CONTROLLING FACTORS

IN GROWTH OF SKULL

PRESENTED BY
PRACHODH C A
1st YEAR MDS
DEPT OF ORTHODONTICS AND
DENTOFACIAL ORTHOPAEDICS
 CONTENTS
INTRODUCTION
GROWTH SITE VS GROWTH CENTRE
CONTROLING FACTORS IN CRANIOFACIAL GROWTH
VON LIMBORGH’S CLASSIFICATION
ENLOW AND MOYERS’ CLASSIFICATION
GOOSE AND APPLETON'S CLASSIFICATION
THEORIES OF BONE GROWTH
 BONE REMODELING THEORY
 GENETIC THEORY
 SUTURAL HYPOTHESIS
 CARTILAGINOUS THEORY
 FUNCTIONAL MATRIX THEORY
 SERVO SYSTEM THEORY
 COMPOSITE HYPOTHESIS BY VON LIMBORGH
 RATE LIMITING RATCHET HYPOTHESIS
 GROWTH RELATIVITY HYPOTHESIS
 ENLOW GROWTH COUNTERPART PRINCIPLE
 ENLOW EXPANDING V PRINCIPLE

 CONCLUSION
 INTRODUCTION

Growth is a dynamic and continously changing process,which is influenced

and controlled by many factors
Since need for orthodontic treatment is created by disproportionate growth
of the jaws, in order to understand the the etiological processes of
malocclusion,it is necessary to learn how craniofacial facial growth is
influenced and controlled
 GROWTH SITE VS GROWTH CENTER
 .
Growth site has been defined as a region of periosteal or sutural bone formation
and modeling resorption adaptive to environmental influences.- BAUME

Proffit defines growth site as merely a location at which growth occurs, whereas
growth center is a location at which independent or genetically controlled growth
occurs


All growth centers are also sites, whereas all growth sites are not centers.

Examples of growth sites - mandibular condyle, maxillary tuberosity,

synchondroses, sutures, alveolar process, etc.

Growth center implies special areas which control the overall growth of
bone. These growth centers have “force” or “energy” within them for bone
growth.
 GROWTH SITE
Is any location or place where
growth takes place
Is a region of periosteal or sutural
bone formation and remodeling
resorption adaptive to environment
Sites of growth when transplanted to
another area, does not continue to
grow
Marked response to external
influences
They do not cause growth of the
whole bone, instead they are simply
places where exaggerated growth
takes place
All growth sites are not growth
centers
Growth sites do not control the
overall growth of the bone
GROWTH CENTRE
Is any location or place where
genetically controlled growth takes
place
Are places of ossification with tissue
separating force
Centers of growth when
transplanted to another area,
continues to grow
Less response to external influence.
More response to functional needs
Cause growth of the major part of
the bone
All growth centers are growth sites
Growth center controls the overall
growth of the bone
 CONTROLLING FACTORS IN CRANIOFACIAL GROWTH

There are different methods of classifying the controlling factors

Von Limborgh’s Classification

Intrinsic genetic factors

Local genetic factors
General epigenetic factors
Local environmental factors
General environmental factors
 Enlow and Moyers’ Classification

 Natural
 Genetic
 Function
 General body growth
 Neurotrophism
 Disruptive Factors
 Orthodontic forces
 Surgery
 Malnutrition
 Malfunction
 Gross craniofacial anomalies
Goose and Appleton's Classification
Endocrinal factors
Multifactorial inheritance
Racial differences
Nutrition
Diseases
Socioeconomic factors
Secular trends
 Von Limborgh’s classification
S. No.
Factor Definition/Explanation
1.
Intrinsic genetic factors Genetic factors inherent to the craniofacial
skeletal tissues.
2.
Local epigenetic factors Genetically determined influences originating
from adjacent structures and spaces (brain, eyes,
etc.).
3.
General epigenetic factors Genetically determined influences originating
from distant structures (sex hormones).
4.
Local environmental factors Local nongenetic influences from external
environment (Muscle force, local external
pressure).
5.
General environmental factors General nongenetic influences originating from
the external environment (oxygen supply, food).
Genetic growth factors and their possible role in endochondral growth
Genetics
Genetic Factor Function

Parathyroid hormone related peptide {PTHrP} Stimulates chondrocyte proliferation,

Indian hedgehog {Ihh}
Bone morphogenetic proteins {BMPS
inhibits chondrocyte hypertrophy.
controls chondrocyte proliferation and
hypertrophy.
Stimulates chondrocyte differentiation,
hypertrophy ,mineralization.

