Theories of growth

Theories of growth
DR. GARIMA BENIWAL
PG 1ST YR.

Growth & development:
GROWTH :-
- Growth refers to an increase in size/ number. (Profitt)
- The self mulplication of living substances. ( J.S Huxley)
- Increase in size, change in proportion and progressive
complexity. ( Krogman)
- An increase in size. ( Todd)
-Quantitative aspect of biologic development per unit of time. (
Moyers )
- Change in any morphological parameter which is
measurable. ( Moss)

DEVELOPMENT:-
- Is progress towards maturity. ( Todd)
- All the naturally occurring unidirectional changes in
the life of an individual from its existence as a single
cell its elaboration as a multifunctional unit terminating
in death. (Moyers)
- Development cannotes a maturation process
involving progressive differentiation at cellular and
tissue level. ( Enlow)

GROWTH CENTER vs GROWTH SITE:
According to BAUME:
Growth Center:
Is a site of endochondral ossification with tissue separating
force, contributing to the increase of skeletal mass.
Growth Site:
Regions of Periosteal or suture bone formation and
modeling resorption adaptive to environmental influences.

According to profitt:
Growth site: It is defined as a location at which growth
occurs.
Growth center: It is a location at which independent or
genetically controlled growth.
All growth centers are also growth sites but reverse is
not true.
According to Enlow and Moyers:
They use a common term growth fields for both growth
sites and centers.

Controlling factors in craniofacial
growth:
Von Limborgh’s classification:
.Intrinsic genetic factors
.Local genetic factors
.General epigenetic factors
.Local Environmental factors.
.General environmental factors.

Goose and Appleton’s classification:
.Endocranial Factors
.Multifactorial inheritance
.Racial differences
.Nutrition
.Diseases.
.Socioeconomic factors
.Secular trends

Enlow and Moyers classification:
Natural factors Disruptive factors
.Genetic .Orthodontic Forces
.Function .Surgery
.General body growth .Malnutrition
.Neurotrophism .Malfunction
.Gross craniofacial
anomalies

Theories of growth
1. Bone remodeling theory
2. Genetic theory
3. Sutural dominance theory
4. Cartilaginous theory
5. Functional matrix hypothesis
6. Composite hypothesis by Von limborgh’s
7. Servo system theory
8. Rate limiting ratchet hypothesis
9. Growth relativity hypothesis

1.Bone Remodeling Theory of Craniofacial
growth:
Given by: BRASH(1930)
.This theory concluded that bone grows only by interstitial growth.
Three fundamental tenets of this theory are:
1. Bone grows only by apposition
at the surfaces.
2. Growth of jaws takes place
by deposition of bone at posterior
surface of maxilla and mandible
this is described as “Huntarian Growth”.
3. Calvarial grows through bone
deposition on the ectocraial surface resorption of bone on the
endocranial surface.

2. The Genetic theory
Given by: A.BRODIE(1941)
Genetic concept stipulates that the genotype supplies all
the information required for phenotypic expression.
.Growth of craniofacial complex is under tight genetic
control.
.Nothing in biologic development that does not have
genomic basis.

.
Brodie noted the persistent pattern of facial
configuration and assumed it was under tight genetic
control.
“ Gene makes us body and mind”

Evidences in favour of theory:
Brodie (1940) noted the persistent pattern of facial
configuration and assumed it was under tight genetic
control.
Consistent with the above is the observation that it is
possible to predict features of children from
cephalometric data of parents.
This was also supported by Weinmann and Sicher.

.
No rational scientist would deny the role of “Gene” in
the development of craniofacial complex.
If it is under tight genetic control it would have been
possible to predict child’s features from cephalometric
data of parents but correlation is only 25 %
Also the facial expressions, body built, obesity may be
acquired due to cohabitational effect

.
Moyers quoted that
“ At the end of all this, it is concluded that the
inheritance of facial dimensions is polygenic”
It is also pointed out that “ it is fallacy that the genome,
the totality of DNA molecules, is the main repository for
the developmental information i.e. there exists a genetic
program or a blueprint, theoretically capable of creating
an entire organism”
(BURDI ,A.J.O. 1995)

3.Sutural Dominance theory
Given by: SICHER and WEINNMAN (1952)
In this sutures ,cartilages and periosteum are responsible for facial
growth and assumed that all these were under tight intrinsic genetic
control.
The primary event in sutural growth is the proliferation of the connective
tissue between the two bones.
The sutural connective tissue proliferates,
it creates the space for appositional growth
at the borders of the two bones.

