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Transcript of Growth and Development/ orthodontic courses by Indian dental academy
GROWTH AND DEVELOPMENT – A Bird’s Eye View
This shall be divided into three parts for the sake of convenient:
a) Growth and development in general.
b) Factors affecting growth and development.
c) Theories of growth and development.
In the first part, titled
Growth and development in general, we shall look at the following aspects:
i) What is growth? What is development?
ii) Why do we need to study about growth development.
iii) Normal features of growth and development.
a. Differentiatial growth.
b. Pattern.
c. Variability.
d. Timing, rate and direction.
e. Normality.
iv) Mechanisms of growth in:
- Soft tissues.
- Hard tissues.
v) Evolution of the human head form.
vi) Measurement and prediction of growth.
vii) Clinical implications.
1
What is growth? What is development? Though closely related growth and
development are not one and the same.
Definition of growth Growth :
- Growth usually refers to an increase in size – Profile (Todd).
- Growth may be defined as the normal change in amount of living
substance – Moyers.
Definition of development Development :
- Development connotes a maturational process involving progressive
differentiation at the cellular and tissue levels – Enlow.
- Development refers to all naturally occurring progressive, sequential and
unidirectional changes in the life of an individual from its existence as a
single cel to its elaboration as a multifunctional unit terminating in death –
Moyers.
- Development is a progress towards maturity (Todd).
- Morphogenesis : A biologic process having an underlying control at the
cellular and tissue levels – Enlow.
- As can be understood from the above definitions, growth and development
are complementary to each other.
- One can also draw certain correlations between growth and development.
2
Co-relation between growth and development:
- Growth emphasizes the normal dimensional changes during development.
- Because growth is mainly anatomic; also quantitative.
Development growth + differentiation + translocation.
- Development is mainly physiologic and qualitative.
- Development implies an increased specialization wit a decrease in
function. Thus, it is the combination of growth and morphogenesis Self
Multiplication.
+ Differentiation.
+ Organization.
Individual phenotype.
Why do we need to study growth and development?
To have an understanding of the following:
a) Normal growth and how it occurs.
b) Patterns of abnormal growth and the reason(s).
c) To distinguish between normal and abnormal.
d) Utilize growth (“working with growth”) to our benefit.
3
Normal Features of Growth and Development :
a) Differential growth – different tissues and in turn different organs grow at
different rates. This process is called differential growth. As depicted in
figure 1, in a normal individual, the neural tissues grow early in life
completing their maturation first, followed by the lymphoid tissues, which
actually diminish in size after puberty. The remaining general body fuses
mature later; the last being the genital tissues. The maxilla and the
mandible follow the general body growth; the mandible slightly slower
than the maxilla initially but catches up later.
It is important to know this because a male child who presently with a
slight mandibular deficiency at age 12 should be expected to have a normal
mandibular size by age 15-16 years.
b) Pattern of growth – pattern is a set of constraints, quantitative or geometric
rules, operating to preserve integration of parts under varying conditions or
through time.
These constraints may be in the form of coordinated transformations,
cybernetic mechanisms and compensations of various sorts.
What this essentially means is that growth demonstrates certain complex
proportionalities which change wit time. For example : At 3 months of
intrauterine life, the human foetus is almost 50% of the total body length.
This, for that particular time is normal. At birth, the trunk and limbs, which
were earlier rudimentary have grown faster than the head and therefore the
proportion of head size to the rest of body length is about 25-30%. Eventually,
at adulthood, the head size is just about 12% (Figure 2); these reflect the
complexity in proportions, which change with time.
4
In relation to differential growth and indicative of a normal growth pattern, is
the cephalocaudal gradient of growth.
- Predictability of growth pattern : as can be inferred from figure 2, a
specific kind of proportionality exists at a particular time and progresses
towards another at the next time frame, with a slight variations.
- This has important implications : In prediction of the future growth pattern
(using growth charts for that population) and to recognize if the individual
has deviated from his original growth pattern.
- This particular gradient connotes the variance of growth between the
cephalic (head end) and the caudal (fail end i.e. limbs and extremities).
This can be amply inferred from figure 2.
- It is interesting that even within the craniofacial skeleton, there exists a
cephalocaudal gradient; The skull of an infant occupies almost 2/3rd –3/4 of
the cranial complex. The maxilla grows next and the mandible (being at
the caudal end) is the last to grow (Figure 3).
In orthodontic, pattern has a morphogenetic as well as a developmental
application.
- Morphogenetic – For ex: the statement he has a Class III facial pattern.
