THEORIES OF GROWTH

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CONTENTS
• Introduction
• Growth fields
• Growth sites
• Growth centers
• The Sutural hypothesis ( Sicher 1941)
• The Cartilaginous theory (Scott 1950s)
• The Remodelling theory(Brash 1930s)
• The Genetic concept(Brodie 1940s)
• The Functional Matrix theory (Moss 1962)

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• The Cybernetics theory
(Alexandre Petrovic1970)
• Conclusion
• References

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INTRODUCTION
✔Growth and development are two integral
process which defines the existence of
life.

✔Growth of an organism is the interplay

between its genetic constitution and
environment in which it thrives.

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✔Assessment of growth revels about the
general health of the individual and can
be used for growth modification
treatments.

✔Growth is a complex process and is not

supported by a single theory but is based
to a large extent on evolving concepts
concerning the biological mechanisms of
craniofacial development.

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GROWTH
FIELDS
🞭 Bone growth is controlled
by growth fields.
🞭 Distributed in a mosaic like
pattern across the surface
of a given bone.
🞭 They have pacemaking
function.
🞭 They are either resorptive
or depository activity.
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🞭 About one half of the
bone is periosteal and
the other half
endosteal.
🞭 If endosteal
surface is resorptive
then periosteal
surface would be
depository.

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 GROWTH SITES
🞭 Growth fields having special role in the growth of the
particular bone ( grows fast) are called growth sites.

⮚ Growth site is merely a location at which growth

occurs.

🞭 e.g. mandibular condyle, maxillary tuberosity,

synchondrosis of the basicranium, sutures and the
alveolar process.

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 GROWTH CENTERS
🞭 Special areas which are believed to control the overall
independent (genetically controlled) growth of the bone
e.g.epiphyseal cartilage .

🞭 Force, energy or motor for a bone resides primarily

within its growth centre.

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All centres of growth also are sites,
but reverse is not true.
THE SUTURAL HYPOTHESIS

⮚ Given by Sicher and Weinmann in 1947 .

⮚ According to this theory, sutures ,cartilages

and periosteum are responsible for facial
growth and were assumed to be under
intrinsic genetic control.

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Essence of the Theory:

According to Sicher, the sutures are the

primary determinants of craniofacial growth.
The craniofacial skeleton enlarges due to
expansible forces exerted by the sutures as
they separate.

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❑ Sicher called this theory as the sutural
dominance theory because he believed
that the primary event in sutural growth is
proliferation of the connective tissue between
the two bones.

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⮚Proliferation of the sutural connective tissue
creates the space for appositional bone growth
between the borders of two bones.

⮚Increase in the size of the cranial vault takes place via

primary growth of the bone at the sutures, which forces
the bones of the vault away from each other.

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⮚Growth of the midface takes place via intrinsically
determined sutural expansion of the circummaxillary
suture system, which forces the midface downward
and forward.

⮚Mandibular growth takes place via intrinsically

determined growth of the cartilage of the mandibular
condyle ,which pushes the mandible downward and
forward.

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⮚There is considerable growth occuring in
suture and hence from this point of view
sutural growth attains significance.

⮚Sicher postulated that bone growth within

the various maxillary sutures produces
pushing of the bone which results in forward
and downward movement of the maxilla.

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⮚If this theory were correct, growth at the sutures should
occur largely independently of the environment and it
would not be possible to change the expression of
growth at the sutures very much.

⮚So few attempts were made to modify facial growth:

Concluded that sutures & periosteal tissues are not

primary determinants of craniofacial growth.

They are not Growth Centres.

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 Two lines of evidence
Second evidence
First evidence
• It can be seen that growth
• When an area of the at sutures will respond to
suture between two facial outside influences under a
bones is transplanted to number of circumstances.
another location (to a • If cranial or facial bones
pouch in abdomen) the are mechanically pulled
tissue does not continue to apart at the sutures, new
grow. bone will fill in, and the
bones will become larger
• This indicates lack of that they would have been
innate growth potential in otherwise
the sutures. If suture is compressed,
growth at that site will be
impeded.
THE GENETIC
THEORY( 1941)
⮚ Genetic theory was given by Brodie.

⮚ The genetic theory simply stated that

genes determine and control the whole
process of craniofacial growth.

⮚ But the mechanism of action by the genetic

unit and the mechanism by which the
traits are transmitted were not understood
until recently.
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⮚ Genetic concept suggests that the genes
supply all the information in growth and
development.

