Growth of the nasomaxillary /certified fixed orthodontic courses by Indian dental academy

GROWTH OF THE
NASOMAXILLARY COMPLEX
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

1

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.

2

 Greater part of floor and lateral
wall of nasal cavity and part of
bridge of nose.
 Greater part of floor of each
orbit.

3

Body  Large and Pyramidal in shape.
Four processes  Frontal
Alveolar
Zygomatic
Palatine

4

Body of maxilla is like a hollow
pyramid.
Base of pyramid is formed by nasal
surface and apex is directed towards
zygomatic process.


5

Frontal Process
Maxillary sinus
Maxillary process
[palatine]
Horizontal plate
of palatine
process of maxilla
Alveolar process

6

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.

7

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


8

Face

Upper

Frontonasal
Prominence

Middle

Maxillary
prominence

Lower

Mandibular
Prominence
9

Head development depends upon inductive
activity of prosencephalic and rhombencephalic
organizing centers.
Prosencephalic  Upper third of face.
Rhombencephalic  Middle and lower
third of face.

10

The branchial arches begin to develop
early in 4th 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.

11

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.


12

3. Paired mandibular prominences Caudal
boundary of stomodeum.

Frontonasal
prominence
Maxillary
prominence
Mandibular
prominence

13

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


14

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

Medial Nasal
Lateral Nasal
Prominence
Prominence

15

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.

16


17

By the end of 5th week.

Maxillary prominence + lateral nasal prominence

continuity between side of nose and cheek region.


18


19

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.


20

 In maxillary
intramembranously
develop.
a.

prominences numerous
ossification
centers

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

 Vomer.


21

b.

In 7th 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.

22

Two intermaxillary ossification centres
generate the alveolar ridge and primary
palate region.
Single centre for each of zygomatic bone
in 8th week.


23

Skeletal Units of Maxilla

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


24

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.


25

POST NATAL GROWTH AND
DEVELOPMENT OF MAXILLA


26

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.

27


28

Enlow and Bang has described the growth
of maxilla by way of it’s 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).

29

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
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rate.

Postnatal growth of maxilla is mainly
because of:
1. Surface apposition.
2. Sutural growth.
3. Nasal septal growth.
4. Sphenooccipital synchondroses.


31

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.

32

HEIGHT
1. In the coronal section, the palate is
‘V’ shaped. Applying the Enlow and
Bang’s ‘V’ principleDeposition on oral side.

Resorption on nasal side.

Increases the height of the nasal
cavity.

33

V principle in sagittal and coronal view


34


35

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


36

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


37

Primary Displacement
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.


38

Primary
displacement


39

Maxillary tuberosity


40

Palato maxillary suture


41

The increase in height of maxilla because of
primary displacement can be explained on the
basis of

Sutural theory

cartilaginous theory Functional
hypothesis

42

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.


43

Sutural theory
explaining the
maxillary growth


44

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.


45

Scott’s 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 septopremaxillary ligament and the fibres which are
embedded in the premaxillary segment.


46

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.


47

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


48

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.

49

Secondary Displacement
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).


50

Secondary
displacement


51

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 midpalatine suture


52

Growth of the mid-palatine suture

Mimics general
growth pattern of
the body

Mutual transverse
Occurs in
rotations separate
response to the posterior
the
region more than
functional the anterior
matrix

U shaped
53
arch

Growth in anteroposterior direction:
1. The increase in the sagittal direction of the
maxilla begins in the 2nd 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.

54

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.

55

The antero-inferior displacement of maxilla

Sutures

nasal septum,
sphenooccipital
synchondrosis


the
orofacial
functional
matrix
56

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.


57

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 crosssectional 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 1st 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
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2nd molars andwww.indiandentalacademy.com
not the 3rd molars.

Growth of Zygomatic region


61

The malar region

anterior surface

Posterior surface

Resorption

Apposition


62


63

 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.


64

Bone deposition

inferior edge
of the zygoma

the fronto-zygomatic suture

increase in
vertical length of
lateral orbital
rim.

vertical growth / increase
in the height of the
anterior part of
zygomatic arch and the

65

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.

66


67

 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.


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Zygoma

displaced
anteriorly

displaced
inferiorly

zygomaticotemporal suture

frontozygomatic suture


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70

Growth and Development of Palate


71

Oral development in the embryo is demarcated
early in life by the appearance of the prechordal
plate in the bilaminar germ disk on 14th 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.


73

Primitive stomodeum
Oronasopharyngeal
chamber
28thday

Oropharyngeal membrane
disintegrates.

