.

GOOD MORNING

1
GROWTH & DEVELOPMENT”
Theories & Principles

DR ANAGHA S
JUNIOR
RESIDENT
PEDODONTICS
2
CONTENTS
 Introduction
 Mechanism of bone growth

 Deposition and Resorption

 Growth fields

 Growth sites

 Growth centers

 Remodeling

 Molecular biology of bone

remodeling 3
 Principle of Area relocation
 Enlow V principle
 Growth movement
1. Cortical Drift
2. Displacement
 Trajectories of bones
1. Trajectories in maxilla
2. Trajectories in mandible

4
Changing concepts & hypothesis of
craniofacial growth-
1. Evolution of theories
2. The Remodelling theory (Brash
1930s)

3. The Genetic concept (Brodie 1940s)

4. The Sutural hypothesis ( Sicher 1941)

5
5. The Cartilaginous theory (Scott 1950s)

6. The Functional Matrix theory (Moss 1962)

7. Neurotrophism

8. The Cybernetics theory

(AlexandrePetrovic 1970)

9. Conclusion

10. References
6
INTRODUCTION
 Growth and development are two integral
process which defines the existence of life.

 Growth of an organism is the interplay

between its genetic constitution and
environment in which it thrives.

7
 Assessment of growth reveals about the
general health of the individual and can be
used for growth modification treatments.

 Growth is a complex process and is not

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

8
MECHANISM OFBONE GROWTH

Bone growth is based on

certain principles .

Bones do not grow symmetrically

but grow by complex differentiation
mechanism .

9
All bone growth is a complicated
mixture of the two basic principles
deposition and resorption .

Deposition and resorption which are

carried out by the growth fields
comprised of the soft tissue investing
the bone.
10
As the fields grows and function
differently on different parts of the bone ,the
bone undergoes remodeling.

When the amount of bone deposition si

greater than the resorption , enlargement of
the bone necessitates its displacement.

11
DEPOSITION AND RESORPTION

Bone grows by addition of new bone

tissue on one side of the bony cortex.

Bone formative changes occurs on bone

surface facing towards the direction of
progressive growth resulting in new bone
deposition.

Deposition is observed on the inside.

12
+ Bone deposition
- Bone resorption 13
BONE RESORPTION
BONE REMODELING

• Bone remodeling involves

independent sites of resorption and
formation that change the size and
shape of a bone.

15
REMODELLING

It involves deposition and

resorption

Four types: Biomechanical

Growth remodelling
Haversian remodelling
Pathologic remodelling

16
1. Biomechanical- continuous deposition
& removal of ions to maintain mineral
homeostasis
2. Growth remodelling- constant
replacement of bone during childhood

3. Haversian remodelling- secondary process

of cortical reconstruction as primary
vascular bone is replaced.
4. Pathologic remodelling- regeneration &
reconstruction of bone during &
following trauma

17
E.g. The ramus
moves posteriorly
by the combination
of deposition and
resorption.

So the anterior part

of the ramus gets
remodeled

18
 FUNCTIONS OF REMODELING
1. Progressively change the size of whole bone
2. Sequentially relocate each component of the
whole bone
3. Progressively change the shape of the bone to
accommodate its various functions

19
4. Progressive fine tune fitting of all the
separate bones to each other and to their
contiguous ,growing, functioning soft
tissues.

5. Carry out continuous structural

adjustments to adapt to the intrinsic and
extrinsic changes in conditions .
20
MOLECULARBIOLOGYOFBONE
REMODELLING
Bone remodeling is accomplished according to the
following phases:

1. Activation phase –
Different inputs such as a microfracture , an
alteration of mechanical loading sensed by the
osteocytes or factors released in the bone
microenvironment including IGF-1, TNF-alfa,
IL-6 .PTH, activate the lining cells ,which are
quiescent osteoblast.
21
 •As a consequence lining cells increase
their own surface expression of
RANKL(Receptor activator of nuclear
ligand) which in turn interacts with its
receptor RANK , expressed by
preosteoclast .

•RANK / RANKL interaction triggers

preosteoclast fusion and differentiation
towards multinucleated osteoclast.
Rucci, N.: Molecular biology of bone remodelling , Clinical cases in
Mineral and Bone metabolism : 2008;5(1): 49-56
22
2. Resorption phase-

• Once differentiated osteoclast polarize , adhere to

the bone surface and begin to dissolve bone.
• This function requires two steps :Acidification of
bone matrix to dissolve inorganic content and release
of lysosomal enzymes such as cathepsin K and
MMP9 both in charge for degradation of organic
content. Once accomplished their function osteoclast
undergo apoptosis.

Rucci, N.: Molecular biology of bone remodelling , Clinical cases

in Mineral and Bone metabolism : 2008;5(1): 49-56 23
 3. Reverse phase:
The reverse cells whose role has not yet been
completely clarified performs this phase.
Indeed it is known that they are macrophage
like cells with a likely function of removal of
debris produced during matrix degradation.

Rucci, N.: Molecular biology of bone remodelling , Clinical cases in

Mineral and Bone metabolism : 2008;5(1): 49-56

24
4. Formation phase:
• Bone matrix resorption leads to the release of
several growth factors herein stored, including bone
morpho- genetic proteins (BMPs), fibroblast growth
factors (FGFs) and
• transforming growth factor β(TGF β), which are
likely responsible for the recruitment of the
osteoblasts in the reabsorbed area.

25
Once recruited, osteoblasts produce the new bone
matrix, initially not calcified (osteoid) and then they
promote its mineralization , thus completing the bone
remodeling process.

Unbalance between the resorption and formation

phases mirror an incorrect bone remodeling ,
which in turn affects the bone mass , eventually
leading to a pathological condition.

Rucci, N.: Molecular biology of bone remodelling , Clinical

cases in Mineral and Bone metabolism : 2008;5(1): 49-56 26

 Bone remodelling process

Rucci, N.: Molecular biology of bone remodelling , Clinical cases in

Mineral and Bone metabolism : 2008;5(1): 49-56
27
 Osteoblastogenesis process

Rucci, N.: Molecular biology of bone remodelling , Clinical cases in

Mineral and Bone metabolism : 2008;5(1): 49-56
28
Boskey, A.L., Coleman, R.:Aging and Bone. J Dental Res 2010 ; 89(12):
1333-1348
29
GROWTH FIELDS

Bone growth is controlled

by growth fields.
Distributed in a mosaic like
pattern across the surface of
a given bone.
They have pacemaking
function.
They are either resorptive
or depository activity.

