Functional matrix theory /certified fixed orthodontic courses by Indian dental academy

FUNCTIONAL MATRIX THEORY

INDIAN DENTAL ACADEMY
Leader in continuing dental education

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INTRODUCTION:
A discussion of the regulation of craniofacial growth
seems an appropriate place to outline the
conceptual milieu within which the functional matrix
hypothesis originated & exists. The hypothesis
derives from the century old work of His & Roux
and is compatible with recent epigenetic concepts
associated with Waddington, Bleschmidt and
Lovtrup. The hypothesis serves as a conceptual
bridge between the concepts of function and
epigenesis.
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BASIS FOR DEVELOPMENT OF THEORIES
It is a truism that growth is strongly influenced by genetic factors,
but it also can be significantly affected by the environment, in the
from of nutritional status, degree of physical activity, health or
illness and a number of similar factors.
Since a major part of the need for orthodontic treatment is
created by disproportionate growth of the jaws, it is necessary to
learn how skeletal growth is influenced and controlled to
understand the etiologic processor of malocclusion and
dentofacial deformity. Great strides have been made in recent
year in improving the understanding of growth control. Exactly,
what determines the growth of the jaws, however remained
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unclear and continues to be the subject of intensive research.
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DEFINITIONS
GROWTH
Growth is defined as a change in size or shape or spatial
position of any living tissue or organ. Krogman defined it as
increase in size, change in proportion and progressive complexity.
Todd defined it as an increase in size, and the development
as progress towards maturity.
DEVELOPMENT
It refers to all the naturally occurring unidirectional changes
in life of an individual from its existence as a single cell to its
elaboration as a multifunctional unit terminating in death. It
encompasses the normal sequential events between fertilization
and death.
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So development = growth +differentiation+translocation.
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DIFFERENTITATION
It is a change from generalized cells or tissues to more
specialized kind during development. It is change in quality or
kind.
TRANSLOCATION
It is the change in position eg. Chin point moves downward
and forward for more than any growth.
MATURATION
Qualitative changes which occurs with ripening or aging.

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GROWTH SITES VS GROWTH CENTRE
A site of growth is merely a location at which growth
occurs, whereas a Centre is a location at which independent
(genetically controlled) growth occurs. In general all centres of
growth also are sites but the reverse is not true.
In cartilage, cells of growth plate are capable of creating a
tissue separating force by virtue of interstitial expansion. When
such units are transplanted to subcutaneous sites the dimensions
continue to increase.
The cells of suture however are not capable of generating a tissue
separating force. When transplanted to subcutaneous site the
transplant no longer grow-apart. So Baume called growth centers
are endochondral ossification with tissue separating force
contributing to increase of skeletal mass and growth sites are
regions of periosteal or sutural bone formation and modeling
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resorption adaptive to environmental influences.
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EPIGENETICS
Epigenetics, as defined here, includes (1) all of the extrinsic (extra
oraganismal) factors impinging on vital structure, including
importantly mechanical loadings and electro electric states and (2)
all of the intrinsic (intraoraganismall) biophysical, biochemical and
bioelectric micro environmental events occurring on, in, and
between individual cells and cells and extracellular substances.
HIERARCHY
Biological structures are hierarchically organized, with
structural and functional complexity increasing “upward” from the
ever – expanding family of subatomic particles to protons,
electrons, atoms, molecules, subcellular organelles and on cells,
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tissue, organs and organisms.
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EMERGENCE
It consist of the appearance, at each successively higher
and structurally and/or operationally more complex level, of new
attributes or properties, not present in the lower levels, whose
existence or functions could not in any way be predicated even
from a complete knowledge of all the attributes and properties of
any or all of the preceding lower organizational levels. This
phenomenon occurs in all natural hierarchies.
For example, full knowledge of all the attribute and
properties of an osteocyte does not permit prediction of the
attributes and properties of any type of bone tissue. And full
knowledge of all attributes and properties of all constituent bone
tissue types does not permit prediction of the form (size and
shape), growth or functions of a macroscopic “bone”.
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FUNCTIONAL MATRIX THEORY
Based on the “functional cranial component theory” of Van
der Kjaauw hi own experimental work and that of others combined
with clinical interpretations and experiences MELVIN L:MOSS in
1960 has formulated the functional matrix theory. This theory can
be described as follows.
It claims that origin, growth & maintenance of skeletal
tissues & organs are always secondary, compensatory and
mechanically obligatory responses to temporally & operationally
prior events and processes occurring in related non-skeletal
tissues, organs and functioning spaces (eg. Functional matrices
either periosteal or capsular.
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There is no direct genetic influence on the size, shape or position
of skeletal tissues only the initiation of ossification. All genetic
skeletogenetic activity is primarily upon the embryonic functional
matrices. In a softer view, neither the cartilage of the mandibular
condyle nor the nasal septum cartilage is a determent of jaw
growth. Instead he theorizes the growth of the face occurs as a
response to functional needs and is mediated by soft tissue in
which the jaws are embedded. In a conceptual view, the soft
tissues grow, and both and cartilage react.
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Moss stresses the dominance of nonosseous structures of
the craniofacial complex over the bony part. Moss claims that the
growth of the skeletal components, whether endochondral or
intramembranous in origin, is largely dependent on the growth of
the functional matrices. The growth of the functional matrix is
primary, that of a skeletal unit secondary. This hypothesis has
initiated many experimental and clinical investigations but also has
given rise to fruitful controversy (Johnston 1976).

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FUNCTIONAL CRANIAL ANALYSIS
Moss says, “the head is a composite structure, operationally
consisting of a number of relatively independent functions
olfactions, respiration, vision, digestion, speech, audition,
equilibration and neural integration.
Each function is carried out by a group of soft tissues which
are supported and/or protected by related skeletal elements. Soft
tissues and skeletal element related to a single function are
termed FUNCTIONAL CRANIAL COMPONENT.
Thus the
component handling speech would consist of the lips,
teeth,tongue,oral cavity, nasal cavity etc., any aspect of the head
that enables a person to speak is part of this functional
component.
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The totally of all the skeletal element associated with a single
function is termed SKELETAL UNIT. The totally of all the soft
tissues associated with single function is termed FUNCTIONAL
MATRIX origin, growth and maintenance of the skeletal unit
depend almost exclusively upon its related functional matrix.