SICHER and WEINMANN advocated that growth of
nasomaxillary complex in a downward and forward
direction is due to growth at sutures- which attach the
complex to cranium and which are parallel.
The bottom line was ‘sutures are the growth
centers and growth is the result of expression of the
genetic program stored here’

Role of nasomaxillary sutures
Sutures:
 Frontomaxillary
 Zygomaticomaxillary
 Zygomaticotemporal
 Pterygopalatine

Sicher’s theory that bones are pushed apart by
connective tissue growth at the sutures, was
contested by Babula, Dixon and Smiley.
They stated
• Bone membrane is pressure sensitive.
• Bone-bone push causes compromised blood
supply.
• Necrosis of osteogenic membrane.

Evidences Against Sutural Theory:
.Trabecular pattern in the bone at the suture changes
with age ,indicating the change in direction of growth.
It can not be accepted that sutures will have the
necessary information foe altering growth.
.Subcutaneous auto transplantation of the
zygomaticomaxillary suture in the guinea pigs has not
been found to grow.(Watanbe M Laskin).
.Extiraption of facial sutures has no appreciable effect on
the dimensional growth of the skeleton(Sarnat,1963).

. Shape of sutures have been found to be depend on functional
stimulus(Moss ,Salentejin,1969).
. Closure of suture appears to be extrinsically determined (Moss ML).
.Sutural growth can be halted by mechanical force like clips placed
across the sutures(Leitunen,1956)
.The parallelism of circummaxillary suture so
as to effect a forward and downward growth
of maxilla is only superficial. Growth at
zygomaticomaxillary suture occurs
predominantly in lateral direction.
The direction of growth of maxilla ranges
from 0 to 82 ֯ in relation to SN plane. It is
practically impossible for sutures running in
the same direction to push the maxilla
parallel to reference plane (Bjork).

Conclusion:
Present evidences indicate sutures as adaptive
growth sites.
Sutural tissues have no tissue separating force
and they are not comparable to growth centers.

4.Cartilaginous Dominance Theory
Also called as Scott Hypothesis/Nasal Septum
theory/Nasocapsular Theory.
Given by: James H Scott
Intrinsic growth controlling factors are present in Cartilage and
Periosteum sutures are secondary.
The cartilage grows while bone merely replaces it.

. Sutures are only responsive and dependent upon the
synchondrosis proliferation as well as local environmental factors.
.In this after recognizing the importance of cartilaginous parts of the
head, nasal capsule, mandible and cranial base in prenatal growth,
Scott felt that cartilaginous development was under tight genetic control
and has opinion that continued to dominant post natal facial growth.
.Scott concluded that nasal septum is mostly active and vital for
craniofacial growth both prenatally and postnatally.
.Anteroinferior growth of nasal septal cartilage which is butteresd
against the cranial base ‘pushes’ the midface downward and forward.

Theory says-
“ pressure accommodating expansion of nasal septal cartilage,
provides the source of physical force that pushes maxilla anteriorly
and inferiorly.
This sets up a field of tension, in all craniomaxillary sutures where the
reactionary growth occurs.”

Anatomic location Controlling factors
Intrinsic genetic factors
Local epigenetic
Local environmental factors
Chondrocranial
Growth
Periosteal
Growth
Sutural Growth Desmocranium

Scott percept these cartilages as growth centers and
pace makers :
Nasal cartilage - nasomaxillary complex
Spheno-occipital synchondrosis - cranial base
Condylar cartilage - mandible

THE CRANIAL BASE:
Mid-ventral segment of the
basicranium characterized by
the presence of synchondrosis.
Spheno-occipital Synchondrosis
is a principal growth cartilage of
basicranium.
Responsible for the antero-posterior
growth of skull

Nasal cartilage at birth and
adulthood

Growth of the septal cartilage pushes
the mid-face downward and forward
relative to anterior cranial base
Separation of midfacial suture system
fills via secondary, compensatory
sutural bone growth

Condylar cartilage:
Scott consider condylar cartilage as the pacemaker or ultimate
determinant of mandibular :-
Growth rate
Amount
Direction
Overall mandibular shape & size

According to Scott , the growth of the condylar
cartilage enables the condyle “to grow upwards
and backwards so as to maintain the contact at
the temporomandibular joint as the mandible is
carried downwards and forwards by the growth of
the upper facial skeleton.”