- Developmental – Mohan ha a vertical growth pattern.
- Patterns can be quantified in terms of craniofacial constants, which show
invariance.
5
Implications of pattern:
- Analysis of morphology.
- Study of stability of treatment.
Variability : No two individuals, with the exception of monozygotic twins are
alike, i.e. variation is the law of nature.
To express variability quantitatively, it is useful to categorize in terms of
deviations from the usual pattern.
This is done using standard growth charts. The growth charts help in:
- Determining whether growth is normal or abnormal.
- To evaluate growth over a period of time.
- Growth charts are available for Indian population through the Indian
Council for medical research and Life Insurance Corporation.
Variability of growth may be seen in terms of:
a) Chronologic age – variation due to timing and because chronologic age is
not a good indicator of growth status.
b) Ethnic group.
c) Sexes.
d) Variance with time – secular trend.
e) Body type.
Normality : Normal refers to what is usually expected, seen or is typical.
6
It is important to distinguish normal from the ideal – because normal
implies a range of small variations from the ideal this ideal being not very
commonly encountered.
Normality can be portrayed.
Statistically – as depicted in figure.
- Functionally.
- Evolutionally.
Therefore, one should understand the term variability and its clinical
implications. Also according to Moyers, misuse of the concept of normality has
led to many problems in clinical orthodontics, particularly in treatment planning.
These are the few additional variables of growth:
- Rate means amount of change / time.
- Direction – this denotes the tendency for growth in a particular plane
space. For ex: The face grows downward and forwad.
- Distance curve v/s velocity curve.
Timing of Growth:
The timing of developmental events vary and are mainly controlled by
genetic factors, yet altered by the environment.
Implications:
There are – sex related difference in timing of events
- Spurts.
- Calcification
- Ossification.
7
Therefore, timing of a particular therapy should take into account these
variations due to timing.
Growth Accelerations (Spurts) – A spurt is defined as growth acceleration upto
a maximum, where the annual amount of growth exceeded the previous one at
least by 0.7mm – Erkstrom.
Normal spurts as given by Woodside (Figure 3).
i) Infantile spurt – at 3 years.
ii) Juvenile spurt – 7-8 years (Females); 8-10 years (Males)
iii) Pubertal spurt – 10-11 years (Females); 18-15 years (Males).
MECHANISMS OF GROWTH
Growth takes place at the cellular level via three mechanisms:
Hyperplasia (Increase in number)
Cell Hypertrophy (Increase in size)
Secretion of extracellular matter.
- Soft tissue growth occurs by a combination of the above two mechanisms
namely, hypertrophy and hyperplasia and is termed as interstitial growth,
which means that growth occurs at all points within the tissues. However,
in hard tissues namely bone, growth takes place by direct apposition i.e. at
the surfaces it must be known that interstitial growth is not possible within
bone. However, interstitial growth is the one which contributes to the
overall skeletal growth as most of the bones are modeled from cartilage. In
bone, the resting cell is termed as osteocyte capable of differentiating into
osteoblast.
8
Osteoblast – bone forming
Osteocyte
Osteoclast – bone removal
Interplay of osteoblastic and osteoclastic activity result in bone remodeling
figure.
In the soft tissues, there is an important interaction between the epithelium
and the mesenchyme:
- Interactive control
- Epithelium
Stimulation
Mesenchyme
Differentiation
This kind of interrelationship is quite significant during the closure of
various facial processes during embryonic development. A classic example to
depict this would be the fusion of the palatal shelves at the midline.
Mechanisms of Growth in Hard Tissues
The bone growth mechanisms are primarily two:
a) Endochondral which is the primary means of ossification in the entire body
which is the chief mode of ossification within the craniofacial complex.
Endochondral ossification – In this variety of ossification, bone forms by
replacing cartilage. This cartilage acts as an intermediary.
Mesenchyme – Cartilage cells Hypertrophy and calcification
9
Invasion by Degeneration of cartilage cells.
Osteogenic tissues Replacement by bone (Figure)
Endochondral bones are seen in areas of compression.
The cartilage bone interfaces is important because :
i) Cartilage offers flexibility pressure tolerance acts as a growth site.
ii) Interstitial growth is possible.
Endochondral bones in the skull and facial regions are:
- Synchondroses at the cranial base.
- Nasal septal cartilage.
- Condylar cartilage.
b) Intramembranous bone formation – This differs from endochondral
ossification in that there is no cartilaginous intermediary and bone
formation can directly proceed from mesenchymal tissue.