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Micro and Macro skeletal units:
Skeletal units may be composed variably of bone, cartilage (or)
tendinous tissues. When such a bone consist of a number of
skeletal units, we call them micro skeletal units. Both maxilla and
mandible are formed of a number of such contiguous micro
skeletal units.
When adjoining portions of a number of neighboring bones
are united to function as a single cranial component, we term this
a macro-skeletal unit. eg: endocranial surface of the calvaria.
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THE FUNTIONAL MATRIX
One Function
Functional cranial component
Functional matrix

skeletal unit

Periosteal Matrix------affects--------------1.Microskeletal
Capsular Matrix--------affects----------2.Macroskeletal
.Masses
.Functioning Spaces
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Mandible is a macroskeletal unit. Capsular matrices act on the
macroskeletal unit that is whole mandible and they bring about
translation or passive growth. They do so by changing the volume
of the capsule within which the functional cranial components are
embedded. Moss speak of the mandible as a group of
microskeletal units. Thus the coronoid process is one skeletal unit
under the influence of temporalis muscle.
The alveolar bone is under the influence of teeth. Teeth are
also a functional matrix, indeed most orthodontic therapy is
based firmly on the fact that when this functional matrix
grows or is moved, the related skeletal unit ( the alveolar
bone) responds appropriately to this morphogenetically
primary demand.
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FUNCTIONAL CRANIAL COMPONENT
(eg: mandible)

Skeletal Unit

Microskeletal

Macroskeletal

Eg : coronoid eg : mandible

Functional Matrices

Capsular
Matrices

Periosteal
Matrices

eg : oral capsule eg : muscles
Act on macro
Act on Macro
Skeletal Unit.

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Skeletal Unit.

Bring about

Bring About

Passive Growth
or Translation

Active growth or
Transformation
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There are two basic types of functional matrices
.Periosteal matrix
. Capsular matrix
PERIOSTEAL MATRIX
This term relates the matrix to those tissues that influence the
bone directly through the periosteum.
Muscles are attached to the periosteum & consequently are
examples of this kind of matrix.

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Periosteal matrix affect a microskeletal unit meaning that the
spare of influence is usually limited to a part of muscles most of
its action on the coronoid process - a micro unit of the mandible.
Coronoid process first arises within the earlier from of anlage of
the temporalis muscle whose contractile abilities are well
developed in prenatal stages. It, subsequent growth also occurs
within this muscular matrix..

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The experimental removal of the temporalis muscle or
its denervation invariably result in the actual diminution of the
size and shape of the coronoid process or even its total
disappearance. Similarly established hyperactivity of the
temporalis muscle produces increase in the size and shape of
the coronoid process
Figure showing the dependence
of the coronoid process
(skeletal unit) upon the
demands of its functional
matrix (temporalis muscle) is
shown in these alterations in
size and shape following
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unilateral muscle
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The total growth change of the coronoid process are at all
times a direct compensatory response to morphogenetic
and functional demand as of the temporalis muscle
function. All responses of the osseous portion of the
skeletal units to periosteal matrices are brought about by
the complementary and interrelated process of osseous
deposition and resorption. The resultant effect of all such
skeletal unit responses to periosteal matrices is to alter
their size and / or their shape. A tooth is responsible for the
alveolar bone that supports it; Extraction of tooth causes
disappearance of microskeletal unit (alveolar process)
In addition to muscles, blood vessels, nerves and glands
also produce morphologic changes in their related skeletal
units in a completely homologous manner.
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CAPSULAR MATRIX
Included in this class of matrix are those
masses and spaces that are surrounded by capsules. All
the functional cranial components (functional matrices
together with the skeletal units) organize in the form of
cranial capsules.
.Neurocranial capsules
.Orofacial capsule

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Each of these capsules is an envelope which contains a
series of functional cranial components which are two covering
layer. In the neurocranial capsule, the covers consists of skin and
duramater.
Figure showing the neurocranial
and orofacial capsular matrices are
shown. The neural capsular matrix
consists of the entire neural mass,
including the dura matter, while
the orofacial capsular matrix
consists of these functioning
spaces. In both cases the skeletal
units exist completely within their
respective capsules.
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Orbital mass is surrounded by the supporting tissues of
the eye. Any enlarged eye or small eye will cause a
corresponding change in the size of orbital cavity. Here
eye is functional matrix.

In the orofacial capsule skin and mucosa form the
limiting layers. Spaces intervening between the functional
components themselves and between them and the
capsule are filled with indifferent loose connective
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tissues.
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Each capsule surrounds and protects capsular
functional matrix – in one case, the neural mass which
consists of brain plus leptomeninges and, most
important, cerebrospinal fluid; in the second case, the
oranoasopharyngeal functioning spaces. The common
factor in both cases is that the capsular matrices exist as
volumes.

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NEUROCRANIAL CAPSULE
In the case of neural skull, it is quite easy to visualize the
calvarial bones as lying within a neurocranial capsule.
The composition of this capsule in the adult is easily
stated; these are so called “five layers” of the scalp, then
the bone itself; and, finally, the two-layer duramatter.

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The calvarial bones consist of a number of contiguous
skeletal units; outer table, inner table, diploid space (and
variably sinuses). Each of these microskeletal units
obviously has its specific periosteal matrix, muscles and
vessels being good examples.

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It has been demonstrated repeatedly that it makes little
difference whether or not this neural mass contains a
“normal” amount of brain tissue. It is the total neural mass
volume which is morphogenetically significant. The
expansion of this enclosed and protected capsular matrix
volume is the primary event in the expansion of the
neurocranial capsule.
The response of the capsule as a whole, is to
expand in a compensatory manner. All of the included and
enclosed functional cranial components that the preinstall
matrices and their microskeletal units, are then obligatorily
carried outward within the capsule in a totally passive
manner.
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It is extremely important to note here that such translations
occur without the necessity of involving the processes of
selective periosteal apposition and resorption. Admittedly,
in “normal” growth it is difficult to determine this point by
superficial analysis, since the activity of periosteal matrices
on their respective micro skeletal units goes on
simultaneously.

