Growth /fixed orthodontic courses

GROWTH

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INDIAN DENTAL ACADEMY
Leader in continuing dental education


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GROWTH
Terms and Terminology in growth

Embryology

Pre and Post natal development of cranial vault

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Terms and Terminology in growth
Growth
- The self multiplication of living substance.
J.S. Huxley
- Increase in size, change in proportion and
progressive complexity.
Krogman

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- An Increase in size.
Todd

- Entire series of sequential anatomic and
physiologic changes taking place from the
beginning of prenatal life to senility.
Meridith

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DEVELOPMENT
According to Todd –
Progress towards maturity.

According to Moyers –
The naturally occurring unidirectional
changes in the life of an individual from its existence
as a single cell to its elaboration as a multifunctional
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unit terminating to www.indiandentalacademy.com
death.

DIFFERENTIATION
It is the change from a generalized cell or tissue
to one that is more specialized. Thus
differentiation is a change in quality or kind.
MATURATION
Is a process by which an individual or system is
fully grown or developed mentally or physically
i.e. it has achieved it’s full potential.

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RHYTHM OF GROWTH

Human growth is not a steady and uniform process
wherein all parts of the body enlarge at the same rate
and the increments of one year are equal to that of
the preceding or succeeding year.
(Hooton)

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RHYTHM OF GROWTH
First wave of growth -Birth to 5-6th year
Slow increase terminating in
10-12th year

Boys

10 years

Girls


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Next period of accelerated growth terminating in14-16 years

Girls

16-18 years

Boys

Final period of growth terminating in18-20 years

Girls

25 years

Boys


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DIFFERENTIAL GROWTH
Different organs grow at different rates to
a different amount and at different times.


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DIFFERENTIAL GROWTH
 Lymphoid tissue proliferates rapidly in late
childhood and reaches almost 200% of adult size.
By 18 years, it undergoes involution to reach adult
size.
 Neural tissue grows very rapidly and almost
reaches adult size by 6-7 years of age. Intake of
further knowledge is facilitated by the very little
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growth that occurswww.indiandentalacademy.com
after this age.

DIFFERENTIAL GROWTH
 General or visceral tissues exhibit or “S’
shaped curve with rapid growth up to 2-3 years,
slow phase between 3-10 years and finally another
rapid growth from tenth year to 18-20 years.
 Genital tissues grow rapidly at puberty
reaching adult size after which growth ceases.

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CEPHALO-CAUDAL
GRADIENT OF GROWTH
It means that there is an axis of increased
growth extending from head towards the feet.


Head- Head takes up about 50% of the total
body length around the 3rd month of I.U. life.
At birth – 30% of body length
In an adult – 12% of total body length

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

Lower Limbs – These are rudimentary around
2nd month of I.U. life
In an adult - 50 % of total body length.



At Birth, cranium is proportionally larger than
the face. Post-natally, the face grows more
than the cranium.

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CEPHALO-CAUDAL
GRADIENT OF GROWTH


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GROWTH SPURTS
 Period of accelerated,incremental,intermittent and
sequential enlargement of skeletal structures associated
with the homeostasis of the individual with the
environment.

Physiological alteration in hormonal
secretion is the believed cause of growth

spurts.
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Timings of growth spurts
1.
2.
3.
4.

Just before birth
One year after birth
Mixed dentition growth spurt
Boys : 8-11 Years
Girls : 7-9 Years
Pre-pubertal growth spurt
Boys : 14-16 Years
Girls : 11-13 Years

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CLINICAL SIGNIFICANCE


Growth modification by means of functional
and orthodontic/orthopedic appliances elicit
better response during growth spurts.



Surgical correction involving the maxilla and
mandible should be carried out only after
correction of growth spurts.

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STRESS TRAJECTORIES

The trajectorial theory of face states
“the lines of orientation of the bony trabeculae
correspond to the pathways of maximal pressure
and tension and that bone trabeculae are thicker in
the region where the stress is greater”.

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Benninghoff studied the natural lines of stress in
the skull by piercing small holes in fresh skull.
Later as the skulls were dried, he observed that
the holes assumed a linear form in the direction
of the bony trabeculae. These were called
Benninghoff’s lines or trajectories which
indicate the direction of the functional stresses.

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STRESS TRAJECTORIES

TRAJECTORIES OF THE MAXILLA

Vertical trajectories

Horizontal trajectories


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STRESS TRAJECTORIES
Vertical trajectories
A. Fronto nasal buttress
B. Malar Zygomatic buttress
C. Pterygoid buttress


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STRESS TRAJECTORIES
A. Fronto Nasal Buttress-This trajectory originates
from the incisors, canines and first maxillary
premolar and runs cranially along the sides of the
piriform aperture, the crest of the nasal bone and
terminates in the frontal bone.


