THEORIES OF GROWTH

Introduction:
Theories of growth :
PART 1:

Bone Remodeling Theory

Genetic Theory
Sutural Theory
Cartilaginous Theory
Functional Matrix Theory
Functional Matrix Hypothesis Revisited
PART 2:
Van Limborghs Theory
Enlows Expanding V Principle
Enlows counterpart principle
Growth relativity Hypothesis
Viscoelastic Stretch
Neurotrophism
Cybernetic theory/Servo System
Light Bulb Analogy
RECENT THEORIES: Aponeurotic tension model of
craniofacial Growth man

• Conclusion

• References
Theories of Growth :
PART 1
Bone Remodeling Theory
Genetic Theory
Sutural Theory
Cartilaginous Theory
Functional Matrix Theory
Functional Matrix Hypothesis Revisited
WHAT IS GROWTH??
an increase in size & number of tissues.(Todd)
refers to anatomic phenomenon & is quantitative in nature.

• Growth may be defined as developmental increase in mass.

• In other words it is a process that leads to an increase in the physical
size of the cells, tissue organs or organisms as a whole.
Introduction:
CRANIOFACIAL GROWTH
The first scientific research on craniofacial growth was in 18th century
by Sir john hunter on Growth of jaw and eruption dentition.

• BASED ON EXPRESSION OF INTRINSIC GENETIC

POTENTIAL.

• THERE ARE VARIOUS THEORIES,CONCEPTS AND

HYPOTHESES.
THEORIES OF GROWTH

 Bone Remodelling Theory- Brash 1930

 Genetic Theory- A. Brodie 1941
 Sutural Theory- Sicher and Weinmann 1952
 Cartilagenous Theory- James H Scott
 Functional Matrix Concept- Melvin Moss 1960
 Remodeling Theory
J. C. Brash (1930’s)

Theories of Craniofacial Growth in the Postgenomic Era - David S. Carlson Seminar Orthod 11:172–183 © 2005 Elsevier
 Remodeling Theory (Brash)
• First theory of craniofacial.
• Introduction Vital staining method by John Hunter helped Brash to
postulate the Bone Remodeling.

• The remodeling theory postulated that all of craniofacial skeletal

growth occurs exclusively by Bone Remodeling—selective addition
and resorption of bone at its surfaces.

• Sutures and the cartilages of the craniofacial skeleton have little or

no role in the growth of the craniofacial skeleton.

Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson

The three fundamental tenets of this theory are:

1. Bone grows only by apposition at surfaces.

2. Growth of the jaws is characterized by deposition of bone at the

posterior surfaces of the maxilla and the mandible.(Hunterian
Growth)

3. Calvarial growth occurs via deposition of bone on the ectocranial

surface of the cranial vault and resorption of bone endocranially.

Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson

 CRANIAL VAULT

 Increase in size of cranial vault occurs by adding bone

• Periosteal deposition of outer Ectocranial surface.
• Resorption of bone on inner Endocranial surface.

Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson

GENETIC THEORY:
(ALLAN G BRODIE -1941)
• GENETIC THEORY States that – Growth
is controlled by Genetic influence.

• states that “Genes determine and control

the whole process of craniofacial Growth”.

• This theory states that genes such

as Homeobox, Sonic hedgehog,
Transcription factor and IHH
(protein) play an important role in
craniofacial growth.
The field of genetics consists of two principle areas:

Transmission Genetics-characterised 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 characteristic

Developmental and Molecular Genetics-

Explains Growth on the molecular basis of Genetics.
Dentofacial disturbances of genetic origin :

DISORDERS

Micrognathia
Macrognathia
 SYNDROMES
Cleft lip and palate
Downs syndrome
Gardner's syndrome
Marfan’s syndrome
Cleido cranial Dysplasia
 MALOCCLUSION
Bimaxillary protrusion
Class II div 1
Class II div 2
Class III
Open Bite
 COMMONLY OCCURING HERITABILITY OF LOCAL
OCCLUSAL VARIABLES:

Supernumerary Ectopic canines Submerged primary molar

teeth
SUTURAL THEORY/Sutural Dominance
SICHER & WEINMANN (1952)

Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson

 According to the theory Suture,cartilages and periosteum are all
responsible for facial growth and were assumed to be under intrinsic
genetic control.

• Sicher came to conclusion that sutures were causing most of the

growth based on studies using vital dyes.

• According to sicher, Craniofacial skeleton enlarges due to the

forces exerted by the sutures as they separate.

Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson

 CRANIAL VAULT

• Increase in size if the cranial vault takes place via primary growth of
bone at the sutures ,which forces the bone away from each other.

Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson

• Sicher postulated that bone growth
within various Maxillary sutures
produces pushing of the bone which
result in forward and downward.

• Mandibular growth takes place via

intrinsically determined growth of
cartilage of the mandibular condyle,
which pushes Mandible downward
and forward.
Theories of Craniofacial Growth in the Postgenomic Era David S. Carlson
 Structure of Sutures (koski-1968)
First school of
Thought
Sicher and weinnman

Suture is a three layered

structure

Connective tissue between

the two bones plays the
same role as cartilage at
the base of skull and like Schematic illustration of structure of the
epiphysis of long bones
suture
A. THREE LAYER CONCEPT
Tissue seperating force
exists in the suture itself

Cranial growth centers: Facts &Fallacies? --- koski 1968

 Schematic illustration of function of the suture
Second school of Thought

Pritchard , Scott and Girgis

Suture is a five layered structure

Each bone at the suture has its A. The concept of a thrusting force
own two layer periosteum on residing in the sutural tissue itself
both sides and the intervening
fifth layer between these
periosteal layer.

This layer plays a role in

adjustment between the bones
during growth , while the active
proliferating role is played by
the cambial layer of the
periosteum of each bone. B. The concept of an outside force seprating
the bone from each other
Cranial growth centers: Facts &Fallacies? --- koski 1968
 EVIDENCES AGAINST SUTURAL THEORY

Untreated cleft palate patients-growth occurs even in absense

of sutures.

Trabecular pattern of bone changes with age, indicating

change in the direction of growth-sutures cannot have the
necessary information for altering growth.

Sridhar premkumar- craniofacial Growth

 Autotransplantation of the zygomaticomaxillary suture in the
guinea pigs has not been found to grow-Experiment done by
(watanabe M Laskin).

Shapes of the sutures have been found to depend on

functional stimulus(Moss and salentejin).

Sridhar premkumar- craniofacial Growth

CLINICAL IMPORTANCE
Rapid Maxillary Expansion
CARTILAGENOUS THEORY:
JAMES SCOTT 1968
SCOTT HYPOTHESIS/ NASAL SEPTUM
THEORY/ NASOCAPSULAR THEORY
States – intrinsic growth controlling
factors are present in
CARTILAGE.(Periosteum with
sutures being only secondary).

Cartilaginous parts throughout head,

nasal capsule , mandible base in
prenatal growth, scott felt that
cartilage develop under tight genetic
control and they continue to dominate
postnatal facial growth.
 The anteroinferior growth of nasal
septal cartilage which is buttressed
against the cranial base “pushes”
the midface downwards and
forward.

Cranial growth centers: Facts &Fallacies? --- koski 1968

NASAL SEPTAL CARTILAGE - pacemaker for growth of the entire
Naso-Maxillary complex.

Mid-face pushed downward & forward relative to anterior Cranial Base.

Separation of mid-face suture filled by new bone.

Cranial growth centers: Facts &Fallacies? --- koski 1968

CONDYLAR CARTILAGE- Growth of mandible
pushes Mandible downward & forward.
Growth of cranial base
Experiments done to prove theory:

 Transplantation

 Surgical removal

TRANSPLANTATION

When a piece of the epiphyseal plate of a

long bone is transplanted it continued to

grow in new location or in culture,

indicating that they did have innate growth

potential.
SURGICAL REMOVAL

Removal of a segment of the Nasal Septal Cartilage in humans and

rabbits showed mid-facial deformities.
Advantages of the theory:
1. In many bones, cartilage growth occurs while bone just replaces
it.

2. There exists innate growth potential of the cartilage.

3. Nasal septal cartilage too has innate growth potential on being

transplanted to other sites.

4. Removal of nasal septal cartilage in rabbits during experiments,

shows retarded mid-face development.
EVIDENCES SUPPORTING THE THEORY

Sarnat-1966 Deficient growth of snout after extirpation of

septal cartilage
Latham and Nasal septum determines anteroposterior growth of
Burstone 1966 upper face
Burstone Importance of septal growth impulse to maxillary
growth in cleft palate cases
Sarnat and Long Found increased proliferative activity of the cells in
posterior regions of nasal septum which reflects
endochondral ossification in this region
Steinler,Kvinslaw Increase in size of autotransplanted nasal septum in
subcutaneousabdominal wall in rats.suggested
intrinsic growth potential in nasal septum
Koshi Found that there is endochondral ossification taking
place at septoethmoidal junction
EVIDENCES AGAINST SCOTT’S THEORY:

Moss and Septal cartilage provides only mechanical

Bloonberg-1968 support for the nasal bones and is not a
primary growth centre

Moss Malformation in snout following excision of

nasal septum is due to trauma following
surgery

Burstone and Reported a case with missing nasal septum.