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It is only when we examine these pathologic, or
experimentally produced, situations in which periosteal
matrices have been prevented from exerting their
morphogenetic activity that we can observe clearly the
passive, non periosteal, translative growth produced by the
capsular matrices.
The expansion of neurocranial cranial capsule is always
proportional to increase in neural mass. The neural skull
does not grow first and thus provide space for the
secondary expansion of the neural mass. Rather, the
expansion of the neural mass is the primary event which
causes the secondary and compensatory growth of the
neural skull.
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This phenomenon can be seen readily in humans in two
experiments of nature.
.when the brain is very small, the cranium is also very small
ad the condition of “MICROCEPHALY” result. In this case
the size of the head is an accurate representation of the
size of the brain.

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.HYDROCEPHALY: in this case reabsorption of the cerebro
spinal fluid is impeded, the fluid accumulates
and
intracranial pressure builds up, which impeded, the
development of the brain. So the hydrocephalic may have
small brain and enormous growth of the cranial vaultcranium two or three times its normal size with enlarged
frontal, parietal and occipital bones.

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OROFACIAL CAPSULE
As the calvarial bones are embedded in a
neurocranial capsule and are translated here by, so are the
oronasomaxillary bones embedded in the orofacial
(splanchno cranial) capsule.

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The primary expansion of functioning oronasopharyngeal
spaces on a morphogenetic stimulus brings about
secondary, compensatory expansion of the orofacial
capsule. The facial bones are passively carried outward by
primary expansion of the enclosed orofacial matrices
(orbital, Nasal and oral matrices). In addition essential
growth of the sinuses and spaces perform important
functions.

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Where the role of functional matrix becomes most difficult
to visualize is, in development of the face. According to moss, the
nasal cartilage and the condyles of the mandible are growth sites
and therefore incapable of tissue separating force. As a
consequence, the translation of the middle and the lower face
downward and forward must be accomplished by the oral-nasalpharyngeal capsules. The soft tissues of these capsules are of
necessity the determinant of their size and position in space.
The skeletal units only respond, offering continually adapting
biomechanical support. The factor that dictates the size of the
facial capsules is the volume of the functioning spaces. The
patency and adequacy of oronasal tubes are so fundamental that
nature programs their size and guarantees that the increased
demands of somatic growth are met by craniofacial expansion.
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Moss contends, then, that all the loci of new bone formation
(sutures, periosteum, spheno-occipital synchondrois,
nasal
cartilages and condyles) are growth sites and not growth centers.
None of these sites contain genetic information that can determine
their ultimate form; all of them are at the disposal of the functional
matrices related to them.

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MANDIBULAR GROWTH
Mandibular
growth
demonstrates
the
integrated activity of periosteal and capsular matrices in
facial growth. Since the condylar cartilages are not primary
sites of mandibular growth but loci with secondary,
compensatory periosteal growth. Bilateral condylar
cartilage removal does not inhibit the spatial translation of
contiguous mandibular functional components. Nor does
the condylectomy inhibit the changes in the form of their
microskeletal units as their microskeletal units as their
individual matrices alter function demands.
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If there are no condylar processes how does the mandible
alter its spatial position? No combination of periosteal
growth changes of microskeletal unit form is capable of
explaining this. It is only by considering that the orofacial
capsule expands in response to the morphogenetically
previous volumetric expansion of the orofacial functioning
spaces that we can comprehend the observed translation
in space.

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Mandibular growth is seen now to be a combination of the
morphologic effects of both the capsular and periosteal
matrices. The capsular growth causes an expansion of the
capsule as a whole. The enclosed and embedded
macroskeletal unit (the mandible) is
passively and
secondarily translated in space to successively new
position.
Under normal conditions then the periosteal matrices
related to the constituent mandibular micro skeletal unit
also respond to this volumetric expansion. Such alteration
in spatial position inevitably causes them to grow. This calls
for direct alteration in the size and
shape of the
microskeletal unit.
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Moss (1973) termed this change in size and in
shape during growth as TRANSFORMATION and the
change in spatial position as Translation. the sum of
translation plus transformation comprise the totality of
mandibular growth.
Only a small percentage of the bone growth in the
facial skeleton is due to pure transformation or pure
translation. A combination of both types of growth is usually
involved, although translation almost always result in bone
transformation.
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REGULATION & CONTROL OF FUNCTIONAL MATRICES
Functional matrices are controlled by neurotrophic
processes.
NEUROTROPHISM
It is a “non-impulse transmittive neuro function,
involving axoplasmic transport, providing, for the long term
interaction between neurons and innervated tissues which
homeostatically regulates the morphological, composition
and functional integrity of those tissues. The nature of the
neurotrophic substances and the process of their
introduction are unknown at present. Moss does indicates
that there are three general categories.
.Neuro-epithelial

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.Neuro-visceral

.Neuro-muscular

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NEURO-EPITHELIAL TROPHISM
It is a quality rather than type of reinnervating axons that
determines whether regeneration will occur. As example
amphibian limb regeneration is initiated only after intimate
neuroepithelial contact. The mitotic activity necessary for normal
epithelial turnover of taste buds the maintenance is being, 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.