30
About one half of the
bone is periosteal and
the other half endosteal.
If endosteal surface is
resorptive then periosteal
surface would be
depository.

31
32
GROWTH SITES
Growth fields having
special role in the growth
of the particular bone
( grows fast) are called
growth sites

e.g. mandibular condyle,

maxillary tuberosity,
synchondrosis of the
basicranium, sutures and
the alveolar process.

33
GROWTH SITES
Baume proposed the
term growth site for
“regions of periosteal
or sutural bone
formation and
modeling resorption
adaptive to
environmental
influences.”
Koski, K. : Cranial growth centres: Facts or fallices?
, AJO-DO : Aug 1968: 566-583
34
GROWTH
CENTERS
Special areas which
are believed to
control the overall
growth of the bone
e.g.mandibular
condyle.

Force, energy or
motor for a bone
resides primarily
within its growth
centre. 35
 The term growth center is widely used in
connection with skeletal growth phenomena.

Baume proposed that the term skeletal

growth center be used to describe “places of
endochondral ossification with tissue
separation forces.”

Koski, K. : Cranial growth centers: Facts or fallices? ,

AJO-DO : Aug 1968; 566-583

47
The definition proposed by Baume already
implies a spatial limitation that is a growth
centre includes only the territory where
endochondral ossification takes place .
The time element also appears important .

Koski, K. : Cranial growth centres: Facts or fallices? ,

AJO-DO :Aug 1968: 566-583,
45
Thus the growth centre should mean a place where
growth of the skeletal is occurring for a sufficient
length of time to make a real contribution to the
increase of the skeletal mass beyond the size of the
model tissue existing at the onset of the growth
centre function.

Koski, K. : Cranial growth centres: Facts or fallices? ,

AJO-DO : Aug 1968 : 566-583

38
 A modified definition would be that a “ growth
center is a site of endochondral ossification
with tissue separation forces , contributing to
the increase of skeletal mass.”

Koski, K. : Cranial growth centres: Facts or fallices? ,

AJO-DO : Aug 1968: 566-583

39
PRINCIPLE OF‘AREARELOCATION’

Due to new bone

deposition on an
existing surface ,all
other parts of the
structure undergo
shifts in relative
position – a
movement
calledrelocation
40
As a result further adaptive bone
remodeling is necessary to adjust the
shape and size of the area to the new
relationship.

•Selective resorption and apposition process

functionally remodel the area to conform to
the new physiological loading.

41
ENLOW’S V PRINCIPLE

Most useful and basic

concept in facial growth as
many facial and cranial
bones have a V- shaped
configuration.

Bone deposition(+) occurs

on the inner side and
resorption (-) occurs on the
outer surface.

42
EXAMPLE WITH VORIENTED
VERTICALLY
Bone deposition on
lingual side of coronoid
process , growth
proceeds and this part
of the ramus increases
in vertical dimension.

43
VORIENTEDHORIZONTALLY
Same deposits of
bone also bring
about a posterior
direction of growth
movement.
This produces a
backward movement of
coronoid processes even
though deposit is on the
lingual side
44
Same deposits carry base of bone in medial direction
.

So, the wider part undergoes relocation into a more

narrow part as the whole v moves towards the wide part .

45
GROWTH MOVEMENTS
 Two kinds of growth movements are seen during
the enlargement of craniofacial bases: cortical
drift & displacement.

 CORTICAL DRIFT: All bones have

one common growth principle that is
drift.

 It was termed byEnlow(1963).

 It is growth movement ( relocation or shifting) of
an enlarging portion of the bone by the
46
remodelling action of its osteogenic tissues.

47
DRIFT
It is remodeling
process and a
combination of
deposition and
resorption.
If an implant is placed
on depository side it
gets embedded.
Eventually marker
becomes translocated
from one side of cortex
to other.

48
The cortical plate can be relocated by
simultaneous apposition
&resorptionprocesess on the opposing
periosteal and endosteal surfaces.

The bony cortical plate drifts by depositing

and resorbing bone substances on the outer &
inner surfaces respectively in the direction of
growth.

49
If the resorption& deposition
takesplace at the same times, the
thickness of the bone remains constant

Should more bone be deposited than

resorbed the thickness of the structure
increases

50
During the developmental period, deposition takes
place at a slightly faster rate than the resorption ,
so that the individual bones slowly enlarge.

The teeth follows the drift of the alveolae while

the jaw is growing & thus maintain their position
within the surrounding bony structure despite the
bone displacement.

51
51
52
DISPLACEMENT
It is the movement of the whole boneas a
unit.

It is a translatory movement of the

whole bone caused by surrounding
physical forces, and is the second
characteristics mechanism of skull
growth.
53
The entire bone is carried away from its
articular interfaces( sutures , synchondroses,
condyle) with adjacent bones.

 Displacement is of two types namely:

Primary displacement- As a bone enlarges

, it is simultaneously carried away from the
other bones in direct contact with it.This
creates space within which bony enlargement
takes place.
54
It is the physical movement of the whole bone
,as the bone grows & remodels by resorption
and apposition.

55
Secondary displacement :It is the
movement of a whole bone caused by the
separate enlargement of other bones which may
be nearby or quite distant.

 It is related to enlargement of other bone.

For example: growth in the middle cranial

fossa results in the movement of the maxillary
complex anteriorly& inferiorly .
56
57
TRAJECTORIESOFBONE
In 1867 an anatomist named Meyer, with the
help of the mathematician Culmann,
propounded the Trajectional theory of bone
formation.

He pointed out that the alignment of the

bony trabeculae in the spongiosa followed
definite engineering principles.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133 58
If lines were drawn following discernible
columns of oriented bony elements, these lines
showed a remarkably similar structure to the
trajectories seen in a crane.

