Theories of growth

“If there were some deep principle that drove
organic systems towards living systems, the
operation of the principle should easily be
demonstratable in a test tube in half a
morning. Needless to say, no such
demonstrahttp://chellescorner.com/wp-
content/uploads/2011/06/New-
Beginnings.jpgtion has ever been given.
Nothing happens when organic materials are
subjected to the usual prescription of showers
of electrical sparks or drenched in ultraviolet
light, except the eventual production of a
system”
Sir Fred Hoyle
GOOD MORNING
www.indiandentalacademy.com

Various theories of growth are based on expression
of intrinsic genetic potential.
Depending on growth centre
1.Genetic theory by BRODIE
2.Sutural dominance theory by SICHER
3.Functional matrix theory by MELVIN MOSS
Various other concepts / hypogheses related to
craniofacial growth are:
1.VON LIMBORGH’s comprimise theory
2.HUNTER & ENLOW’s growth equivalent concept
3.PETROVIC’s cybernatic theory

» It is a truism that growth is strongly influenced by
genetic factors, but it also can be significantly
affected by the environment, in the from of
nutritional status, degree of physical activity, health
or illness and a number of similar factors.
» Since a major part of the need for orthodontic
treatment is created by disproportionate growth of
the jaws, it is necessary to learn how skeletal growth
is influenced and controlled to understand the
etiologic process of malocclusion and dentofacial
deformity.

GENETIC THEORY
» Basic control of growth ,both in magnitude & timing
is located in genes.
» More assumed than proven
» 1950’s – head & face grew from growth centres
- under strict genetic control
» Primary, genetic control determines certain initial
features
» Secondarily,local feedbacks & inner communication
mechanisms between cells & tissues.

» Contradiction : if the face were under rigid genetic
control,it would be possible to predict features of
chjildren from cephalograms of parents.
» Genetic factors - major significance in development
of malocclusion
Occlusal similarities running in families
LIMITATIONS:
1.Not explaining the role of environmental & epigenetic
factors
2.Primary genetic control determines only certain
features and doesn’t have complete influence on
growth

SUTURAL DOMINANCE THEORY(SICHER)
» Primary event – proliferation of connective tissue
between 2 bones – causes growth & functional
maintenance of bone –
suture being primary consideration
» In Sicher’s view, all bone – forming elements, cartilage,
sutures and periosteum are growth centers, which are
responsible for facial growth and assumed all were under
tight intrinsic genetic control.

The principle factors controlling growth and their
relative impact on the two embryologic divisions of the
head according to Sicher are,
Anatomic location Controlling factors
Chondrocranial
growth
Intrinsic Genetic (Major)
Local Environment (Minor)
Intrinsic Genetic (Major)
Local Environment (Minor)
Desmocranial
growth

Limitations:
1.Independence of skull growth – inconsistent
2.Acc. to this theory – bone growth within maxillary sutures –
pushing apart of bones – thrust on whole maxilla anteriorly &
inferiorly.
But any unusual pressure on bone triggers resorption
…..not deposition.
Deposition of new bone is due to displacement
rather than force that cause it.
3.Bone size and shape are profoundly influenced by sutures.
Experimentally, sutures are flexible
4.Transplantation of sutures to another site - no innate growth
potential.

CARTILAGENOUS THEORY(SCOTT’S HYPOTHESIS)
1953, 1954, 1967
» Intrinsic growth contolling factors – present in cartilage
Sutures only secondary
» Prenatal importance of cartilagenous portions of head
Continue to dominate post natally
» Sutures are passive & secondary
responsive to synchondrosis proliferation & local
environmental factors

LATHAM’s elaboration of the theory:
» 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 midfacial & nasal septal growth before birth
NASAL SEPTAL THEORY
OF CRANIOFACIAL GROWTH

Role of primary cartilage during growth:
» 1st appearance – 5th week IU
» 8th week – independent sites coalesce –
chondrocranium(cranial base, nasal & otic structures
» Mid childhood- primary cartilage – replaced by bone
(endochondral ossification)
» Capacity to grow from within (interstitial growth)
» Pressure tolerant, non-calcified,flexible,non-vascular &
no nutrient requirements
» Genetically predisposed, autonomous tissue – direct
influence on craniofacial pattern

Also states that
 All cartilages through out the skull are primary
centres of growth.
 Growth of the maxilla is attributed to the growth of
the Nasal septal cartilage.
 Nasal septal cartilage is the pacemaker of growth
for the nasomaxillary complex.
 The mandible is like the
diaphysis of a long bone
bent with epiphyseal cartilages
at both ends.