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Neuro visceral trophism
Periosteal functional matrices regulate the size and shape
of specifically related skeletal unit. It is apparent that genetic
control of structural functional and chemical attribute of these
same matrices can not reside in the matrices them selves, but
rather reflect constant neurotrophically regulated homeostatic
control of genome. It is also clear that similar trophic control
probably exits for capsular matrices which passively regulate
position of both skeletal unit and periosteal matrices. Some
degree of visceral neurotrophic control is probable. Eg: salivary
glands among other spalanchnocranial viscera are trophically
regulated atleast partially.
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Neuro muscular trophism
Moss indicated that skeletal muscle ontogenesis normally requires
motor neuron innervation to proceed past the stage of myotubes.
Nerve influences give expression in the cell. A qualitatively
different myosin that resemble that of muscle formerly innervated
by the nerve is synthesized in cross innervated muscle, which
indicates species of protein it has been synthesized. Experiments
show that significant morphologic, biochemical and functional
parameters of reinnervated muscle, come to more closely
resemble those of the muscle formerly innervated by the new
ectopically implanted nerve.
DISCULESCU et al state, “The complex chain of events leading
to particular expression of the genetic embryonic potential is not
wholly within the cell but also includes informational elements
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contributed by the nerve”.
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SAMAHA et al writes, “A new species of protein has been
synthesized and we there fore suggest that the nerve influence
gene expression of the cell”.
Moss feels the periosteal matrices reflect constant
neurotrophically regulated homeostatic control of the genome.
Similar trophic control probably exits for capsular functional
matrices, which passively regulates the position of both the
skeletal units and the periosteal matrices.
If some degree of visceral neurotrophic control is probable
then we are close to knowing their ultimate stimulus for growth.
Assuming such role of neurotrophism (neural nourishment)
dictates that at no time any of the nerves is subject to torsion,
compression, tension and shear. Hence with respect to inferior
alveolar nerve with Foramen ovale into the mandibular canal out
of mental foramen, its integrity is never threatened by growth or
functioning of the lower jaw.
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GENETICS, EPIGENETICS AND CAUSATION
It can be shown that the combination of genomic and
epigenetic factor is a necessary cause of craniofacial growth. A
review of some recent literature serves to clarify this conclusion
which is of potential clinical use therapeutic intervention is always
an epigenetic event.
Clinical scientists suggest that “the post fertilization
genome does not contain sufficient information to regulate all
subsequent development. It is postulated that the additional
necessary epigenetic information is self – generated concomitant
with the attainment of increasing structural and functional
complexity”. In this view the interaction of both genomic and
epigenetic factors is required to regulate (or “cause”)
development. The genome is not viewed as containing some prewww.indiandentalacademy.co
existent blueprint that merely requires an appropriate environment
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within which it can become phenotypically expressed.
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As unconformable as the epigenetic hypothesis may seem
to commonly accepted clinical views, Moss suggest that many of
the difficulties are diminished after analysis of the term causation
and after a review of some pertinent data and concept.

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CAUSATION
There are four principal causes of ontogenesis.
.Material (what is acted upon?)
.Formal (by what set of rules?)
.Efficient (how?)
.Final (why?)
These may be categorized as either intrinsic (material & formal)
and extrinsic (efficient): final cause i.e. exiting before the creation
of some specific state or structure. Efficient cause is proximate:
i.e., its operation immediately causes the creation of a new state
or attribute. Material and formal causes are intrinsic. Because they
reside within vital structure (either intracellularly or intercellularly).
(efficient causes are extrinsic – they represent the entire spectrum
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of epigenetic processes, mechanisms and events capable of
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being imposed on vital structures.

In biology material, without reference to any specific
structural (anatomical) arrangement. Formal cause is the genomic
code. They act at the molecular level to regulate the initial creation
of the constituents of material cause. Efficient causes are the
epigenetic factors, whose actions immediately regulate the next
development branching point.
In ontogenesis, genomic (intrinsic, and epigenetic
(extrinsic, proximate) factors are each a necessary cause, but
neither alone is a sufficient cause. Only the interaction of both
provides both the necessary and sufficient cause of
morphogenesis.

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Epigenetics involves the production of new information
during development as structure and function became
increasingly complex. Both structure and function evolve
alterations in the biomechanical, biochemical, biophysical and bioelectrical parameters of the developing organism both intra and
intercellularly. These alteration of state(new information) act
significantly to regulate subsequent development stages, as well
as to result genomic reaction to these –altered environmental
states. In the hypothesis “environment” is not just permissive and
supportive but also regulative.

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EPIGENETIC EVENTS AND PROCESSES
1. The functional matrix hypothesis has demonstrated
repeatedly that the presence, and growth changes in size,
shape and location of all craniofacial skeletal attribute are
epigenetically regulated. In summary from, the functional
matrix hypothesis explicitly claims that the origin, growth
and maintenance of all skeletal tissues are always
secondary, compensatory and obligatory responses to
temporally and operationally prior events or processes that
occur in specifically related non-skeletal tissues, organs or
functioning spaces (functional matrices). In this view,
development could be described as a hierarchical series of
proximate, efficient, extrinsic and necessary causes.
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2. Hierarchical arrays is a description of the way, increasing
structural complexity arises in a developing organism. Any
arbitrary developmental state of an organism may described by
certain attributes. The next higher, more complex state not only
incorporates all of the attributes of the several lower states but
creates newer complexity. Despite an apparently continuous and
uninterpreted developmental process, deeper consideration
reveals marked discontinuities between hierarchical levels. Thus
the phenotype is not merely a surface manifestation of the
genotype which later suffices to regulate development. Rather the
phenotype is the result of a hierarchy of self-regulatory processor
that integrates epigenetic genomic factors into an orderly
sequence of increasingly structured ontogenetic changes.
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3. Position or location of a cell within a developing
organism is significant source of epigenetic information. Here
instructive interactions between cells and the length of time a cell
or cell mass occupies a specific location are among the factors
held capable of locally providing epigenetic information and
regulating genomic expression of cells in the immediate
neighborhood.
4. Neurotrophic regulation of the muscle cell genome is
another type of epigenetic information. Recently in studies of
skeletal muscle fiber, following motor denervation, marked
changes in many of the RNA sequences present in the muscle cell
were noted. These data give strong support to the hypothesis that
the motoneurons are able to control gene-expression of muscle
fibers.
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Development of Functional Matrix Hypothesis
Periodic incorporation of advances in the biomedical,
bioengineering and computer science allow the creation of
increasingly more comprehensive revisions of the
functional matrix theory. Recent work on two topics.

