Theories of craniofacial growth

VISHNU PRIYA

1st yr PG

Department of Orthodontics    and dentofacial Orthopedics

Meghna institute of dental    sciences

Contents

1. Introduction

2. Remodelling theory

3. Genetic theory

4. Sutural theory

5. Cartilagenous theory

6. Functional matrix theory

7. Functional matrix revisited

8. Servosystem theory

9. Neurotrophism

10. Von Limborg`s theory

 11. Enlows principles

12. Modern composite principle

13. Rate limiting ratchet hypothesis

14. Growth relativity hypothesis

15. Conclusion

16. References

INTRODUCTION

Growth-according to todd is “increase in size”.

WHY DO WE NEEDTO STUDY GROWTH….???

Theories

Remodelling theory

Genetic theory

Sutural theory

Cartilagenous theory

Functional matrix theory

Functional matrix revisited

Servosystem theory

Neurotrophism

Von Limborg`s theory

10.Enlows principles

11.Modern composite principle

12.Rate limiting ratchet hypothesis

13.Growth relativity hypothesis

Remodeling theory

Given by Brash in 1930

It provided the foundation for the development of the first general theory of craniofacial

growth.

Genetic theory

This is one of the earliest theories put forward by Brodie (1940).

This theory states that all growth is controlled by genetic influence and is preplanned.

It was more assumed than proven.

Vault sutures were passive while facial sutures were actively forcing bones apart.

Wendell Wylie termed this thinking “ orthodontic calvinism”.

As there was no evident scientific data the theory lacked scientific understanding and

soon was replaced by other theories.

Later research was focused on identifying the growth sites under the genetic control.

The sutures, craniofacial cartilages and periosteum were thought to be under the

genetic control and act as growth sites.

Sutural theory

It was given by Sicher in 1955.

He believed that cranio-facial growth occurs at sutures.

According to him there is connective tissue proliferation between the two.

He stated that paired attached sutures that attach facial areas to the skull and the

cranial base region push the naso-maxillary complex forward to pace its growth with

that of the mandible.

This connective tissue between the sutures of the nasomaxillary complex and cranial

vault produced forces that separated the bone and lead to the growth.
This connective tissue between the sutures of the nasomaxillary complex and cranial

vault produced forces that separated the bone and lead to the growth.

Sicher viewed the cartilage of the mandible somewhat differently stating that it grew

both interstitially as epiphyseal plate and appositionally, as bone grows under

periosteum.

Evidences Against Sicher’s Theory:

Auto transplants of sutures fail to grow in cultural medium though provided with same

environment and conditions.

Extirpation of sutures has no appreciable effect on growth of skull.

The shape and growth within sutures is dependent on external stimuli.

It is possible to bring the sutural growth to halt by mechanical stresses applied across

the sutures.

Cartilaginous theory

Given by James Scott in 1956.

He stated that intrinsic growth controlling factors are present in cartilage and

periosteum with sutures being only secondary.

He specifically emphasized how the cartilage of nasal septum paced with the growth of

maxilla.

The fact that, for many bones of the hand and legs, cartilage does the growing while

bone merely replaces it makes this theory attractive for the bones of the jaws.

According the Scott:-

Spheno-occipital synchondrosis cartilage -responsible for the growth of cranial base.

Nasal septal cartilage – Responsible for the growth of maxilla

Condylar cartilage – Responsible for the growth of mandible

TRANSPLANTATION EXPERIMENTS

Not all skeletal cartilage act same when transplanted.

Epiphyseal plate of long bones continued to grow in new location.

Spheno-Occipital synchondrosis also grows when transplanted but not at same pace.

No growth was seen when mandibular condyle was transplanted elsewhere.

Transplanting nasal cartilage to cultural medium or any other place did not give

equivocal results, that is sometime it grew, sometimes it did not.

CARTILAGE REMOVAL EXPERIMENTS 

Experiments of transplanting condylar cartilage showed little or No growth potential.

Mandibular condyle thus does not have innate growth potential and is not a growth

center.

The fact that after the condylar fracture in children does not all together inhibit growth of

mandible indicates that condyle is not a growth center.

Studies carried out in Scandinavia in 1960’s demonstrated that after the fracture of

mandibular condyle in child, there was an excellent chance that the condylar process

would regenerate to approximately its original size.

Cartilage removal experiment done on rabbits involving removal of the nasal septal

cartilage demonstrated retarded mid face development.           

Functional matrix theory

The concept of functional matrix hypothesis was introduced Melvin Moss(1969).