Latham child had normal resorption and deposition of
palate , height of upper face. only sagittal
development was affected
 FUNCTIONAL MATRIX CONCEPT:
MELVIN L . MOSS- 1962

The primary role of functional matrices in facial growth--

40
Moss and Salentijn . AJO
Based on the original concept of
functional cranial component by
VANDER KLAAW.

Comprehends relationship between

“FORM & FUNCTION”.

Moss :
“ Bones do not grow ; Bones are
grown ”
  FUNCTIONAL MATRIX HYPOTHESIS
Claims that origin, form, position, growth & maintenance of all
skeletal tissues & organs are always secondary, necessary
responses to chronologically & morphologically prior events or
processes that occur in specifically related non-skeletal tissues,
organs or functioning spaces .

“ Soft tissue grow and both Bone & Cartilage react ”

42

William profitt-contemporary orthodontics (6th edition)

PRIMARY GROWTH-capsular matrix (Brain) ENLARGEMENT OF NEUROCRANIUM
SECOUNDRY GROWTH-Sutures and synchondroses (MACROSKELETAL UNIT)

FUNCTION OF THE TEMPORALIS MUSCLE EXERTS PULL OF PERIOSTEAL MATRIX AND

BONE GROWTH OF THE TEMPORAL LINE.(MICROSKELETAL UNIT)
 Functional cranial component is composed of 2 parts

Functional matrix components

Skeletal Unit

FUNCTIONAL MATRIX COMPONENTS COMPONENTS OF SKELETAL UNIT

 SOFT TISSUES  BONE

 ORGANS  CARTILAGE
 FUNCTIONING SPACES  TENDINOUS TISSUE

44

The primary role of functional matrices in facial growth--- Moss and Salentijn. AJO
45
Functional matrix further classified as :
1. Periosteal matrix
2. Capsular matrix

Periosteal matrix- act

directly & actively upon
related skeletal units to
produce secondary
compensatory transformation
of size/ shape of skeletal unit.
Ex. Muscles, vessels, glands,
nerves.

The primary role of functional matrices in facial growth--- Moss and Salentijn . AJO
Capsular matrix: The
organs and space that occupy a
border anatomical complex. Act
indirectly & passively on related
skeletal units producing
secondary , compensatory
translation in space.

 NEURO-CRANIAL
CAPSULER
 ORO-FACIAL CAPSULE

The primary role of functional matrices in facial growth--- Moss and Salentijn . AJO
 NEUROCRANIAL CAPSULE
5 layers of SCALP-
S-skin,
C-dense Connective Tissue.
A-aponeurotic layer.
L-loose Areolar Connective tissue.
P- periosteum.

• BONE

• 2 layers of duramater

The primary role of functional matrices in facial growth--- Moss and Salentijn . AJO
OROFACIAL CAPSULAR

All Functional cranial components

of facial skull arise, grow & are

maintained within Oro-facial

capsule.

Surrounded by skin and mucous

membrane on either side.

Volumetric growth of these spaces

is the primary morphogenetic

event in facial skull growth.

 SKELETAL UNIT

BONE
CARTILAGE
TENDINOUS
TISSUE

TYPES OF SKELETAL UNIT

1. MICROSKELETAL UNIT
2. MACROSKELETAL UNIT

William profitt-contemporary orthodontics (6h edition)

 MICROSKELETAL UNIT
Bones consisting of number of
small skeletal units
Coronoid– temporalis process
Masseter
Medial pterygoid – Gonial angle
Alveolar bone - Presence and
position of teeth.

The primary role of functional matrices in facial growth--- Moss and Salentijn . AJO
 MACROSKELETAL UNIT
When adjoining bones
unite to function as a single
component
Ex. Core of Maxilla, Mandible

The primary role of functional matrices in facial growth--- Moss and Salentijn . AJO
Two Natural Experiments

1.MICROCEPHALY
2.HYDROCEPHALY

1.MICROCEPHALY: When the brain is small , cranium is also small.