Undifferentiated mesenchymal cells
Transformation
Osteoblasts.
Osteoid matrix – secondary osteon
Bone – calcification
This is the :
- Predominant mode of ossification in the skull (cranial vault).
- Periosteal bone is always intramembranous.
- Occurs in areas of tension.
10
- Constant remodeling is possible and therefore forms orthodontic tooth
movement the basis for:
The important regions of intramembranous ossification within the cranial
complex are:
- Cranial vault.
- Bones in the facial complex; ex: zygoma.
- Maxilla.
- Mandible, except the condyle.
Bone Growth Mechanisms
a) Remodelling : A process involving deposition and resorption
occurring on the opposite ends.
b) Displacement
i. Primary due to enlargement of the bone itself.
ii. Secondary due to enlargement of adjacent bones.
c) Rotation – diagonally placed areas of deposition and resorption.
d) Remodelling and displacement combination occurring together are
the basic mechanisms in the enlargement and movement of bone.
Measurement and Prediction of Growth
Types of Growth Data:
a) Opinion – One person’s biased guess. It is the crudest form of data;
however should not be outrightly derided.
11
b) Observations – itself for studying all or none phenomena.
c) Rating and Rankings – comparison with conventional rating scales. The
commonest for there is facial type.
d) Quantitative measurements
Direct data Indirect growth measurements Derived data
Methods of Gathering Data:
A) Longitudinal measurement made of the same person at regular
intervals through time.
Advantages :
a)Variability within a groups is put in proper perspective.
a) Assessment of specific developmental pattern possible.
b) Temporary temporal problems are smoothed out.
12
Disadvantages :
i) Time consuming.
ii) Expensive.
iii) Attrition.
iv) Averaging.
b) B) Cross sectional Data: Measurements of different individuals or different
samples made and studied at different periods.
Advantages:
a. Quick.
b. Cost effectiveness.
c. Statistically significant data for large populations.
d. Repetition of studies is possible.
e. Can be performed on cadavers skeletons etc.
c) Semilongitudinal data – This type of data collection is the preferred one,
since it combines the advantages, longitudinal and cross sectional.
Measurement Approaches:
a) Craniometry – Basic of anthropology
o Precise measurements on dry skulls.
o However, data is always cross sectional.
b) Anthropometry – Measurements of skeletal variables in living individuals
as well; based on various skeletal landmarks.
13
o Longitudinal data
c) Cephalometry – Important clinically to the orthodontist in order to evaluate
a patients skeletal ( and soft tissue) growth at a given period of time.
o Longitudinal data.
o However, only two dimensional representation.
Experiemental Approaches:
a) Vital Staining – Dyes that stain mineralizing hard tissues and occasionally
soft tissues as well.
Introduced by John Hunter ; Belchier in 1736.
o Alizarin.
o Tetracycline.
o Radioactive markers – to a limited extent.
b) Implant Radiography: Implants (inert metal pins) placed in the bone,
which get incorporated.
o Bjork.
o Has remarkable improved the accuracy of longitudinal cephalometric data.
o Rotations of mandible appreciated now, with this technique.
Maturation Indicators
- Hand wrist radiographs.
- Tooth calcification.
o Canine
14
o Third molars.
- Onset of puberty.
- Cervical vertebrae.
- Prediction of growth
- Finite element
Clinical Implications
a) Head form as the basis for malocclusion.
b) Working with growth with the knowledge of growth fields; phenomenon
of relapse.
c) Planning of therapy.
i) To evaluate the causative of the abnormality.
ii) To time the individual and accordingly plan the mode of
therapy.
iii) Phenomena of compensations.
Skeletal Dentoalveolar
d) Predict efficacy of therapy.
e) To understand the evolution of dysmorphogenetic changes.
Evolution of Human Head Form
Human head form varies significantly from its evolutionary predecessors
mainly to accommodate the enlarged brain.
15
Through the overall structure remains the same, the obvious alterations
should be properly understood.
a) Marked flexures in the cranial floor.
b) Vertical deposition of the spinal cord.
c) Orbital positioning.
d) Relative decrease in jaw size.
e) Replacement of snout by an almost hairless integument, with advanced
vasomotor control.
f) Orbital rotation with decreased anatomic region between the eyes.
g) Cheek bones placed in wide bilateral regions.
Functional Matrix Theory of Moss
Moss (1960, 1962, 1964, 1969) proposed that the stimuli of the growing
skeletal tissues lie within the adjacent soft tissues – termed the functional
matrices.