ENLOW’s PRINCIPLE
Two important principles
1.Counterpart principle
2.‘V’ principle
» Growth of any given facial or cranial part relates
specifically to other structural and geometric
‘counterparts’ in the face and cranium.
» If each regional part and its particular counterpart
enlarge to the same extent, balanced growth
between them is the result

Part –Counterpart relationship in the face & cranium:
» Growth process –presented as
1. Deposition & resorption (remodelling)
2. Displacement (actual pacemakers)
Growth of Maxilla & Mandible
» The bony maxillary arch lengthens horizontally in a
posterior direction - by posterior movement of PTM

» DEPOSITION: posterior – facing cortical surface of
the maxillary tuberosity
» RESORPTION: inside surface of the maxilla within
the maxillary sinus.(opposite side of same cortical
plate
» DISPLACEMENT: as maxillary tuberosity lengths
posteriorly, whole maxilla is displaced anteriorly.

counterparts to the bony maxillary
arch :
1. Upper part of the nasomaxillary complex,
2. Anterior cranial fossa,
3. Palate and
4. Corpus of the mandible.

MANDIBLE:
» The mandible is not to be regarded as a single functional
element
» Corpus & ramus are
counterparts to each other
(ramus grows posteriorly
that causes elongation
of corpus)
» The body of the mandible is the
structural counterpart to the body of the maxilla
(The mandibular arch lengthens by an amount that equals
the growth of the maxillary arch)

MIDDLE CRANIAL FOSSA
» Resorption :endocranial side
» Deposition : ectocranially
Sphenooccipital synchondrosis
Endocranial bone growth
Midline part of cranial floor
Facial& cranial parts anterior to middle cranial fossa
Displaced forwards
Secondary displacement

ANTERIOR CRANIAL FOSSA
» Deposition: ectocranially
» Resorption : endocranially
Nasal bones displaced anteriorly
Simultaneous horizontal lengthening of maxillary arch
(counterpart)
Equivalent force increment & balanced form

Ethmoidmaxillary (nasal) region:
» Brain enlarges sutures grow
perimeter of cranial bones increase
Facial area also increases to the same extend
Direct deposition on forward facing cortical surfaces of
ethmoid nasal bones

Vertical lengthening of nasomaxillary complex:
» Deposition: Inferior (oral side)
» Resorption: Superior (nasal side of palate)
Downward growth movement of palate
Relocates it inferiorly & provide for vertical
enlargement of overlying nasal region
» Displacement : sutures of maxilla
Whole maxilla is displaced inferiorly
Primary displacement ( bones own displacement)

“V” – PRINCIPLE
» Useful & basic concept in facial growth
» Most facial & cranial bones have v-shaped
configuration
» Resorption: outer side of “V”
» Deposition : inner side of “V”
» Direction of movement- wide end of “V”
Addition – inside
Removal – outside

The outcome of these
growth processes is,
» Enlargement in overall
size of the ‘V’ –shaped
area.
» Movement of the entire
‘V’ structure toward its
own wide end.
» Continuous relocation

MAXILLA
» Anterior part – resorptive –as it grows downward
» Labial side of premaxilla – resorptive – away from
downward direction of growth
» Lingual side – depository- towards downward growth
direction

Midsagittal section section of maxilla –
palatal side – depository
Floor of the nasal cavity
Surface just above maxillary incisors
- resorptive

MANDIBLE:
» Coronoid process-
inner surface – apposition
outer surface – resorption
backward movement of jaw
» Ramus-
buccal surface- deposition
lingual surface- resorption
drift causing squarer jaw

CONDYLE
» The condylar cartilage
can be visualized as being
situated on the inside of an
ever-expanding ‘V’
» Neck lengthened by
reduction of the bone
situated on the side of the
‘V’ away from the direction
of growth.