In case of the head is accurate present size of the brain.
.

William profitt-contemporary orthodontics (5th edition)

 2.HYDROCEPHALY: Reabsorption of cerebrospinal fluid is
impeded the fluid accumulates and intracranial pressure build up.

Intercranial pressure impeded development of brain.

hydrocephaly has have small brain and mentally retarded,
and this leads to enarmous growth of cranial vault.
• Cranium is 2-3 times bigger than normal; cause enlarge
frontal, occipital, parietal.

Excellent example: the relationship of size of eye is size of orbit,

enlarge eye or small eye will cause change in orbital cavity.

William profitt-contemporary orthodontics (5th edition)

 CLINICAL APPLICATION
As seen in functional appliances:

Dentition is influenced by peri-oral muscle function.

Abnormal peri-oral muscle activity barrier for dento-alveolar

structures

Frankel appliance holds away muscles from dentition

56
Dentofacial orthopedics with functional appliances – Graber, Rakosi, Petrovic
THE FUNCTIONAL MATRIX HYPOTHESIS
REVISITED
MELVIN L . MOSS
1997
Melvin Moss -- 1997 proposed continuation of his classical
Functional Matrix Theory with the new concept.

Published series of articles in American Journal of Orthodontics in 1997.

The functional matrix hypothesis revisited.

1. The role of mechanotransduction ( 8-11).

2. The role of an osseous connected cellular network (221-226).

3. The genomic thesis (338-342).

4. The epigenetic antithesis and resolving synthesis (410-417).

 The functional matrix hypothesis revisited.-

The role of mechanotransduction

CONSTRAINTS OF FUNCTIONAL MATRIX HYPOTHESIS

Methodological Constraints
Hierarchical Constraints

The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
 1. Methodological Constraints

Macroscopic measurement which

use the technique of point
mechanics and arbitary reference
frame.

Example: Roentgenographic
cephalometry

The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
 2.Hierarchical Constraints
The version‘s description did not extended
downward to processes at the cellular,
subcellular or molecular structural domains
or extend upwards to multicellular processes
by which bone tissue respond to lower level
signals.

The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
 THE FUNCTIONAL MATRIX HYPOTHESIS REVISITED 1

MECHANOTRANSDUCTION

IONIC MECHANICAL

STRETCH ACTIVATED CHANNEL INTEGRIN

ELECTRIC EVENTS

ELECTROMECHANICAL ELECTROKINETIC
The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
 Functional Matrix Hypothesis Revisited includes 2 concept

1.Mechanotransduction ---- occurs in single bone cells.

2.Connected Cellular Network ( CCN ) ---- Bone cells are

computational elements that function multicellularly.

63
The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
 MECHANOTRANSDUCTION

The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
64
 Mechanotransduction --- mechanical stimulus is converted into

biological signal to affect a cellular response.

Mechanoelectric & Mechanochemical

Mechanoreception --- transmition of an extracellular physical

stimuli into a receptor cell.(STIMULUS-SIGNAL)

The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
65
 OSSEOUS MECHANOTRANSDUCTION

Static & Dynamic loads are continuously applied to bone

tissues

Deforms extracellular Matrix & Bone cells

Stimulus parameter exceeds threshold values

Tissue responds by triad of cell adaptation processes

DEPOSITION, RESORPTION, MAINTENANCE

The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
66
OSSEOUS MECHANOTRANSDUCTION

67
The functional matrix hypothesis revisited 1. Role of mechanotransduction. –MOSS M L AJODO july 1997, vol.112:8-11
The functional matrix hypothesis revisited-

The role of an osseous connected cellular network(CCN)

The functional matrix hypothesis revisited-

The role of an osseous connected cellular network(CCN)

The functional matrix revisited 2.Role of osseoeus connected cellular network. MOSS AJODO Aug 1997, vol.112: 221-226
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 GAP JUNCTION CONNECTS:

The functional matrix revisited 2.Role of osseoeus connected cellular network. MOSS AJODO Aug 1997, vol.112: 221-226
 REVISITED 3 THE GENOMIC THESIS
The

September 1997
genomic thesis holds that the genome, from
the moment of fertilization, contains all the
information necessary to regulate all
intercellular process and morphogenesis.
“All phenotype features are ultimately
determined by the DNA sequence of the genome”

Moss ML The functional matrix revisited 3. The genomic thesis. AJODO Sep1997, vol.112: 338-342 78
 Craniofacial
development

Activity of
Homeobox
molecular
genes(HOX,PAX)
groups

GROWTH STEROID/THYR
FACTOR OID/RETINOIC
FAMILIES ACID
SUPERFAMILY

Moss ML The functional matrix revisited 3. The genomic thesis. AJODO Sep1997, vol.112: 338-342
HOMEOBOX GENES:

Homeobox genes are regulatory genes that determine

where certain anatomical structures,such as appendages will develop
in an organism during morphogenesis.