He improved on the concept proposed by Vander Klaauw – Bones
composed of various cranial units – “Functional cranial components”, their
growth being relatively independent.
The classic statement of Moss (1981) goes as follows:
“The origin, growth and maintenances of all skeletal tissues and organs are
always secondary, compensatory and obligatory responses to temporarily and
operationally prior events or processed that occurs in specifically related non
skeletal tissues, organs or functioning spaces (functional matrices).
Which implies that:
16
- Skeletal growth occurs passively in response to soft tissue growth. Ex:
Growth of the cranial vault, Growth of the coronoid process, growth of the
orbit.
- The soft tissue growth occurs in response to the functional demands of that
particular region.
Components and Concept: The main philosophy of FMH is based on concept
which visualize the craniofacial areas a set of components.
- The head is a region (operationally) within which certain functions occurs
is specifically associated with the functions for ex: The oral cavity –
mastication, speech, taste etc.
- These functions are carried out by the functional cranial components.
- Functional cranial (periosteal) functional matrix.
- Functional cranial components get arranged and are seen as two capsules
in the craniofacial region namely:
a) Neurocranial capsule.
b) Orofacial capsule.
- These capsules contain capsular matrices which would include non skeletal
tissues – Ex: Brain and leptomeninges or functioning spaces – Ex:
Dronasopharygeal space.
- Growth includes changes in size and shape as well as change in spatial
positions of time.
- Increase in size occurs due to interactions between a periosteal matrix and
its skeletal unit, which is termed as transformation.
17
- Changes in space occurs because of the increase in capsular matrices
termed as translation.
Let us now look at each these components in detail:
Functional Cranial Components:
As mentioned earlier, these are comprised of:
a) Skeletal unit.
b) Functional matrix.
a) Skeletal unit : These may be comprised of bone, cartilage or tendinous
tissue. Their function is to protect and / or support its functional matrix.
Derivatives – If a bone is in turn made up of a number of small skeletal
components, then the bone is termed as a macroskeletal unit. The individual
skeletal components – Microskeletal unit.
For example, Angular microskeletal unit, coronoid microskeletal unit.
- The microskeletal units are relatively independent to a variable extent.
Thus, for the mandible, we can distinguish:
a. Coronoid microskeletal unit.
b. Angular microskeletal unit.
c. Alveolar microskeletal unit.
d. Basal microskeltal unit.
This kind of segregation of a bone is mainly on the basis of the associated
soft tissue attachments or structures within
“FUNCTIONAL CRANIAL COMPONENT”(By Melvin Moss)
18
SKELETAL UNIT FUNCTIONAL UNIT
MICRO-SKELETAL MACRO-SKELETAL PERIOSTEAL CAPSULAR MATRIX MATRIX
E.g., Coronoid e.g. entire e.g. muscles e.g. Neurocranial angular etc. endocranial glands nerves capsule
surface of vessels fat, oro-facial capsulecalvarium teeth etc.
MICRO-SKELETAL UNITS OF THE MANDIBLE
a) Coronoid.
b) Condylar.
c) Angular.
d) Basal.
e) Alveolar.
b) Functional Matrices
Functional matrix : It is the functioning component of a cranial unit. Includes all the
soft tissue (non-skeletal) units. The non skeletal units would include hard tissues like
teeth and cartilage also.
Types of Functional Matrices:
i) Periosteal matrix.
ii) Capsular matrix.
i) Periosteal Matrix : It comprises of all non-skeletal functioning units
adjacent to the skeletal unit. Ex: The muscles, glands, nerves, vessels etc.
19
These functional matrices act to alter either or both size and shape
of the skeletal units per se. ex: Role of temporalis in regulating the size and
shape of the coronoid process.
This means that it is the functioning which occurs first and bone growth is
just in response.
Periosteal matrices are capable of inducing deposition and resorption in the
skeletal unit. Enlow has termed this as growth remodeling, while Moss has
termed this same process as tranformation.
ii) Capsular Matrices : All functional cranial components
are organized in the form of capsules. In the craniofacial region, 4 capsular
can be identified:
1) Neurocranial capsule.
2) Orofacial capsule.
3) Otic capsule.
4) Orbital capsule.
The capsules are envelopes surrounding their respective capsular matrices.
Capsular matrices may exist as volumes.
Capsular are sandwiched between two covering layers.
Growth of skeletal units in space (translation)
results because of the expansion of the capsular matrices.