Supporting views
. Relatively lesser response of endochondral cranial base to the
brain growth, where as intramembranous cranial vault readily
responds.
Pressure and tension have little effect on cartilaginous growth.
On the contrary, intramembranous bone is immediately responsive.
. This indicates different reactions of endochondral and
intramembranous bones to environmental and epigenetic factors.
. Sarnat and Long undertook auto radiographic study with
thymidine to determine levels of proliferative activity of cartilage
cells. They found increased proliferative activity of the cells in the
posterior regions of nasal septal which reflects endochondral
ossification in this region.

.
.Burstone emphasize the septal growth impulse to maxillary growth
in cleft palate cases. where maxillary segment is underdeveloped to
unite with nasal septum in complete unilateral clefts deprives of growth
impulse or energy. The normal contralateral side attained normal
growth.
.Koski after histological study of nasal septal cartilage found that there
is endochondral ossification taking place at Septoethmoidal junction.
. Septomaxillary ligamental traction –
Nasal septum together with septomaxillary ligament b/w
nasal septum and premaxilla is an operative force during prenatal
and early post natal period which causes forward and downward
growth of premaxilla.
Latham’s hypothesis

Latham’s hypothesis:
Septo-premaxillary ligament-later part of fetal life
Role in nasal septal & maxillary growth
Extends from nasal septal cartilage to anterior premaxillary region.
Connection with midface & nasal septal growth before birth.
Nasal septal theory of craniofacial growth.

The effect of removing the cartilaginous nasal septum on
the forward growth of snout in the rabbit.
(Sarnat 1988)

A clinical situation–
In this reported case, the patient got removal of the cartilaginous nasal septum
at the age of 8 years,after an injury.
Obvious midface deficiency after the septum was removed.
Maxilla is often retruded because of restriction of growth of base of skull,
which may produce a relative mandibular prognathism.

Evidences against the theory:
. Moss and Bloonberg found only slight deformity after
extirpation of septal cartilage. They concluded that
septal cartilage provide only mechanical support for the
nasal bone and is not a primary growth center.
.Melson stated that downward sliding of vomar in
relation to anteriosuperior part of nasal septum takes
place throughout craniofacial development making it
unlikely that cartilaginous septum could push the
maxillary complex forward as suggested by Scott.
.

. Moss stated that malformation in snout following
excision of nasal septum is due to trauma following
surgery.
. Burstone and Lantham reported a case of missing
nasal septum. The child has normal resorption and
deposition of palate, height of upper face. Only sagittal
development was affected.

In case of the mandible this
can be explained by
visualizing it as the
diaphysis of a long bone,
bent into a horse shoe
shape, with the epiphysis
removed
so that there is cartilage
representing half an
epiphyseal plate at the ends
of mandibular condyles.

Two studies were carried out by Gillus-Moe in
Scandinavia in 1960’s showed that
there are excellent chances that condylar process
would regenerate to approximately its original size
after trauma
In a few there was even an overgrowth of condyle.
In a few children there is a reduction in growth after
injury maybe due to the trauma to the soft tissues
and resultant scarring
Therefore Scott’s hypothesis does not hold true completely.

Condyle is not a primary center of growth. It does not establish the rate of
overall mandibular growth.
However it has special multidirectional capacity of growth, in response to
various mandibular displacements and this capacity results from, ability of
continued cellular proliferation.

Neither transplantation nor experimental removal studies lend any support
to the idea that condylar cartilage has innate growth potential.
It appears that growth at the condyle is much more analogous to sutures of
maxilla.