Continuity of passage
between mouth and
pharynx.


74

Frontonasal
and maxillary
prominences

Entrance into gut

Horizontal
extensions
Oral
cavity

Nasal
cavity


75

Horizontal
extensions
of
Maxillary
prominence

Frontonasal
prominence

Primary
palate

Central part of
upper
lip(tuberculum)

Lateral
shelves
76


77

Structure of Palate
Palate

Primary palate

Secondary palate

Palatogenesis
5th week I.U to 12th week I.U.
Critical period
end of the 6th week until the beginning
78
th
of the 9 week.

frontal
prominence

medial nasal
prominences

The Primary
Palate

primary palate or
median palatine
process.

fusion

a wedge shaped mass of
mesenchyme between the
internal surfaces of the
maxillary prominences of the
developing maxilla.
deep (internal) part of
the intermaxillary
segment.
79

Primary palate


80

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).


81

The Secondary Palate
internal aspects of the
maxillary prominences
two horizontal
mesenchymal
projections
lateral palatine
processes
Secondary Palate

82

Secondary palate


83

the lateral palatine
processes elongate and
move to a horizontal
position.
Lateral palatine
processes

Nasal septum

Primary
palate

fusion
dorsally or posteriorly in
ventrally or
the region of the uvula by
anteriorly during the
th
the 12th week.
84
9 week.

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 undifferentiated 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.

85

At 8 ½ 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.


86


87


88

Nasal septum
Palatal shelf
Tongue


89

Nasal septum
Palatal shelf
Tongue

90

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.

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5. An intrinsic shelf force.
6. Muscular movement.
7. The withdrawal of the embryo’s 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.


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93


94

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 8th or 9th 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.

95

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.

96

Maxillary width remains stable, allowing
shelf contact to occur.
Also forward growth of Meckel’s
cartilage relocates the tongue more
anteriorly, depressing downward and
laterally thus pushing the palatal shelves
slide medially.

97

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 .

98

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.
99

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


101

Mid palatine
suture/raphe


102

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.


103

Ossification of the Palate:
This proceeds during the 8th 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.

104

infancy
coronal section
is ‘Y’ shaped

Midpalatal suture (10 ½ weeks)
structure
childhood
the junction between
3 bones rises in ‘T’
shape
adolescence

mechanical interlocking and islets of
bone are formed.

105

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.

106

Ossification does not occur in the most superior part
of the palate giving rise to the region of soft palate.


107

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 1st arch, the levator palatini and uvular from the
2nd arch, 4th arch gives rise to the trigeminal nerve
innervation for tensor veli palatini muscle and vagus
nerve for other muscles.

108

Development Period of Muscles:
Tensor veli palatini

-

40 days

Palatopharyngeous

-

45 days

Levator veli palatini -

8th week

Palatoglossus

-

9th week

Uvular muscle

-

11th week


109

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 7th and 18th week intrauterine and
widening occurs from 4th month onward.
In early prenatal life the palate is relatively long,
but from the 4th month intrauterine it widens as a
result of midpalatal sutural growth and
appositional growth along the lateral alveolar
110
margin.

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.


111

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).


112

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.


113

‘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.


114

V principle in sagittal and coronal view


115

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.

116

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


117

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.


118

Epithelial pearls


119

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.

120


121


122


123

3. High arched palate seen in Marfan’s
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.


124


125

Cleft Lip And Palate


126

Orofacial clefts

Most common of all facial malformations
Occur in most racial and ethnic groups
Overwhelming physicological impact


127

Classification
Davis and Ritchies Classification(1922)

Group 1
Pre-alveolar
clefts
unilateral

Group 2
Post-alveolar
involving hard
and soft palates

bilateral

Group 3
Primary and
Secondary
palate
128

Fogh and Anderson Classification(1942)

Type 1
Hare lip
single double

Type 2
Lip and palate
single

Type 3
Only palate

double


129

Kernahan and Stark’s Classification(1958)

Class I
Cleft of
primary palate

Class II
Cleft of
secondary
palate


Class III
Cleft of primary
and secondary
palate
130

Class I


131

Class II


132

Class III


133

Veau and Recamier’s Classification
Cleft Lip
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
134
incomplete or complete.

Cleft Palate
Class I-Cleft involving only soft palate.


135

Class II-Cleft involving hard and soft palate
extending no further than the incisive
foramen.


136

Class III-Complete unilateral or bilateral cleft
extending from uvula to incisive foramen and
then deviating to one side.


137

ClassIV-Complete bilateral cleft similar to
class III with two cleftsd
extending
forward from the incisive
foramen
into the alveolus.