20
This phenomenon of translation has been termed as displacement by
Enlow, we shall limit to the elaboration of the neurocranial and orofacial capsules
only.
1) Neurocranial capsule : It is a capsule between skin and
duramater enclosing the neurocranium.
2) Its capsular matrix is made up of the brain, the
leptomeninges, and cerebrospinal fluid.
3) This capsule originates during the foetal period where in
the foetal neural mass surrounded by the neural capsule.
4) Growth of the neural mass causes expansion of the capsule
– (mitotic activity of the connective tissue elements of the capsule).
5) Due to this growth, the entire composition (all related
cranial elements) gets passively translated.
6) At the same time, transformation is also taking place in
response to this passive displacement.
Oro-facial Capsule:
The oro-facial capsule surrounds and protects the
oronasopharyngeal spaces. These spaces are the capsular matrices for the oro-
facial capsule.
This capsule is surrounded by the skin and the mucous
membrane on either side.
21
The oro-facial capsule originates by the process of
enclosure. The important phases during its origin are as follows:
First arch swellings enclose to form the primordial
oro-nasal cavity, followed by a.
Rupture of buccopharyngeal membrane.
Elevation and fusion of the bilateral palatal processes
then ensues.
The volumetric growth of these spaces that is the
primary morphogenetic event in facial skull growth.
Patency of airway is maintained by the airway
maintenance mechanism.
Growth of the functioning spaces causes an increase
in the size of the capsule (mitosis of both epithelial and mesenchymal
element).
There is a passive movement of the functional cranial
component.
This displacement brings about compensatory
transformation of skeletal units in response to an alteration in the periosteal
matrices. The transformation is necessary to maintain proper articular
contacts.
22
Interaction between of Functional Components
Capsular matrix growth Capsular growth } Translation Total Growth Changes
Periosteal matrix growth Skeletal unit growth } Transformation
In short : Soft tissue growth governs skeletal growth and the related growth
movments.
23
CRANIOFACIAL GROWTH THEORIES
In this concluding section, we shall look at the following:
- Evolution of the various hypothesis.
- The genetic concept, which includes.
a) Sicher’s ‘Sutural Dominance Theory’.
b) Scott’s Cartilagenous Theory.
- Functional Matrix theory of Moss.
- The Servosystem Theory – also called the Cybernetic theory of Petrovic.
As scientists (biologists) started delving more into the question of ‘how’
rather than ‘what’ in relation to growth and development, there was an emergence
of a distinctive field, termed the craniofacial biology.
As defined by Carlson Craniofacial biology is the study of the growth,
function and adaptation, both phylogenetically and ontogenetically, of the
craniofacial skeleton and related structures’.
Evolution of Various Growth Theories : As depicted in the diagram, a theory is a
part of a Paradign Kuhn has defined a Padarigm is a conceptual scheme that
encompasses individual theories and is accepted by a scientific community as a
model and foundation for further research.
- A theory may be defined as a scheme or a system of ideas to explain
observed facts.
- A hypothesis is a supposition made as the basis of reasoning.
- A fact is a recorded scientific observation.
24
Craniofacial biology has had no shortage of theories regarding facial
growth. Generally, these theories occupy a continuum ranging from a complete
emphasis on intrinsic genetic factors as the control mechanisms, to a total denial
of the genetic factors and a total reliance on the functional determinants.
Also, this continuum is also closely related to time, with distinct cras
correlating with distinct paradigms.
I) 1920-1940 – The Genomic Paradigm : Craniofacial
research during this period was based primarily on the study of structure of
the craniofacial skeleton, with little or no emphasis on function. It was on era
essentially static and researchers like Brodie, Sicher etc. stating that growth
of the craniofacial skeleton as being largely genetically predetermined.
II) 1940-1960 – The ‘Pre-revolutionary Era’ – coined
by Pruzansky : During this period, animal experimental research gained
momentum. Craniofacial researchers noted that there is a vast amount of
variation within the facial region than would occur due to genetically
determined patterns and much of this variation could be the results of
modifying influences of the environment.
Though the genomic paradigm, through the researchers like Scott, there was a
dominant shift due to the pioneers works of Melvin Moss. There was also an
increased interrelation developing between craniofacial biology and other
structural sciences like comparative anatomy, embryology etc.; this being termed
as a structures functional approach.