1. Cellular transduction of informational signals.
2. Biologic cellular network theory.
Permit the presentation of this latest revision.
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The conceptual and anatomic basis of revised
functional matrix hypothesis (FMH)
More precisely the FMH claims that epigenetic,
extraskeletal factors and processes are the prior,
proximate, extrinsic and primary cause of all adaptive,
secondary responses of skeletal tissues and organs. It
follows that the responses of the skeletal unit (bone and
cartilage) cells and tissues are not directly regulated by
informational content of the intrinsic skeletal cell genome
per se. Rather, this additional, extrinsic epigenetic
information is created by functional matrix operations.
This new version deals only with the responses to
periosteal matrices and includes the molecular and cellular
processes underlying the triad of active skeletal growth
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processes deposition resorption and maintenance.
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CONSTRAINTS OF THE FMH
Initially FMH provided only qualitative narrative
descriptions of the biologic dynamics of cephalic growth at
the gross anatomic level. It had two explanatory
constraints;
1.
Methodologic
constraint:
Macroscopic
measurements which are the techniques of point
mechanics and arbitrary reference frames e.g.
roentgenographic cephalometry permitted only method
specific descriptions that cannot be structurally detailed.
This constraint was removed by the continuum mechanic
techniques of the finite element method (FEM) and of the
related macro and boundary element methods.
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2. Hierarchical constraint; Even that versions descriptions
did not extend “downward” to processes at the cellular,
subcellular or molecular structural domains or extend
“upwards” to the multicellular process by which bone
tissues respond to lower level signals. All prior FMH version
were “suspended” or “sandwiched” between these two
hierarchical levels.
FMH could not describe how extrinsic, epigenetic,
functional matrix stimuli are transduced into regulatory
signals by individual bone cells.
How individual cells communicate to produce coordinated
multi-cellular responses.

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Experimental and theoretical studies of bone
adaptation consider only the unicellular, unimolecular or
unigenomic levels and their results generally are not
extensible to higher multicellular tissue levels.
Significant
disjunctions
exist
between
the
descriptions at each of the several levels of bone
organization. In hierarchical theory the attributes of
successively higher levels are not simply the sum of all
lower attributes e.g. sum of all lower attributes of a bone
cell cannot predict the higher attributes of a bone tissue.
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This newest FMH version presented herein transcends
some hierarchical constraints and permits seamless
descriptions at and between the several levels of bone
structures and operation from the genomic to the organ
level by the inclusions of two complementary concepts.
1.
2.

Mechanotransduction occurs in single bone cells.
Bone cells are computational elements that function
multicellularly as a connected cellular network.

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MECHANO TRANSDUCTON
All vital cells are irritable and respond to alterations
in their external environment. Mechanosensing processes enable
a cell to sense and to respond to extrinsic loadings by using the
processes of
1.
Mechanoreception
2.
Mechanotransduction
Mechanoreception process: It transmits an extracellular
physical stimulus into a receptor cell.
MechanoTransduction process : It transduces or transform
the stimulus’s energetic and/or informational content into an
intracellular signal.
Eg. Mechanoelectrical, mechanoechemical.
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Osseous MechanoTransduction
When an appropriate stimulus parameter exceeds
threshold values, the loaded tissue responds by the triad of bone
cell adaptation processes like deposition, resorption and
maintenance. Both osteocytes and osteoblasts are competent for
intracellular stimulus reception and transduction and for
subsequent intercellular signal transmission. Osteoblasts directly
regulate bone deposition and maintenance and indirectly regulate
osteoclastic resorption.

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This osseous mechano transduction is unique in four ways
1. Most other mechano sensory cells are cytologically
specialized but bone cells are not.
2. One bone loading stimulus can evoke three adaptational
responses whereas non-osseous processes generally
evoke one.
3. Osseous signal transmission is aneural but all other use
some afferent neural pathways.
4. The evoked bone adaptational responses are confined
within each “bone organ” independently so there is no
necessary “interbone” or organismal involvement.
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Osseous mechanotransduction translates the information content
of a periosteal functional matrix stimulus into a skeletal cell signal,
for eg. it moves information hierarchically downward to the
osteocytes. There are two skeletal cellular mechano transduction
processes.

1. Ionic

2. Mechanical

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IONIC OR ELECTRICAL PROCESSES
This involves some processes of ionic transport through the
bone cell (osteocytic) plasma membrane.
Subsequent intercellular transmission of the created ionic
or electrical signals which are computed by the operation of an
osseous connected cellular network (CCN).
The network’s output regulates the multicellular bone cell
responses. Osteocytic, ionic MechanoTransduction may involve
several possibly parallel cellular processes.
Stretch Activated channel
Plasma membrane stretch activated ion channels, a structure
found in bone cells, which activated in strained osteocytes permit
passage of certain sized ions or set of ions including K+, ca++,
Na+, and Cs+. This ionic flow initiates intracellular electrical
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events such as modulating membrane potentials as well as Ca++
ion flux.
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Electrical Processes
It includes.
1. Electromechanical - involving the osteocytic plasma
membrane, contains voltage activated ion channels and
transmembrane ion flow. Such ionic flows generate
osteocytic action potentials capable of transmission
through gap junctions.
2. Electrokinetic
Bound and unbound electrical charges, many associated
with the bone fluids in the several osseous spaces or
compartments. Electrical effects fluid filled bone are electrokinetic
i.e. streaming potential (SP). SP is a measure of the strain
generated potential (SPG) of convected electric charges in the
fluid flow of deformed bone. SPG of +-2millivolts can initiate both
osteogenesis and osteocytic action potentials.
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Electric Field Strength
Bone responds to exogenous electrical fields in an effective
range of 1 to 10 micro volts per/cm strength that are on the order
of those endogenously produced in bone tissue during normal
(muscle) activity.
MECHANICAL PROCESS
Mechanical properties of the extracellular matrix influence
cell behaviour. Loaded mineralized bone matrix tissue is deformed
or strained. A series of extracellular macromolecular mechanical
levers exits capable of transmitting information from the stained
matrix to the bone cell nuclear membrane.
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The
basis
of
this
mechanism is the physical
continuity of the transmembrane
molecule integrin. This molecule
is connected extracellular with the
macromolecular collagen of the
orgain matrix and intracellularly
with the cytoskeletal actin. The
actin’s molecules in turn are
connected
to
the
nuclear
membrane at which site the
action of the mechanical lever
chain initiates a subsequent
series of intra nuclear processes
regulatory of genomic activity.
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Such a cytoskeletal lever chain connecting to the nuclear
membrane can provide a physical stimulus able to activate the
osteocytic genome. It is by such an interconnected physical chain
of molecular levers the periosteal functional matrix activity may
regulate the genomic activity of its strained skeletal unit bone cell
including their phenotypic expression.