Many of these trajectories crossed at the right

angles – an excellent arrangement to resist the
manifold stresses on the condyle of the femur.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133

59
In 1870’s Julius Wolff carried this theory one
step further. He claimed that the trabecular
alignment was due primarily to functional.

A change in the intensity and direction of these

forces would produce a demonstrable change in
the internal architecture and external form or the
bone.

This concept was referred to as “The law of

orthogonality”.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133 68
In essence , the law stated that the
stresses of tension or pressure on bone
stimulate bone formation.

Endochondral bone may respond

differently at its growth centre than
membranous bone.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133
61
It has been shown that both tension and
pressure can produce loss of bone tissue, that the
trabeculae do not form predominantly straight
lines .

Many of the so called trajectories are irregular and

wavy varying from bone to bone depending on the
stresses encountered .

Graber T.M., Orthodontics-Principles and Practice. 3rd

ed. Philadelphia:Saunders;1992.p.133
62
Abnormal pressures on bone can cause
actual change , as seen on patients with
scoliosis who had been treated with
Milwaukee brace.

Benninghoff showed that the stress

trajectories obeyed no individual bone
limits , but rather the demand of the
functional forces

Graber T.M., Orthodontics-Principles and Practice. 3rd

ed. Philadelphia:Saunders;1992.p.133
63
Changes in functional forces produces
measurable changes in bony architecture.

These changes are within the limit of

inherent morphogenetic pattern.

Lack of function leads to reduction of

density of bone tissue or osteoporosis.

Increased function produces a greater density

of bone in an area or osteosclerosis . An example
is kyphosis
72
TRAJECTORIESOFTHEMAXILLA:

The presence of stress trajectories can be

demonstrated in the maxilla originating from
above the teeth and passing superiorly to the
zygomatic or jugal buttress.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133

65
There are three main vertical trajectories, all
arising from the alveolar process and ending in
the base of the skull :
 The canine pillar .
 The zygomatic pillar .
 The pterygoid pillar

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133
66
  Horizontal reinforcing members
include:
 Trajectories from:
 Hard palate, orbital walls ,
zygomatic arches , palatal bone &
lesser wing of sphenoid.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133 67
68
 “Maxillary
trajectories”

Horizontal
Vertical pillars
pillars

Canine Malarzygo Pterygoid pillar

pillar matic pillar

69
TRAJECTORIESOFTHEMANDIBLE :

The mandible because it is a unit by itself and a

movable bone , has a different trabecular alignment
from that of the maxilla.

Graber T.M., Orthodontics-Principles and Practice. 3rd ed.

Philadelphia:Saunders;1992.p.133
70
Trabecular columns radiate from the beneath the
teeth in the alveolar process & join together in a
common stress pillar or trajectory system, that
terminates in the mandibularcondyle .

The thick cortical layer of compact bone

along the lower border of the mandible offers
the greatest resistance to the bending forces.

Graber T.M., Orthodontics-Principles and Practice. 3rd

ed. Philadelphia:Saunders;1992.p.133
71
Other trajectory patterns are seen at the
symphysis , at the gonial angle & leading
downward from the coronoid process into the
ramus and body of the mandible.

These accessory stress trajectories

probably are due mainly to the direct effect
of the attachment of the muscles of
mastication.

Graber T.M., Orthodontics-Principles and Practice. 3rd

ed. Philadelphia:Saunders;1992.p.133
72
73
EVOLUTIONOFTHEORIES

74
 Paradigm
It is a conceptual scheme that encompasses
individual theories and is accepted by a
scientific community as a model and
foundation for further research.

Moyers R.E.,Handbook of Orthodontics..4th ed. Year Book Medical

Publishers:1988.p.48-50

75
 EVOLUTION OF PARADIGM‟S

Moyers R.E.,Handbook of Orthodontics..4thed.Year

Book Medical Publishers:1988.p.48-50 76
 Various paradigms
1920-1940
• Development of the Genomic Paradigm

• More emphasis on structure rather than function.

• Moss subdivided this period:
1. Preradiologic Phase-Emphasis placed
on craniometry
2. Radiological phase

Moyers R.E.,Handbook of Orthodontics..4thed.Year

Book Medical Publishers:1988.p.48-50 77
Moss- “Classic Triad”
1. Sutures are primary growth sites
2. Growth of the cranial vault
occurs only by periosteal
deposition and
endostealresorption.
3.All cephalic cartilages are primary
growth centers under direct genetic
control

78
1940-1960

•Craniofacial biology saw an increased emphasis on

experimental animal research in an effort to account
for the actual mechanism of facial growth.

•Studies were more methodological and

conceptual.

•Investigators began to recognize that there is much

more variation within the facial region and that this
variation could be the result of modifying influences
during Ontogeny
79
Technological
developments:-
•Use of Radioopaque Implants.
• Vital Dyes.
• Autoradiography.
• In-vivo and In-vitro transplantations.

•By the end of 1950’s two similar approaches were

seen within the single Genomic Paradigm:

• Comprehensive Approach

• Structurofuntional Approach
80
Comprehensive
Approach:
Continued with craniometrics but with
more sophisticated hardware including
radiographs,cephalostatsand software in the form
of statistical models.

Structurofunctional Approach:

Concentrated more on “cause and effect

relationships” within and among the biologic
systems of the Craniofacial complex.

81
 By the end of 1950’s the genomic paradigm was put
into question

Periostealand Sutural bone growth were removed from the

genomic paradigm and given the status of secondary,
compensatory or adaptive phenomena

But due to lack of evidence the genomic paradigm

remained dominant and the alternative view that
“Function” plays a major role continued to gather
momentum.

82
MAINLY
DOMINATE
D BY
GENOMIC
PARADIGM

83
1960-1980

Formulation of an Alternative paradigm.

--Termed as the “Functional Paradigm” stated that the

Craniofacial complex is highly adaptable to the
functional demands placed on it and its
developmental environment.