⮚ This originated with classical Mendelian

genetics.

⮚ Later with the blending of data from

vertebral paleontology created the neo-
Darwinian synthesis which is
accepted phylogenetic
currently of
regulation. paradigm

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⮚The field of genetics consists of two
principle areas :

⮚“Transmission genetics” is characterized

by statistical approach and involved only in
explaining possible method of transmission.

⮚It is based on Mendelian laws and did not

explain about genes or its characteristics.

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⮚ Genetic concept stipulates that
genotype the supplies all the
required forinformation
phenotypic expression.

⮚ Moss also stated in his thesis that the

whole plan of growth, the various
operations carried out , the order and site
of growth and their co-ordination with
other systems are all embossed in the
nucleic acid message.

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CARTILAGENOUS THEORY
Given by scott

This theory implies that the

genetic control resides in
the cartilage and the bone
responds passively.
Cranial base
synchondrosis
• Most authors consider this,
especially sphenooccipital
synchondrosis as growth
centre

• There is no doubt of structural

similarity with epiphysial
growth plate and considerable
growth occurs here
• Koski and Ronning, transplanted cranial base
synchondrosis to a nonfunctional sites and found
not enough growth to effect growth of adjacent
bone as seen in situ.

• Powel and Brodie found sphenooccipital

synchondrosis to close much earlier than once
thought, at about 11-16yrs.

• At present there is no direct evidence to support

the claims that synchondrosis are growth centers.
 Cartilage of nasal septum
Endochondral ossification
at septo-ethmoidal
junction and area of
proliferation at vomeral
edge all suggest its role
to provide thrusting force
to push maxilla
downward and forward.
• Sarnat and Wexler, showed excision of nasal
septum affected upper facial growth considerably
• Report by Latham and Burston 1966 concerning
arhinencephalic 9 month old with missing nasal
septum, states that height of upper face was not
greatly affected although middle one third sagittal
development retarded.
• On the basis of the present evidence we may
conclude that septo-ethmoidal junction possibly
acts as growth center during postnatal life,
although direct evidence of this is lacking and may
indeed be difficult to obtain.
Condylar cartilage of mandible

• Most authors in the 60s accepted the opinion that

growth at condyle moved mandible forward and
downward, so condyle is indispensable for normal
vertical growth of face.

• It was also claimed growth of condyle caused antero-

posterior growth of mandible
• On the contrary Scott had opinion
that cartilage grow upward and
backward so as to maintain
contact at TMJ as mandible is
carried downward and forward by
growth of upper facial skeleton
⮚Research works shows that condylar cartilage are
latecomers.

⮚secondary cartilage with different embryological

precursor as that of epiphysial cartilage.

⮚Condylar cartilage is highly responsive to

mechanical stimulus.
• Transplanted condylar cartilage in nonfunctional sites
did not behave like condylar cartilage in situ (koski
and Ronning)

• Tissue culture study have also demonstrated lack of

growth.

• Even bilateral condylectomy or congenital absence of ramus

(Kazanjian) have no appreciable effect on growth of rest of
mandible.

• Thus the information available appears to very strongly point

towards its subordinate role as site of growth not growth
centre.
 BONE REMODELLING THEORY
By BRASH 1930
✧ This theory states that bone grows only
by interstitial growth.

✧ The fundamental tenets of this theory are:

✧ Bone grows only by apposition at the surface.

✧ Growth of jaws takes place by deposition of bone

at the posterior surfaces of the maxilla and
mandible.
✧ This is described as Hunterian growth.
✧Calvarium grows through bone deposition on the
ectocranial surface of the cranial vault and resorption
of bone on the endocranial surface.

✧Bone remodeling theory postulated that the

craniofacial skeletal growth takes place by bone
remodeling –selective deposition and resorption of
bone at its surfaces.

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ENLOW’S V
PRINCIPLE (1963)
🞭 Most useful and basic
concept in facial growth
as many facial and
cranial bones have a V-
shaped configuration.

🞭
Bone deposition(+)
occurs on the inner side
and resorption (-) occurs
on the outer surface.

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EXAMPLE WITH V ORIENTED
VERTICALLY

🞭 Bone deposition on
lingual side of
coronoid process ,
growth proceeds and
this part of the
ramus increases in
vertical dimension.
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 V ORIENTED
HORIZONTALLY
★Same deposits of
bone also bring
about a posterior
direction of growth
movement.
★This produces a
backward movement
of coronoid processes
even though deposit
is on the lingual side
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HUNTER&ENLOW’S GROWTH
EQUIVALENT
✔The Hunter-Enlow growth equivalents concepts is
an important principle covering the development of
the facial skeleton.

