Growth of The Nasomaxillary / Orthodontic Courses by Indian Dental Academy

1
GROWTH OF THE
NASOMAXILLARY COMPLEX

INDIAN DENTAL ACADEMY

Leader in continuing dental education
www.indiandentalacademy.com

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Anatomy:
The maxillary bone is the second largest
bone of face, the first being mandible.
The maxillary bones are two in number
and when two maxillae articulate, they
form:
a. Whole upper jaw.
b. Roof of oral cavity.
3
Greater part of floor and lateral
wall of nasal cavity and part of
bridge of nose.
Greater part of floor of each
orbit.
4
Body -
Large and Pyramidal in shape.

Four processes -
Frontal
Alveolar
Zygomatic
Palatine

5
Body of maxilla is like a hollow
pyramid.

Base of pyramid is formed by nasal
surface and apex is directed towards
zygomatic process.

6
Frontal Process
Maxillary sinus
Maxillary process
[palatine]
Horizontal plate
of palatine
process of maxilla
Alveolar process
7
Sites of attachment of maxilla to surrounding
bones:

1. By pterygomaxillary fissure and
pterygopalatine fossa between sphenoid
bone of cranial base and palatine bones or
maxillary bones or posterior face.

2. The zygomatic bone is attached to
calvaria at temporozygomatic and
frontozygomatic suture.

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3. The maxillary bone and nasal bones
are attached to calvaria at frontomaxillary
and frontonasal sutures.

9
Face
Upper
Middle
Lower
Frontonasal
Prominence
Maxillary
prominence
Mandibular
Prominence
10
Head development depends upon inductive
activity of prosencephalic and rhombencephalic
organizing centers.

Prosencephalic Upper third of face.

Rhombencephalic Middle and lower
third of face.

11
The branchial arches begin to develop
early in 4
th
week due to migration of
Neural Crest Cells into future head and
neck region.

The first branchial arch, the
primordium of the jaws appears as a
slight surface elevation lateral to
developing pharynx.

12
The five facial primordia appear around the
stomodeum or primitive mouth early in 4
th
week.

1. The frontonasal prominence Forms
cranial boundary of stomodeum.

2. Paired maxillary prominences Lateral
boundary of stomodeum.

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3. Paired mandibular prominences Caudal
boundary of stomodeum.

Maxillary
prominence
Mandibular
prominence
Frontonasal
prominence
14
These facial prominences are active
centers of growth in the underlying
mesenchyme and this mesenchyme is
continuous from one prominence to the other.

15
By the end of 4
th
week
each side of the inferior part of frontonasal
prominence.
bilateral oval thickenings of surface ectoderm
mesenchyme proliferates producing horseshoe
shaped elevations

Medial Nasal
Prominence
Lateral Nasal
Prominence
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The maxillary prominences enlarge.
grow medially towards each other and
towards the medial nasal prominences.
moves the medial nasal prominences towards
median plane and towards each other.
Each lateral nasal prominence is separated from
maxillary prominence by a cleft or furrow
called as Nasolacrimal groove.
17 www.indiandentalacademy.com
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By the end of 5
th
week.
+ lateral nasal prominence
continuity between side of nose and cheek region.

Maxillary prominence
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The facial bones develop intramembranously
from ossification centers in embryonic facial
prominences.

In the frontonasal prominence intramembranously
single ossification centre appear in 8
th
week for each
of nasal and lacrimal bone in membrane covering the
cartilaginous nasal capsule.

21
In maxillary prominences numerous
intramembranously ossification centers
develop.

a. In 8
th
week I.U. Medial pterygoid
plates of sphenoid.

Vomer.

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b. In 7
th
week I.U.

Primary intramembranously ossification
center for each maxilla at termination of
infraorbital nerve just above the canine
tooth dental lamina.

Secondary zygomatic, orbitonasal,
nasopalatine and intermaxillary centres
appear and they fuse with primary centre.

23
Two intermaxillary ossification centres
generate the alveolar ridge and primary
palate region.

Single centre for each of zygomatic bone
in 8
th
week.

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Skeletal Units of Maxilla

1. Basal body Infraorbital nerve.
2. Orbital unit Eye ball.
3. Nasal unit Septal cartilage.
4. Alveolar unit Teeth.

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Nasolacrimal Duct

A solid rod of epithelial cells sinks into the
mesenchyme within the grooves between lateral
nasal and maxillary prominences. These rods
extend from the developing conjunctival sac of
eye at medial corner of forming eyelid. These rods
later canalize to form nasolacrimal duct but these
ducts become patent only after birth.

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POST NATAL GROWTH AND
DEVELOPMENT OF MAXILLA

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As in other regions of the craniofacial
skeleton, growth in maxilla occurs by 2
processes:

1. Extensive appositional and resorptional
surface remodeling.
2. Displacement of the maxilla.

Moss referred to these movements as
transposition and translation respectively.
29
Enlow and Bang has described the growth
of maxilla by way of its sutures that attach it
to the cranial base, by applying the principle
of Area Relocation

- (i.e. specific local areas come to occupy
new actual positions in succession, as the
entire bone enlarges, involving both the
processes, translation and transposition).

30
For the precise assessment of remodelling
processes 2 methods have been used:

1. Cross sectional study using histological
sections of dried skulls.

2. Longitudinal studies using implant
markers and Cephalometric radiographs. Bjork
was the first to use this technique in 1955. In
the first technique it was difficult to note the
individual variability in the growth amount and
rate.