138

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.

139

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.
140

MECHANISM OF CLEFT FORMATION.
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
141
contact of palatal shelves.

Primary Palate
Major portion

Minor portion

Fusion of facial
processes

Formed by
epethelial
invagination
Clefts of
primary palate

142

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)


143

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)


144

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


145

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.

146

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 ↓Mesenchymal
147
proliferation
migration

Distortion or Malposition of Facial Processes
(Transler)
Distortion of M.N.P
Malposition of nasal
placodes
Unequal
mesenchymal
distribution

148

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.


149

Etiology
Heterogenicity
Occurrence in relatives
Other malformations
Environmental factors
Genetic factors

Anatomic and
physiologic variation
in the uterus
Infections

1deg
2deg
3deg

Metabolic alterations
Drugs


X-radiations

Dietary factors
150

Heterogenicity
High percentage with chromosomal
abnormality
Few who live

trisomy D or E

Mostly trisomy 21

Down’s Syndrome

Van der Woude’s Syndrome
Waaldenburg’s Syndrome

151

Van der Woude’s Syndrome
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.

152

Waaldenburg’s 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 www.indiandentalacademy.com
cases are environmentally
influenced.

153

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 Robert’s “Multifactorial
etiology.”Supported by Carter’s and is the most
widely accepted.

154

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.

155


156


157


158

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

159

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)

160

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.

161

-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)

162

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)

163

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
degrees of cleft formation.

variable
164

3.MATERNAL ANTIBODIES

May interfere with placental function

Cleft formation


165

Infections
Viruses-implicated as teratological agentsRubella--cardiac disorders,cataracts,deafness
Cytomegalovirus--microsomia
Protozoans
Toxoplasma-incidence of infestation 2-4
times in mothers of children with facial
clefts over control mothers.
166

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.

167

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.

168

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.

169

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.


170

Types of Facial Clefts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)

171

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)

172

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)


173

Bilateral Complete CL and CP

Growth of nasal septum carries the premaxilla
forward through its attachment to the
septopremaxillary ligament.(Latham 1973)


174

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.

175

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.

176

Anterior crossbites occur which may be unilateral
or bilateral.(Dahl 1970)

Upper incisors are retroclined with increased severity
of the cleft.


177

Musculature
Bilateral clefts

Unilateral clefts

Severe underdevelopment
and atrophy of lip muscle.

Upper lip may be
slightly less protrusive
than normal.


178

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.


179

Post Surgical Growth And Development
Unilateral CL and CP
Tightness of repaired lip

anterior cross bite.

Redundancies.
Tongue thrust
segments.

separation of maxillary


180

Bilateral CL

If the lateral segment of the lip is brought below
philtrum to produce a long lip
crossbite posteriorly.
If short lip develops
premaxilla.

excessive protrusion of


181

Effect on the Palate
Healing after surgery
Lowering of
soft tissue of
palatal vault

Scar tissue

Constricting force on the maxilla
mostly in anterior region

Amount of
alveolar bone

Size of inferior
turbinate and nasal
septum182

Nose

Tip becomes
retrusive.

Columella
becomes
short.

Nasal
bones get
distorted.


Nasal septum
becomes
concavoconvex.

183


184

Long Term Effects
General
Difference in growth timings.
Growth spurt is delayed.
Ross)
Maxilla

(Shibaski and

Retruded but anterior vertical height is normal.
Crossbites occur.
Retrusion of teeth.
↓Arch length.


185

Occlusion
Abnormal position of teeth

palatal
crossbites

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

Protrusion of lower lip.

186

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.

187


188


189

Intrinsic growth defeciency.

Constricting
effect of
palatal scar.

Pressure from tight
upper lip.

↓ maxillary skeletal and
dentoalveolar growth.
Pulls teeth medially.

190


191

Mandible
Nasal septal deviation
Interferance with
nasal breathing
Mouth breathing
Tongue drops

Low
Contracted
maxillary arch palatal
vault
↓ nasal width
Encourages further
collapse of maxillary
arch

Mandible drops
down

192

Mandible
Retrusion of chin.
Upward and forward displacement of
condyle.
Steep mandibular plane angle.
 Decreased body mass at gonial angle.


193

Management Of Cleft Lip And Palate.
Age
Orthodontics
Surgery
0-3 months

Stage 1(a)
Presurgical oral
orthopaedics for lip.

------

3 months

--------

3.5-12 months

Stage 1(b)
-----Presurgical oral
orthopaedics for palate.

Lip repair.

