross
displacement and distortions of landmarks
(i.e. ANS, PNS)
In primary dentition class III molar relationship /
ant.crossbite are of great concern.
Retroposition of the maxillary buccal segments
as a result of scar-mediated “maxillary ankylosis”
as proposed by Ross.

 Clinical significance :
1. Lingual inclination will be more severe in those cases
requiring surgical repair of clefts involving the
premaxilla
2. A-P problems worsen with age
3. Problem compounded by the normal anterior
expression of mandibular growth.
4. Consideration to be given to the rest position of the
mandible at the time of record taking.www.indiandentalacademy.com

5. Vertical problems :
 Vertical contributions to the orthodontic
problem arise during the development of the
mixed dentition
1. Progressively decreasing rate of max. vertical
development by the time of early permanent
dentition.
2. Increased severity due to downward and
backward rotation of premaxilla.
3. Cant in the palatal plane

OCCLUSAL CANTING

4. Altered mandibular posture and ass. Increase
in gonial angle.
5. Excessive freeway space
6. Impeded vertical eruption of maxilla
7. Excess vertical D-A development
8. Local disturbances in the vertical eruption of
teeth adjacent to the cleft.
9. Overclosure of the mandible aggravates Cl III
condition www.indiandentalacademy.com

INCREASED LAFH OVER 3 YEARS

Net result of this complex interaction is that in
occlusal contact the vertical deficiency tends to
accentuate the A-P discrepancy b/w jaws, and
then both problems serve to create a worsening
transverse imbalance.
i.e. the primary dentition cannot be used to
evaluate the magnitude of future problems.

ROLE OF ORTHODONTIST
Starts as early as 2 years of age
 Infant maxillary orthopaedics – birth to 2 years
of age
 Orthodontic considerations of primary
dentition (2 yrs to 6 yrs)
 Mixed dentition (7 to 12 tears of age)
presurgical considerations before alveolar
bone grafting
 Final treatment in permanent dentition

Birth to 2 years
Problems
 Smaller segments displaced laterally
 premaxillary segment rotated forward and far
away from cleft
 Deviation of nasal septum
 Median collapse of the lesser segment
(LESSS FREQUENT)

Nasoalveolar Molding For Infants
In 1686, Hoffman described the use of a
head cap with arms extended to the face
to retract the premaxilla and narrow the
cleft.
Improvements to this method of using the
head as extraoral anchorage and it is
used today to retract the premaxilla
Berkowitz S. Semin Orthod 1996;2:169–84.

The concept of an intraoral device to
reposition the cleft alveolar segments is
attributed to McNeil (1950)
In 1975, Georgiade and Latham
introduced a pin-retained appliance to
simultaneously retract the premaxilla and
expand the posterior segments over a
period of days.
B.H. Grayson, D. Maull / Clin Plastic Surg 31 (2004) 149–158

Hotz described the use of a passive
orthopedic plate to slowly align the cleft
segments.
Grayson et al described a technique to
correct the alveolus, lip, and nose in
infants born with cleft lip and palate
B.H. Grayson, D. Maull / Clin Plastic Surg 31 (2004) 149–158

Original research for molding cartilage
was performed by Matsuo
Recognized that the cartilage in the
newborn is soft and lacks elasticity
believes that the high level of estrogen at
the time of birth correlates with the
increased hyaluronic acid, which inhibits
the linking of the cartilage intercellular
matrix
Matsuo K, Br J Plast Surg 1991;44:5– 11

Rationale / Objectives :
1. To facilitate feeding.
2. To help establish normal tongue posture.
3. Provide a psychological boost to patients/parents.
4. Assist the surgeon in his initial repairs.
5. Stimulate palate bone growth.
6. To restore the oro-facial “functional matrix”.