31
Postnatal growth of maxilla is mainly
because of:

1. Surface apposition.
2. Sutural growth.
3. Nasal septal growth.
4. Sphenooccipital synchondroses.

32
Growth of maxilla can be viewed in 3 aspects:

1. Growth in the Height.
.
2. Growth in the transverse direction.

3. Growth in the anterio-posterior
direction.

33
HEIGHT
1. In the coronal section, the palate is
V shaped. Applying the Enlow and
Bangs V principle-

Deposition on oral side.

Increases the height of the nasal
cavity.

Resorption on nasal side.
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V principle in sagittal and coronal view

36
2.Similarly surface remodeling of bone in
the alveolar process, which increases the
height of palatal vault.

37
3.In addition to surface remodeling the height of
maxilla is increased by displacement process i.e.
primary and secondary.

38
Primary displacement because of apposition at the
tuberosity and palatine sutures which pushes the
maxilla in a forward direction, thus separating the
sutures and further, causing bone apposition in the
connective tissue.
Primary Displacement
39
Primary
displacement

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Maxillary tuberosity
41
Palato maxillary suture
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The increase in height of maxilla because of
primary displacement can be explained on the
basis of

Sutural theory cartilaginous theory

Functional
hypothesis
43
According to Sicher, the growth potential lies in the
sutures themselves and hence their growth would
ultimately push the maxilla in a downward and
forward direction. This is because the sutures are
oblique in nature and there is a sliding effect at the
sutures due to growth taking place.

44
Sutural theory
explaining the
maxillary growth
45
However this contention was disapproved by
the fact that the sutures are pressure
sensitive unlike cartilages, which are tension
sensitive areas. Thus pressure on the sutures
would cause inhibition of growth.
46

Scotts theory tried to prove that it is because of
the innate growth potential of the nasal septum
that its growth pushes the maxilla downward
because of the thrust effect of septo-
premaxillary ligament and the fibres which are
embedded in the premaxillary segment.

47
However, recent research has shown that the
nasal septum plays an important role in
anteroposterior growth of the maxilla than its
vertical growth and experiments in which the
nasal septum was removed surgically, did not
prove the role of the septum in the
development of the mid-face.

48
Animal and human studies showing the effect of
removal of nasal septum on the growth of the
midface

49
Moss used the functional matrix theory(Van
der Klauuw) that each skeletal unit has its own
functional matrix and that the soft tissue
growth is responsible for the growth of the
skeletal units.
Thus the enlarging oro-facial capsule is
responsible for the increase in height of the
maxilla (e.g. increase in nasal airway). Also
the increase in height of the maxilla is seen to
occur because of the remodelling changes in
the orbit.

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Secondary displacement occurs because of
growth of the anterior and middle cranial
fossa and changes in cranial base flexures.
(Also because of increase in length of
cranial base).

Secondary Displacement
51
Secondary
displacement

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Growth in Transverse Direction:
It is finished earlier in postnatal life.
Occurs by two processes:
Alveolar remodeling in the
lateral surface of alveolar
process
Growth of the mid-
palatine suture
53
Growth of the mid-palatine suture
Mimics general
growth pattern of
the body
Occurs in
response to
the
functional
matrix
Mutual transverse
rotations separate
the posterior
region more than
the anterior
U shaped
arch
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Growth in anteroposterior direction:

1. The increase in the sagittal direction of the
maxilla begins in the 2
nd
year of life and ceases
after the increase in width has taken place.

2.The main increase in the length of the maxilla is
because of surface remodeling in the maxillary
tuberosity region (i.e. appositional changes) and in
the sutures between the palate and the palatine
bones.
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3.Cortical drift - The anterior surface of the
maxilla is mostly resorptive, however, the
total growth of the maxilla is seen to be in an
antero-inferior direction. This is because as
the maxilla remodels, it is simultaneously
translated in an antero-inferior direction.
4.Thus, it is both the remodeling and
translatory growth process, which brings
about the change in anteroposterior
direction.
5.The translatory changes - Primary and
Secondary displacement.

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The antero-inferior displacement of maxilla

Sutures nasal septum,
sphenooccipital
synchondrosis

the
orofacial
functional
matrix
57
Discussion of the study conducted by
Sheldon Baumrind (AJO Jan, 87).

In their study, they used implant
markers and computer aided methods
for analyzing the lateral skull
radiographs.

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They used 3 reference points. ANS, PNS and Point
A.
1.In their findings, they found out that there was a
uniform displacement of all the 3 points in the
vertical direction. On an average, the mean
downward displacement was about 0.3mm / year.
2.In the horizontal direction, there was a posterior
displacement of all the 3 landmarks. However, the
displacement of PNS was greater than point A and
ANS. Thus this finding proves that the increase in
length is primarily by growth at the posterior
border.
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3.The backward and downward remodeling of all
the 3 landmarks is reduced after about 13.5
years. This finding was consistent with the cross-
sectional studies on dry skull.

4.They found that the mode of pattern of
remodeling between treated and untreated
patients was different. This, if true, would be of
major biologic and clinical interest.

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Effects on dentition and occlusion
1. Bimolar width in the 1
st
molar area
correlates with vertical growth of maxilla,
growth in midpalatal suture and growth in
height.
2. Dental arch drifts forward on an
average of 5mm by late adolescence in the
molar region and by 2.5 mm in the incisor
region.
3. The shortening of maxilla arch
perimeter is coincident with the eruption of
2
nd
molars and not the 3
rd
molars.

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Growth of Zygomatic region
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The malar region
anterior surface Posterior surface
Resorption Apposition
64
This posterior remodeling is basically
to keep pace and close contact relation with
the maxillary bone. However, the magnitude
of relocation is less as compared to the
maxilla.