This hypothesis did not come into existence in one day but has a long history.
Several papers were published in the subsequent years and it was finally in the year

1981 Moss gave the classical statement ‘THE ORIGIN, GROWTH AND

MAINTAINANCE OF ALL SKELETAL TISSUES AND ORGANS ARE ALWAYS

SECONDARY, COMPENSATORY AND OBLIGATORY TO TERMPORALLY AND

OPERATIONAL PRIOR EVENTS OR PROCESS THAT OCCUR IN SPECIFICALLY

RELATED NON-SKELETAL TISSUES ORGANS OR FUNCTIONAL SPACES

(FUNCTIONAL MATRICES)’

Moss said that head and neck consists of a number of relatively independent and yet

integrate functions – i.e.

Digestion

Respiration   

Speech   

Olfaction

Balance

Vision

Neural integration

Each of this function is completely carried out by a à functional cranial component

Each such component is composed of two parts.

Functional matrix

Skeletal unit

Before going into the details of these 2 components it is important to understand the

basis concept of how growth is brought about.

These are 2 mechanism i.e. transformation and translation.

TRANSFORMATION TRANSLATION
Skeletal unit – composed variably of bone, cartilage or tendinous tissue.

- Macroskeletal unit

- Microskeletal unit

Macroskeletal – when adjoining portion of a number of a number of neighbouring bone

are united to function as a single cranial component.

Example – endocranial surface of calvaria.

Microskeletal units:

When a bone consists of a number of small skeletal units.

Example – Both maxillary and mandibular are formed by number of such contiguous

microskeletal units.

Maxilla – Orbital

Pneumatic

Palatal

Basal
Mandible   

Coronoid –    Temporalis

Angular

Alveolar

Basal

FUNCTIONAL MATRICES

This not only includes “soft tissue” i.e. muscles, gland, nerves, vesicle fat etc but teeth

which are also considered as functional matrix.

Periosteal matrices

Capsular matrices

Periosteal matrices

All the non-skeletal functional units adjacent to skeletal unit form the periosteal

matrices.

These may be attached indirectly to the outer fibrous layer of the periosteum or

sometimes by insertion into skeletal tissue itself.

This is best explained by the taking the example of temporalis muscle and coronoid

process.

The process first arises within the earlier formed analage of temporalis muscle whose

contractile ability are well developed in prenatal stages.

It has been proved experimentally – that whenever there is removal, denervation à

decrease in size post infectively / post traumatically or total disappearance.

Similarly, Functional hypertrophy / hyperactivity à increase in the                 

Size and change in shape.

Finally by altering the much attachment to other mandibular skeletal unit can produce

compensating change in muscle function itself.

CAPSULAR MATRICES

All skeletal units are totally embedded within the functional periosteal matrices.

At the same time this functional cranial component are organized in the form of cranial

capsule.

4 cranial capsules –

Neurocranial

Orofacial

Otic
Orbital

The capsule expands in response to volumetric increase of the capsular matrix.

The embedded bones are passively carried outward by process of growth.

NEUROCRANIAL CAPSULE

Sandwiched between à skin and dura mater

It consists of – 5 layer of scalp

-               -    Bone

-                      -Two layer dura mater

Bone consists of number of contiguous skeletal unit à outer table, Inner table, diploic

space.

Expansion of this enclosed and protected capsular matrix volume is the primary event in

expansion of the capsule.

This volumetric increase causes compensatory expansion of surrounding capsule as a

whole, which takes place by the mitotic activity of connective tissue.

Later the calvarial functional cranial components as a whole are passively and

secondary translated without the process of selective periosteal apposition and

resorption.
In cases of hydrocephaly à passive, non-periosteal translative growth is produced by

capsular matrices.

OROFACIAL MATRIX

Surrounds and protect – oronasopharyngeal spaces.

It is surrounded by skin and mucous membrane on either side.

The capsule originates by process of enclosure.

The volumetric growth of these spaces in the primary morphogenetic event in facial

skull growth.

Growth of these functioning spaces causes increase in size of capsule (by mitosis).

This is followed by passive movement of functional cranial component.

This brings about compensatory transformation of skeletal unit in response to an

alteration in periosteal matrices therefore

Growth = Transformation + Translation.

MANDIBULAR GROWTH

Can be used for demonstrating the integrated activity of periosteal and capsular

matrices of facial growth.

This is done by

A longitudinal series of lateral cephalograms representing mandibular growth is taken 2

assumptions are made.

Anterior cranial base fossa has completed the growth by end of 3rd year, so that

anterior cranial base is constant in shape size.

Position of mental foramen does not alter with time.

First and last series of tracings are taken and superimposition are done

1st superimposition is done on anterior cranial base.

This represents the total growth changes of the mandibular complex during this period.

This is termed as interosseous growth i.e. total growth, which is relative to fixed anterior

cranial base. (Capsular and periosteal matrix).

Second tracing – orient both mandibles so that anterior cranial base outlines are

perfectly parallel and registering both mandibular outline on mental foramen.

This represents change in size and shape independent to the spatial translation termed

as intra osseous growth occurring due to osseous deposition and resorption.