7. To help decrease the number of ear infections.
8. Expand or prevent collapsed segments.
9. To reduce the need for later orthodontic
treatment.
10. To allow soft tissue growth.
11. To guide tooth eruption.
12. Improve esthetics.
13. To reestablish sutural growth patterns

UNILATERAL CLEFT WITH WIDE
NOSTRIL

REDUCTION IN SEVERITY OF
CLEFT DEFORMITY
AFTER PNAM

Frontal View After Primary Surgery

Patient At 2 Years, 5 Months Of Age Showing A Minimally
Detectable Lip Scar

Impression Procedure
Heavy-bodied silicone impression material
is used to take the initial impression as
soon after birth as possible
In case of an airway emergency, the
surgeon is always present to help with the
impression

Infant is held upside down by the surgeon,
and the impression tray is inserted into the
oral cavity
Tray is seated until impression material is
observed just beginning to extrude past its
posterior border.

Infant is kept in the inverted position to
keep the tongue forward and to allow
fluids to drain out of the oral cavity.
Once the impression material is set, the
tray is removed, and the mouth is
examined for residual impression material
that may be left behind.

CHILD IN INVERTED POSITION

Materials of choice:
 Silicon > low fusing compound > Alginate
Elastomeric material records fine detail
Nasal impression is made of clear poly
siloxane

The molding plate is fabricated on the
dental stone model
Made of hard clear acrylic and is lined with
a thin layer of soft denture material
Care is taken to reduce the border of the
plate in the area of the labial frenum
attachments and other areas that may be
likely to ulcerate.

Parents are instructed to keep the plate in
full time and to take it out for cleaning as
needed, at least once a day
The appliance is secured extra-orally to
the cheeks and bilaterally by surgical
tapes which have an orthodontic elastic
band at one end

Infant feeding with bilateral
molding plate in place

Unilateral nasal stent in position
showing lip taping.

The retention arm is positioned
approximately 40 down from the horizontal
to achieve proper activation and to prevent
unseating of the appliance from the palate

Retention Arm Is Positioned Approximately 40 Down From
The Horizontal

In the unilateral cleft, only one retention
arm is used
When the retention arms are engaged by
the tape elastic system, the elastics (inner
diameter 0.25 inch, wall thickness—
heavy) should be stretched approximately
two times the resting diameter for proper
activation force (2 oz)

Retraction of the premaxilla requires
greater elastic traction force than is
required for closure of a unilateral alveolar
gap.
Parents are instructed to place tapes to
approximate the cleft lip segments

Tape should be applied at the base of the
nose (nasolabial angle) and not low on the
lip near the vermillion border
Taping too low can cause undesirable
horizontal lengthening of the lip over time

The tape should be applied to the non-
cleft side first, then pulled over and
adhered to the cleft side; the philtrum and
columella should be brought to the midline

When the cleft alveolus is reduced to 5
mm or less, the nasal stent is added.
The stent is made of 0.036-gauge round
stainless steel wire and takes the shape of
a ‘‘swan neck’’

SWAN HEAD SHAPE

ACRYLIC ADDED TO THE STENT

STENT COATED WITH SOFT
DENTUR LINER

STENT IN PLACE

BILATERAL CLEFT LIP & PALATE

Feeding Plate For Bilateral Cleft
Lip & Palate

Bilateral Cleft Lip & Palate

1 year, 6 months of age.

Primary surgical closure of the lip and
nose is performed from 3 to 5 months of
age
Alveolar segments are in approximation, a
gingivo-periosteoplasty is simple for the
surgeon to perform, avoiding extensive
dissection
Cutting CB,Plast Reconstr Surg 1989;84:409– 17; discussion 418– 9

COMPLICATIONS
Irritation of the oral mucosal or gingival
tissue
Breakdown are the frenum attachments
Intranasal lining of the nasal tip can
become inflamed if too much force is
applied by the upper lobe of the nasal
stent

Area under the horizontal prolabium band
can become ulcerated if the band is too
tight
Poor compliance by the parents can
cause loss of valuable treatment time

PRIMARY LIP REPAIR
Rule of TEN
 10 weeks of age
 10 pounds of weight
 10 gm of Hemoglobin

PRIMARY PALATE REPAIR
Primary bone grafting
Evaluation for SPEECH
Between 14 to 18 months of age

Aim of cleft palate diagnosis :
Cleft palate orthodontic diagnosis must
evaluate potential problems in all three
planes of space, with both skeletal and
dental components.
Must take into account features both
common to and unique for the various
types of clefts, as all tend to get worse
with further growth and development.