✔As the individual components of the skull develop

in different directions ,they must interact directly in
order to compensate for the growth activities.

✔This is achieved by growth equivalents which

act in opposing directions.

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These growth equivalents coordinate the different
movements of the cranial base ,the
nasomaxillary complex and mandible , which are
due to development ,and thus determine the
adaptive changes in relation to individual parts of
the skull.

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For example, elongation of the anterior cranial
base is related with enlargement of the
nasomaxillary complex.
Disturbances during realization of this growth
pattern cause craniofacial anomalies. The
disturbance can be related to disproportions of
the equivalents in the vertical or horizontal
plane

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THE FUNCTIONAL MATRIX
THEORY
⮚Introduction
⮚ Essence of theory
⮚Explanation
⮚Neurotrophism
⮚Constraints of functional matrix
hypothesis

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INTRODUCTION

The concept of this theory was introduced first

by Vander Klaww(1948- 52).
Melvin L. Moss developed the form and
function concept into the functional matrix
hypothesis.
Introduced in 1962.

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 ESSENCE OF THE
THEORY

The functional matrix hypothesis claims that the origin,

form, position, growth and maintenance of all skeletal
tissues and organ are always secondary, compensatory
and necessary responses to chronologically and
morphologically prior events or processes that occur in
specifically related nonskeletal tissues ,organs or
functioning spaces (functional matrices).

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The hypothesis as shown that change in size,
shape, and location (growth) of all craniofacial
skeletal entities are epigenetically( causally
related series of processes in external and internal
environment) regulated.

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✔The epigenetic hypothesis suggests that the post
fertilization genome does not contain sufficient
information ,such as a blueprint, to regulate all
subsequent development.

✔ As structural and functional complexity

increases new regulating information is
generated.

✔The interaction of both genomic and epigenetic

factors is required to regulate or cause development.
Proponents of the functional matrix states that
the expansion of the soft tissue matrix is primary
and the bone growth is purely secondary and
compensatory event.
Translation of the various bones of the face is due
to volumetric expansion of the encapsulated
spaces or tissues.

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Functional
Functional
matrix
matrix
Skeletal unit

Periosteal Capsular
matrix matrix

microskeleton macrosketeto
n
FUNCTIONAL CRANIAL
COMPONENT

One function

Skeletal tissue Neural tissue Muscle tissue Vascular tissue

Functional Cranial Component

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Periosteal functional matrix

• Periosteal Functional Matrix are virtually self

defining. They are best exemplified by the effect of
muscles upon skeletal unit.
• Whether the muscles attach their tendinous
portions directly into skeleletal tissues or indirectly
by fusion with periosteum, they all produce rapid
compensatory response by their specific skeletal
unit.
❑ All periosteal functional matrix act homologously
usually by means of process of osseous
deposition and resorption and such a growth is
termed as transformative growth

❑ Almost all experimental studies like vital staining,

intra osseous implants, histologic sections are
capable of demonstrating the activity of only
periosteal matrix
Insertion of tendon into bone
• But when observing rapid volumetric changes of first
neural and later facial skull, we are forced to accept that
no possible combinations of periosteal apposition and
resorption could account for either rapidity or
magnitude of such growth

• The resolution of this seemingly perplexity was achieved

when full implications of capsular functional matrix was
realized
CAPSULAR MATRIX

Included in this matrix are those masses

and spaces that are surrounded by
capsules.
Example:
Neural mass with scalp and dura.
Orbital mass with supporting tissues of
the eyes.

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Capsules tend to influence macroskeletal
units which means portions of several bones
are simultaneously affected
Inner surface of calvarium.
This sharing of reaction by
several adjacent bones constitutes
a macroskeletal unit.

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Each capsule is an envelope which contains a series of
functional cranial components ,skeletal units and their
related functional matrices and is sandwiched between
two covering layers.
Examples: neurocranial capsule orofacial capsule

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 Neurocranial capsule:

In this cover consists of skin and duramater ,the

neurocapsular matrix consists of the brain ,
leptomeninges and CSF.

The expansion of the enclosed and protected

capsular matrix volume is the primary event in the
expansion of the neurocranial capsule.

