Theories of cranio facial growth /certified fixed orthodontic courses by Indian dental academy

THEORIES OF
CRANIOFACIAL GROWTH
INDIAN DENTAL ACADEMY
Leader in continuing dental education
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HOLY GRAIL OF
CRANIOFACIAL BIOLOGY
The search for a single theory of
craniofacial growth that is both
biologically accurate and clinically
effective


VARIOUS ARGUMENTS
 ROLES

OF HEREDITY AND THE
ENVIRONMENT IN CRANIOFACIAL
GROWTH
 EVOLUTION OF CONCEPTS
REGARDING MECHANISMS OF
CRANIOFACIAL GROWTH
 EMPHASIS ON THE EMERGING FIELD
OF GENETICS

NATURE AND NURTURE
CONTROVERSY
NATURE

NURTURE

Genetics
Genetically Predetermined
Biological Calvinism
Effects of environment with
little or no genomic basis
Functional factors

FORM –FUNCTION PRINCIPAL
It emphasizes the role of biological purpose, behavior,
and the environment, i.e., “function” in the production of
form .
INTRINSIC vs EXTRINSIC FACTORS
Intrinsic
Genetically predetermined
Extrinsic
Systemic influences that are
remote from the cells & tissues
being considered, such as hormones,as
well as effect of environment,like muscles


 GENOMIC

& FUNCTIONAL PARADIGMS
All biological cells & tissues have a degreeof
plasticity at some stage of ontogeny during which
they are capable of being influenced to a variable
degree by factors extrinsic to the genome

 EARLY

CONCEPTS OF CRANIOFACIAL
GROWTH
Vital dye experiments

VARIOUS THEORIES OF
GROWTH
 REMODELLING

THEORY OF GROWTH
The flat membrane bones in the skull vault expand
by accretion on the exposed surface and
absorption on the intracranial surface. It was
formerly supposed that the sutural lines
represent the main region of growth, but this is
by no means the case."
SIR WILFRED LE CLARK(1939)


REMODELLING THEORY
 Bone

only grows appositionally at surfaces
 Growth of the jaws is characterized by
deposition of bone at the posteriorsurfaces
of maxilla and mandible
 Calvarial growth occurs via deposition bone
endocranially


ENLOW’S “V” PRINCIPLE


THE SUTURAL THEORY
 WEINMANN

& SICHER ,1940s
“ The role of proliferating sutural connective
tissue in cranial growth…is identical to that of
the proliferating cartilage in basal
synchondroses” (Weinmann and Sicher, 1947
“The sutures, as well as the cartilages of the
craniofacial skeleton, were essentially the
locations of centers of bone growth at which the
inherited pattern of craniofacial form and
facial type, however determined, was
expressed; and the pattern could not be
changed” (Brodie, 1946).

THE NASAL SEPTUM
THEORY
 GIVEN

BY JAMES H. SCOTT1953,54,56
 The essential primary elements directing
craniofacial skeletal growth are the
cartilages found within the cranial base
and, in particular, the anterior extension
of the chondrocranium, the nasal septal
cartilage.

EPIGENETIC
 All

the extrinsic(extraorganismal) factors
impinging on vital structures , including
mechanical loadings & electroelectric states
 All intrinsic(intraorganismal)biophysical ,
biomechanical, biochemical ,bioelectric
microenvironmental events occuring on ,in
and between individual cells and
extracellular substances.

CRANIAL DIFFERENTIATION
 INTRINSIC

GENETIC FACTORS
 LOCAL EPIGENETIC FACTORS
 GENERAL EPIGENETIC FACTORS
 LOCAL ENVIRONMENTAL FACTORS
 GENERAL ENVIRONMENTAL
FACTORS


CONTROL OF SKULL
GROWTH
CHONDROCRANIAL
GROWTH



INTRINSIC GENETIC
FACTORS
LOCAL
ENVIRONMENTAL
FACTORS

DESMOCRANIAL
GROWTH
INTRINSIC GENETIC
FACTORS
LOCAL
ENVIRONMENTAL
FACTORS


SCOTT’S VEIW ON SKULL
GROWTH
CHONDROCRANIAL
GROWTH
INTRINSIC GENETIC
FACTORS

DESMOCRANIAL
GROWTH
SUTURAL
GROWTH
LOCAL EPIGE
NETIC FACTORS
LOCAL ENVIRON
MENTAL FACTORS


PERIOSTEAL
GROWTH
INTRINSIC
GENETIC
FACTORS

VAN LIMBORGH’S
ESSENTIAL ELEMENTS
 Growth

of the synchondroses & the ensuing
endrochondral ossification is exclusively
controlled by intrinsic genetic factors.
 The genetic factors controlling
intramembranous bone growth are small in
number & of a general nature
 The cartilaginous skull parts must be seen
as growth centers