VON LIMBORGH’S THEORY –
Mutifactorial theory
Factors influencing growth
Intrinsic factors Epigenetic Environmental
Local General GeneralLocal
Soft tissue
matrices – eye ,
brain
Hormones
Action of
muscle
force
Availability
of O2 in
blood

Intrinsic genetic factors: They are the genetic control of the
skeletal units themselves.
Local epigenetic factors: Bone growth is determined by genetic
control originating from adjacent structures like brain, eyes etc.,
General epigenetic factors: They are non-genetic factors
determining growth from distant structures. Eg. Sex hormones,
growth hormone etc.,
Local environmental factors: They are non genetic factors from
local external environment. Eg. Habits, muscle force, etc.,
General environmental factors : They are general non-genetic
influences such as nutrition, oxygen etc.,
5 factors controlling the growth

The views expressed by van Limborgh can be summarized
in the following six points:
» Chondrocranial growth is controlled mainly by the
intrinsic genetic factors.
» Desmocranial growth is controlled by any few intrinsic
genetic factors.
» The cartilaginous parts of the skull must be considered
as growth centres.

» Sutural growth is controlled mainly by influences
originating from the skull cartilages and from other
adjacent skull structures.
» periosteal growth largely depends upon growth of
adjacent structures.
» Sutural and periosteal growth are additionally
governed by local non-genetic environmental
influence

» Based on the “functional cranial component theory” of
Van der Klauw ,his own experimental work and that of
others combined with clinical interpretations and
experiences MELVIN L:MOSS in 1960 has formulated
the functional matrix theory
» The hypothesis serves as a conceptual bridge between
the concepts of function and epigenesis.

» Origin, growth & maintenance of skeletal tissues &
organs are always secondary, compensatory and
mechanically obligatory responses to temporally &
operationally prior events and processes occurring
in related non-skeletal tissues, organs and
functioning spaces (eg. Functional matrices either
periosteal or capsular.

» No direct genetic influence on the size, shape or
position of skeletal tissues
» All genetic skeletogenetic activity is primarily
depends upon the embryonic functional
matrices
» In a conceptual view, the soft tissues grow, and
bone and cartilage react
» stresses the dominance of nonosseous
structures of the craniofacial complex over the
bony part

» MOSS said that head and neck – composite - number
of functions
1.Digestion
2.Respiration
3.Speech
4.Olfaction
5.Balance
6.Vision
Each of these function - completely carried out by
FUNCTIONAL CRANIAL COMPONENT
FUNCTIONAL CRANIAL ANALYSIS

components include
Functional matrix
Skeletal unit
FUNCTIONAL MATRIX
» This consist of soft tissue-
muscle,gland,nerve,vessels,fat and teeth as well
as non skeletal cartilages
DIVIDE INTO TWO TYPES-
1.Periosteal matrices
2.Capsular matrices

» All non skeletal functional units adjacent to skeletal unit
form the periosteal matrices
» They act by bringing transformation of the related
skeletal units
» Example – coronoid process and temporalis muscle
» Removal,denervation,postinfectively-
decrease in the size
or total disappearance
» Functional hypertrophy/
hyperactivity- increase in size
and change in shape

Capsule surrounding spaces & masses
4 cranial capsules are
 Neurocranial
 Orofacial
 Otic
 Orbital
» Sandwitched between two covering layers with
spaces in between, filled with loose connective
tissue
» Capsules expands due to volumetric increase of
capsular matrix- translation of embedded bone

» Sandwiched between-skin and dura mater
» Consists of-5 layers of scalp
-bone
-two layer dura mater
NEURO CRANIAL CAPSULE

1.Volume of the neural mass is important whether
or not it contains “normal” amount brain tissue.
2.Expansion of this closed capsular matrix volume
is primary event in expansion of the capsule.
3.The volumetric increase cause compensatory
expansion of surrounding capsule which is
brought about by mitotic activity.
4.Later the calvarial functional cranial component
as a whole are passively and secondarily
translated
» In hydrocephaly-passive,nonperiosteal
translative growth is produced.