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As the capsule enlarges ,the whole of the
included and enclosed functional components,
that is the periosteal matrices and the
microskeletal units are carried outward in a
totally passive manner.

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The calvarial functional cranial components as
a whole are passively and secondarily
translated in space.

In experimentally induced or pathological

states the periosteal matrices are prevented
from exerting their morphogenetic activity.

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Hydrocephaly
 Hydrocephaly

• It is only when we examine these pathologic, or

experimentally produced, situations in which
periosteal matrices have been prevented from
exerting their morphogenetic activity that we can
observe clearly the passive, translative growth
produced by the capsular matrices.
 In the neurocranium, hydrocephaly is such a
condition. The expansion of the neurocranial capsule
is always proportional to the increase in neural mass.

• But this same increase in intracranial pressure

effectively obliterates vascular flow within the capsule
and so prevents periosteal accretion of bone at
sutural areas, thus producing the characteristic
excessively large fontanelles and other sutural
dehiscences.
Thus the point is simple the neural skull does
not grow first and provide space for the
secondary expansion of the neural mass
rather the expansion of the neural mass is
primary event causing growth of the neural
skull.

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Orofacial capsule:
All the functional cranial components of the
facial skull arise, grow and maintained
within the orofacial capsule.
This surroundsand protects the
orophoryngeal functioning spaces, and the
volumetric expansion of these spaces
serves as a primary morphogenetic extent
in facial skull growth.

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 SKELETAL UNITS

May be composed of bone,cartilage

or
tendinous tissue. Each bone is
composed of several micro skeletal
units

The possible interaction between

periosteal matrix and microskeletal units includes
Medial pterygoid gonial angle, temporalis-
coronoid process, masseter, teeth alveolar –
bone.

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When the adjoining portions of a number of
neighboring bones are united to function as a
single cranial component it is termed as macro-
skeletal unit .

e.g. Endo cranial surface of the calvaria, maxilla,

mandible

The overall skeletal growth is a combination of

changes in microskeletal and macroskeletalunits
due to stimulation of periosteal and capsular
matrices respectively.
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 In the mandible we distinguish the
following micro skeletal units.

🞭 Coronoid micro skeletal unit – related

to functional demands of temporalis.

🞭 Angular micro skeletal unit – related to activity of

both masseter and medial pterygoid.

🞭 Alveolar unit – related to presence of teeth.

🞭 Basal micro skeletal unit – related to 73

These micro skeletal units are relatively
independent of each other. The term functional
matrix is by no means implies only to soft
tissues but also includes muscles,
glands, nerves, vessels fat, teeth etc.

Most of the orthodontic therapy is firmly based

on the fact that when this functional matrix
grows or is moved, the related skeletal unit
responds.
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VAN LIMBORGH’S
COMPROMISE THEORY

Three major viewpoints

considered: Sicher’s
Scott’s

Moss’s

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CONTROLLING FACTORS IN
CRANIOFACIAL GROWTH
INTRINSIC GENETIC Genetic factors inherent to the
FACTOR skull tissues

LOCAL EPIGENETIC Genetically determined influence

FACTORS originating from adjacent
structures and spaces ( brain,
eyes)

GENERAL Genetically determined

EPIGENETIC FACTORS influences originating from
distant structures ( sex
hormones)
LOCAL Local non genetic influences
ENVIRONMENTAL originating from the
FACTORS external environment( local
external pressure, muscle
forces etc)
GENERAL General non genetic influences
ENVIRONMENTAL originating from external 76
FACTORS environment ( food ,oxygen)
Sicher’s view
Cartilage
Sutures
Periosteum
Are all growth centers

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 primitive
cartilaginous
skeletal structure of
the fetal skull.

Mass of mesoderm at the

cranial end of notochord

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Scott postulates
Intrinsic genetic factors affect:
Cartilage
Periosteum
while sutures are passive and reactory.

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Moss is felt to have erred
in denying any intrinsic genetic factors in the
control of chondrocranial growth and…
restricting the control of sutural growth to
local epigenetic and environmental factors.

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 VAN LIMBORG’S
COMPROMISE

Chondrocranial growth is controlled by intrinsic

genetic factors

Desmocranial growth is controlled mainly by local

epigenetic factors.

Desmocranial factors is also controlled by local

environmental factors

General epigenetic and general environmental

factors have very little role to play.
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 LIGHT BULB ANALOGY

Also k/n as GROWTH

RELATIVITY HYPOTHESIS By
(John C Voudouris 2000)
• Growth relativity refers to growth that is relative to
the displaced condyles from actively relocating
fossae.
• John c voudouris introduced this concept to explain
the possible effect of functional appliances on
condyle and the resulting growth.