Timing of orthodontic
treatment
 FISHMAN
1. Pre-dental : (1-18 months )
- prior to the eruption of the primary
molars.
a) Pre-surgical
b) Post-surgical
2. Deciduous dentition : (3-6 yrs)
- after full eruption of the primary
dentition.
3. Early mixed dentition : (7-9 yrs)
- during eruption of permanent maxillary
dentition.
4. Late mixed and early permanent dentition : (9 yrs
onwards)

 PROFFIT
1. In infancy i.e. before the initial surgical repair of
the lip
2. During late primary and early ,mixed dentition.
3. Late mixed and early permanent dentition.
4. In the late teens, after completion of the facial
growth in conjunction with orthognathic
surgery.

According to cooper :
Emphasis on minimizing total active
orthodontic intervention, limiting it to what
is required to achieve the optimum results.
- Against any orthodontic/orthopedic
therapy.
- Patient’s monitored continuously.
- Wolff’s law
- Questioned the claimed advantages of
pre-surgical orthopedics.

Oslo approach ( 1948 ….)
One of the first cleft treatment teams, based at
two places : Bergen / Oslo
Based on the principles given by Egil Harvold
and Arne Bohn.
Wilhelm Loennecken (plastic surgeon) became
a part of the oslo team (1948) and introduced a
standard surgical procedure for all cleft
treatment.

Loennecken’s operative plan
(1948)
1. No pre-operative orthopedics.
2. Closure of cleft lip in infancy.
3. Simultaneous closure of the alveolar cleft by a
one layer vomer flap during primary lip repair.
4. Closure of the remaining cleft palate in early
childhood by a von langenback palatoplasty.

5. Secondary operations when required based on
the current treatment plan and the
requirements of the orthodontist, prosthodontist
and the speech therapist all aiming at a final
rehabilitation by the age of 20 yrs.
6. All surgery to be done meticulously; no parts –
soft or hard – to be unnecessarily harmed or
removed.

Objectives :(Bergland)
1. Provide an aesthetically acceptable and
healthy dentition for life and to contribute
positively to the general facial form and
appearance.
2. Using appliances as simple as possible.

PHASE I ORTHODONTIC
TREATMENT
Early intervention in cases of deep bite
Removal of traumatic cross bites
Avoidance of asymmetric repositionings

Follow up
 Comprehensive assessment of teeth eruption
 Develop good oral hygiene measure
 Maintain teeth in vicinity of cleft
 Early intervention for rotated incisors
 Early maxillary sagittal protraction (4-8 years)
 Not to over expand the arches

Maxillary protraction devices
 Reverse pull head gear ,Delaire face mask
 Rail style face mask
Individual centre of resistance of maxilla
should be determined due to scar
formation
Anterior segmental twin bracket appliance

Delaire Style Face Mask

RAIL STYLE FACE MASK

Orthodontic preparation for alveolar bone
grafting
Correct segmental collapse
Teeth adjacent to cleft are tipped back to
retain (controlled tipping)

Hinged palatal expanders

Double Hinged palatal expander

Maxillary protraction spring

Maxillary protraction spring
Made up of 0.036”CNA wire
600 – 700 gram force is applied for 2-3months

Primary Dentition stage
Case classified according to Goslon score
indicative of treatment
Dental compensation causes
retroclination of lower incisors
Anterior cross bite leading to functional
shift of mandible