» Surround and protect oronasopharyngeal
space.
» Surrounded by skin and mucous membrane on
either side.
» Originates by process of enclosure.
» Volumetric growth of these
spaces is the primary
morphogenetic event
in facial skull growth
OROFACIAL CAPSULE

Increase in size of capsule
Passive movement of functional cranial
component
Compensatory transformation of skeletal unit
Growth
(transformation + translation)

Mandibular growth
» Periosteal + capsular matrices activity.
» Series of lateral cephalograms represented
1.anterior cranial base fossa – completed
growth by the end of 3rd year
-constant in shape and size
2.Position of mental foramen doesn’t alter
with time

» FUNCTIONAL CRANIAL COMPONENT
» (eg: mandible)
Skeletal Unit Functional Matrices
Microskeletal Macroskeletal Capsular Periosteal
Matrices Matrices
Eg : coronoid eg : mandible eg : oral capsule eg : muscles
Act on macro Act on Macro
Skeletal unit Skeletal Unit.
Bring about Bring About
Passive Growth Active growth or
or Translation Transformation

• Orbital mass is surrounded by the
supporting tissues of the eye.
• Any enlarged eye or small eye will cause a
corresponding change in the size of
orbital cavity.
• Here eye is functional matrix
ORBITAL CAPSULE

» Composed of –bone, cartilage and tendinous
tissue
1. MACROSKELETAL UNIT-
Adjoining portions of number of
neighbouring bones carrying out
a single function
eg-endocranial surface of calvaria

2.MICROSKELETAL UNIT
Bones consisting of number of small skeletal units
MAXILLA-orbital
-pneumatic
-palatal
-basal
MANDIBLE-coronoid
-angular
-alveolar
-basal

Functional Matrix Hypothesis Revisited
• Advances in biomechanical,bioengineering
and computer sciences – more revisions of
FMH
• Comprehensive revision Indicate
-portions that are retained,extended or
discarded
-Which prior deficiencies are now resolved
• New version : molecular and cellular processes
underlying skeletal growth processes-
DEPOSITION,RESORPTION & MAINTAINANCE
FMH I

HISTOLOGIC DEMONSTRATION:
1.Adjacent adaptational tissue surface
simultaneously show deposition,resorption and
maintainance
2.Adaptation is a tissue process.Deposition and
maintainance are functions of relatively large
group of homologous osteoblasts,never single
cells
3.A sharp demarcation exists between adjacent
cohorts of active,depository and quiscent
(resting)osteoblasts

1. METHODICAL CONSTRAINTS
macroscopic measurement technique
(radiographic cephalometry) and arbitary
reference planes are now been replaced by
continuum mechanics technique like –
FEM(Finite Element Method)
2. HIERARCHIAL CONSTRAINTS
Earlier versions did not extended “downward” or
“upwards”
ie . Suspended between two levels
CONSTRAINTS OF FMH

Vital cells
Irritable( external environment)
Mechano sensing processes
Mechano reception mechanotransduction
Transmits stimulus transforms stimulus
To receptor cell to signal
Mechanotransduction
Eg: Mechanochemical or mechanoelectrical
transduction in bone

Static & dynamic loading on bone
Deformation of ECM & bone cells
Stimulus exceeds threshold
Response(triad adaptation process)
Osteoblasts(deposition & maintainance
Osteoclasts(resorption)
OSSEOUS MECHANOTRANSDUCTION

UNIQUE IN FOUR WAYS-
1.Most of mechanosensing cells are cytological
specialized, but bone cells are not.
2.One loading stimulus evoke 3 adaptation.
3.Osseous signal transmission is aneural.
4.Responses are confined within “bone organ

1. IONIC-brought about transport of ions through plasma
membrane resulting in creation of electrical signal.
Stretch activated channels
loading S-A get activated passage of certain sized
ions
Electrical processes
+ Electromechanical (voltage activated ion channels)
+ Electro kinetic (streaming potential not piezoelectric)
+ Electric field strength
MECHANOTRANSDUCTIVE PROCESSES -TYPES

2.MECHANICAL PROCESS:
INTEGRIN
(physical continuity)
Extracellularly intra cellularly
With collagen with cytoskeletal actin
nuclear membrane
Activation
regulatory genomic activity (cfos genes)

Osseous connected cellular network(CCN)
All bone cells (except osteoclasts)
Connected by gap junctions(connexin 42),
Canalicular processes
Osseous CCN(true syncyctium)
FMH II

GAP JUNCTIONS CONNECT-
 Osteons and interstitial regions
 Superficial osteocytes to periosteal and
endosteal osteoblasts
 Lateral connection of osteoblast
 Periosteal osteoblast with preosteoblastic
cells,which are interconnected

Stimulus intercellular output/response
signal
Initial output hidden final output
layer
Signals summation output
FLOW OF INFORMATION - NETWORK THEORY
Mechanotransductively activated bone cell –
initiate action potential –stimulus- transmission
through gap junction

i. DEVELOPMENTAL-unstrained,organised,self
adapting,epigenetically regulated.
ii. OPERATIONALLY-stable,dynamic
system,oscillatory behaviour.
iii. STRUCTURALLY- variation in organization
permit discrete processing of different
signals
ATTRIBUTES OF SKELETAL CCN