.
Conclusion:
“ the old concept that ‘growth cartilage’ serves as a
primary regulator for the development of a craniofacial
complex is now regarded as incomplete, because many
more input factors are now known to be involved”
R.E.MOYERS

5. Functional Matrix Theory
Given by Melvin Moss(1969)
.Based on original concept of Van Der Klaaus that is “Form follows
function”
It claims,
the origin form position growth and maintenance, of all skeletal
tissues and organs are always, secondary compensatory & necessary
response, to chronologically and morphologically prior events, that occur
in a specifically related non-skeletal tissue organs and functioning
spaces.

It claims that apart from initiating the process of
development, heredity and genes play no active role
in growth of skeletal structure in general and
craniofacial structure in particular.
Growth is mediated by functional demands and
neurotrophic control and not by periosteum or
cartilage.

MOSS’S VIEW ON CONTROL
OF CRANIAL GROWTH

Functional matrix
1.Pariosteal matrix 2.Capsular matrix
(Muscles,bloodvessels,
nerves,teeth etc.) a.)Neurocranial capsule b.)Orofacial
capsule
Skeletal units
1. Microskeletal unit 2. Macroskeletal units

THE SKELETAL UNIT -
All skeletal tissues associated With single function
Micro skeletal unit –
when bone is composed of several contiguous skeletal units,
these are termed as microskeletal units. Its growth is modulated by
periosteal matrices. This includes : temporalis-coronoid process,
masseter, teeth-alveolar bone.
The change in size and shape of this microskeletal units occurs
independently of change is spatial position. Moss used two terms for
this: Transformation or intraosseous growth. E.g. mandible

Mandible as a microskeletal unit

Macro-skeletal unit –
When the adjoining portions of
a number of neighboring bones
are united to function as a single
cranial component.The capsular
matrix expansion cause the
macroskeletal unit to change
the position.This process is
called as translational growth.
E.g. Inner surface of calvarium.

Functional matrix
1.Periosteal matrix
Consists of muscles, blood vessels, nerves, glands they bring
about changes in their related skeletal units.
Acts directly and actively. process of osseous deposition and
resorption.
The resultant effect transformative
growth i.e. change in size and shape.
In this A – Resorption
B- Deposition

2.Capsular matrix
capsules is an envelope which contains functional cranial
components sandwiched between the covering layers.
It acts indirectly and passively and not by resorption or
deposition. These do not alter the size and shape of skeletal units
instead they change there location in space . This type of growth
process is called “Translation”
Facial skeletal units are passively & secondarily moved in a space
as the capsule expands.
. Example:
Neurocranial capsule – skin & dura mater.
Orofacial capsule – skin and mucous membrane.

Moss termed change in
spatial position “Translation”
No osseous deposition
and resorption

CAPSULES OF OROFACIAL
REGION
1. Neurocranial capsule
2. Orofacial capsule

 The expansion of the
neurocranial capsule is
proportional to the
increase in neural mass.
 This suggests that the
neural skull does not
grow first, rather the
growth of neural mass is
primary and causes
secondary compensatory
growth of the skull.

Orofacial capsule surrounds and protects 3 functioning spaces;-
ORAL, NASAL, PHARYNGEAL.
The volumetric expansion of these spaces serves as a “primary
morphogenic event” in facial skull growth. These spaces are not just
“left over” when all other facial components complete their growth. The
patency of these spaces is related to the metabolic demands of the
body.
The human oronasopharyngeal space increase in size from the third
month of pregnancy.

Functional cranial analysis of Maxilla
.
Moss and Greenberg point out that the basic functional matrix for basic
skeletal unit is infraorbital neurovascular triad.
.In this:
maxillary division of trigeminal
nerve that play the major role in
maintaining the spatial constancy of
the infraorbital canal to the anterior
cranial base.
.The area of infraorbital foramen is the
site of the first ossification of human
maxillary bone.

Bone formation begins at about the end of 6th week in form of
radiating trabeculae.
.The orbital mass functional matrix virtually cease their
volumetric growth by the end of 1st decade. The definitive
height of the nasal cavity is attained at the same time.

Mostly all the functional matrices that might affect the
position of maxillary basal skeletal unit come to rest at this
time and do not participate in further growth of maxillary
complex.
The non basal maxillary matrices related to oral and
dental function continue to grow after 10 years of age.
.Maxillary base is passively carried downward, forward and
laterally as a result of expansion of their capsule.