Anterior Teeth Cross Bite

FACE MASK
For growth modification and redirection
 During the treatment the factors to be
considered are
• Ability of child to cooperate
• Severity of malocclusion
• Timing of secondary bone grafts

FACE MASK

Mixed dentition stage
Eruption of permanent teeth beside the
cleft
 Missing
 Malformed
 Ectopically erupted
 Supernumerary
 Misplaced
 Rotated

EXPANSION
V shaped arch form due to collapsed
arches
Maxillary appliances anchor on first
molars for expansion

Cleft subjects exhibit normal posterior
lateral relationship but collapsed anterior
relation
Collapse is not parallel but inward
maxillary rotation with pterygoid plates as
fulcrum

Palatal Helix Expander

Arnold Expander For bilateral
Crossbite

Anterior Drive Appliance
Drives premaxilla forward
Screw can be incorporated in nance button for
anterior expansion

FAN SHAPED EXPANDER
Anterior region expands like fan
LUCA LEVRINI JCO VOLUME 33 : NUMBER 11 : PAGES (642-643) 1999www.indiandentalacademy.com

QUAD HELIX

NITI EXPANDER

NITI EXPANDER
Available in different sizes from 26mm to
44 mm
Generates forces of 180 to 300 gm
Selection criteria
 Measure distance between the buccal cusps
of 36 & 46
 Measure the distance between the central pits
of 16 & 26
 Difference gives the amount of expansion
needed

NITI EXPANDER
Measure the distance between the lingual
surface of 16 & 26 where the sheath is placed
Add 1.5 to 2mm for over correction
Lingual retainer for a period of 3 months to be
used after expansion

Post operatively the fistula gets widened
providing space for the secondary surgery
Retention is advocated by placing the
same appliance after expansion
Tooth movement is delayed by 3-6 weeks
after the graft placement

Secondary alveolar bone grafting
Restores
 Continuous alveolar ridge
 Allows eruption of teeth through the graft
 Implant placement is possible

CLEFT

SECONDARY BONE GRAFTING

TYPES OF BONE GRAFTING
Primary
 Done after lip surgery
 Done generally at 1½ years of age
Secondary
 Provides support for the unerupted teeth
beside the cleft
 Closes oro-nasal fistula
 Support elevation of the alar base on cleft
side

 Continuous ridge
 Stabilization of the repositioned maxilla

Permanent Dentition
Skeletal discrepancy gets accentuated
Profound psychological effect on the
patient

Permanent Dentition
Growth Considerations
 Maxillary deficiency or mandibular
prognathism
 Vertical maxillary excess
 Postural rest position ( frequently increased)
 Obvious saggital & transverse deficiency

Permanent Dentition
Skeletal facial considerations
 Facial balance and proportions to be achieved
If skeletal discrepancy is mild and esthetic
concerns minimal dental compensation by
orthodontic treatment is recommended

Permanent Dentition
If surgery is indicated presurgical
orthodontics is to be carried out

ORTHOGNATHIC SURGERIES
Case is scored with Goslon Yard stick
To delay the surgeries until growth
Additional problem in the velopharyngeal
mechanism may be compromised by
maxillary advancement

Distraction osteogenesis
“ Biologic process of new bone formation
between the surfaces of bone segments
that are gradually separated by
incremental traction”

MAXILLARY DISTRACTION

Distraction devices
External Internal
Bone Born Intra oral Subcutaneous
Submucosal
Extramucosal
Bone Born
Tooth Born
Hybrid
Unidirectional
Bidirectional
Multidirectional

FRACTURE HEALING
IMPACT
INDUCTION
INFLAMMATION
SOFT CALLUS
GRADUAL TRACTION
HARD CALLUS
REMODELLING

Contemporary method of correction
severe maxillary hypoplasia
Benefit lies in more gentle advancement
of maxilla with osteotomy cuts without
down fracture
Maxillary complex is advanced at 1mm/
day in coordination with speech
Good velopharyngeal mechanism is
achieved

FINAL DETAILING
Skeletal surgery
Orthodontic evaluation
Final prosthetic rehabilitation
Final soft tissue revision
Rhinoplasty

RHINOPLASTY

SPEECH CONSIDERATIONS
Children born with palatal clefts are at risk for
speech/language delay and speech problems
related to palatal insufficiency.
Individuals require regular speech evaluations,
starting in the first year of life and often
continuing into adulthood.