LOADING
Static dynamic
mechanosensing
Mechanoreception
Mechanotransduction
Ionic/electrical mechanical
S-A electro electro field macromolecular
Channel mechanical kinetic strength level
skeletal unit signal
CCN
Response (output)
Deposition resorption maintenancewww.indiandentalacademy.com

Factors contributing to periosteal functional matrices
to regulate the adaptive responses of skeletal units
are:
1.Normalmuscle function strains attached bone
tissue intermittently
2.Dynamics of muscle contraction fit to the bone cell
response
3.Strain frequency of muscle-morphogenetically
osteoregulatory
4.Electric fields produced by muscle and bone similar
morphologically
So bone appears to be closely tuned to skeletal
muscle

FMH III GENOMIC THESIS
» Initially – macroscopic experimental,comparitive & clinica
data
» Revised – hierarchy from gross to microscopic(cellular &
molecular)
» The epigenetic or genomic problem is a dichotomy and
dialectics is one analytical method for its resolution. The
method consist of the presentation of two views, a thesis
and an anti-thesis and of a resolving synthesis

» The genomic thesis holds that the genome, from the
moment of fertilization, contains all the information
necessary to regulate (cause, control, direct).
1. The intra nuclear formation and transcription of
mRNA
2. Succinctly “all (Phenotype) features are ultimately
determined by the DNA”: sequence of the genome
Genomic thesis originated - classic MENDELIAN
genetics(chromosomal)
Recently – extended to all concepts of ontogeny(growth
& development)

The Genomic thesis in orofacial
biology
Prenatal cranio facial development is controlled by two
inter related, temporarily sequential processes:
1. Initial regulatory (Homeobox) gene activity.
2. Subsequent activity of two regulatory molecular groups:
growth factor families and steroid/thyroid/retinoic acid super
family.
Regulatory molecules - can alter the manner of homeobox
genes
- involved in genetic variations causing abnormal
development

» Emergence- appearance of complex higher
levels by self organisation at lower levels.
This can be explained by the concept of
CAUSATION
CAUSATION
THERE IS CONTINUING CONTROVERSY CONCERNING
THE ROLE OF GENOMIC AND NON GENOMIC
PROCESSES IN THE REGULATION OF GROWTH .THIS IS
RESOLVED BY SEVERAL TYPES OF CAUSATION.

CLASSICAL CATEGORIZATION OF CAUSATION
» MATERIAL(what is acted upon?)
» FORMAL(set of rules?)
» EFFICIENT(immediate preceding event?)
» FINAL
MATERIAL FORMAL EFFICIENT FINAL
Cellular and
extracellular
substance
Genomic
regulation
Epigenetic
event
Sufficient
GENETICS EPIGENETICS

Eg: ODONTOGENESIS
Rigid genomic control of odontogenesis
 a. Temporally sequential
b. Spatially restricted
 Epigenetic regulation of odontogenesis
a.experiments on polyphydont chiclid
fish.

EPIGENETIC ANTITHESIS
Entire series of interaction among cells and cell
products which lead to morphogenesis and
differentiation
THESE INCLUDE-
1. All extrinsic,extraorganismal, macroenvironment
factors
2. All intrinsic,intraorganismal,
microenviromental factors
FMH IV - EPIGENETIC ANTITHESIS &
RESOLVING SYNTHESIS

Many different mechanism are capable of modifying
phenotype.
1.Loads may act at –cellular level
tissue level
2.Loads may be – dynamic
static
3.To be effective load may increase,decrease or remain
constant
Epigenetic mechanism at cellular level-
 Deformation of extracellular matrix
 Altering the cell shape
Epigenetic regulation at higher level-
 Regulation of the periosteal matrices.
EPIGENETIC PROCESS OF LOADING

DIALETICAL ANALYSIS
THESIS ANTITHESIS
(GENOMIC) (EPIGENETIC)
RESOLVING SYNTHESIS

A RESOLVING SYNTHESIS
Fundamental argument
» morphogenesis is regulated (controlled, caused) by the
activity of both genomic and epigenetic processes and
mechanisms.
» Both are necessary causes; neither alone are sufficient
cause;
» only their integrated activities provides the necessary
and sufficient causes of growth and development
» . Genomic factors are - intrinsic and prior causes;
epigenetic factors are - extrinsic and proximate causes