This posterior relocation thus ceases
after increase in dental arch length is
achieved during childhood.

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Bone deposition
inferior edge
of the zygoma
the fronto-zygomatic suture
vertical growth / increase
in the height of the
anterior part of zygomatic
arch and the malar
region.
increase in
vertical length of
lateral orbital
rim.

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The lateral growth of the
zygomatic region.
resorption on the inner
aspect of zygoma.

periosteal deposition on
the lateral surface of
zygoma.
Enlarges the temporal fossa and
keeps the cheek bone in proper
proportion to the enlarging face.

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The antero-inferior displacement of the
zygoma occurs simultaneously along with
the maxilla and the magnitude is also the
same. This is basically because of primary
displacement of maxilla.

69

Zygoma
displaced
anteriorly
displaced
inferiorly

zygomatico-
temporal suture
frontozygomatic suture
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Growth and Development of Palate

72
Oral development in the embryo is demarcated
early in life by the appearance of the prechordal
plate in the bilaminar germ disk on 14
th
day of
development. The face derives from 5
prominences that surround central depression - the
stomodeum that constitutes the future mouth. The
prominences are:

1. The single frontonasal prominence.
2. The paired maxillary prominences.
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3. The paired mandibular prominences.
The later two being derivative of the first
branchial arch.
All these prominences and arches arise
from Neural Crest Cell ectomesenchyme.

74
Oronasopharyngeal
chamber
Oropharyngeal membrane
disintegrates.
Continuity of passage
between mouth and
pharynx.
28
th
day
Primitive stomodeum
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Entrance into gut
Frontonasal
and maxillary
prominences
Horizontal
extensions
Oral
cavity
Nasal
cavity
76
Frontonasal
prominence
Maxillary
prominence
Primary
palate
Central part of
upper
lip(tuberculum)
Lateral
shelves
Horizontal
extensions
of
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Palate
Primary palate
Secondary palate
Palatogenesis
5
th
week I.U to 12
th
week I.U.
Critical period
end of the 6
th
week until the beginning
of the 9
th
week.

Structure of Palate
79
frontal
prominence
medial nasal
prominences
deep (internal) part of
the intermaxillary
segment.
primary palate or
median palatine
process.
a wedge shaped mass of
mesenchyme between the
internal surfaces of the
maxillary prominences of the
developing maxilla.
fusion
The Primary
Palate
80
Primary palate
81
The primary palate becomes the premaxillary
part of the maxilla, which lodges the incisors.

The primary palate gives rise to only a very
small part of the adult hard palate (i.e. the part
anterior to the incisive foramen).

82
internal aspects of the
maxillary prominences
two horizontal
mesenchymal
projections
lateral palatine
processes
Secondary Palate
The Secondary Palate
83
Secondary palate
84
the lateral palatine
processes elongate and
move to a horizontal
position.
Lateral palatine
processes
Nasal septum
Primary
palate
ventrally or
anteriorly during the
9
th
week.
dorsally or posteriorly in
the region of the uvula by
the 12
th
week.

fusion
85
Formation and Elevation of palatal shelves:
The coincidental development of the tongue
from the floor of the mouth fills the oronasal
chamber intervening between the lateral palatal
shelves.

At 6 weeks the tongue is a small mass of un-
differentiated tissue pushing dorsally into the
nasal cavity, palatal shelves develop in a
wedge shape and, because of the presence of
the tongue, grow downward into the floor of
the mouth along either side of the tongue.

86
At 8 weeks, the steps in the palatal
development result in the movement of the
palatal shelves from a vertical position beside
the tongue to a horizontal position overlying
the tongue.

89
Nasal septum
Palatal shelf
Tongue
90
Nasal septum
Palatal shelf
Tongue
91
This change in the position probably involves
movement of both the tongue and palatal shelves.
Several mechanisms have been proposed for this
rapid elevation of the palatal shelves.
1. Biochemical transformations of the
connective matrix of the shelves.
2. Variations in vasculature and blood flow
to these structures.
3. A sudden increase in their tissue trigger.
4. Rapid differential mitotic growth.
92
5. An intrinsic shelf force.

6. Muscular movement.

7. The withdrawal of the embryos face from
against the heart prominence by uprighting of the
head facilitate jaw opening. This jaw opening
reflexes have been implicated in the withdrawal of
the tongue from between the vertical shelves.

95
8. Pressure differences between the nasal and
oral regions due to tongue muscle contractions
may account for palatal shelf elevation. This
occurs generally at about 8
th
or 9
th
week after
conception.
9. It is possible that the nerve supply to the
tongue is thus sufficiently developed to provide
some neuromuscular guidance to the intricate
activity of palatal elevation followed by closure.

96
Fusion of the Palatal Shelves:

During palatal closure i.e. following palatal
elevation.

The mandible becomes more prognathic.

The vertical dimension of the stomodeal
chamber increases.

97
Maxillary width remains stable, allowing
shelf contact to occur.

Also forward growth of Meckels
cartilage relocates the tongue more
anteriorly, depressing downward and
laterally thus pushing the palatal shelves
slide medially.

98
Generally the epithelium overlying the edges of
the palatal shelves is especially thickened.

The fusion occurs between the dorsal surfaces
of the fusing palatal shelves and the lower edge of
the midline nasal septum.

It also occurs anteriorly in the hard palate region
with subsequent merging of the soft palate.