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B
Molar-Zygomatic Buttress-This
trajectory transmits the stress from the buccal
group
of teeth in three pathways:
a) Through the zygomatic arch to the
base of the skull.
b) Upward to the frontal bone through
the lateral walls of the orbit.
c) Along the lower orbital margin to join
the upper part of fronto nasal buttress

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C

Pterygoid Buttress-This trajectory transmits
the stress from the second and third molars to
the base of the skull.


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STRESS TRAJECTORIES
Vertical Trajectories


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STRESS TRAJECTORIES
Horizontal Trajectories
A. Hard Palate
B. Orbital ridges
C. Zygomatic arches
D. Palatal bones
E. Lesser wings of sphenoid

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STRESS TRAJECTORIES
TRAJECTORIES OF THE MANDIBLE
DENTAL TRAJECTORY
 The spongy trabeculae surrounding the apical
part of the sockets unite as a trajectory that
runs backward below the sockets and then
diagonally upwards and backwards through the
ramus to end in the condyle.
In this way the masticatory pressure is finally
transmitted to the base of the skull over the

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

This trajectory bulges on the inner surface of
the ramus as a blunt crest, the crest or ridge of
the mandibular neck continuous with the
mylohyoid ridge.


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STRESS TRAJECTORIES

Other trajectories are formed in response to the
forces exerted by the muscles of mastication
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in the region of mandibular angle

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beginning of the coronoid process and fans out
into the mandibular body.

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•

in the chin trajectory of the spongiosa where
the tracts of trabeculae cross each other at
right angles, running from the lower border
of the chin upward to the left into the
alveolar process and vice versa.


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STRESS TRAJECTORIES
TRAJECTORIES OF THE MANDIBLE


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FUNCTIONAL CIRCLES OF STRESS IN
THE UPPER JAW COMPLEX (RICKETS)
• One circle of stress in function is directed to
support of the canine and incisor teeth.
• A second circle of stress may be located from
the molar teeth where the forces of a
transpalatine nature take place through the
palate.
• A third circle of reinforcement runs around the
nasal capsule to terminate as the frontal
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process of the maxilla.

•Force is also transmitted to a fourth, larger circle
passing around the orbits and up through the
frontal bone.
•Through the zygomatic arch and on to the
temporal bone extending backward to the joint and
finally downward into the mandible.

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CLINICAL IMPLICATION AND PRINCIPLES
OF THE UPPER JAW COMPLEX
• A whole complex is involved.
• This type of bone is laminated and passive in
function.
• Analysis of stress can be followed by
reinforcements for transmission of force around
the maxillary sinus.

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• These bones, when connected form capsules.
• The superstructure or base for the upper jaw
complex does not come from the anterior
cranial floor alone.
• The scaffolding for the maxilla is principally
through other bones transmitting force to the
basal skull.

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• The several intermediate bones between the
maxilla and skull base provide a mechanism
capable of slight movement by virtue of
multiple sutures.
• Forces tend to run perpendicular to sutures and
the direction of sutures tends to parallel the
Basion-Nasion plane.
• These sutures provide areas of adjustment and
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mechanisms for adaptation.

• Critical cephalometric points are found in the
upper jaw complex for orientation. Nasion (N),
Orbital(O), Anterior nasal spine (ANS), Point
A (A), Point Jugale (J), Nasal Cavity (NC),
Posterior nasal spine (PNS), Pterygo-maxillary
fissure (PTM)


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• Growth of the maxillay complex is downward
and forward from the Basion-Nasion plane.
• The arrangement of bones within the complex
protects the blood and nerve supply.
• The arrangement of the bones in the upper jaw
complex protects the respiratory tract.

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• The upper jaw complex, while mainly passive
for the forces of mastication, also gives support
for certain functions.
• The upper jaw is connected to the lower jaw
directly through the muscles of mastication and
the muscles of facial expression.


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• The alveolar process has distinct architectural
designs in its organization. The stresses from the
teeth are carried through the alveolar processes
into the basilar portion from which they are
transmitted to the areas of muscle attachment,
which provide the sources of the power for tooth
contact.