--Melvin Moss’s “Functional Matrix Hypothesis” is

believed by most craniofacial biologists to be the
alternative paradigm
84
DEVELOPMENT OF AN ALTERNATIVE PARADIGM

85
Moss 10 yrs later released a third paper on the same.

--From then on the “Functional” hypothesis became a topic

of theoretical debate involving people like:-
• Moorrees(1972)
• Johnston(1976)
• Koski(1977)
• Wayne Watson(1982)

Debate focused on:

•That cephalic cartilages have no intrinsic
growth properties.
•The mechanisms by which the capsular
matrices(oral,nasal,pharyngeal)assert “morphogenic
primacy” 94
--Alexander Petrovic and Associates(1975)
•Proposed the cybernetic models of
mandibular growth.

1980-2000
• This period saw a confluence of both the genomic and
the functional paradigms.

• A more focused view was developed and merits and

demerits of each theory were considered.

87
 FUNCTIONA
L MATRIX
REVISITED

PRESENT

88
 BONE REMODELLING THEORY
BY BRASH (1930)
 This theory states that bone grows only by
interstitial growth.

 The fundamental tenets of this theory are:

 Bone grows only by apposition at the surface.

 Growth of jaws takes place by deposition of boneat

the posterior surfaces of the maxilla and mandible.

 This is described as Hunterian growth.

Carlson ,D.S.:Theories of craniofacial growrth in postgenomic era . Seminorthod
97
2005;11:172-183
Calvarium grows through bone deposition
on the ectocranialsuface of the cranial vault
and resorption of bone on the endocranial
surface

Bone remodeling theory postulated thatthe

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

90
91
THEGENETIC THEORY( 1941)
Genetic theory was given by Brodie.

The genetic theory simply stated simply that

genes determine and control the whole process
of craniofacial growth.

But the mechanism of action by the genetic

unit and the mechanism by which the traits are
transmitted were not understood until recently.

92
Genetic concept suggests that the genes supply
all the information in growth and development.
This originated with classical Mendelian
genetics.
Later with the blending of data from vertebral
paleontology created the neo-
Darwinian synthesis which is currently
accepted paradigm of phylogenetic
regulation.

93
Genetic concept stipulates that the
genotype supplies all the information
required for phenotypic expression.

Mossalso stated in his thesis that the whole

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

94
The field of genetics consists of two
principle areas :

“Transmission genetics” is characterized by

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

It is based on Mendelian laws and did not

explain about genes or its characteristics.

95
THESUTURALHYPOTHESIS

Given by Sicher and Weinmann in 1947 .

According to this theory, sutures

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

Sicher came to the conclusion that sutures

were causing most of the growth based on
the studies using vital dyes.

96
Essence of the Theory:
According to Sicher, the sutures are the primary
determinants of craniofacial growth. The
craniofacial skeleton enlarges due to expansible
forces exerted by the sutures as they separate.

97
98
Theory:
He started that all bone forming elements like
sutures ,cartilages and periosteum are growth
centers like the epiphysis of the long bone.

Sicher called this theory as the sutural dominance

theory because he believed that the primary event in
sutural growth is proliferation of the connective
tissue between the two bones.

99
Proliferation of the sutural connective
tissue creates the space for appositional
bone growth between the borders of two
bones.

Increase in the size of the cranial vault takes

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

100
Growth of the midface takes place via
intrinsically determined sutural expansion of
the circummaxillary suture system, which
forces the midface downward and forward.

Mandibular growth takes place via

intrinsically determined growth of the
cartilage of the mandibularcondyle ,which
pushes the mandible downward and forward.

101
There is considerable growth occuring
in suture and hence from this point of
view sutural growth attains significance.

Sicher postulated that bone growth

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

102
It was believed that the stimulus for
bone growth is tension produced by the
displacement of the bones.

103
Koski (1968) stated there are two different
views regarding the structure of sutures.

The first school or thought (Sicher and

Weinmann ) considers sutures as a three
layered structure.

Koski, K. : Cranial growth centres: Facts or fallices? , AJO-DO :

Aug 1968: 566-583 112
It stated that the connective tissue
between the two bones plays the same role
as the cartilage at the bases of the skull and
like epiphysis of the long bone

There is spreading of sutures due to

proliferation of middle layer of the sutural
tissue.

According to this concept tissue separating

force exists in the suture itself.

105
Thesecond school of thought (Pritchard
,Scott and Girgis,1956) says the suture as a five
layer structure .

Each bone at the suture has its own two

layer of periosteum on both sides ant the
intervening fifth layer between these
periosteal layers.

106
This layer plays a role in adjustment
between the bones during the growth .

while the active proliferating roleis

played by the cambial layers of the
periosteum of each bone.

107
It is very clear now from the histological
evidenced that the sutural structure is not
identical to that of the epiphyseal growth
plate.

Sicher also perceived the mandible asa long

bone and the mandibularcondylar cartilage as
comparable to epiphyseal plate of the long
bone.

108
109
EVIDENCESAGAINST SUTURAL
THEORY
Trabecular pattern in the bones at the suture
change with age ,indicating the changes in the
direction of growth it cannot be accepted that
suture will have the necessary information for
altering growth.

 Extirpation of facial sutures has no appreciation

effects on the dimensional growth of the skeleton
(Sarnat 1963)

110
 Shape of sutures have been found to
depend on the functional stimulus.( Moss
&Salentejin, 1969)

 Closure of sutures to be extrinsically

determined.( Moss ML, 1954)

 Sutural growth can be halted by

mechanical forces like clips placed across the
sutures.
111
 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 degree in relation to SN plane .

 It is practically impossible for the suture running in

same direction to push the maxilla parallel to the
reference plane. (Bjork 1966)
Bjork: Acta odont.scandinav.1966; 24:109-127 120
Conclusion:

Present evidences indicates suture as adaptive

growth sites.

Sutural tissues have no tissue separating forces

and they are not comparable to growth centers.

113
NASAL SEPTUM
THEORY/CARTILAGENOUS THEORY/NAS

James H Scott , an Irish anatomist in 1950

proposed the nasal septum theory as the single
and unified theory of craniofacial growth.

114
Essence of theory:

According to this sutures play little role or

no direct role in the growth of the
craniofacial skeleton .
Sutures are considered as merely passive
secondary and compensatory sites of bone
formation and growth

115
After recognizing the importance of
cartilaginous parts of the head , nasal
capsule ,mandible and cranial base in
prenatal growth.