99
Epithelial adherence between contacting palatal
shelves is facilitated by degeneration of the epithelial
cells and a surface coat accumulation of
glycoproteins.
Only the medial edge of the epithelium of the
palatal shelves (in contrast to their oral and nasal
epithelia) undergoes cytodifferentiation involving a
decline of epidermal growth factors receptors that
lead to cell programmed cell death of fusing epithelia
is essential to mesenchymal coalescence of the
shelves. www.indiandentalacademy.com
100
Fusion of the 3 palatal components initially produces
a flat, unarched roof to the mouth.

The fusing lateral palatal shelves overlap the
anterior primary palate.

The site of junction of the 3 palatal components is
marked by the incisive papilla overlying the incisive
canal.

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Incisive
foramen
Mid palatine
suture/raphe
102
Mid palatine
suture/raphe
103
The line of fusion of the lateral palatal
shelves is traced in the adult by the
midpalatal suture and on the surface by
the midline raphe of the hard palate. This
fusion stitch is minimized in the soft palate
byinvasion of extraterritorial mesenchyme.

104
Ossification of the Palate:

This proceeds during the 8
th
week intrauterine
from the spread of bone in the mesenchyme of
the fused lateral palatal shelves and from the
trabeculae appearing in the primary palate as
premaxillary centres all derived from the
single ossification centre in the maxillae.
Posteriorly the hard palate is ossified by
trabeculae spreading from the single primary
ossification centres of each palatine bone.

105
Midpalatal suture
structure
coronal section
is Y shaped
the junction between
3 bones rises in T
shape
infancy childhood
mechanical interlocking and islets of
bone are formed.

adolescence
(10 weeks)
106
Structure of the midpalatal suture has been
traced by Melson at 3 different stages:

Infantile -- Y shape.

Juvenile -- T shape serpentine course.

Adulthood-- Iigraw possle.
107
Ossification does not occur in the most superior part of
the palate giving rise to the region of soft palate.

108
Musculature of the Palate:

The myogenic mesenchyme of the first, second and
fourth branchial arches migrate into this faucial
region supplying the musculature of the soft palate
and fauces. The tensor veli palatini is derived from
the 1
st
arch, the levator palatini and uvular from the
2
nd
arch, 4
th
arch gives rise to the trigeminal nerve
innervation for tensor veli palatini muscle and vagus
nerve for other muscles.

109
Development Period of Muscles:

Tensor veli palatini - 40 days
Palatopharyngeous - 45 days
Levator veli palatini - 8
th
week
Palatoglossus - 9
th
week
Uvular muscle - 11
th
week

110
Growth in the Dimensions of the Palate:
The hard palate grows in length, breadth, and
height becoming an arched palate. The fetal palate
increases in length more rapidly than in width
between 7
th
and 18
th
week intrauterine and
widening occurs from 4
th
month onward.

In early prenatal life the palate is relatively long,
but from the 4
th
month intrauterine it widens as a
result of midpalatal sutural growth and
appositional growth along the lateral alveolar
margin.

111
At birth the length and breadth of the hard palate
are almost equal. The postnatal increase in
palatal length is due to appositional growth in the
maxillary tuberosity region.

112
During infancy and childhood bone apposition
occurs on the entire inferior surface of the palate and
superior (nasal) surface undergoes resorption. This
remodeling results descent of the palate and
enlargement of the nasal cavity (i.e. to keep pace
with the increasing respiratory requirements).

113
The appositional growth of the alveolar processes
contributes deepening and widening of the vault of
the bony palate and also increases the height and
width of palate. A variable number of transverse
palatal rugae develop in the mucosa covering hard
palate. They appear even before the fusion, which
occurs at 56 days intrauterine.

114
V Principle of Bang and Enlow in the
Remodelling of the Palate:
As mentioned earlier the palate grows in an inferior
direction by subperiosteal bone deposition on its
entire oral surface and corresponding resorptive
removal on the opposite side. The entire V shaped
structure thereby moves in a direction towards the
wide end of the V and increases in the overall size
at the same time.

115
V principle in sagittal and coronal view

116
Factors in Normal Development of Palate:
1. Elevation of head and lower jaw, opening
of the mouth and movement of tongue.
2. Deficiencies of oxygen, various foodstuffs
or vitamins have been reported causing cleft lip
and palate.
3. Excess of endocrine substances, drugs, and
irradiation has teratogenic effect on the
developing palate.

117
4. In regards to vascularity, which of course
controls the amount of oxygen and nutrition
determines the normal development of palate.

5. Failure of degeneration of the epithelium
during fusion leads to failure of fusion of the
prominences
118
Anomalies of Palatal Development:

1.Epithelial Pearls: Entrapment of epithelial
rest or pearls in the line of fusion of the palatal
shelves, (particularly in the midline) gives rise
to median palatal rest cysts.

119
Epithelial pearls

120
2. Delay in elevation of palatal shelves
from vertical to the horizontal while head is
growing results in widening gap between the
shelves so they cannot meet leading to cleft
of the palate.

Variations in Clefting of Palate: Cleft palate
is part of number of syndromes like
Mandibulofacial dysostosis (Treacher Collin
Syndrome), Micrognathia (Pierre Robbin
Syndrome) and Orodigito facial dysostosis.

124
3. High arched palate seen in Marfans
Syndrome, Cleidocranial dysostosis Crouzon
syndrome.

2. Torus Palatinus Genetic anomaly of the
palate is a localized mid palatal overgrowth of
bone of varying size. If prominent, may interfere
with the seating of removable Orthodontic
appliance or upper denture.