Hence, cranial growth is combination of morphogenetically primary activity of both types

of matrix.

Growth is accomplished by both spatial translation and change inform.

FUNCTIONAL MATRIX REVISITED:

FMT hypothesis revisited 1: The role of mechanotransduction.

This newest FMH version, transcends some hierarchical constraints and permits

seamless descriptions at several levels of bone structure and operation-from the

genomic to the organ level.

It does so by the inclusion of two complementary concepts:

(1) that mechanotransduction occurs in single bone cells

(2) that bone cells are computational elements that function multicellularly as a

connected cellular network.

All vital cells are "irritable" or perturbed by and respond to alterations in their external

environment.

Static and dynamics loadings are continuously applied to bone tissues

tending to deform both extracellular matrix and bone cells.

When an appropriate stimulus parameter exceeds threshold values, the loaded tissue

responds by the triad of bone cell adaptation processes.

Osseous mechanotransduction is unique in four ways:

(1) Most other mechanosensory cells are cytologically specialized, but bone cells are

not
(2) One bone-loading stimulus can evoke three adaptational responses, whereas

nonosseous processes generally evoke one

(3) Osseous signal transmission is aneural, whereas all other mechanosensational

signals use some afferent neural pathway

(4) The evoked bone adaptational responses are confined within each "bone organ"

independently

This process translates the information content of a periosteal functional matrix stimulus

into a skeletal unit cell signal, for example, it moves information hierarchically downward

to the osteocytes.

There are two skeletal cellular mechanotransductive processes: ionic and mechanical.

A) IONIC PROCESSES.

This involves ionic transport through the bone cell plasma membrane.

There is a subsequent intercellular transmission that are computed by the operation of

an osseous connected cellular network.

That network's output regulates the multicellular bone cell responses.

Ionic- mechanotransduction may involve several, possibly parallel, cellular processes.

Several types of deformation may occur in strained bone tissue.

These involve the plasma membrane stretch-activated (S-A) ion channels, a structure

found in bone cells, significantly in fibroblasts.

When activated in strained osteocytes, they permit passage of a certain sized ion or set

of ions, including K+, Ca2+, Na+, and CS+

ELECTRICAL PROCESSES:

These include several, non-exclusive mechanotransductive processes involving the

plasma membrane and extracellular fluids.

1. Electromechanical: In most cells, the osteocytic plasma membrane contains voltage-

activated ion channels, and transmembrane ion flow may be a significant osseous

mechano-transductive process.

Such ionic flows generate osteocytic action potentials capable of transmission through

gap junctions.

2. Electrokinetic: Bound and unbound electric charges exist in bone tissue associated

with the bone fluids in the osseous spaces or compartments.

It is generally agreed that electrical effects in fluid-filled bone are not piezoelectric, but

rather of electrokinetic, that is, streaming potential (SP) origin.

The SP is a measure of the strain-generated potential (SGP) of convected electric

charges in the fluid flow of deformed bone. The usually observed SPG of +2 mV can

initiate both osteogenesis and osteocytic action potentials.

3. Electric field strength: Bone responds to exogenous electrical fields.

Although the extrinsic electrical parameter is unclear, field strength may play an

important role.

Bone responds to exogenous electrical fields in an effective range of 1 to 10 υV/cm,

strengths that are endogenously produced in bone tissue during normal (muscle)

activity.

B) MECHANICAL PROCESSES

The mechanical properties of the extracellular matrix influence cell behavior.

Loaded mineralized bone matrix tissue is deformed or strained.

A series of extracellular macromolecular mechanical levers transmit information from

the strained matrix to the bone cell nuclear membrane.

The basis of this mechanism is the physical continuity of the transmembrane molecule

integrin.

This molecule is connected extracellularly with the macromolecular collagen of the

organic matrix and intracellularly with the cytoskekeletal actin.

The molecules of the latter is connected to the nuclear membrane, at which site the

action of the mechanical lever chain previously noted initiates a subsequent series of

intranuclear processes regulatory of genomic activity.

FMT hypothesis revisited 2: The role of an osseous Connected Cellular Network.

Gap junctions that form an osseous CCN extensively interconnect all bone cells, except

osteoclasts.

In these junctions, connexin 43 is the major protein.

Each osteocyte, enclosed within its mineralized lacuna, has many cytoplasmic

processes, _+15 ~m long and arrayed three-dimensionally, that interconnect with similar

processes of up to 12 neighboring cells.

These processes lie within mineralized bone matrix channels.

In compact bone, the canaliculi cross "cement lines," and they form extensive

communications between osteons and interstitial regions.

Gap junctions also connect superficial osteocytes to periosteal and endosteal

osteoblasts.

Vertically, gap junctions connect periosteal osteo- blasts with preosteoblastic cells, and

these, in turn, are similarly interconnected

Effectively, each CCN is a true syncytium.