The expression of Homeobox genes result in the production of a

protein Homeodomain that can turn on or switch off other genes.

These genes act as transcription factors.

80
In humans the Homeobox gene family contains an estimated 235
functional genes and 65 pseudogenes.

These genes often appear as 4 clusters, labelled as A,B,C,D.

Each cluster is situated on different chromosome.

Each Homeotic cluster consists of 13 homeotic genes numbered

sequentially from 1 to 13.

Examples are:HOX,PAX,MSX,DLX.

81
82
 Critical Definitions:

Epigenetics Hierarchy Emergence Causation

The functional matrix revisited 3. The genomic thesis. AJODO Sep1997, vol.112: 338-342
83
Epigenetics:
Includes(1)all the extrinsic factors impinging on vital structures
including mechanical loading and electroelectric states (2)all of the
intrinsic, biophysical, biomechanical, biochemical and bioelectric
events occuring in on and between individual cells , extracellular
materials and cells.

Hierarchy :
Structural and functional complexity increasing “upwards” from the
ever expanding family of subatomic particles to protons, electrons,
atoms ,molecules,subcellular organelles, and on to cells, tissues
,organs and organisms.

Moss ML The functional matrix revisited 3. The genomic thesis. AJODO Sep1997, vol.112: 338-342
84
 • Emergence :
Appearance , at each higher level , of new attributes or properties ,
not present in lower levels , whose existence or functions could
not in any way be predicted , even from a complete knowledge of
all of the attributes and properties of any or all the preceding
lower organisational levels.

• Causation :
How the attributes of a given biological structural level
”cause”(control , regulate, determine)the attributes of the next
higher level.

The functional matrix revisited 3. The genomic thesis. AJODO Sep1997, vol.112: 338-342 85
REVISITED 4 THE EPIGENETIC ANTITHESIS AND
RESOLVING SYNTHESIS

“It is a fallacy that the genome, the totality of DNA molecules, is the
main repository for developmental information; i.e. there exists a genetic
program, or blueprint, theoretically capable of creating an entire
organism”

Moss ML The functional matrix revisited 4.The epigenetic antithesis and the resolving synthesis. AJODO Oct 1997, vol.112: 410-417.
• Genomic thesis is denied because it is both reductionist and
molecular.

• EPIGENETIC PROCESSES AND MECHANISMS:

Process : series of actions or operations that lead towards a

particular result.

Mechanism : physical or chemical processes involved in , or

responsible for ,an action ,reaction, or other natural phenomenon.

Moss ML The functional matrix revisited 4.The epigenetic antithesis and the resolving synthesis. AJODO Oct 1997, vol.112: 410-417. 87
 • Loading results in:

Extracellular matrix deformation.

Cell shape changes.
Epigenetic cell signalling processes.
Chains of intracellular molecular levers.

Moss ML The functional matrix revisited 4.The epigenetic antithesis and the resolving synthesis. AJODO Oct 1997, vol.112: 410-417. 88
 REFERENCES
• William profitt-contemporary orthodontics (5th edition).
• Textbook of craniofacial growth- Sridhar Premkumar.
• Theories of Craniofacial Growth in the Postgenomic Era -
David S. Carlson Seminar Orthod 11:172–183 © 2005 Elsevier
• Dentofacial orthopedics with functional appliances – Graber,
Rakosi, Petrovic.
• Enlow, latham, harvold, - Text research on control of craniofacial
morphogenesis.

89
• Moss ML the functional matrix hypothesis revisited 1. Role of
mechanotransduction .AJODO july 1997, vol.112:8-11
• Moss ML The functional matrix revisited 2.Role of osseoeus
connected cellular network. AJODO Aug 1997, vol.112: 221-226
• Moss ML The functional matrix revisited 3. The genomic thesis.
AJODO Sep1997, vol.112: 338-342
• Moss ML The functional matrix revisited 4.The epigenetic antithesis
and the resolving synthesis. AJODO Oct 1997, vol.112: 410-417.

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