Early evaluations
Velopharyngeal function in infants or
toddlers can be assessed indirectly by
asking parents questions about speech
and swallowing.
Child’s speech has a nasal quality or tone
during babbling or early speech attempts.

A mirror held under the nose during
speech also may show fogging, indicating
visible nasal emission during oral sounds.
Examination may be completed, often in
conjunction with the cleft
palate/craniofacial team’s pediatrician and
plastic surgeon.

Speech evaluations before and after palatal
surgery
History is an important part of any speech
evaluation, irrespective of age
Clefting or velopharyngeal insufficiency in family
members
Adenotonsillectomy or other orofacial and nasal
procedures
Feeding or swallowing problems, including nasal
regurgitation
Speech problems
Frequent ear infections

Concerns about patency of air way,
possible nasal obstruction to be
considered

Patient and parent education
Key component of the evaluation is
educating or counseling parents and
patients.
Parents are also counseled about normal
speech/language development, as
indicated

Parents are counseled about instrumental
measures of palatal function and their role
in determining the presence and
magnitude of palatal defects.

Evaluation of velopharyngeal
function for speech
Determination of velopharyngeal function for
speech is a primary component of the speech
evaluation
Knowledge of normal velopharyngeal function
provides the basis for evaluating patients in the
clinical setting.

Characteristics of normal
velopharyngeal function
During normal speech production,
 the velum and pharyngeal walls act as a
valve, closing off the nose from the mouth to
prevent airflow and acoustic energy from
going into the nose during the production of
oral sounds

The open velopharynx allows airflow and
acoustic energy into the nasal cavities for
nasal consonant production
The ability to appropriately and rapidly
open and close the velopharynx during
conversation constitutes velopharyngeal
competence for speech

ARTICULATIONARTICULATION
DISORDERSDISORDERS
Formation ofFormation of
sounds withinsounds within
the mouththe mouth

LOCATION OF SOUNDSLOCATION OF SOUNDS
WITHIN THE MOUTHWITHIN THE MOUTH
Bilabials (p,b,m)Bilabials (p,b,m)
Lingua-Alveolars (t,d,m,l)Lingua-Alveolars (t,d,m,l)
Velars (k,g)Velars (k,g)
Labio-Dental (f,v)Labio-Dental (f,v)
Lingua-Dental (th)Lingua-Dental (th)

MANNER OF SOUNDMANNER OF SOUND
PRODUCTIONPRODUCTION
Stop Plosives (p,b,t,d,k,g)Stop Plosives (p,b,t,d,k,g)
Fricatives/Affricates (s,z,sh,ch,j)Fricatives/Affricates (s,z,sh,ch,j)
Glides (l, r)Glides (l, r)

SUMMARYSUMMARY
LOCATION OF ARTICULATIONLOCATION OF ARTICULATION
MANNER OF ARTICULATIONMANNER OF ARTICULATION
VOICE OR VOICELESSVOICE OR VOICELESS

EXAMPLES OF SOUNDSEXAMPLES OF SOUNDS
BilabialBilabial
Stop-PlosiveStop-Plosive
/P/ and /B//P/ and /B/
Lingua-AlveolarLingua-Alveolar
Stop-PlosiveStop-Plosive
/T/ and /D//T/ and /D/