Gap junctions are electrical synapses; they permit bidirectional signal traffic, e.g.,

biochemical, ionic.

Mechanotransductively activated bone cells, e.g., osteocytes, can initiate membrane

action potentials capable of transmission through interconnecting gap junctions.

The primacy of ionic signals rather than secondary messengers is suggested here,

because, although bone cell transduction may also produce small biochemical

molecules that can pass through gap junctions

A CCN is operationally analogous to an "artificial neural network.

It consists of a number of relatively simple, densely interconnected processing

elements, with many more interconnections than cells.

In network theory, these cells are organized into "layers":

An initial input

Intermediate or "hidden" layers

A final output

In the initial layer, these represent the loadings; all the weighted inputs are then

summed.

This sum is then compared, within the cell, against some liminal or threshold value.
If this value is exceeded, an intracellular signal is generated, i.e., successful

mechanotrans- duction occurs.

This signal is then transmitted identically to all the "hidden" layer cells to which each

initial layer cell is connected by gap junctions.

Next, similar processes of weighted signal summation, comparison, and transmission

occur in these intermediate layers until the final layer cells are reached.

The outputs of these anatomically superficial cells determine the site, rate, direction,

magnitude, and duration of the specific adaptive response, i.e., deposition, resorption,

and/or maintenance, of each osteoblasts.  

A skeletal CCN displays the following attributes:

(1) Developmentally, it is an untrained self-organized, self-adapting and epigenetically

regulated system.

(2) Operationally, it is a stable, dynamic system that exhibits oscillatory behavior

permitting feedback.

It operates in a noisy, nonstationary environment, and probably uses useful and

necessary inhibitory inputs.

(3) Structurally, an osseous CCN is nonmodular, i.e., the variations in its organization

permit discrete processing of differential signals.

It is this attribute that permits the triad of histologic responses to a unitary loading event.

Each osteocyte is potentially able to transmit three different adaptational signals, in

three different directions-some stimulatory and some inhibitory.

The morphogenetic primacy of periosteal functional matrices on their skeletal units is

consensually accepted.

As a muscular demand alters, e.g., myectomy, myotomy, neurectomy, exercise,

hypertrophy, hyperplasia, atrophy, augmentation, or reposition- ing, the triad of active

bone growth processes correspondingly adapts the form of its specifically related

skeletal unit.

A classic example is the regulation of coronoid process form by the temporalis muscle.

The tension in the tendon of this contracted muscle, transmitted through intertwined

periosteal fibers inserted into subjacent bone, deforms the loaded skeletal unit.

Periosteal functional matrices to regulate the adaptive responses of their skeletal units

by ionic mechanotransductive processes are related to several factors.

These are that

(a) normal muscle function strains attached bone tissue intermittently

(b) the dynamics of skeletal muscle contraction fit rather nicely with the energetic

requirements for bone cell responsiveness;

(c) the range of specific strain- frequency harmonics of muscle dynamics are also those

found to be morphogenetically competent   

(d) normal skeletal muscle activity produces intraosseous electric fields on the order of

extrinsic fields found to be similarly morphogenetic

(e) bone cells may be stimulated by two mechanisms-directly by strain-activated plasma

membrane channels and indirectly by electrokinentic phenomena.

FMT hypothesis revisited 3: The genomic thesis.

The genomic thesis holds that the genome, from the moment of fertilization, contains all

the information necessary to regulate

(1) The intranuclear formation and transcription of mRNA

(2) To regulate also all of the intracellular and intercellular processes of subsequent, and

structurally more complex, cell, tissue, organ, and organismal morphogenesis

In this thesis, morphogenesis is but 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.

Each dental replacement cycle involves identical odontogenic stages, it is postulated

that

(1) mechanical forces, related to differential diet "hardness," generate epigenetic

signals, mechanotransductively processed by dental papilla cells.

(2) these signals control at least the temporal and spatial expression of genomic

products related to the development of differential tooth form, such as size and shape.

Recently, molecular genetics extended the claims of the thesis to the regulation of all

aspects of "growth and development".

The mega-human genome project, called "the ultimate triumph of genetics, explicitly

intends to:

(1) describe the complete human genome;

(2) demonstrate genomic controls of all developmental processes, at all structural

levels, from the subcellular to the organismal

(3) in a societal context, possibly lead to some type of neoeugenics.

Many human activities now are claimed to be genomically regulated: e.g., psychological

behavior, personality, alcohol and drug abuse, chronobiological cyclic behaviors,

smoking, obesity, alcoholism, drug abuse, food-binging—indeed any attention-

deficiency disorder,.

Two interrelated, temporally sequential, processes control craniofacial development:

(1) initial regulatory (homeobox) gene activity

(2) subsequent activity of two regulatory molecular groups:

growth factor families   

steroid/thyroid/retinoic acid super-family.