EVOLUTION OF THE HYPOTHESIS
PARADIGM
25
THEORY
HYPOTHESIS
Paradigms in Craniofacial Biology :
- 1920-1940
- 1940-1960
- 1960-1980
- 1980-onwards
III) 1960-1980 – Evolution of the Functional Paradigm :
The functional matrix hypothesis (FMH) proposed by Moss and Young and
Moss and Salentijin paved way for the new paradigm, termed as the
functional paradigm. Also the serious questioning of the rationale of the
genomic paradigm by basic scientist helped the functional paradigm to
establish itself.
This does not imply that the genomic paradigm has completely lost
ground. In fact, it is beyond doubt that genes do play a major role in craniofacial
growth.
Thus, there existed two mutually conflicting paradigms, each on trying to
establish its supremacy.
IV) 1980’s onwards – The Era of Rational Confluence :
As the two paradigms refuted each other completely, the entire jigsaw could
not be put together entirely.
26
FACT
This led the craniofacial biologists to seek a composite explanation for the
growth mechanisms. For ex: Van Limbhorg tried to integrate both genetic and
epigenetic mechanisms together. Also the fact that Moss himself in 1997, stated
that both the genetic and epigenetic factors are equally important and put forth a
new theory called the “Complexity Theory’, underlines this congregation of ideas.
We shall now sequentially assess critically each of the prominent theories
that have been put forth.
Growth Centres:
Places of endochondral ossification with a tissue separation force – Baume.
Contributing to the increase of skeletal mass – Koshi.
Prototype – Epiphyseal plate.
Assumed cranial growth centers:
a) Sutures.
b) Cartilage of the nasal septum.
c) Condylar cartilage.
d) Cranial base synchondroses.
Criteria for terming a growth center:
i) Inherent growth potential.
ii) Independence
iii) Extirpation should cause profound altered and depleted growth.
iv) Should be similar to the prototype.
27
Sicher’s Theory of Sutural Dominance
Weimann and Sicher (1947) inferred from their studies using vital dyes
that sutures were causing most of the growth. In Sicher’s words. “The primary
event in sutural growth is the proliferation of the connective tissues between the
two bones. If the sutural tissue proliferates, it creates the space for oppositional
growth at the borders of the bones”.
Other proponents of sutures as growth centers were Massler, Baer, Prabl
etc.
Their visualization of the suture was as a three layered structures and that
interstitial connectives tissues growth caused separation and replacement
of the proliferating connective tissues was necessary for the functional
maintenance.
Sicher also proposed that mandibular growth is controlled by a similar
intrinsic genetic potential for growth of the mandibular condyles.
Their visualization of growth in the nasomaxillary area was:
‘Growth at the sutures moves the nasomaxillary complex downward and
forward and growth of condyles keep pace in the same directions, thereby
creating space for alveolar process growth and the eruption of teeth’.
Thus, the primary importance was given to sutural growth, which was
assumed to be under genetic control. The remnant mandibular growth was again
believed to be determined genetically, the principal area being the condyle. Little
or perhaps no role was attributed to the environmental factors.
28
This theory was quite popular at that time; so much so that people gave
up the idea of altering growth, even to a small extent. However, with experiments
which disproved the idea of sutures being growth centers and the surge in the
functional dogma, this theory lost ground.
Evidences against Sicher’s Theory :
- Autotransplants of sutures fail to growth.
- The shape and growth within this sutures is dependent on external stimuli.
Ex: sutural expansion or closure can be attempted.
- Extirpation of sutures does not show appreciable alterations in growth in
the areas from where they have been removed. This was demonstrated by
Moss.
- Finally, sutures do not resemble epiphyseal plates – both histologically or
biochemically.
- The present concept about sutures is that : sutures are growth sites, they are
five layered structures, show adaptability to extrinsic stimuli.
29
PROCESS CONTROL
CRANIAL DIFFERENTIATION
Intrinsic Genetic Factors
Local Epigenetic Factors
General Epigenetic Factors
Local Environmental Factors
General Environmental Factors
30
PROCESS CONTROL
CHONDROCRANIAL GROWTH
Intrinsic Genetic Factors
Local Epigenetic Factors
General Epigenetic Factors
Local Environmental Factors
General Environmental Factors
DESMOCRANIAL GROWTH
SUTURAL GROWTH
PERIOSTEAL GROWTH
SCOTT’S VIEW
Scott’s Cartilaginous Theory
Scott (1956) suggested that hyaline cartilage has certain properties which
allow it to determine growth in the cranial base and the nasal areas, and this
growth establishes an under pinning for the shell of the face to be formed
intramembraneously around this cartilage.