Three Main Foundations :

 FORCE
NEUROMUSCULAR
DISPLACEMENT TRANSDUCTION
VISCOELASTIC
OF CONDYLE AND NEW BONE
TISSUE STRETCH
FORMATION
DISPLACEMENT OF CONDYLE
• The glenoid fossa promotes condylar growth with the use of
orthopedic mandibular advancement therapy. Initially, that
displacement affects the fibrocartilaginous lining in the
glenoid fossa to induce bone formation locally.

• This is followed by the stretch of nonmuscular viscoelastic

tissues. Viscoelasticity refers to all noncalcified tissues.
• Specifically, viscoelasticity addresses the viscosity and
flow of the synovial fluids, the elasticity of the
retrodiskal tissues, the fibrous capsule and other
nonmuscular tissues including LPM perimysium, TMJ
tendons and ligaments, other soft tissues, and bodily
fluids.

• Due to viscoelastic stretch there is influx of nutrients

and other biodynamic factors into the region, through
engorged blood vessels of the stretched retrodiscal
tissue that feed into the fibrocartilage of the condyle.
 FORCE TRANSDUCTION AND NEW BONE
FORMATION

BONE FORMATION takes place at some distance from actual

retrodiscal tissue attachments in the fossa.
The glenoid fossa and the displaced condyle are both
influenced by the articular disk, fibrous capsule, and
synovium which are contiguous.

Thus condylar growth is affected by viscoelastic tissue forces

through attachments of the fibrocartilage that covers the
head of the condyle.
 Effect of three growth stimuli

Voudoris and Kuftinec compares this process to light bulb

analogy.
 When growing condyle is continuously
advanced, it lights up like a light bulb on a
dimmer switch.

When the condyle is released from the anterior

displacement, the reactivated muscle activity dims the
light bulb and returns it close to normal growth activity.
 upper open coil shows potential of the
anterior digastric muscle and other
perimandibular connective tissues to
reactivate and return the condyle back in
the fossa once the advancement is
The open coil above released.
the yellow condylar
light bulb
represents the
effects of the
stretched
retrodiskal tissue
The lower coil represents the
shortened inferior LPM.
 CYBERNETIC THEORY
PART 2
• The term “CYBERNETICS” (Greek kybernetes means
steersman) was coined by mathematician Norbert
Wiener in 1948 to encompass the entire field of
control and communication theory, whether in the
machine or in the animal.
INTRODUCTION
• The concept of cybernetics and control theory was
put forth by Petrovic (1977, 1982) to describe the
craniofacial growth mechanisms and the method of
operation of functional and orthopedic appliances.
The theory demonstrates a qualitative and
quantitative relationship between observationally
and experimentally collected findings.
• Cybernetics is based on the communication of
information. Any cybernetically organized system
operates through signals that transmit information
(which may be physical, chemical or
electromagnetic in nature)
Understanding the cybernetic approach

• Input and outputs represented by arrows.

In study of time dependant phenomena each arrow
represent a signal that at some point may become a
message

• The physiologic system under investigation

represented by a black box.
PHYSIOLOGICAL CYBERNETIC SYSTEMS

• OPEN LOOP SYSTEM

has no feedback or comparator. Output has no
effect on the input action

• CLOSED LOOP CONTROL SYSTEM

Has two variations
1) The regulator
2) The servosystem
•THE REGULATOR
The input is constant.

TRANSFER
Input COMPARATOR FUNCTION

REGULATION OF INPUT

Eg: Temperature regulation system of

the body
 CHANGE IN BODY TEMPERATURE
(input)

TEMPERATURE HYPOTHALAMUS
brought to (comparator)
normal

PILOERECTION AND SHIVERING

(action)
• SERVOSYSTEM
In this system the input is not constant but varies
across time.
 Definitions of various components of the servosystem
COMMAND Signal established independent of
feedback system.

REFERENCE INPUT ELEMENTS Establish relationship between

command and reference input.
REFERENCE INPUT Signal established as a standard of
comparison.
CONTROLLER Located between deviation signal
and actuating signal.
ACTUATING SIGNAL Correspond to output signal of
controller.
CONTROLLED SYSTEM Part of control system between
actuating signal and directly
contolled variable.