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.

Specific orthodontic implications of the genomic thesis include claims that "poorly

coordination-ordinated control of form and size of structures, or groups of structures

(e.g., teeth and jaws) by regulator genes should do much to explain the very frequent

mismatches found in malocclusions and other dentofacial deformities

And "single regulatory (homeobox) genes can control the development of complex

structures indicating that single genes can determine the morphology of at least some

complex structures," including "how characteristic noses or jaws are inherited from

generation to generation.
FMT hypothesis revisited 4: The epigenetic antithesis and the resolving synthesis.

The dialectic process concludes here with an epigenetic antithesis and a resolving

synthesis, following two additional definitions:

(1) A process is a series of actions or operations that lead toward a particular result.

(2) A mechanism is the fundamental physical or chemical process involved in, or

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

The epigenetic antithesis, detailing both processes and mechanisms, is integrative,

seeking to clarify the causal chain between genome and phenotype.

Its goal is to identify and describe comprehensively the series of initiating biological

processes and their related underlying responsive mechanisms that are effective at

each hierarchical level of increasing structural and operational complexity.

Epigenetics refers to the entire series of interactions among cells and cell products

which leads to morphogenesis and differentiation.

Thus all cranial development is epigenetic.

Epigenetic factors include

(1) all of the extrinsic, extraorganismal, macroenvironmental factors impinging on vital

structures (for example, food, light, temperature), including mechanical loadings and

electromagnetic fields.

(2) all of the intrinsic, intraorganismal, biophysical, biomechanical, biochemical, and

bioelectric microenvironmental events occurring on, in, and between individual cells,

extracellular materials, and cells and extracellular substances.

In terms of clinical orthodontics, and of the FMH, all therapy is applied epigenetics, and

all appliances (and most other therapies) act as prosthetic functional matrices.

In craniofacial morphogenesis, more is known presently about processes than about

mechanisms.

Epigenetic processes of "intrauterine environment" can regulate fetal mandibular

growth.

The future aim must be to elucidate the molecular, genomic, mechanisms whose

activation underlies the adaptive growth processes of the mandibular functional cranial

components

that is, of the mandibular skeletal units and their related functional matrices.

SERVOSYSTEM THEORY

The concept of cybernetics and control theory was put forth by Petrovic (1982)
To describe the craniofacial growth mechanisms and the method of operation of

functional and orthopedic appliances.

The theory demonstrates a qualitative and quantitative relationship between

observationally and experimentally collected findings.

It helps in a broader understanding of orthodontic problems as the language of

cybernetics is compatible with the rapidly expanding use of computers among clinicians.

Cybernetics is based on the communication of information.

Any cybernetically organized system operates through signals that transmit information

(which may be physical, chemical or electromagnetic in nature).

Any cybernetic system, when provided an input (or stimulus), processes such an input

and produces an output.

The output is related to the input by a transfer function

Servo-system- In this, the main input is constantly changing with time, and the output is

constantly adjusted in accordance with the input.

Various Components of a Servo-System

Command- A signal established independent of the servosystem, and is not affected by

the output of the system.

Hence, as the name suggests, it tells the system what is to be done.

Reference Input- The input into the servo-system (which is brought about by the

command).

The command created a reference input through the action of a reference input

element. 

So the design of the servo-system so far is –

Comparator (Peripheral) - The input is fed into the comparator which is the component

that analyses the reference input and judges the performance of the system through

performance judging elements.

Central Comparator- The performance judging elements then transmit a deviation signal

to the central comparator which sends a signal to various components – the actuator,

the coupling system and the controlled system.

This ultimately brings about an output.

Growth of the Face – As Explained by the Servosystem Theory 

Types of Cartilage and influence of growth factors on them.

Role of the lateral Pterygoid and retrodiscal pad in condylar growth.

Types of Cartilage: 

a) Primary Cartilage

The zone of growth is comprised of functional chondroblasts, which divide, and

synthesize a cartilaginous matrix.

Chondroblasts undergo maturation and are later transformed into hypertrophied

chondroblasts.

Deeper in the cartilaginous matrix, calcium is deposited and endochondral ossification

begins.

b) Secondary Cartilage

The zone of growth includes skeletoblasts and perchondroblasts – cells that divide but

do not synthesize a cartilaginous matrix.

Once the prechondroblasts mature into chondroblasts, they become surrounded by

cartilaginous matrix and do not divide.

Primary cartilages are seen in:-

Epiphysial cartilages of long bones

Cartilages of synchondroses of cranial bones

Nasal septal cartilage

Lateral cartilaginous masses of ethmoid

Cartilage between greater wings and body and sphenoid.