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• The upper jaw complex is important to the
esthetics of the face
• The maxillary complex is the target of Le Fort
surgical procedures. It is considered as a nasal
operation.
• Early orthodontics has capability of orthopedic
alteration of the upper jaw complex in three
planes of space.
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WOLFF’S LAW
It states that a bone grows and develops in such a
manner that the composite of physiologic forces
exerted on it are accommodated by bones
developmental process, thereby adopting its structure
to its complex of functions.
Enlow (1899)


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Thus not only is the quantity of bone tissues the
minimum that would be needed for function
requirements, but also its structure is such that it is
best suited for the forces exerted upon it
e.g. if a long bone such as the femur is cut open, it
will be found that dense cortical bone is on the
outside in such a way that they support its cortical
bone along well defined paths of stress and strain.
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Internal architecture of bone
1. Osteone, 2. Cortical and medullary bone 3. A long bone

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ENDODERM
The cells of the inner cell mass differentiate into
flattened cells, that come to line its free surface.
These constitute the endoderm (the first germ
layer). It gives rise to living epethelium of
alimentary canal between the pharynx & anus,
lining epethelium of respiratory system, secretary
cells of liver and pancreas.

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ECTODERM
The remaining cells of the inner cell mass become
columnar. There cells form the second germ layer
on the ectoderm. It gives rise to cutaneous system
= skin + appendages , oral mucous membrane +
enamel of teeth
Neural system = CNS , PNS


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MESODERM
The cells of the trophoblast give origin to a mass of
cells called extra embryonic mesoderm or primary
mesoderm. These cells come to lie between the
trophoblast and the flattened endodermal cells living
the yolk . It gives rise to CVS, locomotor system,
connective tissues + pulp , dentine, cementum, PDL

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OSTEOGENESIS
The process of bone formation is called
osteogenesis. Bone formation takes place
in two ways :1. Endochondral bone formation
2 Intra-membranous bone formation


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ENDOCHONDRAL BONE
FORMATION
Undifferentiated Mesenchymal Cells
Chondroblasts
Hyaline Cartilage
Cartilage Cells

Perichondrium


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Cartilage Cells

Perichondrium

Alk. Ph.
Intercellular substance
gets calcified

Blood
Vessels

Osteogenic
Cells

Primary Areolae
Formation of Bars due to eating
away of the calcified matrix
Secondary Areolae

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Secondary Areolae
Osteogenic
cells become
osteoblasts
Osteoid
Lamella of bone

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INTRAMEMBRANOUS BONE FORMATION
Undifferentiated Mesenchymal Cells

Collagen
fibres

Gelationous
Matrix

Osteoblasts
Ca2+

Trapping

Osteocytes
Bone Lamella

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INTRAMEMBRANOUS
OSSIFICATION
•Frontal
•Parietal
•Zygomatic
•Palatine
•Nasal
•Lacrimal
•Maxilla
•Vomer

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ENDOCHONDRAL
OSSIFICATION

BOTH

•Ethmoid
•Inferior nasal conchae

•Occipital
•Sphenoid
•Temporal
•Mandible


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PRIMARY CARTILAGE – Cartilage of the
pharyngeal arches such as Meckel’s cartilage
and the definitive cartilages of the cranial base.
SECONDARY CARTILAGE – It does not
develop from the established primary cartilage of
the skull e.g. condylar cartilage.

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Primary Cartilage
New cells are formed within existing tissues.
(Interstitial growth)

e.g. epiphyseal, spheno-occipital, synchondrosis,
nasal septal

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Secondary Cartilage
New cells are added from exterior.(Appositional
growth)

e.g. condylar, coronoid, angular

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TERMS & TERMINOLOGIES
GROWTH
DEVELOPMENT
DIFFERENTIATION
MATURATION
RHYTHM OF GROWTH
DIFFERENTIAL GROWTH
GROWTH SPURTS

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STRESS TRAJECTORIES
ENDODERM, ECTODERM, MESODERM
OSSIFICATIONENDOCHONDRAL
INTRAMEMBRANOUS
PRIMARY CARTILAGE
SECONDARY CARTILAGE

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FACTORS AFFECTING
PHYSICAL GROWTH
HEREDITY
NUTRITION
ILLNESS
RACE
SOCIO ECONOMIC FACTORS
FAMILY SIZE AND BIRTH ORDER
SECULAR TRENDS
CLIMATIC AND SEASONAL EFFECTS
PSYCHOLOGICAL DISTURBANCES
EXERCISE www.indiandentalacademy.com

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EMBRYOLOGY

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EARLY EMBRYONIC DEVELOPMENT
The development of the embryo may conveniently be
divided into three main periods during the 280 days of
its gestation (10 lunar months of 28 days each).
The period of the ovum extends from conception until
the 7th or 8th day.
.

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The embryonic period, from the second through
eighth week, may be subdivided into presomite,
somite and postsomite periods.
The final period of the foetus encompasses the 3rd
to 10th lunar months

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The presomite period extends from the 8th to the
20th days of development.
The somite period covers the 21st to 31st days of
development. During this ten-day period, the basic
patterns of the main systems and organs are
established


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The postsomite period from the 4th to 8th week, is
characterized by rapid growth of the systems and
organs established in the somite period and by the
formation of the main features of external body
form.
During the foetal period, from the 3rd month until
birth, there is little organogenesis or tissue
differentiation, but there is rapid growth of the
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foetus.