Scott felt that this cartilaginous development

was under genetic control and was of the
opinion that they continued to dominate
postnatal facial growth also.

116
Scott concluded that nasal septum is
mostly active and vital for craniofacial
growth both prenatally and postnatally.

The anterioinferior growth of the nasal septal

cartilage which is buttressed against the cranial
base “pushes” the midface downward and
forward.

The cranial base synchondroses causes the

growth of the cranial base and Scott
compared the condylar cartilage to the cranial
base cartilage 117
Discussion:
 Numerous experimental studies were conducted to address the
validity of Scott’s hypothesis .

 This theory is based on the fact that cartilage is a pressure adapted

tissue and expansion of cartilage provides the force to displace
downward and forwards.

118
According to Scott ,bone separation must
precede before the adaptive sutural bone
growth occurs .

The bone separation is because of growth of

organs like brain , eyeball or cartilage.

119
Scott is of the opinion that there are two suture
system:
 Posterior suture system lies behind the maxilla
and separates it from palatine ,lateral mass of
ethmoid , lacrimal , zygomatic and vomer bones.

 Anterior suture system separates premaxila

nasal and vomer bone.

120
 Scott said that the nasal cartilage is an
extension of the cranial base cartilage and as
it grows further, it separates the facial bones
from one another and also from the cranial
portion .

 Thus it allows bone growth to take place at the

sutures (frontomaxillary , frontonasal ,
frontozygomatic and
frontozygomaticomaxillary) by surface
deposition.
121
Evidences supporting the theory:

Experimental research on rats by Ohyama(1969) -

removal of septal cartilage produces deficient growth of
snout.

Also supported by research of Burdi , Petrovic , Baume,

Latham (1965,1967-1968,1968,1972)
respectively .

130
EXPERIMENT BYBURDI , PETROVIC,
BAUME, LATHAM (1965 ,19 67 -
1968,1968,1972) RESPECTIVELY

123
The importance of the septal
growthwas also seen in impulse to
maxillary growth in cleft palate cases.

Failures of the underdeveloped

maxillary segment to unite with nasal
septum in complete unilateral clefts
deprives it of the growth impulse or
energy. The normal contra lateral side on
the other hand, attained normal growth.

124
Sarnat in (1988)from experiments on rabbit
snout concluded that deformity of snout after
resection of nasal septum was the result of lack
of growth.

Latham (1974) described the role of

septomaxillary ligament passing from
anterioinferior border of nasal septum to
anterior nasal spine and inter maxillary
suture in premaxillary region.
He stated that the traction through the ligament
will exert downward and forward growth of
maxilla. 133
Koski(1968) after histological study of nasal
septal cartilage found that there is endochondral
ossification taking place at septoethmoidal
junction.

Hunter and Enlow(1968) –in their growth

equivalent theory –emphasizes on relatively lesser
response of the endochondral cranial base as
opposed to immediate response of the
intramembranous cranial vault to external
influences

126
Evidence against the theory:

Moss and Bloonberg(1968), Brigit

Thilander(1970) found only slight deformity
after extirpation of septal cartilage

They concluded that septal cartilage

provides only mechanical support for the
nasal bones and is not a primary growth
center.

127
Two studies were carried out by Gilhus-Moe and
Lund in Scandinavia in 1960’s showed that
There are excellent chances that condylar process
would regenerate to approx. its original size after
trauma
In a few there was even a overgrowth of condyle.
In a few children there is a reduction in growth
after injury maybe due to the trauma to the soft
tissues / scarring

Therefore Scott’s hypothesis does not hold true

completely.

128
CONCLUSION:
At present ,nasal septum theory is stil
accepted as a reasonable explanation for
craniofacial growth.
Nasal septum may be important
anterioposterior growth of face because of
endochondral growth process occurring at its
posterior border.
It is not considered to be an active
contributor for vertical development of face.
129
HUNTER &ENLOW’S GROWTHEQUIVALENT

 The Hunter-Enlow growth equivalents

concepts is an important principle covering the
development of the facial skeleton.

 As the individual components of the skull

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

 This is achieved by growth equivalents

which act in opposing directions.
130
These growth equivalents coordinate the different
movements of the cranial base ,the nasomaxillary
complex and mandible , which are due to
development ,and thus determine the adaptive changes
in relation to individual parts of the skull.

131
For example, elongation of the anterior cranial base
is related with enlargement of the nasomaxillary
complex.
Disturbances during realization of this growth pattern
cause craniofacial anomalies. The disturbance can be
related to disproportions of the equivalents in the
vertical or horizontal plane

140
133
134
THEFUNCTIONALMATRIX THEORY
Introduction

 Essence of theory
 Explanation
 Neurotrophism
 Constraints of functional matrix
hypothesis

135
INTRODUCTION

The concept of this theory was introduced

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

136
ESSENCEOFTHE THEORY

The functional matrix hypothesis claims that the origin

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

137
The hypothesis as shown that change in
size, shape, and location (growth) of all
craniofacial skeletal entities are
epigenetically( causally related series of
processes in external and internal
environment) regulated.

138
 The epigenetic hypothesis suggests that the
post fertilization genome does not contain
sufficient information ,such as a blueprint, to
regulate all subsequent development.

 As structural and functional complexity

increases new regulating information is
generated.

 The interaction of both genomic and

epigenetic factors is required to regulate or
cause development. 147
Proponents of the functional matrix states that the
expansion of the soft tissue matrix is primary and the
bone growth is purely secondary and compensatory
event.
Translation of the various bones of the face is due to
volumetric expansion of the encapsulated spaces or
tissues.

140
141
150
FUNCTIONALCRANIAL
COMPONENT

One function

Skeletal tissue Neural tissue Muscle tissue Vascular tissue

Functional Cranial Component

143
 Functional Cranial Component

A related skeletal unit that

acts biomechanically to protect and/or support its fun
Tissues and spaces that
completely perform a function

Functional matrix Skeletal cranial

component

Periosteal matrix
Capsular matrix
144
PERIOSTEAL
MATRIX
Relates the matrix to those tissues that influence the
bone directly through the periosteum.
Examples of periosteal matrices includes: Muscles.
Blood vessels and nerves lying in grooves or entering
or exiting through foramina.
Teeth.