In the maxilla: orofacial matrix expand
Than maxilla would carried away from adjacent bones
Than bone fill in response
In the orbital floor:
It is secondary and compensatory growth following the passive
movement of maxilla.
Orbital mass is surrounded by the supporting by the supporting tissues
of the eye.
Here eye is functional matrix.

Moss and Greenberg states that three types of
bone growth are seen in maxilla:
Firstly, primary expansion of the orofacial capsule.(these changes help
to maintain anatomical and functional continuity between maxilla and
adjacent bones.
Secondary, there are changes in bone morphology associated with
alteration in absolute volume, size, shape or spatial position of any or all
of the several relatively independent maxillary functional matrix like
orbital mass.
Finally, there are bone changes associated with the maintenance of the
form of bone itself. Example: Posterior repositioning of zygomatic arch
which have forward movement of arch.

Functional cranial analysis in
mandible:
The mandibular matrix consists of:
. All muscles with mandibular attachments.
. Neurovascular triads
.Associated salivary glands
.The teeth
.Fat, skin and connective tissue
.The tongue
.The oral and pharyngeal spaces.

The basal tubular portion serves as a protection for the
mandibular canal and it follows a logarithmic spiral in its
downward and forward movement from beneath the cranium.
This is called “Unloaded nerve concept”.
The most constant portion of mandible is the arc from
foramen ovale to mandibular foramen and mental foramen.

According to moss, three important phenomenon
occurs during growth of mandible:
1. constancy of relative position of mental foramen in mandibular
corpus:
2. Absolute migration of the dentition through the alveolar bone:
This movement happens during the 1st two decades.

3. Change in the direction of mental foramen:

Transmission of functional stimuli to the bone,
Neurotrophism:
Neurotrophism:
It is defined as “non-impulsive, transmitive neurofunction involving
axoplasmic transport providing for the long term interaction between
neurons and innervated tissues, which homeostatically regulate the
morphological, compositional and functional integrity of those tissues”.
“the nervous system is also concerned with the integrity of body
structure”
(SINGER,1963 )
“Interaction between nerves and other cells that controls,
molecular modifications in other cells”
(GUTH,1969 )

Neurosecretory mechanism
A presumed pathway
for transport of
neurotrophic substance
from the site of origin to
the innervated tissue.
Mechanism is same in
both afferent & efferent
neuron.

3 types
NEUROEPITHELIAL TROPHISM
NEUROVISCERAL TROPHISM
NEUROMUSCULAR TROPHISM

1. THE NEURO EPITHELIAL TROPHISM
The neurological work of neurotrophism first began with the field of
dermatology.
The factors which contributes neuro epithelial trophism are:
.Local mechanism operating in area of high mitotic activity.
.Epithelial growth factors.
.Types of feedback mechanism between dermis and epidermis:
Taste bud Following denervation,degeneration of his
specialized epithelium occurs. not only the taste buds cell, but adjacent
epithelium also becomes thinner, following gustatory nerve section,
Indicating a “neural influence” governing epithelial thickness.
Amphibians limb regeneration is an example for neuro
epithelial trophism.

2. NEUROVISCERAL TROPHISM :
Trophic control probably exist for capsular matrices which
passively regulates position of both skeletal unit and periosteal
matrices.
Salivary glands are regulated by neurotrophism.
Hypertrophy and hyperplasia of gland cells seem to be under
neurotrophic control partially.

3. NEUROMUSCULAR TROPHISM :
Moss says that nerve influences the gene expression of
the cell.
Skeletal muscle ontogenesis normally requires motor
neuron innervation to proceed past the stages of
myotubes.
Periosteal muscular functional matrices regulates the size
of microskeletal units through neuromuscular trophism.

Embryonic myogenesis, is independent of neural
innervation however, at myoblast stage of
differentiation, neural innervation is established without
which further myogenesis usually cannot continue.
The complex chain of events leading to particular
expression of the genetic embryonic potential is not
wholly within the cell but also includes informational
elements contributed by the nerve. (Disculescu et
al)

Muscle denervation and renervation
Guttmann showed that when motor neuron
conduction is blocked effectively by pressure, no muscle
atrophy occurs.
studitsky reconstructed functioning muscle from
minced muscle fragments and demonstrated that such
fragment will form a functional muscle if they are
supplied by motor nerve
without such innervation a mass of connective
tissue will form.