Secondary cartilages are seen in:-

Coronoid cartilage

Condylar cartilage

Midpalatal suture cartilage

Post fracture callus

According to studies carried out by Charlier, Petrovic and Stutzmann on organ cultures,

at the Strasbourg Laboratory of Craniofacial Growth Mechanisms, France:-

Dividing chondroblasts (in primary cartilage) are more susceptible to general extrinsic

factors, especially growth hormone, somatomedin, sex hormones and thyroxinel.

The cartilage matrix surrounding the mature chondroblasts isolates them from the effect

of local factors.
Local Biomechanical factors (like functional appliances) can only modify the direction of

growth.

In the secondary cartilages, where prechondroblasts ate the dividing cells, general and

local extrinsic factors can affect the growth.

The amount of growth of these cartilages can be modulated by using orthopedic

appliance

Role of Lateral Pterygoid muscle and retrodiscal pad on condylar growth.

Lateral pterygoid muscle is involved in 2 important aspects:-

Blood Circulation

Biomechanical effects

The blood supply to condylar cartilage is mainly from the lateral pterygoid muscle and

the retrodiscal pad.

On surgical excision of these 2 structures the growth rate of the condyle is significantly

diminished.

Biomechanical effects:-

Contraction of the lateral pterygoid muscle places the condyle in a more anterior

position.

This causes a stretching of the retrodiscal pad.

Repeated contraction causes increases activity of the retrodiscal pad, resulting in an

increased blood supply and increases washing away of metabolites, which tend to

inhibit growth.

Increase in the blood supply increases the supply of nutritive factors as well as growth

factors such as stomatomedin, testosterone, and other hormones.

Rat experiments by Stutzmann and Petrovic have shown that proper function of these

two structures is essential for proper mandibular growth.

Growth of the Face

The growth of the maxilla is brought about by the release of hormones (esp. STH-

Somatomedin).

These hormones have various direct and indirect effects which result in the growth of

the maxilla.

Somatomedin induces growth of primary and secondary cartilages which results in an

outward and forward growth of the maxilla.

Another important action of somatomedin is the increase in the size of the tongue,

which also facilitates the outward and forward growth of the maxillary dental arch.
Once the maxilla increases in length and width, the position of the maxillary dental arch

is changed.

THE POSITION OF THE MAXILLARY DENTAL ARCH FORMS THE REFERENCE

INPUT OF THE SERVOSYSTEM.

The release of somatomedin represents the COMMAND (command to grow).

The hormone itself is the REFERENCE INPUT ELEMENT.

The OCCLUSION between the upper and lower teeth forms the COMPARATOR.

Owing to the forward and outward growth of the maxilla there is an obvious change in

the relation of the teeth.

What was originally a cusp to fosse relationship becomes a cusp to cusp relationship.

Hence the PERIPHERAL COMPARATOR (occlusion) senses this due to a change in

PERFORMANCE or the efficiency of mastication.

Due to improper mastication, there is increased force on the periodontium, teeth,

muscles and TMJ, which serve as the PERFORMANCE ANALYSING ELEMENTS.

The performance analyzing elements send signals to the CENTRAL COMPARATOR

which is represented by the central nervous system.

The CNS is equipped with a SENSORY ENGRAM which is a record of ideal tooth

relations, and a record of the ideal muscular posture which can help to attain proper

mandibular position.

Details on the development and functioning of the sensory engram are given

subsequently. 

The CNS compares the present muscular position with the ideal muscular position

stored in the sensory engram.

It then sends a DEVIATION SIGNAL to correct this discrepancy.

The deviation signal is sent to an ACTUATOR which is represented by the motor cortex.

The actuator then sends an ACTUATING SIGNAL to the COUPLING SYSTEM of the

lateral pterygoid muscle and the retrodiscal pad.

The LPM positions the mandible forward and the activity of the retrodiscal pad induces

mandibular growth at the condyle (THE CONTROLLED SYSTEM)

The resultant output or CONTROLLED SYSTEM is the forward growth of the mandible

which results in an ideal cusp to fossa dental relation.

Growth at the Posterior Border of the Mandible

Once growth occurs at the condyle, the posterior border of the mandible becomes more

concave in shape.  
This causes a negative piezoelectric effect to develop at the posterior border of the

mandible, and bone apposition results.

At the same time, the anterior border of the condylar process becomes more convex,

causing a subsequent POSITIVE piezoelectric current to develop and a subsequent

resorption of bone occurs.

This accounts for an increase in length of the mandible.

Clinical Implications

According to the principle of optimality of function, a condition which results in maximum

efficiency is one that is instilled into the brain.

So, all orthodontic treatment must strive to reach the optimal functional situation, or, if

this is not possible, the post treatment functional condition should be better than the

pretreatment condition.

If this is established, the tendency for relapse is less.  

A functional appliance should be removed only when growth is completed, or if growth is

not completed, it should achieve a good intercuspal relation (the attractor).

This ensures a stable result.