Fibroblast growth factors {Fgf} Inhibits chondrocyte proliferation.

Transforming growth factor beta {Tgf-β} Stimulates chondrocyte differentiation,
inhibits chondrocyte proliferation
hypertrophy and mineralization.

Hyaluronan and CD 44 Controls lengthening of cranial

base.
 sutures
growth factors such as 1 (Tgf-β1), Tgf-β2, Tgfβ3 , 2(BMP 2), BMP 7, (Fgf4),
(Igf-1) and sonic hedgehog (Shh) are found in the sutures and duramater
Mutation in genes for fibroblast growth factor receptors 1, 2 and 3 (Fgfr1,
Fgfr2 and Fgfr3) is associated with craniofacial synostosis in humans.

multifactorial

In Multifactorial inheritance, the likeness of parents and offspring can be

expressed by correlation coefficients.
Function
Lack of function results in retarded growth in relation to that area. Classical
examples include condition like microglossia, TMJ ankylosis, and muscle
dysfunction

General Body Growth

General body growth (somatic growth) and craniofacial growth are
interrelated, but this relationship cannot be precisely predicted.
Neurotrophism

Neurotrophism has been defined as “the nonimpulsive transmittive

neurofunction involving axoplasmic transport, providing for the long term
interactions between neurons and innervated tissue, which homeostatically
regulate the morphological, compositional and functional integrity of those
tissues”.
Disruptive Factors
These factors do not contribute to variations, but they can induce changes
in growth. Examples include:
Orthodontic/orthopedic forces when used to alter growth.
Surgical procedures interfering with growth.
Malnutrition.
Malfunction
Endocrinal control

growth hormones produced by pituitary gland are essential for normal

growth

somatomedins are mainly produced in liver. somatomedin act on growing

cartilage cells

Thyroxin is essential for development in early fetal life, nervous system

development and also for general growth . Puberty or adolescence is the
..
result of interplay of various hormones like follicle stimulating hormone (fsh)
and luteinizing hormone (lh).
Racial Differences
There is difference in the growth among various races. Asians are
generally shorter than Europeans

Nutrition
Malnutrition causes retarded as well as delayed growth in children.

Diseases
Minor diseases in normal children does not have any effect on growth,
but is found to alter the mineralization of teeth.
Socioeconomic status

children from different social groups display variation in size and speed of
their growth. children who belong to lower strata have delayed growth.

Secular trend

with evolution, there is a trend towards children growing larger than their
parents and also maturing earlier.
 THEORIES OF BONE GROWTH

The theories are based on the fact where the intrinsic genetic potential or
growth center is expressed.

The various theories of growth are:

Bone remodeling theory (Brash (1930)

Genetic theory (A R BRODIE-1941)
Sutural hypothesis (Sicher and Weinnman)—1952
Cartilaginous theory (James H Scott -1953)
Functional matrix theory (Melvin Moss 1962)
Neurotrophism (Behrent and Moss 1976)
Servo system theory (Alexandre Petrovic 1974
Composite hypothesis by von Limborgh 1970
Rate limiting ratchet hypothesis (Johnson)
Growth relativity hypothesis. (John C Voudouris 2000)
Enlows –Part counterpart principle
-Expanding V principle
Bone Remodeling Theory of Craniofacial Growth by Brash (1930)

This theory postulated that the craniofacial skeletal growth takes place by
bone remodeling—selective deposition and resorption of bone at its
surfaces.
The three fundamental tenets of this theory are:
1. Bone grows only by apposition at the surfaces.
2 .Growth of jaws takes place by deposition of bone at the posterior
surfaces of the maxilla and mandible. This is described as "Hunterian
growth".
3. Calvarium grows through bone deposition on the ectocranial surface of
the cranial vault and resorption of bone on the endocranial surface
Diagrammatic representation of the remodeling theory of craniofacial growth using the cranial
vault as a model. Increase in the size of the cranial vault occurs by adding bone via periosteal
deposition on the outer, ectocranial surface and resorption of bone on the inner, endocranial
surface of the vault (Source: Seminars in orthodontics
December 2005)
The Genetic Theory (A. Brodie—1941)
The genetic theory simply stated that genes determine and control the
whole process of craniofacial growth
Gregor Mendel (1822- 84) opened up the field of genetics
Weisman - concept of "germ plasm
Two principle areas of interest in genetics