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THE ROLE OF BONE AN OSSEOUS
CONNECTED
CELLULAR
NETWORK
(CCN).
All bone cells, expect osteoclasts are
extensively interconnected by gap junctions
that form an osseous CCN. Gap junction are
found where the plasma membranes of a
pair of markedly overlapping canalicular
processes meet. Gap junctions also connect
superficial to periosteal and endosteal
osteoblast. All osteoblasts are similarly
interconnected laterally. Vertically gap
junctions connect periosteal osteoblasts with
preosteoblastic cells and these in turn are
similarly interconnected. Each CCN is a free
synctium m a very real sense bone “hard
in
wired”.

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Gap junctions permit intercellular transmission of ion and small
molecules and electrical and fluorescent dye transmission. Gap
junctions are electrical synapses- they permit bi-directional 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. A CCN is operationally
analogous to an “artificial neural network” in which massively
parallel or parallel– distributed signal processing occurs. It
computationally processes in a multi–processor network mode,
the intercellular signal created by an electrical type of
mechanotransduction of periosteal functional matrix stimulus.
Subsequently, the computed network output informational signals
move hierarchically “upward” to regulate the skeletal unit
adaptational responses of the osteoblasts.
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In network theory these cells are organized into “Layers”
an initial input, a final output, and one or more intermediate or
hidden layers. Regardless of the actual physiological stipulatory
process, each cell in any layer may simultaneously receive
several “weighted’ inputs (stimuli).
In the initial layer these represent the loadings within each
cell independently 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 mechanotransduction occurs. This
signal is then transmitted identically to all the “hidden” layer cells
(adjacent osteocytes) to each initial layer cell is connected by gap
junctions.
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Next similar processes of weighted signal summation,
comparison and transmission occur in these intermediate layers
until the final layer (osteoblasts) cells are reached. The output of
these anatomically superficial cells determines the site, rate,
direction, magnitude and duration of the specific adaptive
response i.e. deposition, resorption and/or maintenance of each
cohort of osteoblasts.
Information is not stored discretely in a CCN, rather it is
distributed across all or part of the network and several types of
information may be stored simultaneously. The instantaneous
state of CCN is a property of the state of all its cells and of all their
connections. Accordingly, the informational representational of
CCN is assuring that the network is fault or error tolerant i.e. one
or several inoperative cells causes little or no noticeable loss in
network operations” matter of useful clinical significance.
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The CCNs show oscillation, i.e. iterative reciprocal
signaling (feedback) between layers. This attribute enables them
to adjustively self-organize, this behavior is related to the fact that
biologic CCNs are not preprogrammed; rather they learn by
unsupervised or epigenetic “training” a process probably involving
structural or conformational changes in the cytoskeleton. The
structurally more complex network attributes and behavior of a
CCN gradually or epigenetically self-organize and emerge during
operation. Gap junctions permitting bi-directional flow of
information are the cytological basis for the oscillatory behavior of
CCN. A skeletal CCN displays the following attributes:

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1. Developmentally, it is an untrained self-organized, selfadopting and epigenetically regulated system.
2. Operationally, it is a stable, dynamic system exhibits
oscillatory behavior permitting feedback.
3. Structurally, an osseous CCN is non-modular i.e.,
variation in its organization permit discrete processing of different
signals.

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THE ROLE OF PERIOSTEAL FUNCTIONAL MATRICES:- NEW
INSIGHT
The Morphogenetic primary of periosteal functional
matrices on their skeletal unit is consensually accepted. As a
muscular demand alters, e.g., myectomy, myotomy, neurectomy,
exercise, hypertrophy, hyperplasia, atrophy, augmentation, or
repositioning, the triad of active bone growth processes
correspondingly adapts the form of its specifically related skeletal
unit.
Presently excluding the stimulation of neural afferents in
muscle, tendon, and periosteum, extrinsic physical loading tend to
deform bone tissue and to invoke skeletal unit (bone) adaptation
responsive processes. 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
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intertwined periosteal fibers inserted into subjacent bone, deforms
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the loaded skeletal unit.

Although some periosteal osteoblasts may be directly stimulated,
extant data suggest osteocytic primary in mechano sensory
processes. Their three dimensional array of extensive canalicular
cell processes is architecturally well suited to sense deformation
of the mineralized matrix.
Strain plays a primary role in all bone adaptational or
remodeling responses and is a competent stimulus. Skeletal
muscle contraction is typical periosteal functional matrix loading
event and frequency is one of its critical parameters. Of particular
significance to the FMH is the close similarity of muscle stimulus
frequencies to bone tissue response frequencies.

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MECHANO TRANSDUCTION: A TENTATIVE SYNTHESIS
Ability of periosteal functional matrices to regulate the
adaptive response of their skeletal units by ionic
mechanotransduction processes is related to several factors.
These are.
1.
Normal muscle function strains attached bone tissue
intermittently.
2.
The dynamics of skeletal muscle contraction fit rather
nicely with the energetic requirements for bone responsiveness.
3.
The range of specific strain frequency harmonics of muscle
dynamics are also those found to be morphogenetically
competent (i.e. osteo-regulatory).
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4.
Normal skeletal muscle activity produces intra osseous
electric fields on the order of extrinsic fields to be similarly
morphogenetic.
5.
Bone cells may be stimulated by two mechanism – directly
by strain activated plasma membrane channels and indirectly by
electro kinetic phenomena.
These factors strongly suggest that bone appears to be closely
tuned to skeletal muscle i.e., skeletal units are tuned to their
periosteal functional matrices.

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When both the ionic membrane and the mechanical (molecular
lever) transductive processes are conceptually and operationally
combined with the data of both electric field effects and of
contraction frequency energetics, they provide a logically sufficient
biophysical basis of support for the hypothesis of epigenetic
regulation of skeletal tissue adaptation. These two processes
share a common final pathway, i.e. they eventually produce
signals regulatory of osteoblastic activity.