145
 Lack of contraction leads to atrophy of the bone.

All the periosteal matrices act homogeneously by

means of osseous deposition and resorption.

The muscles are attached either into the skeletal tissue

or indirectly by fusion with the outer fibrous layer of
periosteum.

Functioning muscles influence developmental changes

in the form of skeletal tissue to which they are attached.

146
The periosteal matrices stimulation causes growth of
the micoskeletal units.

Affects a microskeletal unit, sphere of influence is

usually limited to a part of one bone
Temporalis – coronoid process.
Tooth - alveolar bone.

They act to alter the size or shape or both of the

bones.
The growth process that occurs due to periosteal
matrix stimulation is called Transformation.

147
CAPSULAR
MATRIX

Included in this matrix are those masses and

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

148
Capsules tend to influence macroskeletal units
which means portions of several bones are
simultaneously affected
Inner surface of calvarium.
This sharing of reaction by several adjacent
bones constitutes a macroskeletal unit.

149
Each capsule is an envelope which contains
a series of functional cranial
components ,skeletal units and their related
functional matrices and is sandwiched
between two covering layers.
Examples: neurocranial capsule orofacial
capsule

150
Neurocranial capsule:

In this cover consists of skin and duramater

,the neurocapsular matrix consists of the
brain , leptomeninges and CSF.

The expansion of the enclosed and

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

151
.As the capsule enlarges ,the whole of the
included and enclosed functional
components, that is the periosteal matrices
and the microskeletal units are carried
outward in a totally passive manner.

160
The calvarial functional cranial components
as a whole are passively and secondarily
translated in space.

In experimentally induced or pathological

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

153
The expansion of the neurocranial
capsule is proportional to the increase in
neural mass. This can be shown by
considering hydrocephaly as an
example.
This suggests that the neural skull does not grow
first and thus provide space for the expansion of
the neural mass rather the growth of neural mass
is primary and causes secondary compensatory
growth of the skull.
154
Thus the point is simple the neural skull does not
grow first and provide space for the secondary
expansion of the neural mass rather the expansion
of the neural mass is primary event causing
growth of the neural skull.

155
Orofacial capsule:
All the functional cranial components of the facial
skull arise, grow and maintained within the
orofacial capsule.
This surrounds and protects the orophoryngeal
functioning spaces, and the volumetric
expansion of these spaces serves as a primary
morphogenetic extent in facial skull growth.

Moss ML,SalentijinL.:The primary role of functional matrices in facial growth:

Am J Orthodjune 1969; 55;566-77

156
These spaces are left over as it were, when facial bones,
muscles blood vessels and nerves complete their growth.
The patency of these spaces are vital in the metabolic
demands of the body.

E.g. airway passage (accomplished by a dynamic

musculoskeletal postural balance the mechanism) open
masticatory cavity

157
SKELETAL UNITS

May be composed of bone, cartilage or

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

The possible interaction between

periosteal matrix and microskeletal units
includes pterygoid –
gonialangle,temporalis-coronoid process,
masseter

158
When the adjoining portions of a number of
neighboring bones are united to function as a single
cranial component it is termed as macro- skeletal unit .

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

mandible

The overall skeletal growth is a combination of changes

in microskeletal and macroskeletalunits due to
stimulation of periosteal and capsular matrices
respectively.

159
In the mandible we distinguish the following
micro skeletal units.

Coronoid micro skeletal unit – related to

functional demands of temporalis.

Angular micro skeletal unit – related to activity of both

masseter and medial pterygoid.

Alveolar unit – related to presence of teeth.

Basal micro skeletal unit – related to inferior

alveolar neurovascular bundle.
160
These micro skeletal units are relatively independent
of each other. The term functional matrix is by no
means implies only to soft tissues but also
includes muscles, glands, nerves,
vessels fat, teeth etc.

Most of the orthodontic therapy is firmly based on

the fact that when this functional matrix grows or is
moved, the related skeletal unit responds.

161
AGAINST
Spheno-occipital synchondrosis
Demonstrates autonomous growth
Nasal cartilage
Scott- midfacial growth not responsive to external
influence
Removal - deficient growth
Destruction of cell proliferation potential
without cicatrization – Deficient growth
Craniostenosis – premature stenosis of sutures
inhibits growth – sutures have some capacity to
regulate the activity of functional matrix
170
 TRANSMISSION OFFUNCTIONAL STIMULUS TOTHE
BONE-NEUROTROPHISM

• Neurotrophism is a non impulsive

transmittiveneurofunction involving axoplasmic
transport providing for long term interaction
between neurons and innervated tissue , which
homeostatically regulate the morphological
compositional and functional integrity of those
tissues.

163
 Types of neurotrophism:
1. Neuromuscular
2. Neuroepithelial
3. Neurovisceral
Neuromuscular trophism:
Neural innervations are established at myoblast
stage. The genetic control cannot reside solely in
the functional matrices alone and there is
neurotropically regulated homeostatic control of
genome and similar neurotrophic mechanism exist
for capsular matrix which passively regulate the
functional cranial component.

164
Muscle denervation-reinnervation: muscle
denervation and reinnervation enable us to
diffrentiate effect on muscle tissue associated
with loss of impulse conduction and
contraction from those due to loss of
neurotrophic factors.
If motor neurons are sectioned and the
muscle subsequently becomes reinnervated
there is reformation of neuronal conductive
function, this demonstrates neuromuscular
trophism.
165
Neuroepithelialtrophism:
The neurological work of neurotrophism first
began in dermatology. The factors which
contribute to neuroepithelialtrophism are:
1. local mechanism operating in areas of
high mitotic activity
2. Epithelial growth factors.

166
Neurotrophic control of genetic activity:
neurotrophic control of genetic activity is
demonstrated in many tissues under
experimental conditions:
Protein synthesis in oral epithelial cells and
specific enzymatic sysnthesis in taste buds
epithelium appear to be neurotrophically
regulated.