1. "Transmission genetics“-involved only in explaining possible method of

transmission
2. Developmental and molecular genetics.
• SUPPORTING FINDINGS

Malocclusions are inherited eg-skeletal class II,class III

cleft lip and palate

CONTRADICTORY FINDINGS

Habits like thumb sucking( environmental influence) Affect maxillary growth

Hydrocephaly and microcephaly

Genes controlling growth- indian hedge hog, sonic hedge hog,homeobox,

transcription factors
The Sutural Hypothesis/Sutural Dominance Theory (Sicher and Weinnman)—
1952
According to this theory, sutures, cartilages and periosteum are all
responsible for facial growth and were assumed to be under intrinsic genetic
control.
Essence of the Theory
According to Sicher, the sutures are the primary determinants of craniofacial
growth. The craniofacial skeleton enlarges due to the expansible forces
exerted by the sutures as they separate.
THEORY
sicher stated that all bone forming elements like sutures, cartilage and
periosteum are growth centers like the epiphysis of long bones
this theory is called "sutural dominance theory" because he believed that
the primary event in sutural growth is the proliferation of the connective
tissue between the two bones.
Diagrammatic representation of the sutural theory of craniofacial growth using the cranial vault as
a model. Increase in the size of the cranial vault takes place via primary growth of bone at the
sutures, which forces the bones of the vault away from each other (Source: Seminars in
orthodontics December 2005)
Koski (1968) stated that there are two different views regarding the structure of
sutures.

The first school of thought (Sicher and Weinnman) considers sutures as a three
layered structure. It stated that the connective tissue between the two bones
plays the same role as the cartilage at the base of the skull and like epiphysis of
long bones.

The second school of thought (Pritchard, Scott and Girgis, 1956) sees the suture as
a five layer structure (each bone at the suture has its own two layer periosteum
on both sides and the intervening fifth layer between these periosteal layers.
Evidences against Sutural Theory

Trabecular pattern in the bones at the suture change with age, indicating
the changes in the direction of growth

Subcutaneous auotransplantation of the zygomaticomaxillary suture in the

guinea pigs has not been found to grow (Watanabe M Laskin).

Extirpation of facial sutures has no appreciable effect on the dimensional

growth of the skeleton (Sarnat, 1963).
Shape of sutures have been found to depend on functional stimulus (Moss &
Salentejin, 1969).

Closure of suture appears to be extrinsically determined (Moss ML).

Sutural growth can be halted by mechanical force like clips placed across
the sutures (Leitunen, 1956).
Scott Hypothesis/Nasal Septum Theory/
Cartilagenous Theory/Nasocapsular Theory

James H Scott, an Irish anatomist proposed the nasal septum theory as the
single and unified theory of craniofacial growth.

According to the nasal septum theory,

Sutures are considered as merely passive, secondary and compensatory sites
of bone formation and growth
Scott is of the opinion that there are two suture systems:

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 premaxilla, nasal and vomer bone. It

disappears in the human face during later part of fetal period and or after
birth.
Evidences supporting the Theory

Extirpation of septal cartilage in growing rats resulted in deficient growth of

the snout (Sarnat, 1966).
Latham and Burstone (1966) - nasal septum has a role in determining
anteroposterior growth of upper face.

Burstone emphasized the importance of the septal growth impulse to

maxillary growth in cleft palate cases.

Sarnat and Long - auto radiographic studies with thymidine to determine

levels of proliferative activity of cartilage cells.
Sarnat (1988) from experiments on rabbit snout concluded that deformity of
snout after resection of nasal septum was the result of lack of growth.

Steinler, Kvinslaw compared the increase in size of autotransplanted nasal

septum in subcutaneous abdominal wall in rats.

Latham (1974) - role of septopremaxillary ligament passing from

anteroinferior border of nasal septum to anterior nasal spine and inter
maxillary suture in the premaxillary region.

Koski - histological study of nasal septal cartilage ,found that there is

endochondral ossification taking place at septoethmoidal junction.
Evidences Against the Theory

Moss and Bloonberg (1968), Brigit Thilander (1970) that - septal cartilage
provides only mechanical support for the nasal bones and is not a primary
growth center.