EXAMPLES OF SOUNDSEXAMPLES OF SOUNDS
Lingua-velarLingua-velar
GlideGlide
/R//R/
Labio-dentalLabio-dental
FricativeFricative
/F/ and /V//F/ and /V/

MOST COMMON ERRORSMOST COMMON ERRORS
/S/ and /R//S/ and /R/
(Common in other languages as well)(Common in other languages as well)

Velopharyngeal insufficiency
Peterson-Falzone et al reported that the term
velopharyngeal insufficiency
Velopharyngeal insufficiency results
 Speech problems
 hypernasality,
 Audible/visible nasal emission
 Weak pressure consonant

Audible nasal emission is caused by
turbulent airflow through the nasal cavities
during oral speech (consonant)
production.
A complete evaluation involves obtaining
speech (perceptual) judgments and
anatomic and physiologic information
related to velopharyngeal function.

Perceptual evaluation
 Perceptual judgments made by an experienced
speech/language pathologist form an essential part of
the evaluation of velopharyngeal function for speech
 Judgments include results of standardized speech sound
articulation testing and judgments of oral-nasal
resonance balance.

 Standardized articulation tests usually can be
administered to children as young as 2 to 3 years
 Patient’s speech sound development and the presence
of errors related to velopharyngeal insufficiency or nasal
obstruction.

ARTICULATION TESTARTICULATION TEST
 InitialInitial (Puppy)
 MedialMedial (Puppy)
 FinalFinal (Pup)

Anatomic evaluation
Information about oral structures,
including information about the presence,
location, and size of palatal fistulas and
the presence and size of tonsillar tissue.
It allows clinicians to visualize dentition,
dental hygiene, and unusual positions of
teeth

Deviations in dentition or occlusion that
result in abnormal surfaces for lingual or
labial contacts could result in speech
sound
Velopharyngeal closure is evaluated by
the visual endoscope

CLOSURE PATTERNS

Cephalometric roentgenography can
provide information about the relationship
of the velum to the posterior pharyngeal
wall

Acoustic rhinomanometry is also used to
provide metric cross-sectional areas along
the entire length of the nasal cavities,
localizing sites of obstruction to better
guide corrective nasal surgery

ACOUSTIC RHINOMETRY
Representative pressure-flow tracing for /pi/ syllables
produced by a normal speakerwww.indiandentalacademy.com

ACOUSTIC RHINOMETRY
Pressure-flow tracing for /pi/ syllables indicating inappropriate
velopharyngeal openings during oral speechwww.indiandentalacademy.com

Prosthetic treatment
3.5 to 5.5 years patient is referred to
prosthodontist for speech bulb
Speech bulb can help in obtaining
velopharyngeal competency
If no development surgery is indicated

Thorough speech assessments by an
experienced speech pathologist working
with the cleft palate/craniofacial team can
best determine treatment approaches in
difficult and complex cases.

Surgical repair
Optimum age – 4.5 years
Hyper nasality can be corrected by
pharyngeal flap
After surgery complication
 Extensive scar tissue
 Non functional uvula
Sphincter pharyngoplasty to be done for
extensive scar

PNAM

PRIMARY LIP REPAIR

PRIMARY PALATOPLASTY

SPEECH THERAPY

PHASE I ORTHODONTICS

SABG

COMPREHENSIVE ORTHODONTICS

PROSTHETIC REHABILITATION

DISTRACTION OSTEOGENESIS

ESTHETIC CORRECTIVE SURGERY

CONCLUSION
Orthodontist as a part of cleft team plays a
key role in determining the timing of the
treatment
Helps in the psychosocial rehabilitation of
the cleft patient

CONCLUSION
The basic understanding of the etiology,
prevention application of the genetic
counseling & modulation, prevention of
the clefts constitute the major future of
cleft treatment
Orthodontic strategies continue to evolve
as new methods and treatment concepts
more directly address the specific
problems of patients who have clefts