126
Cleft Lip And Palate
127
Orofacial clefts
Most common of all facial malformations
Occur in most racial and ethnic groups
Overwhelming physicological impact
128
Davis and Ritchies Classification(1922)
Group 1 Group 2 Group 3
Pre-alveolar
clefts
unilateral bilateral
Post-alveolar
involving hard
and soft palates
Primary and
Secondary
palate
Classification
129
Fogh and Anderson Classification(1942)
Type 1 Type 2
Type 3
Hare lip Lip and palate
Only palate
single
double
single
double
130
Kernahan and Starks Classification(1958)
Class I
Class II
Class III
Cleft of
primary palate
Cleft of
secondary
palate
Cleft of primary
and secondary
palate
131
Class I
132
Class II
133
Class III
134
Veau and Recamiers Classification
Class I-Unilateral and bilateral cleft of the
vermillion border not extending into the lip.
Class II-Unilateral or bilateral notching of
vermillion extending into the lip,but not
including the floor of the nose.
Class III-Unilateral and bilateral clefting of the
vermillion border involving lip and extending
into the floor of the nose.
Class IV-Any bilateral cleft of the lip whether
incomplete or complete.
Cleft Lip
135
Cleft Palate
Class I-Cleft involving only soft palate.
136
Class II-Cleft involving hard and soft palate
extending no further than the incisive
foramen.
137
Class III-Complete unilateral or bilateral cleft
extending from uvula to incisive foramen and
then deviating to one side.
138
ClassIV-Complete bilateral cleft similar to
class III with two cleftsd extending
forward from the incisive foramen
into the alveolus.
139
The International Confideration for
Plastic and Reconstructive
Surgery(IPRS) Classification(1968)
Group I Clefts of anterior (primary) palate
(a) lip:right and/or left.
(b) alveolus:right and/or left.
Group II Clefts of anterior and posterior palate
(a) lip:right and/or left.
(b) alveolus:right and/or left.
(c) hard palate: right and/or left.

140
Group III Clefts of posterior(secondary)palate
(a) hard palate:right and/or left.
(b) soft palate : median.
Rare Facial Clefts(Topographic)
(a) median clefts of upper lip with or without
hypoplasia or aplasia of the premaxilla.
(b) oblique clefts(oro-orbital);
(c) transverse clefts(oroauricular);
(d) clefts of lower lip,nose and other very rare defects.
141
Clefts of hard and soft palate result from the
defective development of embryonic secondary
palate.
Most clefts of primary palate are due to
variable degrees of mesenchymal defeciencies
in facial processes(or)distortion of the
processes.
Clefts of secondary palate are associated
with grown distortions subsequent to cleft
formation in the primary palate which prevent
contact of palatal shelves.
MECHANISM OF CLEFT FORMATION.
142
Primary Palate
Fusion of facial
processes
Formed by
epethelial
invagination
Clefts of
primary palate
Major portion
Minor portion
143
Cleft Lip

-- persistence of a temporary phase of embryonic
development.(Longacre 1970;Wiiliam Harvey 1651)
--persistence of epethelial wall between frontonasal and
maxillary processes.(Hochestetter and Veau)
--mesenchymal insufficiency in the region of
consolidation.(Tondury 1964)

144

Cleft Palate

--delay in timing of palatal shelf alignment.(Tondury)
--tissue breakdown subsequent to fusion.(Kraus 1970)
--Failure of epethelial breakdown due to non
contact of the shelves.(Burdi 1977)

145
Patten(1961) stressed the importance of the primordial
ground substance which controlled the migration of
the mesenchymal cells.

146
Poswillo(1968) investigated cleft palate with
micrognathia in rats and concluded that cleft palate
is caused due to-

--interference with intrinsic shelf force.
--excessive head width or diminuitive palatal shelves.
--excessive tongue resistence.
--non-fusion of the shelves.
--fusion of shelves with subsequent breakdown.

147
Increased facial width
Tendency for
defeciency
Aggravated by
increase in
forebrain
width
Increased interorbital
width
Because upper face presses
too firmly against the heart

Mesenchymal
proliferation
Mesenchymal
migration
148
Distortion or Malposition of Facial Processes
Distortion of M.N.P
Malposition of nasal
placodes
Unequal
mesenchymal
distribution
(Transler)
149
Associated Clefts of Secondary Palate
(Transler and Fraser)
Tongue remains high in primary clefts.
Tongue gets wedged in the cleft.
Other abnormal forces delay shelf elevation
and lead to secondary palate clefts.
150
Heterogenicity
Genetic factors
Environmental factors
Occurrence in relatives
Other malformations
1deg
3deg
2deg
Metabolic alterations
Drugs
Dietary factors
Infections
X-radiations
Anatomic and
physiologic variation
in the uterus
Etiology
151
Heterogenicity
High percentage with chromosomal
abnormality
Few who live trisomy D or E
Mostly trisomy 21 Downs Syndrome
Van der Woudes Syndrome
Waaldenburgs Syndrome
152
variable combination of cleft lip and
palate,cleft lip with lower lip pits.
caused by a single gene.
when one parent has the expression of the
gene then 50% of the offsprings have the
same manifestations.
1-2% of the cleft lip and palate cases
belong to this group.
Van der Woudes Syndrome
153
Waaldenburgs Syndrome
High incidence.
if single cases occur it suggests cause is
environmental.
if unexpected high uncidence in a family it
suggests cause is genetic.
Only small number of cases have
chromosomal abnormalities and single gene
defects.
Vast number of cases are environmentally
influenced.
154
Genetic Factors
Occurrence in relatives
Fogh Anderson in 1942 did pedigree studies
and quoted The mode of inheritence is recessive
with variable expressivity.
According to Roberts Multifactorial
etiology.Supported by Carters and is the most
widely accepted.
155
Classification of relatives with the defect
First degree one half of the same genes are
inherited e.g siblings,parents and offspring.
Second degree one quarter of the same genes are
inherited e.g aunts,uncles,neices,nephews.
Third degree one-eighth of the same genes are
inherited e.g first cousins.
This significance is consistent with Falcon
Multifactorial Threshhold model.