Melson (1977) stated that downward sliding of vomer in relation to

anterosuperior part of nasal septum takes place throughout craniofacial
development

Moss - malformation in snout following excision of nasal septum is due to

trauma following surgery.
 Neurotrophism (BEHRENT ,MOSS 1976)
 Neurotrophism is defined as a nonimpulsive transmittive neurofunction
involving axoplasmic transport providing for the long-term interaction
between neurons and innervated tissue, which homeostatically regulate
the morphological, compositional and functional integrity of those tissues.
 Types of neurotrophism: Moss classifies neurotrophism into three types
arbitrarily:
 Neuromuscular

 Neuroepithelial

 Neurovisceral
Neuromuscular trophism:
Normal contractility of skeletal muscle depends on its ability to transmit an
efferent impulse

Neural innervations are established at the myoblast stage of differentiation.

Moss states that after this stage, skeletal muscle ontogenesis cannot proceed
without innervations..
Muscle denervation—reinnervation:
Muscle denervation and subsequent reinnervation enable us to differentiate
effect on muscle tissue associated with the loss of impulse conduction and
muscle contraction from those due to loss of neurotrophic factor.

 Cross innervations: Previttt and Safesky

NEUROEPITHELIAL TROPHISM
Epithelial mitosis and synthesis are nuerotrophicaly controlled

 Ifthe neurotrophic process is lacking abnormal epithelial growth and

orofacial hyperplasia ,malformations occur

Eg- tastebuds in tongue are dependant on intact innervation

The factors which contribute to neuroepithelial trophism are:

Local mechanism operating in areas of high mitotic activity.

Epithelial growth factors.

Type of feedback mechanism between dermis and epidermis.

 Neurovisceral trophism:

 In the orofacial region, salivary gland is partially trophically regulated.

 Increase or decrease of mature salivary gland, under neurotrophic

influence have been experimentally demonstrated.
 Functional Matrix Hypothesis (FMH)—
Melvin Moss
The concept that "form follows function" was first proposed by vander
klaaw (1948-52)


melvin moss and his co-workers developed the form and function concept
into the "functional matrix hypothesis".

Functional matrix hypothesis claims that the origin, growth and

maintenance of all skeletal tissues and organs are always secondary
compensatory and obligatory responses to temporally and operationally
prior events or processes that occur in specifically related nonskeletal
tissues, organs or functioning spaces (functional matrices).
 Functional Cranial Component

The totality of all the skeletal structures, soft tissues and functioning spaces
(nasal, oral, etc.) necessary to carry out a specific function is collectively
called a "functional cranial component".

Each functional cranial component consists of a skeletal unit and a

functional matrix (soft tissues and spaces).

Functional matrix consists of two distinct types: the periosteal matrix and the
capsular matrix.
 Functional Matrix

The functional matrix refers to all the soft tissues and spaces that perform a
given function

Examples of periosteal matrices include muscles, blood vessels, nerves, teeth

etc. The effects of periosteal matrices are best exemplified by the effect of
muscles upon the skeletal units. Lack of contraction leads to atrophy of the
bone.
Functioning muscles influence developmental changes in the form of
skeletal tissues to which they are attached. This is achieved through muscle
bone interface (Moss, 1971)

The growth process that occurs due to periosteal matrix stimulation are
called "transformation"
 Capsular matrix

The ‘capsular matrix’ is defined as the organs and spaces that occupy a
broader anatomical complex

Each capsule is an envelope that contains a series of functional cranial

components, skeletal units and their related functional matrices and is
sandwiched between two covering layers
 Neurocranial capsule:

In the neurocranium, it is the volume of the total neural mass which is

morphogenetically significant.

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

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.
 Orofacial capsular matrix:

The orofacial capsular matrix or oropharyngeal functioning spaces is

surrounded by the orofacial capsule .

The human oronasopharyngeal space increases in size from the third

month of pregnancy. It produces a compensatory increase in the size of
the orofacial capsule.
 Asthe capsule enlarges, both the periosteal matrices along with the
respective skeletal units are passively and secondarily translated to a new
position in space.

 Theenclosed capsular matrices act indirectly on the macroskeletal units

or on entire functional cranial component.

 They do not alter the size or shape of the skeletal units; instead they
change their location in space. This type of growth process is called
"translation
THE NEUROCRANIAL AND OROFACIAL CAPSULAR MATRICES ARE SHOWN. THE NEURAL
CAPSULAR MATRIX CONSISTS OF THE ENTIRE NEURAL MASS, INCLUDING THE DURA MATER, WHILE
THE OROFACIAL CAPSULAR MATRIX CONSISTS OF THESE FUNCTIONING SPACES. IN BOTH CASES,
THE SKELETAL UNITS EXIST COMPLETELY WITHIN THEIR RESPECTIVE CAPSULES. (SOURCE: MOSS
AND SALENTIJN. AJO 1969;20-31): THE PRIMARY ROLE OF FUNCTIONAL MATRICES IN FACIAL
GROWTH
 Skeletal Unit

 Theskeletal unit refers to the bony structures that support the functional
matrix There are two types of skeletal units:

1. Microskeletal,

2. Macroskeletal units.
Microskeletal units are parts of the bone whose growth is modulated by the
periosteal matrices..
 The change in size and shape of microskeletal units occur independently
of the changes in spatial position. Moss uses two terms for this:
“transformation” or “intraosseous growth”.