If the treatment ends with the teeth in poor occlusion (repeller), relapse is more likely to

occur.

An understanding of how functional appliances affect the servosystem is important to

know how long the appliance is to be worn.

The first group of appliances should be worn full time.

The second group of appliances should be worn part time.

Proper function of the LPM – RDP is essential for growth.

This was shown by rat experiments by Petrovic and Stutzmann.

Ideal functioning of LPM-RDP not only increases the amount of growth of the mandible,

but also improved the response to functional appliances, as was seen in breast fed

versus gavage fed rats.

This is important to know for counseling purposes.

The sensory engram in children is poorly developed.

Hence younger children respond better to functional appliance therapy than older

children, and the results are more stable.

Hormonal activity is highest at puberty, during the pubertal growth spurt.

Since hormones are very important for growth, one must take full advantage of the

increased hormonal activity if any growth modulation is required.

Drawbacks

The theory places a lot of importance on the condyle as the growth centre.

Hence if the condylar cartilage is lost subsequent to a fracture, growth should seize.

But studies done in Scandinavia show that this does not happen.

The author places a lot of importance on the role of hormones in controlling growth.

In all probability, they do not have such a large role to play.

The peripheral comparator, the occlusion, itself, is unstable.

Discrepencies in the occlusion can easily be overcome by dentoalveolar changes,

rather than by growth of the mandible.

According to the theory, an end on relation is a repeller.

Still, end on relation of the molars and other teeth are often seen.

The theory does not explain the action of the reverse pull headgear.

NEUROTROPHISM

Given by Melvin Moss

Neurotrophism is a non impulsive transmittive neurofunction

It    involves axoplasmic transport providing for long term interaction between neurons

and innervated tissue ,

which homeostatically regulate the morphological compositional and functional integrity

of those tissues.

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

there is neurotropically regulated homeostatic control of genome and similar

neurotrophic mechanism exist for capsular matrix which passively regulate the

functional cranial component.

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.
Neuroepithelialtrophism:

The neurological work of neurotrophism first began in dermatology.

The factors which contribute to neuroepithelial trophism are:

1. local mechanism operating in areas of high mitotic activity

2.Epithelial growth factors.

 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.

3.Neuro visceral trophism

In the orofacial region salivary gland is partially trophicaly regulated.

Increase or decrease of mature salivary gland under neurotrophic influence have been

experimentaly demonstrated.

VON LIMBORGH’S THEORY

5 FACTORS

INTRINSIC GENETIC FACTORS- control of skeletal unit themselves

LOCAL EPIGENETIC FACTORS- Bone Growth Determined by genetic control

originating from other structures

GENERAL EPIGENETIC FACTORS Genetic factors determining growth from distant

Structures. Eg:hormones

LOCAL ENVIRONMENTAL FACTORS Non genetic factors from local external

Environment. Eg: habits, muscle force

GENERAL ENVIRONMENTAL FACTORS General non genetic influences such as

nutririon, oxygen etc.

ENLOW’s PRINCIPLE

Two important principles

1.Counterpart principle

2.‘V’ principle

Growth of any given facial or cranial part relates specifically to other structural and

geometric ‘counterparts’ in the face and cranium.

If each regional part and its particular counterpart enlarge to the same extent, balanced

growth between them is the result

Counterpart relationship in the face & cranium:

Growth process –presented as

1. Deposition & resorption (remodelling)

2. Displacement (actual pacemakers) Growth of Maxilla & Mandible » The bony

maxillary arch lengthens horizontally in a posterior direction - by posterior movement of

PTM.

DEPOSITION: posterior – facing cortical surface of the maxillary tuberosity

RESORPTION: inside surface of the maxilla within the maxillary sinus.

(opposite side of same cortical plate

DISPLACEMENT: as maxillary tuberosity lengths posteriorly, whole maxilla is displaced

anteriorly.

counterparts to the bony maxillary arch :

1. Upper part of the nasomaxillary complex,

2. Anterior cranial fossa,

3. Palate

4. Corpus of the mandible.

MANDIBLE:

The mandible is not to be regarded as a single functional element

Corpus & ramus are counterparts to each other (ramus grows posteriorly that causes

elongation of corpus)

The body of the mandible is the structural counterpart to the body of the maxilla (The

mandibular arch lengthens by an amount that equals the growth of the maxillary arch)

ANTERIOR CRANIAL FOSSA

Deposition: ectocranially

Resorption : endocranially

Nasal bones displaced anteriorly

Simultaneous horizontal lengthening of maxillary arch (counterpart)

Equivalent force increment & balanced form

Ethmoidmaxillary (nasal) region:

Brain enlarges

sutures grow

perimeter of cranial bones increase

Facial area also increases to the same extend

Direct deposition on forward facing cortical surfaces of ethmoid nasal bones

Vertical lengthening of nasomaxillary complex:

Deposition: Inferior (oral side)

Resorption: Superior (nasal side of palate)

Downward growth movement of palate

Relocates it inferiorly & provide for vertical enlargement of overlying nasal region

Displacement : sutures of maxilla

Whole maxilla is displaced inferiorly

Primary displacement ( bones own displacement)

 MAXILLA
Anterior part – resorptive –as it grows downward

Labial side of premaxilla – resorptive – away from downward direction of growth

Lingual side – depository- towards downward growth direction

Midsagittal section of maxilla

palatal side – depository Floor of the nasal cavity Surface just above maxillary incisors -

resorptive

Modern composite theory

It tries to explain the growth of the mandible and maxilla

It divides the facial skeleton into the desmocranium, chondrocranium and

splanchnocranium

The calvarium forms the desmocranium, tha nasal spetum and cranial base form the

chondrocranium and the rest of the midface and the mandible form splanchnocranium.

Chondrocranium is considered the dominant factor in craniofacial growth

Post natal remanants,cranial basal cartilages and nasal cartilages act as growth

centres.

Which are influenced by intrinsic genetic factors

S-O synchondrosis exhert a direct action on the desmocranium

Local epigenic factors (capsule) and local environmental (periosteal matrix) control the

calvarium

Sutures are only growth sites

The growth of nasal cartilage pushes the maxilla forward and downward

The growth of the maxilla is controlled by both local epigenic factors and local periosteal

factors

The position of the mandible is also effected by the cranial base flexion and growth by

altering the posture of the glenoid fossa

Ventral position of maxilla with respect to the    glenoid fossa also effects the mandible

by rotating it forward or backward

Rate limiting ratchet hypothesis

It was given by johnson

It views the condyle as an opportunist

It is suggested that the condyle is infact a dunctional rectifier, a ratchet whose whose

growth is ultimate determinant of downward and forward mandibular translation

It is based on a finding that the condyle has an inherent ability to grow and pressure will

arrest their growth

Functional loading controls mandibular growth whereas functional unloading stimulates

mandibular growth

The condyle is therefore considered as “rate limiting ratchet”

According to this theory any therapeutic appliance that increases the time of unloading

of the condyles would be expected to increase condylar growth.

Growth relativity hypothesis

Given by John C Voudouris in 2000

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

relocating fossae

The main foundations rae

Displacement of condyle

Neuromuscular viscoelastic tissue stretch

Force transduction beneath the fibro cartilage of the glenoid fossa and condyle add new

bone formation

1) Displacement of condyle

Displacement that takes place initially following the mandibular advancement affects the

fibrocartilaginous lining in the glenoid fossa to induce bone formation locally.

2)Viscoelastic stretch

Once the condyle is displaced it is followed by the stretch of non muscular viscoelastic

tissues.

Viscoelastic refers to all the non- calcified tissues

It addresses the viscosity and flow of synovial fluids, the elasticity of retrodiscal tissues

the fibrous capsule and other non muscular tissue.

Due to viscoelastic stretch there is influx of nutrients and other biodynamic factors into

the region through engorged blood vessels

Alteration of synovial fluid dynamic also takes place

3)force transduction and new bone formation

New bone formation takes place at some distance from actual retrodiscal tissue

attachments in fossae

The glenoid fossa and displaced condyle are both influenced by the articular disk,

fibrous capsule and synovium which are contagious

Thus condylar growth is affected by viscoelastic tissue forces

Conclusion

Identifying the primary trigger mechanism for growth of the dentofacial region will help

the orthodontist in proper planning of the treatment.

It allows the orthodontist to either enhance or inhibit the maxilla or mandible.

Hence, proper knowledge of how growth occurs is essential to the orthodontist.

Refferences

Essentials of facial growth- Enlow and Hans

The human Face- Enlow

Contemporary orthodontics – Proffit 5th edition

Textbook of craniofacial growth- Sridhar prem Kumar

Dentofacial orthopedics with functional appliances- Graber,Rakosi and Petrovik

Theories in craniofacial growth- seminars in orthodontics – David S Carlson

The capsular matrix- Melvin Moss & Letty Salentijn    AJODO 1969

The primary role of functional matrices in facial growth- Melvin Moss & Letty Salentijn

The functional matrix revisited    1- the role of mechanotransduction

The functional matrix revisited 2-the role of an osseous connected cellular network

The functional matrix revisited 3- the genomic thesis

The functional matrix revisited 4 – the epigenic antithesis and the resolving synthesis

A procedure for the analysis of intrinsic facial form and growth an equivalent balance

concept- Enlow,Moyers, Hunter & Mcnamara

Improved clinical use of twin block and herbst as a result of radiating viscoelastic tissue

forces on the condyle and fossa in treatment and long term retention: Growth relative-

John Voudouris & Kuftinechy