If muscle tissue, is experimentally prevented from
becoming efferently innervated motor end plate will
never develop.
Organs require afferent innervations for their
development are muscle receptors, muscle spindles and
tendon organs.
The conformational features of myosin are determined
by the nature of the innervation.

Crossinnervation
following cross innervation of motor nerve, between
slow-fast pair of functioning muscle the result suggest
that the changes in the speed are brought about by a
neural influence.
Therefore, these parameters of skeletal muscle are
nerve-specific, not muscle specific.
Hyperneuralization
It is not simply the number of nerve fibers that is
important but rather the total amount of neurosecretory
material is also critical. Such a muscle increase in
weight by 10-20%.

Neurotrophism controlling genetic activity
Protein synthesis in oral epidermal cells and
enzymatic synthesis in taste bud cells appear to be
neurotrophically regulated .
The forelimb of the adult frog, which normally will not
regenerate following its amputation, will regenerate if the
quantity of the nerves in the fore limb stump is
augmented, by the surgical addition of the ipsilateral
sciatic nerve.
[SINGER, 1954]

Regeneration of amputed amphibian limb suggest
that regenerating nerves may be exerting a direct
control over the synthesis of DNA, RNA& protein.
Also when aberrant peripheral nerve generation
occurs supernumerary limbs are formed.

LIMITATIONS OF F.M.H
Methodological constraint
Hierarchical constraint
1. Methodological constraint : Macroscopic measurements, permitted
only method specific description that cannot be structurally detailed.
experimental bases of FMH were cephalometric follow up of individuals.
2. Hierarchical constraint :
F.M.H couldn’t describe the downward (i.e. cellular, sub cellular) or
upward processes( i.e., multicellular) taking place during growth.
F.M.H. couldn’t describe that how extrinsic, epigenetic Functional matrix
stimuli are transduced into regulatory signals at cellular, multicellular
and molecular level.

The new version of F.M.H. tries to bridge the gap between
hierarchical constraints and explains the operation from
genome to organ level by two concepts:
1. Mechanotransduction occurring in single cells.
2. That bone cells function multicellularly as a connected
cellular network.

Functional matrix hypothesis
revisited:
.Advances in biomechanical, bioengineering and
computer sciences allows the creation of more
comprehensive revision of the functional matrix
hypothesis.
In F.M.H. revisited inclusion of two topics:
1. Mechanism of cellular mechanotransduction.
2. Biological network theory.
(AJODO 1997)
Melvin Moss.

F.M.H. Revisited:
1.F.M.H. Revisited 1:The role of mechanotransduction.
2. F.M.H. Revisited: The role of an osseus connected
cellular network.
3. F.M.H. Revisited: The genomic thesis
4. F.M.H. Revisited: The epigenetic antithesis and the
resolving synthesis.
(Melvin moss AJODO 1997)

1. The functional matrix hypothesis
revisited.1: The role of mechanotransduction:
The mechanotransduction is a process by which a mechanical
stimulus is converted into a biological signal to affect a cellular
response.
All vitals cells respond to alternations in their external environment, by
process called:
a. Mechanoreception :
Transmit an extra cellularly physical stimulus into a “receptor
cells”.
b. Mechanotransduction :
Transform the stimulus “informational content” into an
intracellular signal.

PROCESS OF
MECHANOTRANSDUCTION

Osseous Mechanotransduction:
Bone is subjected to constant loading, both static and dynamic. This is
essential for normal homeostasis of bone.
When the threshold value of the force is exceeded, the loaded tissue
responds to the stimulus by the triad of bone cell adaptation.
The triad includes:
1. Bone deposition
2.Maintenance
3.Bone resorption

The osseous mechanotransduction has four unique properties:
1. Bone cells are not cytologically specialized like other
mechanosensory cells.
2. Single bone loading stimulus evoke three adaptional responses,
where as non osseous process generally evokes one.
3. Osseous signal transmission is aneural, it doesn’t involve neural
pathway unlike other mechanosensory signals.
4. The adaptational response is confirmed within the individual bone.