Macroskeletal units - core of maxilla, mandible and neurocranium.

Moss and Greenberg - the basic maxillary unit is the core which supports
and protects the infraorbital neurovascular triad and in mandible, the basal
tubular portion which protects the mandibular canal.
DIAGRAMMATIC REPRESENTATION OF FUNCTIONAL MATRIX THEORY.
PRIMARY GROWTH OF THE CAPSULAR MATRIX ( BRAIN) RESULTS IN A
STIMULUS FOR SECONDARY GROWTH OF THE SUTURES AND
SYNCHONDROSES, LEADING TO OVERALL ENLARGEMENT OF THE
NEUROCRANIUM (MACROSKELETAL UNIT). FUNCTION OF THE TEMPORALIS
MUSCLE EXERTS PULL ON THE PERIOSTEAL MATRIX AND BONE GROWTH OF
THE TEMPORAL LINE (MICROSKELETAL UNIT) (SOURCE: SEMIN ORTHOD
 Constraints of Functional Matrix Hypothesis

FMH provided only qualitative description of the biologic dynamics of

cephalic growth at gross anatomic level

 Methodological

 Hierarchial
 Functional Matrix Revisited

Tries to bridge the gap between hierarchical constraints and he

explains the operation from genome to organ level by two concepts:

 Mechanotransduction occurring in single cells.

 2.That bone cells function multicellularly as a connected cellular

network.
 Mechanotransduction
 Role of Osseous Connected Cellular Network (CCN)
All the bones are extensively interconnected by gap junction
and form an osseous connective cellular network

Gap junctions are found where the plasma membranes of a pair

of canalicular processes meet.

It is said that mechanotransductively activated bone cells like

osteocytes can initiate membrane potential which gets
transmitted through CCN
CCN is an untrained, self organized, self adapting and epigenetically
regulated system.

Exhibits oscillatory behavior permitting feedback

The functional stimuli after intercellular activation goes hierarchically

upward again through histological levels to the event of gross bone form
adaptational changes
 Von Limborgh’s Compromise Theory (1970)

Von Limborgh has summarized tat

 Intrinsic genetic factor controls chondrocranial growth.
 Epigenetic factors originating from skull cartilages and head tissues control
desmocranial growth.
 Local environmental factors like tension forces and pressure influences the
growth of desmocranial growth.
 General epigenetic and general environmental factors are less significant
in craniofacial growth
DIAGRAM SHOWING THE LIMBORGH’S VIEW ON THE CONTROL OF
EMBRYONIC SKULL DIFFERENTIATION.
 Modern Composite Theory

The composite theory tries to explain the growth of maxilla and mandible. It
separates the facial skeleton into desmocranium, chondrocranium and
splanchnocranium. Calvarium forms the desmocranium, the cranial base
and nasal septum as chondrocranium. Remaining part of middle face and
mandible constitute the splanchnocranium
Essence of the Theory

CRANIOFACIAL GROWTH AS EXPLAINED BY COMPOSITE THEORY

Servo System Theory: Alexandre Petrovic 1974

 Petrovic, using the language of cybernetics explained that the growth

of various craniofacial regions is the result of interaction of a series of
causal changes and feedback mechanisms
 two principal factors:

 (1) The hormonally regulated growth of the midface and anterior

cranial base, which provides a constantly changing reference input
via the occlusion.

 (2) The rate-limiting effect of this midfacial growth on the growth of the
mandible.
 Cybernetics

Weiner defines cybernetics as the science of control and communication

in the animal and machine

 Cybernetics 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.
 CYBERNATICS IN CRANIOFACIAL GROWTH

APPROACH TO SERVO SYSTEM CONCEPT

 Elements of Servo System Theory

 Command
 Reference input elements
 Reference input
 Controller
 Comparator
 Actuating signal
 Controlled system
 Controlled variable
 The gain:
 The disturbance:
 The attractor
 The repeller
 Explanation of the Theory

Anterior growth of the midface (A) Results in a slight occlusal deviation between the maxillary and mandibular
dentitions (B) Perception of this occlusal deviation by proprioceptors (C) Triggers the protruder muscles of the
mandible to become more active tonically (D) In order to reposition the mandible anteriorly. The muscle
activity and the protrusion in the presence of appropriate hormonal factors (E) Stimulate growth at the
mandibular condyle (F). (Source: After David Carlson. Semin Orthod 2005;11:172-83)
 Evidences Against the Theory

Goret-Nicaise, Awn (1983) - resection of the lateral pterygoid muscle fails

to diminish condylar growth.