PERIOD OF THE OVUM
Sperm + Secondary Oocyte

(Fertilization)

Zygote

Cleavage (30 Hrs.)

Bastocyst

4th Day

Morula

4th Day


Blastomeres
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After 6 days
Bastocyst
Trophoblast

Attaches to the
endometrial
epithelium
Inner Cytotrophoblast
Outer Syncytiotrophoblast


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After 7 days
Blastocyst

Hypoblast
(Primitive
Endoderm)

Trophoblast
differentiates
into 2 layers

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EMBRYONIC PERIOD
Presomite Period
Primiordium of amniotic cavity
Aminoblast
(from epiblast)
Amnion
(Membrane)

Amniotic
cavity
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Embryoblasts
Embryonic
disc
Epiblasts
(High Columnar Cells)

Hypoblasts
(Cuboidal Cells)


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Surrounds
Hypoblast
blastocyst cavity

Excoelomic Cavity

Extraembryonic
mesoderm
Extraembryonic
Coelom

Primary Yolk Sac
in size

in size

Secondary Yolk Sac


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Extraembryonic
Coelom

Splits

Extraembryonic Mesoderm

Extraembryonic
Somatic
Mesoderm

Extraembryonic
Splanchic
Mesoderm

+2 layers of
trophoblast

Chorion


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At 14 th day
Bilaminar embryonic disc
Hypoblastic Cells
Columnar Cells
Prechordal plate
(cranial end of embryo)

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Third Week
Gastrulation
(Bilaminar embryonic disc

Primitive
Streak

Ectoderm

Trilaminar embryonic disc)

Endoderm


Mesoderm

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Primitive Streak

Addition of
cells to Caudal
end
Cloacal
membrane
Anus

Cranial end
Proliferates
Primitive node
or knot
Primitive Pit


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Cells of Primitive Streak

Displace
hypoblast

Displace
epiblast

Form a
loose
network

Intraembryonic Intraembryonic Intraembryonic
endoderm
ectoderm
Mesoderm

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Primitive node
Cells migrate cranially

Notochord
Process
Notochord
canals
reach

Prechordal Plate
Oropharyngeal Membrane

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Notochordal Process

Communication
with yolk sac
Notocanal
disappears

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Notochordal cells

Notochordal
plate
infolds

Notochord detaches from endoderm

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Notochord
Neural Plate
18thday
Neuralation Neural Groove + Neural folds

Neural tube


Neural Crest
Cells
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SOMITE PERIOD
Neural Tube

Brain

Spinal cord


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MESODERM

Lateral
Plate
Pleural,
Pericardial
cavities

Intermediate
Gonads,
kidneys,
adrenal
cortex

Paraxial
Somites
(42-44 paired)
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SOMITE

Ventromedial
(Sclerotome)
Vertebral
Column,
Occipital Skull

Lateral Aspect
(Dermatome)
Dermis of Skin

Intermediate
(Myotome)

Muscles of trunk,
limbs, orofacial
region
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



Most of the organ systems start to develop
i.e. cardiovascular,alimentary,respiratory
genitourinary and nervous systems develop.
The part of yolk sac endoderm incorporated in
cranial end is called foregut while that in the
caudal end of the embryo is called hindgut.


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Foregut-laryngeotracheal diverticulum(bronchi,lungs)

-hepatic and pancreatic diverticula(liver,pancreas)
-pharynx,pharyngeal pouches (oesophagus,
stomach, 1st part of duodenum)


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Midgut-rest of the duodenum
-small intestine
-ascending and transverse colon of L.I
Hindgut -descending colon
-terminal parts of the alimentary canal

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THE POSTSOMITE PERIOD
 The predominance of the segmental somites as an
external featureof the early embryo fades during
the 6th week i.u..
 The head dominates much of the development of
this period.
 The earliest muscular movements are first
manifest at this time.

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 Facial features become recongnizableears,eyes,nose and neck become defined.
 Body stalk condenses into a definitive
umblical cord.


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Thoracic cavity enlarges as the developing heart
is accompanied by rapidly growing liver.
The long tail at the beginning of embryonic period
regresses.


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SUMMARY


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NEURAL CREST
CELLS

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EMBRYOLOGY
Characteristics of Neural Crest Cells:
1.Pleuripotent capability – These cells are
capable of giving rise to several types of precursor
cell which are required in formation of different
structures.