» COMPLEXITY AND SELF ORGANIZATION
(COMPLEXITY THEORY)
» CT provides description of the behaviour of complex
biological systems that exist as “ensembles” of
several tissues and organs and not as clusters of
individual cells and extracellular substances. –
COMPLEX ADAPTIVE SYSTEM
» The highly ordered morphological properties of
adult complex biological system (e.g.; functional
matrices and skeletal units) result from the operation
of a series of spontaneous and self-organizing events
can create phenotypic variability under constant
genetic and other extra organismal epigenetic
conditions

“Enviromental factors play a decisive role in all
ontogenetics processes.But it is the organism itself
that ,as an integrated system ,dictates the nature of
each and a very developmental response.
The living organism self organizes on the basis of its
own internal structuring,in continuous interaction
with the environment in which it finds itself”
OPERATION OF COMPLEXITY

NEUROTROPHISM
It is a “non-impulse transmittive neuro function,
involving axoplasmic transport, providing, for the long
term interaction between neurons and innervated tissues
which homeostatically regulates the morphological,
composition and functional integrity of those tissues.
Moss does indicates that there are three general
categories.
Neuro-epithelial
Neuro-visceral
Neuro-muscular

NEURO-EPITHELIAL TROPHISM
There is growth after intimate neuroepithelial
contact.
Eg : amphibian limb regeneration.
This is neuroepithelial trophism
Few patients with facial hypoplasia ,cleft palate –
exhibit sensory deficits – show neuroepithelial
trophism

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

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 stage of
myotubes
» Periosteal muscular functional matrices regulate the size
of microskeletal units through neuromuscular trophism.
» 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

» Based on a factorial qualitative analysis which
takes into account various factors which
determine a coordinated growth of the
craniofacial complex as a whole.
Alexandre Petrovic, Charlier,and Jeanne
Stutzmann of Louis Pasteur School of
Medicine.
Servosystem theory

Study’s in Otosclerosis by
Petrovic revealed that
cartilage surrounding the
cochlea never grew in organ
culture but epiphyseal
cartilages grew well.
Petrovic and coworkers:
Chronobiological aspects
of cartilage and bone
growth
Petrovic and Charlier in
1967-69- Jaw Growth rate
and direction can be
modified by functional
appliance
Jeanne Stutzmann-1976 The
role of LPM and retrodiscal pad
-mediator role
SERVOSYSTEM
THEORY

» Craniofacial growth - multifaceted process
where the connections and interrelationships
are complex with interactions and feedbacks.
» uses the Cybernetic language of information
and communication as a tool to explain the
influence of various factors - extrinsic and
intrinsic on Craniofacial growth

» “Cybernetics” derived from a
greek word meaning ‘steersman’
by Dr.Rosenbleuth and Norbert
Weiner and others in 1947.
» “The language used to describe
control and communication in
man and machine.”
» Can also be used in Biological
Biomedical sciences to explain
negative and positive feedback
loops, self regulation, gain and in
the process explain physiological
processes.

» CYBERNETICS:
• A Cybernetically organised system operates
through signals transmitting information.
• Signals can be physical, chemical or
electromagnetic in nature and of low energy.
• Advantages: not static, sophisticated.

INPUT
(STIMULUS)
ORTHOPEDIC
AND
FUNCTIONAL
APPLIANCES
BLACK BOX
•GENETICALLY
DETERMINED AND
CYBERNETICALLY
ORGANISED GROWTH
•MAXILLA LENGTHENING
AND WIDENING
•MANDIBLE LENGTHING
WIDENING
•TEETH MOVEMENT
OUTPUT
CORRECTION
OF
MALOCCLUSION
AND
INTERMAXILLAY
RELATION
CYBERNETIC ORGANISATION OF
CRANIOFACIAL GROWTH

PHYSIOLOGICAL
SYSTEMS
OPEN
LOOP
CONTRO
L SYSTEM
CLOSED
LOOP
CONTROL
SYSTEM
REGULATOR
SYSTEM
SERVOSYSTEM

COMMAND
REFERENCE INPUT
ELEMENT
COMPARATOR
PERFORMANCE
ANALYSING ELEMENTS
CONTROLLED
SYSTEM
CONTROLLER
ACTUATOR
AMPLIFIER
REFERENCE
INPUT
PERFORMANCE
Output
COMPONENTS OF THE CRANIOFACIAL SERVOSYSTEM