159
If a large no. of individuals
of a family are affected
Presence of a large no. of predisposing factors +
environ.conditions
Amount of mesenchyme
Insufficient for facial processes to form and fuse
Partial or complete clefts
160
Other malformations
Incidence of serious malformations in relatives
of cleft lip and palate patients cannot be much
above general population.
(Fogh and Anderson)
Incidence is greater in families with a negative
history.
(Drillen)
161
Environmental Factors
Anatomical variations in uterus leads to
isolated cleft palate.These variations may be due
to :
Uterine physical manipulations.
Alteration in blood supply(hypoxia).
Uterine pressure.
Amount of uterine fluid.
162
-Mothers of children suffering from CL and CP tend
to be relatively elderly,less fertile,to have a high
casuality rate among pregnancies and a higher
proportion of abnormal offspring than general
population.(Wallace 1968)

-Habitual aborter and emotional stress was implicated
as a cause of CL and CP by Haight and Stark.(1968)
163
Metabolc Alterations
Greater significance since most hormones and
metabolic products transverse the placenta and
influence the embryo.
1. DIABETES
-If mother is diabetic,chances of child
being a diabetic is 3 times higher.
(Fogh-Anderson)
164
Evidence of increased resistence to action of
insulin in some diabetics anti-insulin factor .
(Vallance-Owen)
Study showed 15 of 22 mothers with cleft lip
and palate in children had this factor.

2.THYROXINE DEFECIENCY
Partial thyriodectomy in rats variable
degrees of cleft formation.
165
3.MATERNAL ANTIBODIES

May interfere with placental function
Cleft formation
166
I nfections
Viruses-implicated as teratological agents-
Rubella--cardiac disorders,cataracts,deafness
Cytomegalovirus--microsomia
Protozoans
Toxoplasma-incidence of infestation 2-4
times in mothers of children with facial
clefts over control mothers.
167
Drugs
Thalidomide--role +ve in animals,man
unlikely.
Aminopterin--severe effects on embryo,
causing cleft lip and palate.
Anticonvulsant drugs--cleft lip and palate
teratogens.
Hadacidin
Aspirin

Capable of producing clefts.
168
Dietary Factors
Vitamin excess in rats.
Not proven in humans.
X-Radiation
Capable of producing clefts in animals.
not proven in human beings although
incidence of mental retardation and
microcephaly is increased.
169
Clinical Features Of Cleft Lip And Palate
Natal and Neonatal Teeth.
Congenital absent Teeth.
Supernumery Teeth.
Ectopic Eruption.
Hypoplasis,Microdontia,Macrodontia.
Rotations.
Posterior Cross Bites.
170
Protuberant,mobile premaxilla.
Nasal septum deviated to normal side.
Teeth adjacent to cleft have poor periodontal
support which makes these teeth
--susceptible to premature loss.
--anchorage problems.
171
Clefts between M.N.P
Oblique facial clefts (maxillary process on
one side and M.N.P on the other side.)
Lateral Facial Clefts (between maxillary
and mandibular processes)
Median Facial Cleft (development failure
of frontonasal process derivatives)
Types of Facial Clefts-
172
Facial Growth in Unrepaired
Cleft Lip and Palate
Unilateral CL and CP
Neonatal size of palate remains within normal
limits.(Miyazaki 1975)
High frequency of asymmetry between affected and
unaffected sides due to tissue discrepancy in the
anterior end of the minor palatal segment.(Mapes et al
1974)
173
Width of maxilla is greatly increased.(Subtelny
1955)
Forward rotation and protrusion of premaxilla
due to forces of the tongue.This protrusion
increases with age.(Longacre 1970)
Medial collapse and flattening of alveolar
process on affected side.(Van Limborgh 1964)

174
Bilateral Complete CL and CP

Growth of nasal septum carries the premaxilla
forward through its attachment to the
septopremaxillary ligament.(Latham 1973)
175
Dental Occlusion
Maxillary buccal teeth are usually in normal
buccolingual relatiomship with mandibular
teeth but maxillary incisors are protruded.

In bilateral clefts,incisors show excessive
eruption and canines are inclined towards the
cleft.
176
Supernumery teeth and Aplasia occur more frequently.
Supernumery Teeth
--more common in decidous dentition.
--incidence is decreased as the extent of cleft increases.
--greatest in cases of cleft lip.
Aplasia
--lowest in isolated cases of CL and CP.
--increases with increased complexity of cleft.
177
Anterior crossbites occur which may be unilateral
or bilateral.(Dahl 1970)

Upper incisors are retroclined with increased severity
of the cleft.
178
Musculature
Unilateral clefts
Bilateral clefts
Severe underdevelopment
and atrophy of lip muscle.
Upper lip may be
slightly less protrusive
than normal.
179
Conclusion
Excluding the initial tissue defect and
distortion,facial growth proceeds in
reasonably normal fashion in children with
unrepaired clefts,but the existing
normal growth potential must proceed on the
abnormal substrate.

180
Post Surgical Growth And Development
Unilateral CL and CP
Tightness of repaired lip anterior cross bite.
Redundancies.
Tongue thrust separation of maxillary
segments.
181
If short lip develops excessive protrusion of
premaxilla.
Bilateral CL
If the lateral segment of the lip is brought below
philtrum to produce a long lip crossbite posteriorly.