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EMBRYOLOGY
2.Migratory property – NCC break free during
neuralization from neural folds by losing their
lateral connections to adjacent epidermal and
neural ectodermal cells and by dissolution of
underlying basement membrane as these cells
begin their migration away from the developing
neural tube and towards future craniofacial
regions of the embryo.

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EMBRYOLOGY
This migration is brought about by two means:
Active (Cohen and Konigsberg 1975)
Passive (Nuden, 1986)


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EMBRYOLOGY
Active – Cells readily migrate away without the
ectoderm which is present superficially.
Passive – In which lateral and ventral
translocation of superficial ectoderm take place
along with NCC.
NCC migrates as a single cell dividing as
they go, so that by the time they reach their final
destination, they represent a much larger
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population than was present at the outsets.

EMBRYOLOGY
Factors affecting migration :
Molecules – Especially fibronectin which is
encountered along the way are used by NCC to
govern their migration. This is supported by work
of (Rovasio et al 1983) – in which they found out
when NCC are confronted with either fibronectin
coated or fibronectic free substrates in vitro, they
preferentially with great precision choose the
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fibronectin coated surface.

Vitamin A –
Acts as a teratogen, it is shown to slow the
migration of neural crest cell maintained in vitro
by inhibiting their interactions with extracellular
matrix products.
Administration of vit. A in pregnant mice leads to
formation of craniofacial structures in abnormal
position. Defects analogous to either Treacher
Collins Syndrome or Hemifacial Microsomia can
by produced by varying the dose of Vit. A
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between 50,000-100,000iu

Drugs:
Isotretenion – cause severe facial
malformation by effecting neural crest cell
migration.


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EMBRYOLOGY
3) Regulation
Refers to ability of an embryo to compensate
for the loss of cells. This compensation is brought
about by two ways:
• Either via migration of neural crest cell across
the midline (if defect is unilateral).
• By increasing proliferation of the remaining
neural crest cells.

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This was shown in study done by Bonner-Fraser
(1986) – in the CSAT antibody, which was used as
an antibody to a cell surface receptor that recognizes
fibronectin and laminin, both of which are involved
in control of neural crest cells migration.


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This antibody was injected in embryonic chicks
just before initiation of NCC migration. 24 hours
later she observed  decrease in number of NCC (defective
proliferation),
 accumulation of NCC within neural tube
(defective initiation of migration) and
 neural crest cells in abnormal position
(defective directionality of migration).
However 36-48 hours of after injection of CSAT
antibody, neural crest derivatives had developed
normally.

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4) Cessation:
For neural crest derived craniofacial
mesenchyme, which is migrating into the position
of future craniofacial structure, some message
must signal these cells to cease migration, which
is a prerequisite for condensation. The best signal
is type II collagen. Migrating NCC possess
specific receptors for collagen which inhibit the
further migration and they accumulates at site
where later cytodifferentiation will take place.

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STRUCTURES DERIVED BY THE
NEURAL CREST CELLS
Connective tissueEctomesenchyme of facial prominences and brachial
arches
Bones and cartilages of facial visceral skeleton.
 Dermis of face and neck
 Stroma of salivary, thymus, thyroid, parathyroid and
pituitary gland.
 Corneal mesenchyme.
Aortic arch arteries.
Dental papilla
Portions of periodontal ligament
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Cementum

Muscle tissueCiliary muscles
Covering connective tissue of branchial arch
muscles


140

STRUCTURES DERIVED BY
THE NEURAL CREST CELLS
Nervous tissue
Leptomeninges.
Schwan sheath cells.
Sensory gangliaAutonomic ganglia.
Spinal dorsal root ganglia.
ANS Sympathetic ganglia.
 Parasympathetic ganglia

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Endocrine tissueAdrenomedullary cells
Calcitonin ‘c’ cells
Carotid body
Pigment cellsMelanocytes
Melanophores


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Dental context
The initiation of the tooth formation.
The determination of the tooth's crown pattern.
The initiation of dentinogenesis.
The initiation of amelogenesis.
The determination of the size,shape and number
of the tooth roots.
The determination of the anatomy of the
dentogingival junction

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EMBRYOLOGY
Clinical Implications
Mandibulofacial Dysostosis (Treacher Collins
Syndrome):
Maxillary and mandibular undercuts,
Lack of mesenchymal fissures.
Lt orbital and zygomatic area.
Ears may be affected.

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EMBRYOLOGY

Etiology: excessive cell death in trigeminal ganglion

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Hemifacial Microsomia:
Lack of tissue of affected side.
Both ramus & soft tissue is deficient / missing.