167
CURRENTCONCEPTSOFFMH:
THEMOLECULARBASIS

The fmh failed to explain the sequences of events

through which the extrinsic stimuli caused adaptive
responses in the skeletal structures i.e. the flow of
the signals that generated required response.

The new researches focused on intercellular

signaling, communication and signal transduction
from the molecular matrix to micromolecular
matrix.

168
CONCEPTOFMECHANOTRANSDUCTION

Mechanotransduction signifies cellular signal

transduction.

It is the process by which macromolecular

extrinsic stimuli are converted into cellular
signals, which can be internalized by a cell and
processed so that a suitable adaptive response
can be generated.
.

169
170
 Altered external environment

Vital cells are pertrubed and leads to

Mechanoreceptors transmits an
extracellular physical stimulus into a
receptor cell

Mechantransduction –transduces or tarnsforms the

stimulus into an intracellular signal

171
Intracellular activation

172
 BONEASAN OSSEOUSCONNECTED
CELLULAR NETWORK

•The term ccn implies a network exists between the

adjacent cells of a tissue through specialised structures
in the cell membranes.

•The specialized structures includes the tight

junction ,gap junctions in cell membrane. These
junctions spread stimuli very fast across the
connected cell.

•Extensive ccn exists in the bone and that the

principle component is the gap junction.
173
•Connexin 43 ,a cytoskeleton protein is the
major constituent this network.

•Gap juction not only connects the osteocytes to the

nighbouringosteocytes but the superficial osteocytes
to periosteal and endostealosteoblasts too.

•Gap junction allows passage of ionic currents

molecules signals.

174
•All osteoblast are also interconnected
laterally.

•Vertically they connect

periostealosteoblast with preosteoblastic
cells and this in turn is interconnected
,thus each ccn is like a true syncytium
and are electrically active.

175
THEFMH AND EPIGENETICS
This concept of moss aims to find a middle path to
solve the controversy of genomic versus epigenetic
control of biologic processes.

Epigenetics is a term which includes : the sum of all

the biochemical, bioelectrical and biophysical
parameters-instantaneously present intra ,inter and
extracellularly- all of which are produced by the
functioning of the cell, tissue, organ or organism
itself.

176
It should be noted that these same
epigenetic factors serve as an internal
environment and must be considered in
addition to the classical external
environment of genetics.
Moss M.L.:The functional matrix hypothesis and
epigenetics:GraberT.M.:Physiologic principles of
functional appliances,STLouis;CV Mosby, 1985;3-4

177
It is postulated that epigenetic factors act upon
the products of the genome to regulate all
developmental processes leading to the
production ,increase and maintenance of
biological structural complexity and provides
feedback regulation of genome itself.

190
•The fmh denies that the genome of
skeletogenic cells contain in and of itself
sufficient information to regulate the type,
site ,rate, direction and duration of skeletal
tissue growth.

•But to be sure the modern epigenticist

accepts both the data and fundamental
concepts of modern molecular biology.

178
In opposition epigenetics views the genome as
providing a set of formal prior intrinsic and
necessary causal factors which when combined
with efficient proximate extrinsic and necessary
epigenetic causal factors together are sufficient to
account the regulation of development.

179
VANLIMBORGH’S COMPROMISE
THEORY

Three major viewpoints considered:

Sicher’s
Scott’s
Moss’s

180
CONTROLLING FACTORS IN
CRANIOFACIAL GROWTH
INTRINSIC GENETIC Genetic factors inherent to the
FACTOR skull tissues
LOCAL Genetically determined influence
EPIGENETIC originating from adjacent structures
FACTORS and spaces ( brain, eyes)
GENERAL Genetically determined
EPIGENETIC influences originating
FACTORS from distant structures
( sex
hormones)
LOCAL Local non genetic influences
ENVIRONMENTAL originating from the external
FACTORS environment( local external
pressure, muscle forces etc)
GENERAL General non genetic influences
ENVIRONMENTAL originating from external environment
FACTORS ( food ,oxygen)
181
Sicher’s view
Cartilage Sutures
Periosteum
Are all growth centers

182
183
Scott postulates
Intrinsic genetic factors affect: Cartilage
Periosteum
while sutures are passive and
reactory.

184
185
Moss is felt to have erred
in denying any intrinsic genetic factors in the
control of chondrocranial growth and…
restricting the control of sutural growth to local
epigenetic and environmental factors.

186
187
 VANLIMBORG’S
COMPROMISE
Chondrocranial growth is controlled by intrinsic genetic
factors

Desmocranial growth is controlled mainly by local

epigenetic factors

Desmocranial factors is also controlled by local

environmental factors

General epigenetic and general environmental factors

have very little role to play.
188
189
SERVOSYSTEM THEORY/CYBERNETICS
THEORY(1972)
 AlexandrePetrovic, explained that the growth of
various craniofacial regions is the result of
interaction of a series of causal changes and
feedback mechanisms.

 Based on a series of experiments , Petrovic and

coworkers have formulated a cybernetic model
for the control of mandibular growth.
190
Essence of the theory:
According to the theory ,control of primary
cartilages (mid face) takes a cybernetic form of
“command” whereas control of secondary cartilages
like condyle is comprised of both direct effect of
cell multiplication and also indirect effects.

191
Simply stated, the servo system theory is
characterized by the following two
principal factors:

(1) The horizontally regulated growth

of the midface and anterior cranial base,
which provide a constantly changing
reference input via the occlusion

192
(2) the rate limiting effect of this midfacial
growth on the growth of the mandible.

While growth of the mandibularcondyle and

of the sutures may be affected directly and
indirectly by systemic hormones, growth of
these structures is clearly more compensatory
and adaptive to the action of extrinsic factors,
including local function as well as the growth
of other areas of the craniofacial complex.

193
This theory starts with the explanation of
cybernetics.

cybernetics is the science of control and

communication in the animal and machine.

194
The theory postulates that every thing
affects everything and therefore organized
living systems never operate in an open loop
manner.

Open loop is a type of feedback

mechanism. The other type of feedback is
closed loop mechanism.