Osseous mechanotransduction translates the
periosteal functional stimulus into a skeletal unit cell
signal by two skeletal cellular mechanotransductive
processes:
. Ionic
.Mechanical
1. The ionic or electrical processes involve some form
of ionic transport through the bone cell plasma
membrane. There is a subsequent intercellular
transmission of created ionic signal in turn are
computed by osseous connected cellular network.

Stretch activated channels:
These involves the plasma membrane stretch activates(S-A) ion
channels.Which activated in strained osteocytes, they permit passage of
a certain sized ions.
Electrical processes:
These include several non exclusive mechanotransductive process,
these are:
1.Electromechenical(voltage activated ion chhanel)
2.Electro kinetic(streaming potential not piezoelectric)
3.Electric field strength(bone respond to exogenous electrical field)

6.Multifactorial theory
Von Limborg in 1970
According to Limborg
The genetic theory, sutural theory and cartilage theory were not
satisfactory, yet each contains elements of significance that cannot
be denied.
Limborg explains the growth and development in a view that
combines all the existing theories.

Van Limborg explains the growth and development in a view that
combines all the three existing theories and suggested five factors
that he believed control growth:
1. Intrinsic genetic factors :
Genetic expression observed in bone and cartilage
2. Local epigenetic factors :
Genetically determined influences originating from adjacent
structures and spaces e.g. : brain, eye etc.

3. General Epigenetic factors :
They are genetically determined factors determining growth from
distant sites e.g.: Sex hormones, growth hormones etc..
4. Local environmental factors : They are non genetic factors from
Local external environment
E.g.. Habits and muscle force.
5. General environmental factors : They are non genetic external
influences such as food oxygen.

Controlling factors Anatomic location
Local epigenetic
Local environmental
Direct effect
Intrinsic genetic
Local environmental
Indirect
effect
Local epigenetic
Local environmental
Local epigenetic
Local environmental
Desmocranium
(Calvarium)
S-O Synchondroses
(Chondrocranium)
Nasal septum
Splanchocranium
(mandible)
Splanchocranium
(middle face)

SUMMARY OF VON LIMBORGS HYPOTHESIS
Chondrocranial growth is controlled by intrinsic genetic factors.
The desmocranial growth is controlled mainly by many epigenetic
factors that originate from skull cartilages and other head tissues.
Ventral surface of maxilla w.r.t. glenoid fossa also affects the mandible
by rotating it forward or backward.

The growth of the desmocranium is influenced by local environmental
factors occurring in the form of tension forces and pressures.
General epigenetic and general environmental factors are of
minor importance.

7. Servo System Theory:
Given by: Petrovic
Cybernetics explained that the growth of various craniofacial regions is
the result of interaction of a series of causal changes and feedback
mechanisms.
“Cybernetics” derived from a Greek word meaning “steersman” by Dr.
Rosenbleuth and Norbert Weiner in 1947.
“The language used to describe control and communication in man and
machine”.
A cybernetically organized system operates through signals
transmitting information.

Principle factors:
1.Hormonally regulated growth of the midface and anterior cranial base,
which provide a constantly changing the reference input via the
occlusion.
2.The rate limiting effect of this midface growth on the growth of
mandible.
While growth of the mandibular condyle and of sutures may
affected directly and indirectly by hormones.

Craniofacial growth is extremely complex process. Complexity results
from organization of different constituents of craniofacial skeleton.
The physiologic properties of craniofacial skeleton are not simply
related to the cells but originate from tissues and organ system as a
whole with all its interactions and feed back mechanism.

Only cybernetic language may accurately explain the complexity of
craniofacial morphogenesis.
In fact it is a major break through in decision making process and
problems solving in orthodontics and Dentofacial orthopedics.
Input Measure of effect Return of modified information
Regulation of effect.

According to this theory, the behaving organism is not seen as a passive
respondent called into action by changing environmental stimuli but as
a dynamic system which continuously generates intrinsic activity for
organized interaction with environment.

Cybernetics in craniofacial growth:
Cybernetics demonstrate the
relationship between observational
and experimental findings.
Feedback signal: It is function of
controlled variable that is compared
to reference input.
Closed loop system: If a
physiological system is designed to
maintain a specific correspondence
between inputs and outputs, in spite
of disturbances.