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EMBRYOLOGY
Etiology: Early loss of NCC.
Limb abnormalities – thalidomine.
-Isotretenion


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SUMMARY OF EVENTS
ZYGOTE

MORULA
(30 HRS.)
NEURAL CREST CELLS

BLASTULA
(4th Day)

AMNIOTIC
CAVITY

NEURAL PLATE AND TUBE (End of 3rd Week)
NOTOCHORD (Middle of 3rd Week)

PRIMITIVE
STREAK
(3rd Week)

GERM LAYERS
(2-3 Weeks)

IMPLANTATION
( 7th Day)

BILAMINAR EMBRYONIC DISC

CHORIONIC SAC
(End of 2nd week)


YOLK SAC
(1-2 Weeks)
148

Pre and Post Natal
Development of the Cranial
Vault


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Introduction
Conventionally, the craniofacial region is
divided into 4 major regions, in order to better
understand growth. These regions are:1. The Cranial Vault
2. The Cranial Base
3. The Naso-maxillary
complex
4. The Mandible

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The growth of each region is further divided into:1. Pre natal
2. Post natal
To understand how the growth occurs we need to
pay attention to the following aspects:1. The sites and location of growth.
2. The type of growth.
3. The determinant and controlling factors.

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Anatomy of the Cranial Vault
Synonyms –
1.
2.
3.
4.

Calvaria, and not Calvarium
Cranial vault
Desmocranium
Calva


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The skull may be viewed from different angles:1.
2.
3.
4.
5.

Above – Norma Verticalis
Below – Norma Basalis
Side – Norma Lateralis
Behind – Norma occipitalis
Front – Norma frontalis

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The cranial vault spans from the superciliary
ridges and glabella of the frontal bone, upto and
including the squamous occipital bone. It also
includes part of the squamous temporal bone,
laterally.
When seen from above:The vault is roughly ellipsoid, with the greatest
width at its occipital end. The bones that make up
the vault arewww.indiandentalacademy.com
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The frontal bone – It forms the forehead. It
passes back to meet the two parietal bones at the
coronal suture.


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Anatomy of the Cranial Vault


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At birth, a suture is seen between the 2 halves of the
frontal bone – the frontal or metopic suture. It usually
closes early in life, but may persist into adulthood in
10-15% of cases.
The parietal bones- form most of the cranial vault.
They articulate in the midline at the saggital suture.
Posteriorly, the parietal bones articulate with the
occipital bone at the lambdoid suture (named after the
Greek letter ‘lambda’, which it resembles in shape).
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Laterally, the parietal bones extend upto the
greater wing of the sphenoid – anteriorly, and
squamous temporal bone- posteriorly.
The junction of the coronal and saggital suture is
known as the ‘bregma’ and
The junction of the lambdoid and saggital suture is
known as the ‘lambda’.
Also, there is a parietal eminence on each side and
a frontal eminence anteriorly.
158

The vault is covered by the SCALP which
has 5 layers1.
2.
3.
4.
5.

Skin
Subcutaneous tissue
Aponeurosis of the occipito-frontalis
Loose areolar tissue
Pericranium.

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Pre-natal Growth
The cranial vault is a derivative of the
mesenchyme, which is initially arranged in the
form of a capsular membrane around the
developing brain.
The membrane has 2 parts:Endomeninx- derived from neural crest cells
Ectomeninx – derived from neural crest cells and
paraxial mesoderm

160

The ectomeninx deferentiates into :


Inner dura mater
Outer superficial membrane with osteogenic
properties

The part of the superificial membrane which is
over the dome of the brain ossifies
intramembranously and forms the vault.
The part that is below the brain, ossifies
endochondrally and forms the cranial base.

161

The endomeninx differentiates into: Piamater
 Arachnoid.
During their development, the 2 layers (ectomeninx
and endomeninx) remain in close apposition, except
in areas where the venous sinuses will develop. The
duramater shows distinctly organized fiber bundles,
which later develop into the various folds – falx
cerebri, falx cerebelli and tentorium cerebelli.

162

These bands also, to an extent , control the shape
of the brain, which would expand as a perfect
sphere if it were not for them.


163

Sites of ossification
Type of Ossification
Controlling factors

Sites of the future bones.
Intra membranous.
Brain


164

Ectomeninx gives rise to the following bones –
Mesoderm – frontal, parietal, sphenoid, petrous
temporal and occipital.
Neural crest – lacrymal, nasal, squamous temporal,
zygomatic, maxilla & mandible.
The individual bones form from various primary
and secondary ossification centers.

165

Frontal bone
Single primary center in the region of the
superciliary arch. This appears in the 8th week of
intrauterine life.
3 secondary ossification centres appear in the
zygomatic process, nasal spine and trochlear
fossae.
Parietal bones
1 primary center each in the region of parietal
eminence. These do not fuse with each other, and a
166

Occipital bones
Squamous portion ossifies intramembranously –
primary center appearing just above the
supranuchal lines.
Squamous part of temporal bone
Single ossification center appearing at the root
of the zygoma.