CONTROLLED VARIABLE Output signal of the system

FACE AS A SERVOSYSTEM
SERVOSYSTEM THEORY

• Stutzmann(1976) emphasized the following

• Primary cartilage: existing in the axial skeleton, skull

base and limbs where the dividing cells are
surrounded by cartilaginous matrix that isolated
them from local factors able to restrain
cartilaginous growth.
• Secondary cartilages: existing in the condylar and
coronoid processes and in suture, the dividing cells,
prechondroblasts, are not surrounded by
cartilaginous matrix and thus are not isolated from
local factor influences.
Primary and secondary growth cartilage
 The following dissimilarities concerning different
growth cartilages were detected in the organ culture

FACTOR PRIMARY SECONDARY

INFLUENCING CARTILAGE CARTILAGE
GROWTH
Hormones yes yes
Local factors NO( Chondroblast YES( Chondroblas
s surrounded by ts not surrounded
matrix) by matrix)
Orthopedic Direction of growth Direction and
appliances amount of growth
• According to this theory influence of the STH
somatomedin complex on the growth of primary
cartilages has a cybernetic form of command

• The influence of STH-somatomedin complex on the

growth of secondary cartilage has direct and
indirect effects on cell multiplication
BIOLOGIC FEATURES OF PRIMARY AND
SECONDARY CARTILAGES
• In primary cartilages the chondroblasts divide and
synthesise intercellular matrix.
• In secondary cartilage the precohondroblasts are
not yetsurrounded by cartilagenous matrix.
When the secondary prechondroblasts from local
factors able to restrain or stimulate the growth
cartilage.
Nature of cells belonging to the mitotic
compartment of secondary cartilage

↑Na conc
↓Ca conc
•Normally when skeletoblasts multiply , some differentiate into
prechondroblasts .
•If LPM is resected they no longer differentiate.
•The skeletoblast increase at detriment of prechondroblast
•When prechondroblast are exhausted skeletoblast differentiate
into preosteoblast and osteoblast
•Increase in size through periosteal growth
Role of retrodiscal pad and lateral pterygoid
• Blood supply to condylar cartilage originate directly
from lateral pterygoid muscle and indirectly through
retrodiscal pad.

• The biomechanic effect that is partly responsible for

posterior growth rotation and supplementry growth
of mandible.
Biomechanic component governs bone apposition and
condylar growth direction at the posterior border of the
ramus. Increase in the activity of the retodiscal pad
produces increase accentuation of ramus posterior
concavity and local increase in bone apposition and
number of negative charges at ramus posterior concave
surface

Ramus anterior convexity present

And local increase in bone
resorption.
And no. of +ve charges
FACE AS A SERVOSYSTEM

• GROWTH OF MAXILLA
Important as position of maxilla acts as the input.
STH somatomedin, testosterone and estrogen play
primary roles in extrinsic control of postnatal
growth of upper jaw.
Has direct and indirect effects
DIRECT EFFECTS
Hormones have a direct
effect on the
responsiveness of the
preosteoblasts to regional
and local factors,
stimulating skeletal growth
multiplication rate in cranial
and facial sutures.
The direct effect represents
almost the entire influence
of STH somatomedin on
the growth of
sphenoccipital
synchondrosis and nasal
septal cartilage, the lateral
masses of ethmoid bone
and between the body and
greater wings of sphenoid.
 INDIRECT EFFECTS
produces 4wd thrust effect of
Forward growth of septal cartilage premaxillary bone leads to
increase in growth of
premaxillomaxillary suture.

Thrust effect
Nasal septal cartilage spreads laterally
on both sides Of the median line
to penetrate into premaxillary bone.
 Septomaxillary ligament traction
Growth of nasal septal cartilage
Traction effect on the premaxillary bone
Through the septomaxillary ligament.

Traction of the labionarinary muscle traction

Traction of premaxillary bone through this muscle.
Biomechanic promotion of the forward growth of upper jaw.
Absence of labial muscle attachment on the nasal septum-
cleft lip – bone deformation.
Direct action
Premaxillo maxillary
suture
Direct effect
• GROWTH OF MANDIBLE
• The variation in direction and magnitude of condylar
growth is partly a quantiative response to
experimentally effected changes in lengthening of
maxilla
• The upper arch is constantly changing reference input
and lower arch is the controlled variable.
• The physiologic adaptation of mandibular length to
maxillary length occurs through a variation in both
growth rate and direction.
• The operation confrontation between dental arches
elicit in certain cases a deviation signal that modifies
activity of LPM and other muscles of mastication.