 Extent

of sutural growth is controlled both
by the cartilaginous growth &the growth of
the other head structures.
 The extent of periosteal bone growth
largely depends on growth of adjacent
structures.
 The intramembranous processes of bone
formation can be additionally influenced by
local environmental factors ,muscles
inclusive.

CONTROL OF SKULL
GROWTH (LIMBORGH)
CHONDROCRANIAL
GROWTH

DESMOCRANIAL
GROWTH

Intrinsic genetic factors
General epigenetic
factors
General environmental
factors

Intrinsic genetic
Local epigenetic
Local environmental
General epigenetic
General environmental


HEREDITY,GENETICS &
THE GENE
 The

mechanisms by which traits are
transmitted
 The units of heredity
 The mechanisms of action by those units of
heredity
 Mendel’s Laws of Inheritance: mechanism
of inheritance & transmission of traits

Earlier Concepts
 Bateson

coined the term “genetics”as the new field
of heredity in 1905
 Weismann’s concept of “germplasm”:the
cytoplasm found with germ cells is comprised of
“determinants”that transmit traits from parents to
offspring.
 W.L.Johannsen used the term “GENE” to refer to
the presumed unit of heredity in1909.

 Waddington

thought of genes as organisers
and evocators of development
 Watson & Crick in 1953 discovered that
DNA is arranged structurallyas a double
helix
gene replication
 Operon Theory of Jacob &Monod(1963):
genes and whole groups of genes operate
within common regulatory sequencesthat
can be turned on and turned off to control
transcription of mRNA and gene expression


“The study of development transformed
in large part into a study of how gene
action underlies and governs
developmental processes”


THE GENETIC CONTROL
THEORY OF GROWTH
 The

whole plan of growth,the whole series
of operations to be carried out ,the order
and site of synthesis and their co-ordination
are all written down in the nucleic acid
message


Within the fertilized egg lies the information
necessary to generate a diversity of cell
types in the precise pattern of tissues and
organs that comprises the vertebrate body
All features (phenotype) are ultimately
determined by the DNA sequence of the
genome


THE GENOMIC THESIS
The genome from the moment of fertilization
contains all information to regulate
i.e.cause,control,direct:
1.the intranuclear formation & transcription of
mRNA
2. To regulate all of the intracellular& intercellular
processes of subsequent,&structurally more
complex,cells,tissues & organismal
morphogenesis.

Morphogenesis is the predetermined reading
out of an intrinsic and inherited genomic
organismal blueprint where, in addition to
molecular synthesis, the genome also
regulates the geometric attributes of cell,
tissue, organ, and organismal size,shape and
location


GENOMIC REGULATIONS :
1.Psychological behaviour
2.Personality
3.Alcohol & drug abuse
4.Smoking
5.Obesity


THE BIOLOGIC BASIS FOR
THE GENOMIC THESIS
 The

somatic cells of an individual inherit
two classes of molecular information:
1. An identical diploid DNA
2. The maternal cytoplasmic constituents of
the of the egg ,e.g.mitochondria,membranes


 Human

genome has approx. 100,000 genes
 Only 10% seems related to phenotypic
ontogenesis
 All somatic cells commonly share
approximately 5000 different polypeptide
chains
 But ,each specific cell type is characterized
only by approx. 100 specific proteins


Thus it is claimed that “these quantitative
protein differences are related to differences
in cell size ,shape and internal
architechture”


 The

encoding 10% of the DNA exists in two
families :
1. “ housekeeping genes” : regulate
(a)common energetic (metabolic,respiratory)
activities of all cells and the specific activities of
special cell types e.g. neurons, osteoblasts,
ameloblasts etc
(b)the synthesis of specific molecular gene products,
whose presence,absence,or abnormal
configuration are associated with the human
pathologic conditions like marfan syndrome,
achondroplasia,osteogenesis imperfecta etc
2. “ structural genes” : relatively nonabundant