167

Tympanic ring of the temporal bone
4 centres on the lateral wall of the
tympanum.
Also, the development of sutural bones
occurs if any unusual ossification sites develop.
Most centers of ossification appear during the 7 th
or 8th week intrauterine, but ossification is not
complete until after birth. Apart from fontanelles,
the sutures themselves are wide, with syndesmotic
168
articulations.

The fontanelles are named according to ther
relation with the parietal bonesAnterior, posterior, 2 – antero-lateral, 2 – posterolateral.
These close at varied times between 2 months
after birth (post. And ant.lateral) and 2 years
(ant. And post.lateral).

169

Pre-natal Growth

170
Sutures continue to ossify until they fuse, sometime in adult life.

Van Limbourgh poses 3 questions in relation to
control of morphogenesis (prenatal growth)of
the skull –
1. Is there a relationship between
development of the skull and presence of
primordial of other organs?
2. How is endochongral and
intramembranous growth coordinated?
3. How is growth of the skull and growth of
other organs coordinated?

171

Three major controlling factors come to mind:1. Intrinsic Genetic factors – or direct hereditary
influence of genes
2. Epigenetic factors – indirect genetic control
through intermediary action on the associated
structures (eye, brain etc)
3. Environmental factors

172


173

Earlier a totally genetic influence was thought
to control the cranial differentiation
But various observations have served to swing the
pendulum more in favor of epigenetic influences.
Example – If the primordial of the eye does not
develop, usually, the orbits do not develop. The
number of orbits that develop correlates with the
number of eyes that develop.
•If no brain develops, no cranial vault develops
(anencephaly).

174

Generally accepted 



Role of genetics to a small extent.
More acceptance to local epigenetics.
Also consideration of general epigenetics
and local and general environmental factors.


175

Post-natal Growth
1. Growth of the skull vault is closely related to
growth of the brain.
2. Due to rapid growth of the CNS up to the 5 th year of
life, it is seen that the calvaria is relatively bigger at
birth than in adulthood. This reflects the
cephalocaudal gradient of growth.


176



There is a different explanation of growth of
the vault according to different theories of
growth. In order to understand the site of
growth of the cranial vault, the type of growth
and controlling factors, it is important of look
at some of the theories of growth and how
different theories have interpreted cranial
growth in different ways.

177

Theories of growth and how they relate to the
growth of the cranial vault.
Sutural growth theory
Sicher said that skull growth was genetically
determined that growth occurred at the sutures.
Local factors, like muscle activity had only a
mild effect.


178

Scott’s Theory
Scott gave importance to cartilage growth. He said
that cartilage had inherent growth potential and
sutures grew in response to cartilaginous growth.
Therefore, sutures respond to growth at
synchondrosis and to environmental factors.


179

Moss’ FMH
Moss postulated the role of functional matrices
which are formed by non osseous tissue. Hence,
this is an example of epigenetic control and
environmental control.


180

Post-natal Growth
Combination of the Theories
Sicher claimed that the growth was under intrinsic
genetic control, but from the work of Moss, we
know that this is not a direct control, but
epigenetic control. Hydrocephaly, microcephaly
and anencephaly are testimony to this.


181

What Scott’s experiments showed, is that cartilages
are not responsive to pressure or tension, but
intramembranous bone is. Therefore one could
deduce that as the synchondroses grow, there is
tension created at the sutures, and bone deposition
occurs. This view is supported by others – Sarnat,
Burdi, Baume,, Petrovic etc.

182

This also explains why growth of the cranial base
is influenced less by brain growth as compared to
the cranial vault.
We are familiar with Moss’ explanation for control
of bone growth by brain growth. He especially
based his theory on the fact that in the synostosis
syndromes, though the cranium cannot grow, the
brain continues to grow. The growth is seen in
many ways – example, bulging of the eyes.

183

But it is interesting to see that if growth were to
be explained entirely on the basis of the FMH, in
hydrocephaly or anenchphaly, even the cranial
base would be relatively large or small, as the
growing brain would exert equal force in all
directions.


184


185

But what is seen, is that the cranial base remains
more or less normal. (Burdi, Van Limborgh, Sarnat,
Latham, Baume, Petrovic & others.)
Thus there is some support for Scott’s theory, that
cartilage growth is under genetic control.


186

So the modern view should be a rational
amalgamation of these theories. This has been
summarized by Van Limborgh as under:-

1. Intrinsic control of growth is exhibited at the
synchondroses.
2. The intrinsic control of sutural growth is less
3. The Synchondroses should be considered as growth
centres.
5. Sutural growth is controlled, in part, by growth at the
synchondroses.