COMMAND
• A signal established
independent of the
Servosystem.
• It affects the behaviour
of the control system
without being affected
by the consequences of
the behaviour.
• Growth hormone,
Testosterone, Oestrogen
CONTROLLER
ACTUATOR
REFERENCE INPUT ELEMENT
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

REFERENCE INPUT
• A signal established
as a standard of
comparison.
• Ideally should be
totally independent
of the feed back.
• The sagittal position
of the maxilla
CONTROLLER
ACTUATOR
COMPARATOR
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT
COMMAND

REFERENCE INPUT
ELEMENT
• They establish the
relationship between
the COMMAND(Growth
hormone) and the
REFERENCE
INPUT(Saggital position
of the maxilla).
• Septal cartilage,
Septopremaxillary
frenum, Labionarinary
muscle, Premaxilla and
Maxilla.
CONTROLLER
ACTUATOR
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

COMPARATOR
• Serves to establish the
relationship between the
REFERENCE INPUT and
the
CONTROLLEDVARIABLE.
• The “operation of
confrontation”- Occlusal
contact between the
upper and lower jaw.
• Any deviation from
optimal occlusal contact
detected by the
comparator leads to
correction signals to
reestablish optimum
occlusal contact.
CONTROLLER
ACTUATOR
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

CONTROLLER
• Located between the
deviation signal and
the actuating signal.
• Lateral pterygoid
muscle and the
Retrodiscal pad.
CONTROLLER
ACTUATOR
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

ACTUATOR
• Output signal from
the controller-
actuator complex.
• Activity of the LPM
and Retrodiscal pad.
CONTROLLER
ACTUATOR
REFERENCE INPUT
ELEMENT
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

CONTROLLED
VARIABLE
• Final output.
• Sagittal position of
the mandible.
CONTROLLER
ACTUATOR
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

GAIN
• OUTPUT / INPUT.
• > 1 - AMPLIFICATION .
• < 1 - ATTENUATION.
• Pterygomandibular
coupling.
• Genetically
determined but can be
amplified by GH and
Testosterone
CONTROLLER
ACTUATOR
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT

REPELLER
• a state of unstable
equilibrium.
• Tries to change to a stable
steady state- ATTRACTOR.
• Cusp to cusp occlusal
contact
CONTROLLER
ACTUATOR
REFERENCE INPUT
ELEMENT
COMPARATOR
COMMAND
PERFORMANCE
ANALYSING
ELEMENTS
CONTROLLED
SYSTEM
PERFORMANCE
AMPLIFIER
REFERENCE
INPUT
OUTPUT
ATTRACTOR
•Structurally stable steady
state.
• What the Servosystem tries to
achieve.
•Full interdigitation type of
Class I, II, III.

FACTORIAL QUANTITATIVE ANALYSIS OF GROWTH
CARTILAGES
» Growth- due to differentiated chondroblasts
(primary cartilages) – general extrinsic factors-
STH(somatomedin),sex hormones & thixonel.
-has cybernatic form of a command
» Growth – due to prechondroblasts (secondary
cartilages)-local extrinsic factors.
-in this case modulated by functional /orthopedic
devices.

Influence of STH on growth of secondary cartilages
Growth of maxilla
Length
1.premaxillomaxillary & maxillopalatine sutures.
2.subperiosteal depposition in anterior region.
Primary role: STH,testosterone,estrogen.
Direct effect indirect effect
Direct effect:
on responsiveness of osteoblasts
On resposiveness & multiplication of
preosteoblasts

Indirect effect:
1.Forward growth of septal
cartilage(premaxillomaxillary suture)
2.Thrust effect(naso septal cartilage)
3.Labionarinary muscle(septal cartilage)
THRUST EFFECT
LIGAMENT TRACTION
MUSCLE TRACTION

UPPER JAW GROWTH

FRANKEL APPLIANCE MECHANISM
» Superior labial frenum
Labionarinary muscles
effect on sagittal growth of maxilla
» Lateral cartilagenous masses of ethmoid
Cartilage between body &
greater wing of sphenoid
Effect on outward growth of maxilla
» Pressure from cheeks in dentoalveolar area
Influence on eruptive path of succedaneous teeth
Frankel retrolabial lip
pads
Frankel lateral
vestibular sheilds
Frankel buccal
sheilds