THUS ,ALTERATIONS IN THE
GENOMICALLY REGULATED
PROCESSES OF MOLECULAR
SYNTHESIS CAN PRODUCE AN
EVENTUAL “STRUCTURAL COLLAPSE”
AT THE HIERARCHICALLY HIGHER
LEVEL OF A MACROSCOPIC BONE


HOMEOBOX GENES
These are genes that contain within their coding
regions a sequence of some 180 nucleotides
called as HOMEOBOX
 8 homeobox genes are linked in a cluster on one
Drosophila chromosome.
 All of them (Hox Cluster) :
1. Encode transcription factors
2. Act in sequential zones of the embryo in the
same order that they occur on the chromosome.
Approx. 60 aminoacids encoded by the homeobox
are called a Homeodomain.


THE HOX CLUSTER
Mice & Humans have 4
Hox clusters located
on four different
chromosomes
Genes in the mammalian
Hox clusters show
strong sequence
homology to
equivalent genes in
Drosophila

HOMEODOMAIN



DROSOPHILA(Fruit Fly)
THORAX
SEGMENTS:
T1
T2:- a single pair of
wings
T3:- halteres(balance)
Each carries a pair of
legs



DROSOPHILA HOMEOBOX
GENES
 Ultrabithorax

: acts within the cells of T3 to
suppress the formation of wings
 Antennapedia : is normally turned “on” in
the thorax and turned “off” in the cells of
the head.
These genes are called as selector genes or
master switches as they regulate the
expression of other genes.

Mutations in a single gene were able to cause the
reprogramming of the building of T3 and the Head
of the Drosophila.
Human Dlx5 and Dlx6 genes have been identified as
homeobox genes
Inactivation of these genes in the mice results in
severe CRANIOFACIAL,axial ,and appendicular
skeletal abnormalities,leadind to perinatal
lethality.
These genes are also believed as possible candidate
genes for the autosomal dominant form of the
split-hand/split-foot malformation,characterized
by missing central digits and claw-like distal
extremeties

ROLE OF HOMEOBOX
GENES IN CRANIOFACIAL
DEVELOPMENT
 It

is believed that “homeobox genes coordinate the development of complex
craniofacial structures and in both normal
and abnormal development,much of the
regulation of the development of virtually
all of the skeletal and connective tissue of
the face is dependent on a cascade of
overlapping activity of homeobox genes”

FUNCTIONAL MATRIX
HYPOTHESIS
“The origin,growth and maintainence of all
skeletal tissues and organs are always
secondary,compensatory,and obligatory
responses to temporally and operationally
prior events for processes that occur in
specifically related non-skeletal tissues,
organs or functioning spaces”

THE FUNCTIONAL
MATRIX HYPOTHESIS
 MELVIN

MOSS ,1962,68,69

FUNCTIONAL
CRANIALCOMPONENT

FUNCTIONAL
MATRIX

SKELETAL
UNIT


FUNCTIONAL MATRIX

PERIOSTEAL MATRIX CAPSULAR MATRIX
(muscles,blood
(organs & spaces e.g.
vessels,nerves)
brain,globes of
eyes,oropharynx)


CAPSULAR MATRIX
 NEUROCRANIAL

CAPSULAR
MATRIX
 OROFACIAL
CAPSULAR
MATRIX


SKELETAL UNIT

MICROSKELETAL
UNITS
(tuberosities,coronoid
process of
mandible,other muscle
attachment ridges)

MACROSKELETAL
UNITS
(neurocranium,
maxillomandibular
complex)


SKELETAL UNIT







Condylar process:-Lateral
pterygoid muscle
Coronoid :-Temporalis
Alveolar process:- Teeth
Angular process:
Massetor,medial pterygoid
Symphysis :- Mentalis,
geniohyoid, genioglossus
Basal portion:- blood
vessels,nerves in IA canal

FUNCTIONAL MATRIX
REVISITED
those portions that are retained,
extended or discarded
which prior deficiencies are now
resolved
The new revision deals mainly with the
responses to periosteal matrices

CONSTRAINTS OF FMH
METHODOLOGIC
CONSTRAINT
Macroscopic
measurements used
e.g. roengenographic
cephalometry
Removed by use of FEM
continuum mechanic
techniques

HIERARCHICAL
CONSTRAINT
The prior FMH could
not establish a link
between the signals
given to cells and the
responses by
individual cells;thus
no link could be given
between the
hierarchical levels


Actively adapting osseous tissues demonstrate
that :
1. Adjacent adaptational tissue surfaces
simultaneously show deposition,resorption,
and maintenance
2. Adaptation is a tissue process.Deposition
and maintenance are functions of relatively
large groups of osteoblasts,never single
cells
3. A sharp demarcation exists between
adjacent cohorts of active,depository,and
quiescent (resting) osteoblasts

 Attributes

of successively higher levels are
not simply the sum of lower level attributes
 Rather at each higher level,new and more
complex structural and operational
attributes arise that cannot be predicted,
even from a complete knowledge of those
of the lower levels.