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THE GENOMIC THESIS
The initial version of the FMH claiming epigenetic control of
morphogenesis was based on macroscopic (gross) experimental,
comparative and clinical data. Recently revised it now extends
hierarchically from gross to microscopic (cellular and molecular)
levels and identifies some epigenetic mechanisms capable of
regulating genomic expression.
The epigenetic or genomic problem is a dichotomy and
dialectics is one analytical method for its resolution. The method
consist of the presentation of two views, a thesis and an antithesis and of a resolving synthesis.
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The genomic thesis holds that the genome, from the moment of
fertilization, contains all the information necessary to regulate
(cause, control, direct).
1.
The intra nuclear formation and transcription of mRNA and
2.
Importantly, without the later addition of any other
information, to regulate also all of the intracellular and intercellular
processes of subsequent and structurally more complex cell,
tissue, organ and organismal morphogenesis: Succinctly “all
(Phenotype) features are ultimately determined by the DNA:
sequence of the genome.
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In this thesis, morphogenesis is the predetermined readingout of an intrinsic and inherited genomic organismal blue
print where, in addition to molecular synthesis, the genome
also regulates the geometric attributes of cell, tissue, organ
and organismal size, shape and location.
The
genomic
thesis
originated
with
classical
(Chromosomal) Mendelian genetics. Recently molecular
(gene) genetics extended the claims of the thesis to
regulation of all aspects of Ontogeny (i.e. growth and
development).

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The Genomic thesis in orofacial biology

Genomic thesis claims that prenatal cranio facial
development is controlled by two inter related, temporarily
sequential processes:
1.
Initial regulatory (Homeobox) gene activity.
2.
Subsequent activity of two regulatory molecular groups:
growth factor families and steroid/thyroid/retinoic acid super
family.

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For example “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”.
It is claimed that regulatory molecules can (1) alter
the manner in which homeobox genes coordinate cell
migration and subsequent cell interactions that regulate
growth (2) be involved in the “genetic variations causing, or
contributing to the abnormal development of relatively
common cranio facial malformations… perhaps modifying
box gene activity”.
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Specific orthodontic implications of the genomic thesis
includes claims that “poorly coordination- ordinated control
of form and size of structures or group of structures (e.g.
teeth, 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 atleast some complex
structures” including “How characteristic noses or jaws are
inherited from generation to generation”. In the genomic
thesis morphogenesis is reduced to molecular synthesis. It
proposes no pathways from molecules to morphogenesis.
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EPIGENETIC ANTITHESIS AND THE RESOLVING SYNTHESIS
DEFINITIONS
PROCESS: It is a series of actions or operations that lead toward
a particular result.
MECHANISM : It is the fundamental physical or chemical process
involved in, or responsible for an action, reaction or other natural
phenomenon.
Mechanism underlie processes specific steps of the
activation and deactivation of appropriate portions of the bone cell
genome, associated with the triad of possible osteoblastic
responses to loading (deposition, resorption or maintenance of
bone tissue) are epigenetic mechanisms that control the genome.
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EPIGENETIC ANTITHESIS
The genomic thesis is denied because it is both
reductionist and molecular; that is descriptions of the causation
(control, regulation) of all hierarchically higher and structurally
more complex morphogenetic processes are reduced to
explanations of mechanisms at the molecular (DNA) level.
For example the genomic thesis of craniofacial ontogenesis
passes directly from molecules to morphogenesis: directly from
DNA molecules to adult morphology, ignoring the roles of the
many epigenetic processes and mechanism competent to control
(regulate, cause) the large number of intervening and increasingly
more structurally complex, developmental stages particularly, and
there are additional similarly reductionist views of odontogenesis.
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The epigenetic antithesis detailing both processes and
mechanisms seeking to clarify the casual chain between genome
& phenotype. Its goal is to identify and describe comprehensively
the series of initiating biological processes and their related
underlying (biochemical, biophysical) responsive mechanisms that
are effective at each hierarchical level of increasing structural and
operational complexity.

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CRANIOFACIAL EPIGENETICS
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” by
definition. This views is supported here, despite continued
expressions of genomic regulation of craniofacial morphogenesis.
Epigenetic factors include
1.
All of the extrinsic extra organismal macro environmental
factors impinging on vital structures including mechanical loadings
and electromagnetic fields.
E.g. food, light, temperature
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2.
All of the intrinsic, intra organismal, biophysical,
biomechanical, biochemical and bioelectric micro environmental
events occurring on, in & between individual cells, extracellular
materials and cells and extracellular substances.
In terms of clinical of orthodontics, and of the FMH all
therapy is applied epigenetics, and all appliances act as prosthetic
functional matrices. Clinical therapeutics includes a number of
epigenetic processes whose prior operations evoke a number of
corresponding epigenetic mechanism. These in turn, underlie the
observed processes of tissue adaptation by both skeletal unit and
functional matrices.

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EPIGENETIC PROCESSES AND MECHANISM
LOADING: - Among the numerous epigenetic factors
influence the vertebrate face is mechanical loading. It is
useful to consider epigenetic process of loading and some
of the epigenetic mechanisms this process evokes is as
follows.
Loading per se
While clinical observations usually are macroscopic, the
loading, act microscopically, at molecular, and or cellular levels.
Loadings are able to regulate several alternative molecular
synthetic pathways of many tissues including bone. Mechanical
loading is known to influence gene expression. Of FMH interest,
extrinsic muscle skeletal loading can rapidly change 1) both
articular cartilage intercellular molecular syntheses and
mineralization. 2) Osteoblastic (skeletal unit) gene expression.
Epigenetic loading process include gravitational variations that
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evoke unique mechanism of molecular synthesis.
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EXTRA CELLULAR MATRIX (ECM) DEFORMATION
Musculoskeletal tissue loading inevitably deforms an extra
cellular matrix (ECM) that is not developmentally inert. In several
ways ECM regulates the formation, development and
maintenance of all its included cells that synthesize the ECM.
ECM can regulate multicellular tissue
morphogenesis and
contribute to genomic regulation of its enclosed cells.
Cell – shape changes: - tissue loading can alter the cell shape
and deforms intracellular constituents including cytoskeleton. The
epigenetic process of changing cell shape invokes the epigenetic
mechanisms of mechanotransduction of biophysical forces into
genomic and morphogenetically regulatory signals.
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Cells shape change process can also activate other
epigenetic mechanisms, for eg stretch – activated ion channels in
cartilage and other mechanically initiated cell signaling
mechanisms. Cell shape change may lead to nuclear shape
deformation which is a mechanism that can directly cause a
consequent alteration of the mechanisms of genomic activity.
Epigenetic cell signaling processes: - Can regulate
genomic expression.