Growth of mandible
Influence of maxillary lengthening on condylar growth
- resection of nasal septal cartilage
-GH/Testosterone administration
-orthopedic appliances
Servo system
maxilla – changing reference input
mandible – controlled variable
LPM activity – operation of confrontation
& muscles of mastication (deviation signal)
Intermediaries influencing mandible:
» Elastic retro discal pad &condylar attachm ent
» Absence of LPM – same response(CLASS II)

» Peripheral comparator – adjusts sagittal
anterior growth & maintains optimal occlusal
relation
» central comparator(sensory ingram)-postural
activity of masticatory muscles-habitual
anteroposterior mandibular position.

LOWER JAW

Functional appliance
Increased contractile activity of the LPM
Intensification of the repetitive activity of the
retrodiscal pad (bilaminar zone)
Increase in growth stimulating factors
Enhancement of local mediators
Reduction of local regulators
Change in condylar trabecular orientation
Additional growth of the condylar cartilage
Additional subperiosteal ossification
Supplementary lengthening of the mandible
APPLICATION IN CLINICAL
ORTHODONTICS

MALFUNCTIONING OF SERVO SYSTEM
» The malfunctioning of the servosystem appears to
involve mainly the peripheral comparator, which
may be morphologically defective or
morphologically acceptable but have an
inadequate reference basis
» the control system operates faultlessly but is
unable fully to correct the discrepancy between
the growth rates of the upper and lower jaws.

Petrovic’s growth categories
First level:
» Quantitative determination – difference between
maxillary & mandibular sagittal growth
70% - mandible & maxilla in quantitatively same range
25%-mandible > maxilla
3% - mandible < maxilla
Second level:
Variation in direction of growth
Relates to growth inclination & rotation of both the jaws.

Third level:
» Occlusal relationship as peripheral comparation
» Subdivisions aggravation/melioration of malocclusion
(Aborization levels)
stable class I & II intercuspation
» Association
unstable cusp-cusp relation

BIFURCATION TYPE OF SITUATIONS
UNSTABLE
OCCLUSION
STABLE
CLASSI
STABLE
CLASSII
At the moment the Servosystem theory is the only theory
which can explain the role of intrinsic and extrinsic factors in
growth.

CONCLUSION
"Nothing is easier than to admit in words the
truth of the universal struggle for life, or more
difficult--at least I have found it so--than
constantly to bear this conclusion in mind."
— Charles Darwin (The Origin of Species)
It is important for the clinician to know the normal
and the abnormal ranges of growth for proper
diagnosis, treatment planning and selecting
appropriate clinical procedures.
Orthodontic treatment irrespective of appliance
depends to a great extent on adaptive capacity of
alveolar process, growth and remodelling.

References
» Craniofacial development – SPERBER
» Concepts of facial growth - ENLOW
» Contemporary orthoontics – PROFFIT
» Textbook of orthodontics – GRABER PREMKUMAR
» Textbook of embryology & oral histology – AVERY
» Textbook of embryology & oral histology – TENCATE

» Textbook of embryology – LANGMAN’S –SADLER;
8TH EDITION
» Sutures and forces – wagemans, van de velde& kuijpers-
jagtman; AJODO, Vol 1988,Aug (129 – 141)
» Growth of human face – proceedings of royal society of
medicine ,JAMES H.SCOTT; Nov 1953,Vol 47,91-100
» The function matrix hypothesis revisited I.The role of
mechanotransduction, MELVIN L.MOSSAJODO,1997,112,8-
11
» The function matrix hypothesis revisited II.The role of an
osseous connected cellular network,MELVIN
L.MOSS;AJODO,1997,112,221-6

» The function matrix hypothesis revisited III.The genomic
thesis- MELVIN L.MOSS;AJODO 1997,112,410-7
» The function matrix hypothesis revisited IV.the epigenetic
antithesis and resolving synthesis-MELVIN L.MOSS;AJODO
1997,112,338-42
» Neurotrophic process in orofacial growth,MELVIN L.
MOSS;journal of dental research; no.6 ,1492 – 1494.

Theories of growth

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Theories of growth

Similar to Theories of growth (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

Theories of growth