195
The feedback closes the regulation loop of a
given system in the following way..

196
 According to cybernetics theory ,the
behaving organism is not seen as a passive
respondent called into action by the
changing environmental stimuli but as a
dynamic system which continuously
generates intrinsic activity for organized
interaction with the environment.

210
Cybernetics in craniofacial growth:
cybernetics demonstrate the relationship
between observational and experimental
findings.

• Black box: The physiologic system under investigation is

represented by the block box .The contents of the black box
is usually not known.

198
 Feedback signal:It is the function of
controlled variable that is compared to
the reference input
 It is negative in regulator and servo
system.

199
 Closed loop system: If a physiologic
system is designed to maintain a specific
correspondence between inputs and outputs,
in spite of disturbance .

 It is called as closed loop system .

 It is characterized by the presence of a

feedback loop and comparator state.

200
Closed loop has two variations namely regulator
and servo system.
Open loop system has no feedback loop or
comparator.
The regulator: The main input is a constant
feature in this system .The comparator
detects disturbances and their effects.

201
 The servo system : It is also
called as follow up system .
 The main input is not a constant in
this system but varies across in time.

202
Elements of the theory:
Command is a signal established
independently of the feedback system
under scrutiny.
It affects the behavior of the controled
system without being affected by the
consequences of this behavior.

203
Examples :
secretion rates of growth hormones ,
testosterone ,estrogen , stomatomedin.
They are not modulated by variations of
craniofacial growth.

204
o References input elements : establish the
relationship between the command and
reference input. Includes septal cartilage,
septo-premaxillary
ligament, premaxillary and maxillary bones.

o Reference input is the signal established as a

standard of comparison ,eg. Sagittal position
of maxilla. Ideally it should be independent
of the feedback.

205
The controller is located between the deviation
signal and the actuating signal.

The confrontation between the position of the

upper and lower dental arch is the comparator
of the servosystem.

Activity of the retrodiscal pad and lateral

pterygod constitutes the actuating signals. The
elastic meniscotemporal and
meniscomandibularfrenum of the condylar form
the retrodiscal pad.
206
 The controlled system is between the actuator
and controlled variable, i.e. growth of the
condylar cartilage through retrodiscalpad
stimulation .
Controlled variable is the output signal of the
servosystem . Best example is a sagittal
position of mandible.

220
The gain: the gain of a system is the output
divided by input . Gain value greater than
one it is called amplification and if its less
than one it is called attenuation. The
pterygocondylar coupling is an example for
gain

208
The disturbance: any input other than the
reference required is called a disturbance. It
results in deviation of the output signal .for
example: increase in hormone secretion results in
supplemental lengthening of mandible.
The attractor: this is the final structurally stable
state in a dynamic system.
The repeller: this includes all unstable equilibrium
states like cusp to cusp occlusal relationship.

209
 Theory:

According to this the midface grows downward and

forward under the primary influence of the
cartilaginous cranial base and nasal septum ,
influenced principally by the intrinsic cell tissue
related properties common to all primary cartilages
and mediated by the endocrine system.

Carlson D.S.:Growthmodification:from molecules to mandible: reprinted from:

McNamara J.A.:Growthmodification:Whatworks,whatdosen,t and why?,Craniofacial
growth series 35,The University of Michigan,Ann Arbor,1999
210
The influence of somatotrophic hormones on
the growth of cartilages of nasal septum,
sphenooccipitalsynchondroses and other follows
that of a cybernetic form of command pattern.

211
•Related to this event the maxillary dental arch is
carried into a slightly more anterior position. this is
the first and primary event.

•This causes a minute discrepancy between the

upper and lower arches ,which Petrovic referred to
as the comparator that is the constantly changing
reference point between the positions of the dental
arches.

212
 Upper arch is the constantly changing
reference input.
Second propriorecptors within the periodontal
regions and TMJ perceive even a very small
occlusal discrepancy and tonically activate the
muscles responsible for mandibular protrusion.

Petrovic says the functional appliances will

work in the same way when given to stimulate
mandibular growth in class 2
malocclusions. 226
Third activation of jaw protruding muscles
(retrodiscal pads and lateral pterygoid) acts directly
on the cartilage of the mandibularcondyle and
indirectly through the vascular supply to the Tmj
stimulating the condyle to grow.

The growth in secondary cartilage is like condyle

corresponds to local and environmental factors (epigenetic
control). Lower arches constitutes the controlled variable

214
Finally the effect of the muscle function and
responsiveness of the condylar cartilage is influential both
directly and indirectly by the hormonal factors acting
principally on the condylar cartilage and on the
musculature.

215
This entire cycle is continuously activated as a
servomotor as long as the midface upper dental arch
continues to grow and mature and appropriate extrinsic
hormonal and functional factors remain supportive .

This affects position of mandible .The sagittalpostion

of mandible depends on the modification of condylar
growth by the activity of the retrodiscal pad and
lateral pterygoid muscle stimulation.

229
EVIDENCESAGAINST THETHEORY
•Goret-Nicaise, Awn (1983) found that the
resection of lateral pterygoid muscle fails to
diminish condylar growth.

•Das, Meyer, Sicher (1965) found that the

occlusion remained unaffected in
condylectomy studies.

217
CONCLUSION

Craniofacial growth and development are based to large

extent on evolving concepts .
At the start these concepts were based on naïve
assumptions about the perceived competing roles of
heredity and environment ,often framed within the
context of the age-old “nature nurture” controversy.

218
The craniofacial biologist tend to believe that there
was a single ,overiding mechanism governing the
growth of the face and jaw tended to focus on a
search for what might be called the HOLY GRAIL of
CRANIOACIAL BIOLOGY, a
single theory that is both biologically accurate and
clinically effective.

219
REFERENCES

•Moyers R.E.,Handbook of Orthodontics..4thed.Year

Book Medical Publishers:1988.p.48-50

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

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

220
•Orthodontic diagnosis –Thomas Rakosi , I.Jonas ,
Thomas Graber ,1stediton

•Orthodontics diagnosis and management of

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

221
•Graber T.M., Orthodontics-Principles and Practice. 3rd
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