194

Age

Orthodontics

12 months

------

Surgery
Palate repair

8 years

Stage 2
Orthodontics
(6 months)

-------

10-12 years

Stage 3
Orthodontics
(18 months)

-------

13-14 years

-----www.indiandentalacademy.com

Secondary surgical
procedures
195

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.

196

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.

197

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
198
gap orthodontically.

MAXILLARY TUBEROSITY


199

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.

200

Tuberosity
grows posteriorly lateral surface
+++
Maxilla carried
anteriorly

endosteal side of the
+++
cortex(interior surface)
Arch
--widening

Maxillary Sinus
increases in size

Cortex moves
posteriorly and
laterally
201


202

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.


203

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.

204

Lacrimal Suture


205

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.


206

Lacrimal Suture

Collagenous linkage within sutural cartilage.
Slippage of bones along
perilacrimal sutural interface.

Maxilla displaced
inferiorly.

207


208

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.


209


210

Nasal Airway


211

Nasal Airway
resorption

deposition

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 212


Ethmoidal Conchae
deposition
lateral and inferior
sides

resorption
superior and medial
surface

downward and lateral movement

213

Inter Nasal
Septum
Bony portion

lengthens vertically at its
sutural junctions.

wraps in relation to
variable amounts and
directions of septal
deviation.


214

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.


215


216

MAXILLARY SINUS


217

MAXILLARY SINUS

The largest of
paranasal sinuses.

Pyramidal cavity in the
body of the maxilla.

Borders
Antero-Posteriorly
posterior to roots of
maxillary canine

area of 3rd molar

218

Supero Inferiorly
Floor of the orbital
cavity.

Root tips of
maxillary
posterior teeth.

Communication:
maxillary ostium
Posterior part of the
hiatus in the middle
meatus.

219

Physiology:
It is lined by mucous membrane
(pseudostratified
columnar
ciliated
epithelium).
Mucociliary mechanism provides the
means for removal of particulate matter
and bacteria.

220

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.

221

Growth of Maxillary Sinus
PRENATAL

AT BIRTH

3rd month I.U
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.


222

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 5th month intrauterine.

223

Postnatal Growth
Maxillary Sinus
resorption

deposition

maxillary internal walls
(except medially)

medial wall
nasal surface
resorption
↑ Nasal Cavity


224

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.


225

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.


226


227

Size: Average sinus is 7mm in length and
4mm in height & width and it expands 2mm
vertically and 3mm anteroposteriorly each
year.


228

ORBITAL GROWTH


229

ORBITAL GROWTH
Orbit

Greater and
Lesser wings
of Sphenoid

Maxilla
Ethmoid

Zygomatic

Lacrimal
Frontal

230

Growth of the
Orbit

Remodeling
growth

Displacement
among bony
elements

231

Orbit
deposition
Roof Lining
remodels
anteriorly and
inferiorly

Floor
Frontal lobe of the
cerebrum expands
forward and downward
resorption on endocranial
side and deposition on the
232
orbital side.

Remodeling
changes in
the orbital
region


233

The growth of the orbit can be explained as:
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.


234


235

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.


236

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..

237


238

Clinical Implications
Of
Maxillary Growth


239

Cessation of maxillary growth in 3 planes
of space is in the following order:
1.
2.

Tranverse
Anterio-posterior

3.

Vertical


240

Transverse growth of maxilla
In narrow palatal vault posterior cross bites are
usually seen.

Skeletal

Dental


241

Skeletal

Unilateral

Bilateral

Present in CO and CR

present at centric occlusion
but not in centric relation


242

Dental crossbite

Quadhelix

‘W’ arch Cross elastics Archwire to
some extent

243

Anteroposterior growth of maxilla
Class II skeletal malocclusion can be due to 3
reasons
1.
2.
3.

Prognathic maxilla.
Deficient mandible.
Or combination.


244

Maxillary excess

Head gear

Cervical
HG

Functional appliances

Occipital HG Removable


Fixed

245

Removable

Activator

Bionator

Twin Block

Fixed

Herbst

Jasper Jumper

246

Maxillary deficiency

Face Mask

Petit

Delaire

Reverse pull
head gear

Reverse functional
appliance
Class II
frankel


Twin
blocks
247

Vertical growth of maxilla
Long face Class II treatment

HP headgear to
functional
appliance
Bite blocks
on functional
appliance

High pull head gear
to molar.
High pull
headgear to
maxillary
splint


248

References
1.Contemporary Orthodontics-William R. Profitt
2.Human Anatomy-Gray
3.Facial Growth-Enlow
4.Human Embryology-Sperber


249

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


250

THANK YOU


251

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