CONCLUSION
By continual review of treatment
outcomes and comparing outcomes with
patients’ problem lists and treatment
objectives, clinicians will identify areas of
treatment needing improvement and
formulate hypotheses for future research

BIBLIGRAPHY
Contemporary Orthodontics 4th
Ed –
William R Proffit
Current Principles & techniques – 4th
Ed
Graber, Vanarsdall, Vig
Text Book of Orthodontics – TM Graber –
3rd
Ed
Contemporary treatment of Dentofacial
Deformity – Proffit, Sarver & White – 2nd
Ed

BIBLIGRAPHY
Human Embryology – Inderbir Singh 4th
Ed
New Insights into Facial Development –
Sperber 3rd
Ed
Maxillofacial Prosthesis for Dentofacial
deformity – Taylor 2nd
Ed

BIBLIOGRAPHY
 Current concepts in the embryology and genetics of cleft lip and cleft palate
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 Three-dimensional technology for documentation and record keeping for
patients with facial clefts A.C. Da Silveira et al / Clin Plastic Surg 31 (2004)
141–148
 Mazaheri M, Sahni PP. Techniques of cephalometry,photography, and oral
impressions for infants. J Prosthet Dent 1969;21:315– 23.
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Modified nasal alveolar molding appliance for management of cleft lip
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 Kusnoto B, Evans C. The reliability of a 3D surface laser scanner for
orthodontic applications. Am J Orthod Dentofacial Orthop 2002;122:342–8
 Farkas LG, Cheung G. Facial asymmetry in healthy North American
Caucasians: an anthropometric study. Angle Orthod 1981;51:70 – 7.
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anomalies: perspectives in management. San Diego, CA: Singular; 1996.
 Warren DW, DuBois AB. A pressure-flow technique for measuring
velopharyngeal orifice area during continuous speech. Cleft Palate J
1964;1:52–7.
 Kunkel M, Wahlmann U, Wagner W. Acoustic airway profiles in unilateral
cleft palate patients. Cleft Palate Craniofac J 1999;36:434–40.
 Standardized Facial Photography of Cleft Patients: Just Fit the Grid?
Cleft Palate–Craniofacial Journal, September 2000, Vol. 37 No. 5

 Haydar B, Ciger S, Saatchi P. Occlusal contact changes after the active
phase of orthodontic treatment. Am J Orthod Dentofacial Orthop.
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 Orlagh Hunt, Donald Burden, Peter Hepper and Chris Johnston The
psychosocial effects of cleft lip and palate: a systematic review European
Journal of Orthodontics 27 (2005) 274–285
 Adam B. Weinfeld, MD, et al International trends in the treatment of cleft lip
and palate Clin Plastic Surg 32 (2005) 19 – 23
 William C shaw et al A six center international study of tretament outcome in
patients with cleft lip and palate Cleft palate Cr Fac Sept 1992, Vol 29 No5
 Molsted et al A six center international study of tretament outcome in
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 Mc Dade et al A six center international study of tretament outcome in
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in patients with cleft lip and palate Cleft palate Cr Fac Sept 1992, Vol 29
No5
 Mars et al Golson Yard Stick: A New system fo assessing dental arch
relationships in children with unilateral cleft lip and palate Cleft palate Cr Fac
1987 vol 24 No 4
 John B. Thornton, Sue Nimer, and Paul S. Howard The Incidence.
Classification, Etiology, and Embryology of Oral Clefts (Semin Orthod
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 Samuel Berkowitz 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.)

 Sally J. Peterson-Falzone 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.)
 Peter D. Waite and Daniel E. Waite Bone Grafting for the Alveolar Cleft
Defect (Semin Orthod 1996;2:192-196.)
 Christos C. Vlachos Orthodontic Treatment for the Cleft Palate Patient
(Semin Orthod 1996;2:197-204.)
 Jeffrey C. Posnick Orthognathic Surgery for the Cleft Lip and Palate Patient
(Semin Orthod 1996;2:205-214.)

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