Whetten and Johnston (1985) used a bilateral condylotomy model in

young rats and removed the lateral pterygoid muscle unilaterally. They
found no difference in condylar growth between the two sides.

Das, Myer and Sicher (1980) - the occlusion remained unaffected in

condylectomy studies.
 Rate Limiting Ratchet Hypothesis (Johnson)

The hypothesis is based on the finding that condyles have an inherent ability
to grow and pressure will arrest their growth.

It is suggested that the condyle is in effect a functional rectifier, a ratchet

whose growth is the ultimate determinant of downward and forward
mandibular translation
Johnston (1986) suggests therefore that the pattern of condylar loading is the
only signal necessary to control condylar growth.
 Anything or any therapeutic appliance that increases the amount of time
a condyle is unloaded would be expected to increase the condylar growth
and ultimately the length of the condyle.

 Conversely any appliance that increases the amount of time condyle is

loaded would be expected to decrease the condylar growth and thereby
results in a shorter mandible.
 Growth Relativity Hypothesis ( John C Voudouris 2000)

Growth relativity refers to growth that is relative to its displaced condyles

from actively relocating fossae.
 The main foundations of growth relativity hypothesis are:
 Displacement of condyle
 Nonmuscular viscoelastic tissue stretch
 Forcetransduction beneath the fibrocartilage of the glenoid fossa and
condyle add new bone formation
GROWTH RELATIVITY HYPOTHESIS FOR CONDYLAR AND GLENOID FOSSA
GROWTH WITH CONTINUOUS ORTHOPEDIC DISPLACEMENT)
. (SOURCE: AM J ORTHOD DENTOFACIAL ORTHOP 2000;117:247-66
 GROWTH EQUIVALENTS CONCEPT/ENLOW COUNTERPART PRINCIPLE

According to Enlow, the growth activity in one region is invariably accompanied by

complementary growth in other regions.

Enlow pointed out, both the dimensions and alignment of the craniofacial components
are important in determining the overall facial balance.
GROWTH EQUIVALENTS CONCEPT OF ENLOW. (A) COMPONENTS OF CRANIOFACIAL REGION (A= ANTERIOR CRANIAL BASE; B=
SPHENO-OCCIPITAL SYNCHONDROSIS; C= NASOMAXILLARY COMPLEX; D= MANDIBLE) (B) ELONGATION OF ANTERIOR CRANIAL
BASE (A) CAUSES SIMULTANEOUS ENLARGEMENT OF NASOMAXILLARY COMPLEX(C). (C) LENGTHENING OF SPHENO-OCCIPITAL
REGION (M) IS THE GROWTH EQUIVALENT FOR UNDERLYING PHARYNGEAL REGION (P) AND INCREASING LENGTH OF RAMUS
DISTANCE (D). THESE GROWTH EQUIVALENTS CAUSE NORMAL POSITIONING OF MANDIBLE RELATIVE TO NASOMAXILLARY
COMPLEX. (D) COMBINED VERTICAL LENGTHENING OF CLIVUS (B) AND MANDIBULAR RAMUS (D) IS THE GROWTH EQUIVALENT FOR
THE TOTAL VERTICAL ELONGATION OF NASOMAXILLARY REGION
 ENLOWS EXPANDING V PRINCIPLE

Many facial and cranial bones have ‘V’ configuration or ‘V’ shaped regions

Deposition on the inner side due to the concept of surface growth

depending on growth direction. Resorption takes place on the external
surface of the ‘V’. The ‘V’ moves away from its tip and enlarges
simultaneously
GROWTH OF MANDIBLE ACCORDING TO V PRINCIPLE
 Conclusion

 An intimate knowledge about the anatomy and growth of head is of

foremost important in the practice of orthodontics .
 Thereare a number of treatment modalities that can regulate the growth
of the jaws and dention
 Understanding the growth of the orofacial region and their controlling
factors are vitally important when planning such treatment procedures
THANK YOU