In other words, the cephalic cartilages, namely the synchondrosis, the
septal cartilage and the condylar cartilage have inherent growth potential. Added
to this is the adaptive role of sutures, which adjusts as these aforementioned areas
growth.
The remaining intramembraneous growth that occurs around this template
passive.
Evidence favouring this theory:
- Disturbances in the nasal septum affects growth of the midface
considerably
31
o Rabbit experiments.
o Cleft palate – in human (Injury)
- On autotransplantation, some growth may occur – Study by Koski and
Ronning.
Recent Concepts in Functional Matrix Hypothesis
Revised Statement
The developmental origin of all cranial structural elements and all their
subsequent in size and shape, as well as their maintenance in being are always,
without exception, secondary, compensatory and mechanically obligatory
responses to temporally and operationally prior demands to their related cephalia
non-skeletal cells, tissues, organs and operational volumes.
Moss, initially points out the constraints of the previous version of the
Functional Matrix Hypothesis is (FMH) and goes on to explain how, in these
years (1980 onwards) they have been overcome.
The constraints according to Moss are:
- Methodological constraint – due to macroscopic measurements which use
arbitrary reference phases like the : SN or FH plane – These have been
overcome by the use of Finite Element Method (FEM).
- Hierarchical Constraint – all previous FMH versions were suspended or
sandwiched between the two hierarchical levels of multicellular and
subcellular. This has been overcome in the version by the establishment of
a linkage between all levels.
32
- This present version (new) deals with the responses of the periosteal
mtrices only.
This new version can be understood better if one understands the following
cellular events:
a) Adaptation is a tissue process consisting of deposition and maintenance are
functions of relatively large groups (whorts) of osteoblasts.
- Adjacent adaptational tissue surfaces simultaneously show deposition,
resorption and maintenance.
It is well known that the previous version implies that skeletal unit
adaptation takes place in response to stimulation of the functional matrices.
- But ho does the stimulation, which occurs at the periosteum reach the
functioning cell units?
- How is it interpreted and what is the resultant?
- How is this output expressed at the tissue level?
All these and pertinent questions seem to be clarified by:
a. The process of mechanotransduction.
- Bone cell functioning multicellularly as a connected cell network.
Mechanotransduction
Vital cells are ‘irritable’ and respond in alteration in their external
environment. This mechanosensing property requires.
- Mechanoreception – transmission from ‘extra’ to ‘intra’
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- Mechanotransduction – transformation of energetic and / or informational
content into an intracellular signal.
When external loadings are applied to the bone tissue there is some
deformation of the bone matrix (extracelular) and bone cells.
- Osteocytes and osteoblasts are competent for intracellular stimulus
reception; transduction and for subsequent intercellular transmission.
Osseous mecanotransduction may involve the complementary process of:
i) Mechanical transduction.
ii) Ionic transduction.
i) Mechanical transduction : It has been shown that a series of
macromolecular mechanical levels exist, which are capable of transmitting
information from the strained matrix to the bone cell nuclear membrane.
This molecules is supposed to be physically continuous from the
extracellular collagen matrix to the intracellular cytoskeletal actin; which in turn
is connected to the nuclear membrane.
The so-described molecular lever chain can provide a physical stimulus
able to activate the osteocytic genome.
ii) Ionic transduction : Osteocytes may contain two types of ionic
channels.
A) Voltage activated ionic channels, which allow certain ions
to flow across the membrane and this transmembrane flow acts as a
transductive process by generating osteocytic action potentials (Figure).
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B) Stretch activated ionic channels – In strained bone tissues
and in fibroblasts too, stretch activated channels exist. When active, they
permit passage of a certain sized ion(s) like Ca++ , K+ , Na+ etc. Such ionic
flow may modulate membrane potential and also to some extent regulate
Ca++ influx (Figure).
The other possible Ionic transduction mechanisms are:
1) Electric field strength – Bone responds to exogenous
field strengths and there seems to be a parallel between these and
endogenously produced fields by muscles.
2) Electrokinetic – These are bound and unbound
charges which exist in bone field(s) and are of streaming potential origin.
These charges can initiate both osteoclastic and osteocytic action
potentials.
Considerations in Mechanotransduction - Mechanotransduction principle is
based on the following factors:
- Normal skeletal muscle strains are attached intermittently.
- Dynamics of skeletal muscle contraction fit nicely with energetic
requirements for bone cell responsiveness.
o Both stimulatory and regulatory.
- Bone cells may be stimulated directly via the channels or indirectly by
electrokinetic phenomena.
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‘Bone seems to be “tuned” to the skeletal muscle’ (Skeletal Units) –
Periosteal Matrix.