• Change in LPM activity influence growth rate of

condylar cartilage.
Cybernetic model of the control mechanisms of the condylar
cartilage growth rate
• peripheral comparator (occlusion), senses change in
performance or efficiency of mastication.
• central comparator (controller) represented by the
CNS. The CNS is equipped with a SENSORY ENGRAM.
Collection of feedback loops Blueprint of ideal
muscular function/position
CNS tends to operate along these feedback loops
Semihypothetical diagram of multiplicative system
between STH somatomedin or testosterone secretion
rates and lateral pterygoid activity on condylar cartilage
growth rate
• Generally if the blood level of STH or testosterone
increases the supplementry lengthening of mandible
is relatively greater than lengthening of maxilla.

• However the operation of confrontation between the

two arches showed a tendency to anterior positioning
of mandible, that reduced the activity of LPM resulting
in decreased condylar cartilage growth rate.
• STUTZMANN ANGLE:the angle formed between main
axis of endochondral bone trabeculae in condyle with
mandibular plane as viewed on lateral cephalogram.

Dividing cells posteriorly

Dividing cells superior part of Opening of angle
condylar
Closing angle
•Experimental findings suggest

Increased Posterior location

Opening of
stimulation of of mitosis in
stutzmann angle
retrodiscal pad condylar cartilage
 Less Posterior
Decreased location of Vertically
Closing of the
stimulation of mitosis in oriented
angle
retrodiscal pad condylar trabeculae
cartilage

There is consequent anterior growth rotation.

This further corresponds to smaller increase in

mandibular length
The lengthening of mandible is measured from the
posterior edge of condylar cartilage to mental
foramen.
FACTORS AFFECTING CONDYLAR CARTILAGE
GROWTH

• Lateral pterygoid muscle & retrodiscal pad tissue

• Effect of hormones Intrinsic regulation of condylar
cartilage growth rate
• Other hormonal & humoral factors
• c-AMP
ACTION OF FUNCTIONAL APPLIANCES
POSTURAL HYPERPROPULSOR
It was observed that during the growth period sagittal
deviation produced by postural hyper propulsor
decreases through the supplementry growth of the
mandible
Increase in LPM
Periodic increase in activity and
thickness of retrodiscal pad
hyperpropulsor

Increase in rate
and amount of
condylar cartilage
growth
• Treatment with hyperpropulsor leads to posterior
growth rotation of the condyle.

Because newly formed endochondral bone trabeculae oriented in a

more horizontal direction, opening the stutzmann angle
• If appliance removed after growth completed – little
or no relapse.

• If removed before growth completed- no relapse if

good intercuspation. If good intercuspation has not
been achieved before the growth is completed - then
the comparator of Servosystem imposes an increased
or decreased growth rate until state of good
intercuspation achieved.
• CLASS II ELASTICS

The stimulating action of class II elastics on lengthening

of condyle is primarily through the retrodiscal pad.
(and its role as a metabolic pump).
• HERREN(L.S.U) ACTIVATOR
2 step effects
1) During the time the appliance is worn the forward
positioning of the mandible is the cause of reduced
increase in the length of LPM.
A NEW SENSORY ENGRAM IS FORMED.

2)When appliance not worn, mandible functioning in

more forward position so that the retrodiscal pad is
more stimulated than it is in controls. Increased
activity cause early hypertrophy of chondroblasts.
Repetitive activity of pad leads to earlier onset of
condylar chondroblasts hypertrophy.

Decrease in no of functional chondroblasts.

Decrease in prechondroblasts multiplication restraining

signal.

Increase in condylar cartilage growth

FRANKEL LATERAL VESTIBULAR SHIELD

• The appliance acts by stimulating midpalatal suture

growth & to lesser extent by increasing bone
apposition on external subperiosteal layer of maxilla.

• Buccal shield --- eruptive pathway of teeth at the

critical time in their development. The relief of
pressure from the cheeks in the dentoalveolar area
seems to allow a more downward and outward
eruptive path at a time of maximal variability,
permitting horizontal and vertical adjustment of
osseous tissues involved
Summary of method of operation of functional
appliances

• Class II elastics, postural hyperpropulsar, Frankel

regulator, Balters bionator, Clark twin block all exert
effects mainly through movement of mandible. Their
stimulating effects are produced mainly during
wearing of appliance.