The new FMH version includes two
complementary concepts :1. Mechanotransduction occurs in single
bone cells
2. Bone cells are computational elements
that function multicellularly as a
connected cellular network


 Gap

junctions are found where the plasma
membranes of a pair of markedly
overlapping canalicular processes meet.
 Gap junctions also connect superficial
osteocytes to periosteal and endosteal
osteoblasts
 All osteoblasts are similarly interconnected
laterally
 Vertically,gap junctions connect periosteal
osteoblasts with preosteoblastic cells which
are in turn similarly interconnected

MECHANOTRANSDUCTION
Mechanosensing processes enable a cell to sense and
to respond to extrinsic loadings by using two
processes:1.Mechanoreception:-transmits an extracellular
physical stimulus into a receptor cell .
2.Mechanotransduction:-transduces or transforms the
stimulus’s energetic and/or informational content
into an intracellular signal.E.g. mechanoelectrical,
mechanochemical

OSSEOUS
MECHANOTRANSDUCTION
It is unique in four ways:
 Most other mechanosensory cells are cytologically
specialized, but bone cells are not
 One bone-loading stimulus can evoke three
adaptational responses
 Osseous signal transmission is aneural
 The evoked bone adaptational responses are
confined within each “bone organ” independently
so there is no “interbone” or organismal
involvement

Types of
Mechanotransduction
1.IONIC OR ELECTRICAL:(a) Strech-activated channels
(b) Electromechanical
(c) Electrokinetic
(d) Electric field
2. MECHANICAL

MECHANOTRANSDUCTION:
A TENTATIVE SYNTHESIS

 Normal

muscle function strains attached bone
tissue intermittently
 The dynamics of skeletal muscle contraction fit
rather nicely with the energetic requirements for
bone cell responsiveness
 The range of specific strain-frequency harmonics
of muscle dynamics are also those found to be
morphogenetically competent i.e. osteoregulatory
 Normal skeletal muscle activity produces
intraosseous electric fields on the orderof extrinsic
fields found to be similarly morphogenetic
 Bone cells may be stimulated by two mechanismsdirectly by SA plasma membrane channels and

BONE AS AN OSSEOUS
CONNECTED CELLULAR
NETWORK (CCN)

 All

bone cells (except osteoclasts) are
interconnected by gap junctions that form an
osseous CCN
 Connexin 43 is the major protein
 Each osteocyte,enclosed within its mineralized
lacuna, has many cytoplasmic processes(15mic
m)long that interconnect with similar processes of
up to 12 neighbouring cells.
 These processes are arrayed three-dimensionally
 They lie within mineralized bone matrix channels

GAP JUNCTIONS
 Permit

the intercellular transmission of ions
and small molecules
 Exhibit both electrical and fluorescent dye
transmission
 Gap junctions are electrical synapses thus
bidirectional


THE CONNECTIONIST
THEORY
A

CCN is operationally analogous to an “artificial
neural network” in which massively parallel or
parallel-distributed signal processing occurs
 It computationally processes the intercellular
signals created by an electrical type of
machanotransduction of periosteal functional
matrix stimuli
 Computed output signals move hierarcally upward
to regulate the skeletal unit adaptational responses
of the osteoblasts

 Initial

input(loadings)
all loadings are
weighted inputs
they are summed
if
exceeds threshold value
an intracellular signal
is generated
signal is transmitted to adjacent
osteocytes
until final osteoblastis layer which
responds to the stimulus
 The CCNs show oscillations i.e. interactive
reciporcal signalling between layers.This enables
them to adjustively self organise .This behaviour
is relayed to the fact that biologic CCNs are not
pre-programmed rather they learn by unsupervised
or epigenetic training.