As Moss Puts it :
“When both ionic and mechanical 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 support for the hypothesis of epigenetic regulation of skeletal tissue
adaptation”.
Bone as an Osseous Connected Cell Network (CCN)
All bone cells, except osteoclasts are extensively connected by gap
junctions.
Gap junctions are seen where the plasma membranes of markedly
overlapping canalicular processes meet.
These canaliculi are extensions of the osteocytes which lie in the bony
matrix.
The canalicular processes are seen to interconnect neighbouring cells
processes.
Gap junctions also connect superficial osteocytes to periosteal and
endosteal osteoblasts; and vertically the periosteal osteoblasts with preosteoblastic
cells.
Gap junctions are seen to permit movement of the ions, small molecules
and even the fluorescent dyes.
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They can be termed ‘electrical synapses’, which permit bi-directional
signal traffic.
Bone tissue seems to be interconnected through layers as a network, where
parallel distributed signal processing occurs.
The CCN cells are organized into layers, the chief units being ‘input’ layer,
an output layer and a series of intermediate or ‘hidden’ layer(s).
Each cell in any layer may simultaneously receive several (weighted)
stimuli.
Within each cell, all weighted inputs are summed independently.
This sum, if it crosses certain threshold values, successful mechano-
transduction occurs.
This signal is transmitted identically to all the hidden layers.
Similar processes of weighted summation, comparison and transmission
occur in the intermediate cells, till the final layer of osteoblasts is reached.
The outputs of these superficial cells determine the site, rate, direction,
magnitude and duration of the specific adaptive response.
Epigenetic process of loading
Loading as a process loading is unquestionably of greatest importances at
the clinically significant structural levels.
Loading acts not only at the tissue levels, but also at cellular and
subcellular levels.
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The epigenetic mechanisms involved include:
- Regulation of multicellular tissue morphogenesis – via extracellular matrix
and transduction.
- Controlling osteoblastic gene expression through mechanical layers
altering cell shape.
At the tissue levels also, epigenetic mechanisms have been noted for ex: in
cartilage.
At the organ level, the vital role of articular function is well known.
Regulation of periosteal matrices:
- Mechanical loads – Phenotype.
- Neutrophism – Genotype.
New Insight into the Role of Periosteal Matrices :
Considering that the morphogenetic primacy of the periosteal matrices is
accepted, one can logically deduce the following:
- Physical loading tends to deform bone tissue and invoke the skeletal unit
adaptive response. Ex: temporalis.
- Mechanoreception occurs chiefly, through some periosteal osteoblasts may
be directly stimulated.
- Strain is believed to be a competent stimulus and the attributes may vary
with:
o Type of loading.
o Fine tuning.
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- Mechanotransduction, either of ionic or mechanical nature occurs
throughout the osseous CCN.
- Output or the adaptive response is via the signals which get transduced
through summation.
Evolution of the Complexity Theory of the FMH
Complexity theory provides description of the behaviour of complex
biologic systems which exist as ‘ensembles’ and not as clusters of individual cells
and extracellular substances.
In this system a functional cranial unit is termed as Complex Adaptive System
(CAS):
Complexity Theory (CT) involves processing of both genomic and
epigenetic information by the CAS.
It also implies that growth and development, to a significant extent exhibit
random behaviour – therefore, are nonlinear processes and is not fully
predictable.
The highly ordered morphological properties of adult biologic system
result from a series of spontaneous and self organized processes and mechanisms.
Such self organizing events can create phenotypic variability under genetic and
epigenetic conditions.
The operation of complexit has been termed by him as “Environmental
factors thus play a decisive role. But it is the organism itself that, as an integrated
system dictates the nature of each and every developmental response”.
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‘The living organism self organizes on the basis of its own internal
structuring, in continuous interaction with the environment in which it finds
itself’.
Moss has also compared between the genetic and epigenetic mechanisms.
- He rebukes the geneticists claim of high genetic control – odontogenic
regulation by epigenesis.
- The genetic thesis is denied because it is reductionist and molecular.
- He says that the epigenetic antithesis as of how is integrative, seeking to
clarify the causal chain between phenotype and the genoms.
- The resolving synthesis, however, he says is to consider both the intrinsic
(genetic) and the extrinsic (epigenetic) processes and mechanisms integrate
and provide the necessary and sufficient causes of growth and
development.
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Thesis (Genetic) Antithesis (Epigenetic)
Resolving Synthesis
Complexity Theory
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