182
Effect on the Palate
Healing after surgery
Scar tissue
Constricting force on the maxilla
mostly in anterior region
Amount of
alveolar bone
Size of inferior
turbinate and nasal
septum
Lowering of
soft tissue of
palatal vault
183
Nose
Tip becomes
retrusive.
Columella
becomes
short.
Nasal
bones get
distorted.
Nasal septum
becomes
concavoconvex.
185
Long Term Effects
General
Difference in growth timings.
Growth spurt is delayed. (Shibaski and
Ross)
Maxilla
Retruded but anterior vertical height is normal.
Crossbites occur.
Retrusion of teeth.
Arch length.
186
Occlusion
Abnormal position of teeth

Abnormalities of reattachment of labial
frenum
delayed eruption of anterior teeth.
open bite tendency.

Protrusion of lower lip.
palatal
crossbites
187
Forward Growth of Maxilla
Scar tissue formation which joins maxillary palatine
bones,pterygoid plates Maxillary Ankylosis.
Dentoalveolar Retrusion
1.Scar tissue formation in anterior region due to
surgical palatography.
2.Decreased tongue support.
3.increased lip pressure.

190
Intrinsic growth defeciency.
Pressure from tight
upper lip.
maxillary skeletal and
dentoalveolar growth.
Constricting
effect of
palatal scar.
Pulls teeth medially.
192
Mandible
Nasal septal deviation
Interferance with
nasal breathing
Mouth breathing
Tongue drops
Mandible drops
down
Contracted
maxillary arch
Low
palatal
vault
nasal width
Encourages further
collapse of maxillary
arch
193
Mandible
Retrusion of chin.
Upward and forward displacement of condyle.
Steep mandibular plane angle.
Decreased body mass at gonial angle.
194
Management Of Cleft Lip And Palate.
Age Orthodontics Surgery

0-3 months Stage 1(a) ------

3 months -------- Lip repair.

3.5-12 months Stage 1(b) ------

Presurgical oral
orthopaedics for lip.
Presurgical oral
orthopaedics for palate.
195
Age Orthodontics Surgery
12 months ------ Palate repair
8 years Stage 2 -------

Orthodontics
(6 months)
Orthodontics
(18 months)
10-12 years Stage 3 -------
13-14 years ------ Secondary surgical
procedures www.indiandentalacademy.com
196
Orthodontic Management
1.Presurgical Orthopaedics
(a) in preparation of the repair of the lip,
(b) in preparation for the palatal surgery.
2. Early Mixed Dentition Orthodntics
--the correction of gross irregularities causing
functional disturbances of the occlusion.
3. Orthodontic Treatment in the established
Permanent Dentition
--the final correction and detailing of any
malocclusion.
197
Aims Of Orthodontic Management
Phase 1
To facilitate surgery and enhance the functional
and aesthetic result.
To provide support to the parents at a critical time.
To ensure the development of a good facioskeletal
form(dental base relationship) with an acceptable
decidous occlusion and with the potential for easy
correction of irregularities in either the mixed or the
permanent dentition.
198
Phase 2
Abolition of any displacement activities either
anterior or lateral.
Phase 3
The speedy corrections of malocclusions
found,using a system of controlled tooth movements
and where necessary the placement of permanent
teeth in a good relationship for the construction of
fixed or removable prosthesis to replace any missing
permanent teeth where it is not possible to close the
gap orthodontically.
199
MAXILLARY TUBEROSITY
200

Horizontal lengthening of the bony maxillary arch.

Maxillary growth in posterior direction.

Posterior boundary of anterior cranial fossa.

Remodeling at the tuberosity region produces the
lengthening.
201
grows posteriorly
Maxilla carried
anteriorly
Tuberosity
lateral surface
Arch
widening
endosteal side of the
cortex(interior surface)
Cortex moves
posteriorly and
laterally
Maxillary Sinus
increases in size
+++ +++
---
203
The stimulus for sutural bone growth
(remodeling) relates to the tension produced by
displacement of that bone and deposition of new
bone is tandem to the displacement and not due
to the new bone on the posterior surface of the
elongating maxillary tuberosity which push the
maxilla against the pterygoid plate as was earlier
thought.

204
Clinical Significance:

1. The depository growth potential of the
tuberosity allows the clinician to expand the
arch by moving the teeth posteriorly into the
area of bone deposition.
2. In a Class II molar relation, such distal
molar movement aid in achieving the
treatment goal of a Class I molar
relationship.

205
Lacrimal Suture
206

Lacrimal bone is a diminutive flake of a bony
island with its entire perimeter bounded by
sutural connective tissue contacts, separating it
from the many other surrounding bones.

207
Lacrimal Suture
Collagenous linkage within sutural cartilage.
Slippage of bones along
perilacrimal sutural interface.
Maxilla displaced
inferiorly.
209
Remodeling Rotation of Lacrimal bone
Medial superior part
Inferior part
Remains with lesser
expanding nasal
bridge.
Moves markedly outward
to keep pace with
expansion of ethmoidal
sinuses.
211
Nasal Airway
212
Nasal Airway
lining surface of the bony
wall and floor
nasal side of the
olfactory fossae
lateral and anterior
expansion of the nasal
chamber
downward
relocation of the
palate
resorption
deposition
213
Ethmoidal Conchae
lateral and inferior
sides
superior and medial
surface
deposition
resorption
downward and lateral movement
214
Inter Nasal Septum
lengthens vertically at its
sutural junctions.
wraps in relation to
variable amounts and
directions of septal
deviation.
Bony portion
215
Individually variable remodeling changes are seen
and the thin plate of bone show alternate fields of
deposition and resorption on right and left sides
producing a buckling to one side or the other.