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Chains of intracellular molecular levers
A second epigenetic cellular process begins with
deformation of ECM. This matrix has an epigenetic regulatory
role in morphogenesis, by virtue of integrin molecules that
physically interconnect the several molecular components of the
intra cellular and the extra cellular environment.
The epigenetic mechanism evoked consists of a physical
array of intracellular macromolecular chains, acting as levers,
extending from the cell membrane to multiple specific sites on
each chromosome. The molecular chain acts as an information
transfer system between the extra cellular environment and the
genome, transmitting signals generated by deformations of the
ECM directly to the intra nuclear genome. Such informational
transfer between cells and ECM is dynamic, reciprocal and
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continuous.
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EPIGENETIC
LEVELS

REGULATION

OF

HIGHER

STRUCTURAL

At the tissue level, there are several causal, strain specific
differences in bone tissue microstructure. Closely similar
epigenetic mechanisms and processes are observed in the
adaptational responses of all connective tissue, including
cartilage, to loading.
At the organ level, the ability of the processes of motion
and of articular function to regulate joint morphology and physical
activity processes regulate organismal skeletal adaptational
responses. Other epigenetic processes affecting bone tissue
include local vascular factors.
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REGULATION OF FUNCTIONAL MATRICES
Mechanical loads regulate skeletal muscle (periosteal
functional matrix) phenotype: and chronic muscle stimulation can
change its phenotype. For muscle as for bone, mechanical
epigenetic factors termed function (or exercise) significantly
control musculoskeletal development and maintenance of
structural and physiological attributes.

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A RESOLVING SYNTHESIS
The fundamental argument of this resolving synthesis
based on an analysis of causation argues that morphogenesis is
regulated (controlled, caused) by the activity of both genomic and
epigenetic processes and mechanisms. Both are necessary
causes; neither alone are sufficient cause; and only their
integrated activities provides the necessary and sufficient causes
of growth and development. Genomic factors are considered as
intrinsic and prior causes; epigenetic factors are considered as
extrinsic and proximate causes.
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COMPLEXITY AND SELF ORGANIZATION

Epigenetic processes and mechanisms are best
explained as examples of Complexity theory (CT). CT
provides description of the behaviour of complex
biological systems that exist as “ensembles” of several
tissues and organs and not as clusters of individual cells
and extracellular substances.
Such an ensemble
(identical to a functional cranial component in the FMH) is
termed here as a complex adaptive system (CAS). CT
provides compact statistical descriptions of the collective
growth behavior of such CAS continuity.
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An algorithm for control of such a CAS requires that it is
able to alter itself in response to the epigenetic information
produced by the system it is trying to control. In a CAS, minor
changes in the epigenetic input can cause huge fluctuations in the
morphological output.
CT, as it utilized information theory, assumed that
CAS processes information both genomic and epigenetic in
a parallel, not a serial, manner, where most previous
biological theories of development were based on the
deterministic
(genomically
predetermined)
classical
mechanics, information theory and CT are probabilistic
(epigenetically self organized and emergent) and are based
on m methods of statistical mechanics.
the
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The highly ordered morphological properties of adult
complex biological system (e.g.; functional matrices and skeletal
units) result from the operation of a series of spontaneous and
self-organizing events can create phenotypic variability under
constant genetic and other extra organismal epigenetic conditions.
The operation of complexity can be suggested as
follows: “ Environmental factors thus play a decisive role in
all ontogenetic process. But it is the organism itself that, as
an integrated system, dictates the nature of each and every
developmental response.
The living organism selforganizes on the basis of its own internal structuring, in
continuous interaction with the environment in which it finds
itself”.
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CURRENT CLINICAL
FUNCTIONAL MATRIX

APPLICATIONS

OF

THE

Orthodontic therapy involves a change in
1.

Periosteal matrix(Teeth)

Skeletal Unit (Alveolar
bone)

And/or
2. Capsular matrix
(Orofacial Orthopedics)

Several Skeletal Units (The Jaws)

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Forces exerted on teeth or jaws do influence their
functional matrices; and there are skill other matrices that
determine the stability of the corrected malocclusions.
To modify one functional matrix at the expense of another
invites trouble. Relapse or perpetual retention is often the choice
following orthodontic therapy.

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The following is a list of current clinical practices that reflect
some aspect of functional matrix modification.
1. Frankels appliance:The larger part of the Frankels appliance is confined to the oral
vestibule. The buccal shields and lip pads hold the buccal and
labial musculature away from the teeth and investing tissues,
eliminating any possible restrictive influence from the functional
matrix.

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Frankels conceives his vestibular constructions as
an artificial “ought-to-be” matrix that allows the muscles to
exercise and adapt. It the buccinator - mechanism pressures are
screened from the dentition significant expansion may occur in the
intecanine dimension. This relieves the crowding often seen in the
lower anterior segment which often leads to the removal of four
first premolars in a fixed multi attachment mechanotherapy.
The Frankel Regulator buccal shields prevent the pressure
of the buccinator being exerted on the dento alveolar area both
during deglutition and at rest. The net effect is outward expansion
to the “ought-to-be” acrylic shield functional matrix.

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2.
Enucleated orbit: The replacement of eyes with
prostheses that are periodically replaced by larger versions
promotes growth of the orbit.
3.
Widening mid palatal sutures a form or orofacial
orthopedics.
4.
Repositioning of the maxillary segments of cleft
patients—involve the change in macro units.

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5.
Bilateral condylectomy—when anklosis of the
condyles occurs in the growing child, condylectomy
removes the restrains and allows the maximum
development of the mandible in space.
6. Oblique bite plane – intra oral devices that hold the
mandible in a protruded position for the purpose of
stimulating condylar growth.
7.
Monobloc functional therapy: Intra oral appliance
used in conjunction with bone grafting to stimulate
mandibular bone remodeling following subtotal mandibular
resection.
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Conclusion:
Using a popular phrase genomic and epigenetic processes
are “apples and pears”. More correctly they are the examples of
totally different types of causation-genomic formal cause and
epigenetic efficient cause. Individually both are necessary causes
but neither are sufficient causes alone. Together they provide both
necessary and sufficient causes for the control (regulation) of
morphogenesis.

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Thank you
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