187

•Some amount of periosteal growth also takes
place in the cranial vault, this is controlled
epigenetically.
•Growth of the cranial vault is also controlled, to
some extent by local environmental factors
(muscle forces inclusive).


188


189

Growth of the Cranial Vault
Growth of the cranial vault is directly influenced by
pressure from the neurocranial capsule.


190

As the brain expands the cranial vault bones are
separated, at the sutures and the resulting space is
closed by proliferation of connective tissue at the
suture and its subsequent ossification. BUT the
bones are NOT PUSHED outwards.


191

Each bone is enmeshed in a stroma, which is
continuous with the meninges and skin. Hence, as
the brain grows, this connective tissue stroma
separates the bones at the sutures.


192

Another change taking place is periosteal growth.
In general, deposition occurs both, at the inner
table and outer table of the bones of the vault, and
resorption occurs at the endosteal surface. The
effect is twofold:-


193

1. To flatten the bones.At birth, the bones are
quite curved. The remodeling serves to flatten
the bones and hence arrange them along a
bigger arc. There may be certain areas of
reversal of the resorption – deposition pattern
mentioned earlier, in order to achieve this.

194


195

2. This also helps to increase the thickness of the
bones.
At birth the bones are thin and lack the spongy
diploë between the inner and outer table.
According to Sicher, the thickening is not
uniform, as the inner table is influenced by the
growth of the brain, while the outer table is
influenced by mechanical force, especially of
muscles in the supraorbital, otic and mastoid
196
regions

Another response to functional stresses is the
development of the frontal sinus(Benninghoff). As
the thickness of the bone increases, the supraorbital
ridges develop due to more thickening of the outer
table. Then, the spongy bone between the inner and
outer table is slowly filled in by the developing
sinus.


197

90% of the cranial vault growth of completed by the
age of 5 – 6 years, as has been shown by Davenport.
This is in accordance with Scammons curve for brain
growth as well as the cephalocaudal gradient.


198

Clinical Implications
1. Synostosis Syndromes
These syndromes result from early closure of the
sutures between the cranial and facial bones.
This is obvious since growth occurs at the
sutures, cranial growth will be extremely limited.
Apart from limited cranial growth, maxillary
growth is also limited due to synostosis of the
circum-maxillary sutures. The orbits are bulging
– due to a combination of increased intracranial
pressure and underdevelopment of the maxilla.

199

Treatment – Surgery to release sutures

2. Hydrocephaly, Microcephaly and Anencephaly
Change in the size of the vault due to increased
CSF or absence of the brain.

200

MICROCEPHALY


201

3. Herniation of the dura into the nose. For some
time, the dura covering the forebrain and the
ectoderm remain in contact at the surface, in the
region of the anterior neuropore. When the
frontonasal process bends ventrally, the dura lies
near the future frontonasal process. Then, the
nasal capsule forms around it. A midline canal is
formed, which later develops into the foramen
caecum, when the dura separates from the
202
ectoderm.

•The foramen caecum, then closes. If this fails to
happen, it leaves an area from where the dura can
herniated into the nasal cavity. It can also lead to the
formation of dermoid cysts, sinus, or encephalocele.


203


204

4. Distortion of the head during birth which is
possible due to the presence of Fontanelles.

5. Development of the outer superstructure of the
vault due to muscular forces esp. mastoid, temporal
and nuchal line, coronoid process etc. Direct
205
dependence on muscular activity.

6. In various conditions ,cretinism, progeria, trisomy
21, cleidocranial dysostosis – there is delayed –
ossification of the frontal suture, and anterior
fontanelles remain open into adult life. It results in
a brachycephalic skull and ‘bossed’ forehead, and
highly curved frontal and parietal bones and
hypertelorism.


206


207

REFERENCES
Craniofacial Embryology - G.H. Sperber
Essentials of Facial Growth - D.H.Enlow
Anatomy – Gray
Abnormalities of Cleidocranial Dysostosis –
Kreiborg,, Bjork & Skeiller (AJO May;1981)
Cranial Base Growth For Dutch Boys & Girls –
M. Herneberke, B.P. Andersen (AJO
208
November; 1994)

Contemporary Orthodontics - W.R. Proffit
The Developing Human - Moore & Persaud
Craniofacial Morphogenesis & Dysmorphogenesis
– Katherine and Alphonse
Oral Histology – Tencate


209

Provocation and Perception in Craniofacial
Orthopaedics- Ricketts, Robert M.
Orthodontics- Art And Science-Bhalaji


210

THANK YOU
Leader in continuing dental education


211

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