• Herren & L.S.U activators & extraoral forward traction

on mandible seem to exert their effects mostly
through sagittal repositioning of mandible
 Postural hyperpropulsor Increased activity
of LPM
Function regulator New engram for
(small shields labial to lower incisors) mandibular
Loosly fitted activator position

Increased Increased
iterative activity growth rate
Increased activity of LPM of the of the
Class II New engram for mandibular
retrodiscal pad condylar
elastics position
Forward movement of lower
cartilage and
dental arch increased
lengthening
of the
Activators fixed on Decreased growth of
Movt of the mandible
maxilla or on mandible LPM causing a more fwd
positioning of the
mandible are Temporary
Characterised mainly by far forward
positioning of the mandible mandible effectuated in opening of
Extra oral forward New engram for more forward stutzmann
traction mandibular position position angle

Forward Periodontal inflow of

Activators fixed on the extrinsic boneresorption
maxilla movement of and bone formation cell
Characterised primarily by high lower dental precursors
molar bite plate arch
BIFURCATIONS DURING FACIAL GROWTH
• Occlusal relationships play a significant role in the
process of controlling facial growth.
• The peripheral comparator has several stable
positions, each corresponding to some type of class
I, II or III intercuspations.
• Any given occlusal relationship is stable with respect
to limited fluctuations and disturbances.
• Each cusp to cusp unstable position corresponds to
a functional discontinuity-a topologic bifurcation
type instability, described by Thom(1972)and
Zeemann(1976).
• Occlusal development involves two phases.
• First phase consists of all morphogenetic process
leading to a stable occlusion, during this phase all the
parts of the servosystem are already existent and
functional, but stable occlusal relationship capable of
serving as a peripheral comparator has not yet been
achieved. A reference point for the development of
sensory engram is not possible Hence mandibular
morphogenesis cannot be regulated through
information originating from occlusal relationships
• The beginning of the second phase coincides with the
establishment of a stable occlusion to serve as a
peripheral comparator – required for the development
of a sensory engram. The subsequent morphogenesis
of the face is regulated to minimize possible
deviations from achieved stable occlusal adjustment,
regardless of whether this corresponds to a class I, II
or III intercuspation.
• Depending on the relationship of maxilla to
mandible, the dentition as a whole or in part
(peripheral comparator may be located near molars
or incisors, sometimes near canines.) may be
operating as a peripheral comparator of the servo
system. In posterior rotating mandible - molars In
anterior rotating mandible - incisors and canines.
The action of the peripheral comparator is an
important part of both orthodontic and orthopedic
treatment
 CONCLUSI
ON
Craniofacial growth and development are based to
large extent on evolving concepts .
At the start these concepts were based on naïve
assumptions about the perceived competing roles of
heredity and environment ,often framed within the
context of the age-old “nature nurture” controversy.

151
The craniofacial biologist tend to believe that there
was a single ,overiding mechanism governing the
growth of the face and jaw tended to focus on a
search for what might be called the HOLY GRAIL of
CRANIOACIAL BIOLOGY, a
single theory that is both biologically accurate
and clinically effective.

152
 The treatment of dentofacial mal relations require
considerable insight into the modalities of
craniofacial growth.
The potential pathogenesis of interjaw malrealtions
should therefore be sought at all levels of biologic
organization.
REFERENC
ES
•Moyers R.E.,Handbook of Orthodontics..4 thed.Year
Book Medical Publishers:1988.p.48-50

• Contemporary orthodontics-William.R.Proffit
,W.Fields,David.M.Sarver,5th edition

• Essential of faciial growth,3thed – H.Enlow, Hans

154
•Orthodontic diagnosis –Thomas Rakosi , I.Jonas ,
Thomas Graber ,1stediton

•Orthodontics diagnosis and management of

malocclusion and dentofacialdeformaties-
O.P.Kharbanda 2nd edition

155
•Graber T.M., Orthodontics-Principles and Practice.
3rd ed. Philadelphia:Saunders;1992.p.133

•Moss ML.:Growth of the calvaria in the rats: The

determination of osseous morphology: Am J
Anat 1954:94;333-62

• Sarnat BG:Postnatal growth of the upper

face:Some experimental considerations: The
Angle Orthodontist:1963 July:vol 33(3);139-61
156
•

voudoris john c, kuftinec .Improved clinical use of Twin-

block and Herbst as a result of radiating viscoelastic tissue
forces on the condyle and fossa in treatment and long-
term retention: Growth relativity 2000;117:247-66.

241