217
MAXILLARY SINUS
218
MAXILLARY SINUS
The largest of
paranasal sinuses.
Pyramidal cavity in the
body of the maxilla.
Antero-Posteriorly
posterior to roots of
maxillary canine
area of 3
rd
molar
Borders
219
Supero Inferiorly
Floor of the orbital
cavity.
Root tips of
maxillary
posterior teeth.
Communication:
Posterior part of the
hiatus in the middle
meatus.
maxillary ostium
220
Physiology:

It is lined by mucous membrane
(pseudostratified columnar ciliated
epithelium).

Mucociliary mechanism provides the
means for removal of particulate matter
and bacteria.

221
Function:

Imparts resonance to the voice during
speech.

Lightens the skull or overall bone weight
by being hollowed cavities.

Warms the air as it passes into respiratory
system.
222
Growth of Maxillary Sinus
PRENATAL AT BIRTH
Lateral evagination or
pouch of mucous
membrane of the
middle meatus of the
nose.
Shallow cavity 2cm A-P
in length,1cm in width
and 1cm in height.
3
rd
month I.U
223
Primary pneumatisation early paranasal
sinuses expand into the cartilage walls and
root of the nasal fossae by growth of mucous
membrane sacs into maxillary, sphenoid,
frontal and ethmoid bones.
Starts in 10 weeks I.U from the middle
meatus.
Secondary Pneumatization sinus enlarges
into bone from their initial small outpocketing
always retaining communication with nasal
fossa through ostia..
Starts in the 5
th
month intrauterine.
224
Postnatal Growth
maxillary internal walls
(except medially)
medial wall
Maxillary Sinus
resorption deposition
Nasal Cavity
nasal surface
resorption
225
The rapid and continuous downward
growth of this sinus after birth brings its
walls in close proximity to the roots of
buccal maxillary teeth and its floor below
its osteal opening.

226
As each tooth erupt, the vacated bone becomes
pneumatised by the expanding maxillary sinus
whose floor descends from its prenatal level above
the nasal floor to its adult level below nasal floor.

Into adult hood the roots of molar teeth
commonly project into sinus lumen.

228
Size: Average sinus is 7mm in length and
4mm in height & width and it expands 2mm
vertically and 3mm anteroposteriorly each
year.
229
ORBITAL GROWTH
230
ORBITAL GROWTH
Orbit
Maxilla
Ethmoid
Lacrimal
Frontal
Zygomatic
Greater and
Lesser wings
of Sphenoid
231
Growth of the
Orbit
Remodeling
growth
Displacement
among bony
elements
232
Orbit
Roof Lining
Floor
deposition
remodels
anteriorly and
inferiorly
Frontal lobe of the
cerebrum expands
forward and downward
resorption on endocranial
side and deposition on the
orbital side.
233
Remodeling
changes in
the orbital
region

234
i. Orbit grows by V principle
The cone shaped orbital cavity moves (relocation
to remodeling) in a direction towards its wide
opening. Deposits on the inside, thus enlarge the
volume rather than reducing it.
The growth of the orbit can be explained as:
236

ii. Enlarging displacement is directly involved.
Sutural bone growth at the many sutures within and
outside the orbit. Orbital floor is displaced and
enlarges in progressive downward and forward
direction along with the rest of maxillary complex.

237
Previous studies by Enlow, Bang and Bjork
have shown that in addition to the lowering of
the nasal floor by downward growth
displacement of the maxillary body, the nasal
floor is further lowered by resorption and
apposition taking place on the oral surface of
hard palate.
The floor of the nasal cavity in adults is
positioned much lower than floor of the
orbital cavity, whereas in child they are at the
same level..

239
Clinical Implications

Maxillary Growth
Of
240
Cessation of maxillary growth in 3 planes
of space is in the following order:

1. Tranverse
2. Anterio-posterior

3. Vertical
241
Transverse growth of maxilla

In narrow palatal vault posterior cross bites are
usually seen.

Skeletal Dental
242
Skeletal

Unilateral
Bilateral
Present in CO and CR
present at centric occlusion
but not in centric relation
243
Dental crossbite
Quadhelix W arch
Cross elastics Archwire to
some extent
244
Anteroposterior growth of maxilla
Class II skeletal malocclusion can be due to 3
reasons
1. Prognathic maxilla.
2. Deficient mandible.

3. Or combination.
245
Maxillary excess
Head gear
Functional appliances
Cervical
HG
Occipital HG
Removable

Fixed
246
Removable
Activator
Bionator
Twin Block
Fixed
Herbst
Jasper Jumper
247
Maxillary deficiency
Face Mask
Reverse pull
head gear
Petit
Delaire
Reverse functional
appliance
Class II
frankel
Twin
blocks
248
Vertical growth of maxilla
HP headgear to
functional
appliance
Bite blocks
on functional
appliance
High pull
headgear to
maxillary
splint
.

High pull head gear
to molar.
Long face Class II treatment
249
References
1.Contemporary Orthodontics-William R. Profitt
2.Human Anatomy-Gray
3.Facial Growth-Enlow
4.Human Embryology-Sperber

250
5. Quantitation of maxillary remodeling
(A description of osseous changes relative
to superimposition on metallic implants)
AJO1987:Baumrind, Korn,and Ben-Bassat

6. Oral Orthopaedics And Orthodontics for Cleft
Lip And Palate.-N.R.E Robertson

251
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