NEUROTROPISM
It is a non- impulse transmitted neurofunction,
involving axoplasmic transport , providing for the
long term interactions between neurons and
innervated tissues which homeostatically regulate
the morphological, compositional and functional
integrity of those tissues.
The nature of neurotropic substances & the process
of their introduction into the target tissue are
unknown at present

THREE GENERAL
CATEGORIES
 Neuro-epithelial

Trophism
 Neuro-visceral Trophism
 Neuro-muscular Trophism


NEURO-EPITHILIAL
TROPHISM
The mitotic activity necessary for normal
epithelial turnover of taste buds,their
maintenance, the expression of their
genomic potential in such processes as
DNA,and enzymatic synthesis are all under
the direct and continuous afferent gustatory
neurotrophic control.

NEUROVISCERAL
TROPHISM
 Experimental

data have shown an increase
and decrease of mature salivary glands
under trophic influence
 There is a consensus developing that
normal rate of growth , expressed in part as
regulation of cell size and number ,is under
neurotrophic control

NEUROMUSCULAR
TROPHISM
 “Skeletal

muscle ontogenesis requires
motorneuron innervation to proceed past the stage
of myotubes”
 Cross innervation experiments show that
significant morphologic,biomechanical,and
functional parameters of re-innervated muscle
come to more closely resemble those of the
muscle formerly innervated by now ectopically
implanted nerve i.e. these parameters of skeletal
muscle are nerve specific not muscle specific.

SERVOSYSTEM THEORY
 INPUT

– orthodontic appliances
 BLACK BOX – genetically determined and
cybernetically organized biologic features of
phenomena characterising,inducing,or controlling
spontaneous & appliance modulated growth eg:
maxilla lengthening,mandible lengthening
 OUTPUT – correction of malocclusion and
intermaxillary relation
 OPEN & CLOSED LOOP SYSTEM
 PERIPHERAL AND CENTRAL
COMPARATOR

command
Reference input
elements

Actuator

Controller

Coupling
System
(amplifier)

Controlled
System

X

Performance
Analysing
elements

Performance


Fwd traction by
septopremaxillary ligament

Forward growth
Of septal
cartilage

Fwd traction by
labionarinary muscles

Growth of
premaxillo maxillary
suture

Protrusion of
upper incisors

STM

somatomedine

Increase
of
Tongue
volume

Outward growth
of lateral mass
of ethmoid

Growth of
Cartilage
B/w greater
Wings, and body
Of sphenoid

Appositional growth
of ant premaxillary
extremity

Posteroanterior
shift of
premaxillary
bones

GROWTH OF
LENGTH
OF UPPER
JAW

Growth of
maxillopalatine
suture

Protrrusion of
lower incisors

Outward shift
of
alveolar border &
upper molar
groups

Transverse
separation
of two
premaxillary bones

Growth of
interpremaxillary
suture

Growth of
midpalatal suture
Transverse
separation
of horizontal
maxillary and
palatine plates

Outward growth
of two
maxillary bones


Outward
appositional
bone growth

GROWTH
OF
WIDTH OF
UPPER
JAW

GROWTH
HORMONE

Septal cartilage growth

Somatomedin &
Other GHmediators

Other
Masticatory
muscles

X

Activity of
lateral
pterygoid
muscle

GROWTH
OF
CONDYLAR
CARTILAGE

X
Appositional
Growth of
Posterior border
Of ramus

Local
Biomechanical
factors

Center for
Command of Mandibular
movements

MOVEMENTS OF
MANDIBLE

C

CENTRAL NERVOUS SYSTEM

Direct
thrust

LabioNarinary
muscles

Forward
Growth of
Maxilla

Shape
Reference
(mandible)

Iterative activity
Of retrodiscal
pad

Superior
head
Number of
sarcomeres
in series
Inferior
head

Superior
Labial frenum
And septoPremaxillary
ligament

Tongue

Position of upper dental
Arch (constantly changing
Reference input)

Mandibular angle
CondyleDental arch
distance
Forward growth
Of mandible

Sagittal
Position of
Lower
Dental arch
(controlled
Variable)

X

SAGITTAL POSITION
OF MANDIBLE

Detectors of occlusal
Adjustment (perodontal,
dental,
Articular, and muscular)


Occlusal
Adjustment

Location
Of teeth

Interaction between STH,
testosterone &LPM on
condylar cartilage growth
c4
c2

retrogn

M

grw rotation

c3

progn

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