Open loop system: It has no feedback loop or comparator.
The regulator: It is a negative feedback system ,disturbances cause
change that tend to restore the normal state of disturbed system to
initial state.
The servo system: It is called as follow up system.

Elements of servo system theory:

Command : Is a signal established independently of feedback system
under scrutiny.
Eg. Secretion rate of growth hormone.
Reference input element: Establish the relationship between command
and reference input.
E.g. septal cartilage, septo premaxillary ligament etc.
The controller is located between the deviation signal and the actuating
signal.
E.g. activity of retrodiscal pad and lateral pterygoid.
The confrontation between the position of upper and lower dental arch
is the comparator of the servo system.
The gain: it is the output divided by input.
Gain value > 1 than called as amplification
Gain<1 is called as attenuation.

The disturbance: any input other than the reference required is called as
a disturbance.
E.g. Increase in hormone secretion result in lengthening of mandible.
The attractor: This is finally structurally stable state in dynamic system.
E.g. full cusp class I molar relationship.
The repeller: This includes all unstable equilibrium states
e.g. cusp to cusp occlusal relationship.

Evidence against the theory:
. Goret-nicaise, Awn(1983) found the resection of the lateral pterygoid
muscle fails to dimmish condylar growth.
.Whetten and Johnston(1985) used a bilateral condylotomy model in
young rats to test the extent which direct muscle traction can alter the
rate of condylar growth and remove the lateral pterygoid muscle
unilaterally.
They found no difference in condylar growth between rwo sides.
.Das, Myer and Sicher(1980) found that the occlusion remained
unaffected in condylectomy studies.

Conclusion:
“Functional paradigm” states simply that the
craniofacial complex is highly adaptable. The
primary focus of craniofacial growth research should be
on those factors that can be modified experimentally
and treated clinically.
This statement of the paradigm does not preclude
the influence of genetic factors on the growth and form
of the craniofacial skeleton.

Similarly, No rational scientist denies that the genes
are essential for normal development. both the genomic
and the alternative functional paradigm recognize this.
Then why should these two paradigms be in
conflict?
with the helping hand from cybernetics we can
focus our attention more on providing sound treatment
to the orthodontic patients.
As far as theoretical debate is concerned, future will
recall this as one of the most complicated problem of
our times.

8. Rate limiting ratchet hypothesis:
Given by: Johnston
.This theory explains that when condyle is unloaded than it is able
to grow
while when condyle is loaded than it is unable to grow.
Johnston suggests that the pattern of condylar loading is the only
signal necessary to control condylar growth.
Mandibular distraction unloads the condyle and permits its
intrinsic ability to grow.
In this the “Condyle” is considered as a rate limiting ratchet.

9. Growth relativity hypothesis:
Given by: John C Voudouris(2000)
.This refers to growth that is relative to its displaced condyle
from actively relocating fossa.
The main foundations of growth relativity hypothesis are:
. Displacement of condyle.
.Non muscular viscoelastic tissue stretch
.Force transduction beneath the fibrocartilage of the glenoid
fossa and condyle add new bone formation.

Displacement of condyle: The displacement takes place initially
following mandibular advancement effects the fibro cartiligenous linning
in the glenoid fossa to induce bone formation locally.
Viscoelastic stretch: Once condyle is displaced it is followed by
the stretch of non muscular viscoelastic stretch. Viscoelasticity refers to
noncalcified tissues.
This stretch addresses the viscosity and flow of the synovial fluids,
elasticity of retrodiscal tissues, including LPM, perimysium, TMJ
tendons and ligaments, other soft tissues and bodily fluids.
Due to this there is influx of nutrients and other
biodynamic factor into the region, through blood vessels of stretched
retrodiscal tissue that feed into fibrocartilage of condyle.

Force transduction and new bone formation:
New bone formation occurs
at same distance from actual
retrodiscal tissue attachments
in the fossa. The glenoid
fossa and displaced condyle are
influenced by the articular disk,
fibrous capsule and synovium
which are contiguous.

Effect of three growth stimuli:
Displacement, viscoelasticity and transduction of force.
Voudoris and Kufinec compares this with light bulb
anology.
The resultant increase in new bone formation appears
to radiate as multidirectional finger like process beneath
condylar fibrocartilage and significant aapositional bone
formation is seen in fossa.

Theories of growth

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