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THEORIES OF

GROWTH
CONTROL

drg. Lina Hadi, Sp. Ort


INTRODUCTION
• Growth is influenced by :
– genetics,
– environment,
– nutrition,
– physical activity,
– Health or illness, and
– a number of similar factors.
INTRODUCTION
• Since much of orthodontic treatment
is created by disproportionate growth
of the jaws, & to understand the
etiologic processes of malocclusion
& dentofacial deformity, it is vital to
learn how facial growth is influenced
and controlled.
INTRODUCTION
• 3 major theories in recent years have attempted to explain
the determinants of craniofacial growth:
– Bone as primary determinant of its own growth  genetic
control in bone
– Cartilage is primary determinant of skeletal growth, while
bone responds secondarily & passively  genetic control in
cartilage, & bone indirectly controlled epigenetically
– Soft tissue matrix in which the skeletal elements are
embedded is primary determinant of growth, and both bone &
cartilage are secondary followers  genetic control mediated
largely outside skeletal system, and both bone and cartilage
controlled epigenetically
• First view has been discarded. Today truth found in second
and third view.
GROWTH CONTROL

Picture illustrates the change in overall body proportions that occurs


during normal growth and development:
- There is progressive reduction of the relative size of the head (from
almost 30% of the total body lenght at birth to about 12% of the
adult)and
- -faster growth of the trunk and limbs ( lower limbs grow more than
upper limbs). At birth, the legs represent about one third of the total
body length, while in the adult, they represent about half.
GROWTH CONTROL

The infant has a relatively much larger cranium and a much smaller face
- after the age of 6 years, there is little further growth of the cranium
because the brain has nearly reached its adult size
- the facial skeleton grows much longer and thus in the adult forms a
much larger proportion of the skull than in the child.
- when the facial growth pattern is viewed against the perspective of
the cephalocaudal gradient, the mandible, being farther away from
the brain, tends to grow more and longer than the maxilla, which is
closer.
Other theories
The major theories
related to
explaining growth
craniofacial growth
Genetic Theory
Enlow’s expanding ‘V’
Remodelling Theory principle
Sutural Theory
Enlow’s counterpart
Cartilageneous Theory
principle
Functional matrix Theory
Sevosystem Theory Neurotrophic process
in oro-facial growth
Van Limborgh’s Theory
GENETIC THEORY
• The classic approach attributed control of
skull growth largely to intrinsic genetic
factors.
• Van Limborgh (1970), who analysed the
controlling and modifying factors in the
growth of the skull.
• The genetic theory simply said that genes
determine all.
REMODELING THEORY
• The research by Brash (1930) on bone provided the
foundation for the development of the first general theory of
craniofacial growth
• The remodeling theory were that:
– bone only grows appositionally at surfaces.
– growth of the jaws is characterized by deposition of bone at the
posterior surfaces of the maxilla and mandible, sometimes described
as “Hunterian” growth of the jaws.
– calvarial growth occurs via deposition of bone on the ectocranial
surface of the cranial vault and resorption of bone endocranially.
SUTURAL THEORY
• Proposed by Weinmann and Sicher
(1940)
• According to this theory, the connective
tissue and cartilaginous joints of the
craniofacial skeleton, much like
epiphyses of long bones, are the
principal locations at which intrinsic,
genetically regulated, primary growth of
bone takes place.
SUTURAL THEORY
• Growth of the cranial vault is caused by the intrinsic pattern
of expansive proliferative growth by sutural connective
tissue that forces the bones of the vault away from each
other; indicating “the primacy of sutural growth for the
determination of adult skull form”
• Similarly, proliferation of sutural connective tissue in the
circummaxillary suture system surrounding the maxillary
skeletal complex forces the midface to grow downward and
forward.
• The mandible was perceived as essentially a bent long
bone, with the mandibular condyar cartilage being
equivalent to the epiphyseal plates of long bones whose
growth forces the mandible downward and forward, away
from the cranial base.
SUTURAL THEORY
• It is clear now that sutures are not primary
determinants of craniofacial growth.
• Two lines of evidence lead to this conclusion.
– The first is that when an area of the suture between two facial
bones is transplanted to another location (to a pouch in the
abdomen, for instance), the tissue does not continue to grow.
This indicates a lack of innate growth potential in the sutures.
– Second, it can be seen that growth at sutures will respond to
outside influences under a number of circumstances. If cranial
or facial bones are mechanically pulled apart at the sutures,
new bone will fill in, and the bones will become larger than
they would have been otherwise. If a suture is compressed,
growth at that site will be impeded. Thus sutures must be
considered areas that react-not primary determinants.
CARTILAGENEOUS THEORY
• Cartilageneous theory/ Nasal septum theory (1950)
• The Irish anatomist, James H. Scott, proposed an
alternative explanation, the nasal septum theory, as
the single and unified theory of craniofacial growth.
Schematic representation of the nasal
septum theory of craniofacial growth
Growth of the nasal septal cartilage
pushes the midface downward and
forward relative to the anterior cranial
base. This results in a separation of the
midfacial suture system, which then fills
in via secondary, compensatory sutural
bone growth.
CARTILAGENEOUS THEORY
• Intrinsic, growth-controlling factors were present
only in the cartilage and in the periosteum
• Growth in the sutures was secondary and
entirely dependent on the growth of the cartilage
and adjacent soft tissues
• Scott’s hypothesis could explain the coordinated
growth that had been observed within the skull,
and between the skull and the soft tissues. He
introduced the concept of cartilaginous ‘growth
centers’.
Functional Matrix Hypothesis

• Melvin Moss introduced the functional matrix


hypothesis to the orthodontic world in 1962.
• Called ‘method of functional cranial analysis’
• He was inspired by the ideas of Van der
Klaauw (1952) that ‘bones’ were in reality,
composed of several ‘functional cranial
components’ the size, shape and position of
which were relatively independent of each
others.
THE FUNCTIONAL MATRIX HYPOTHESIS
One
Function

Functional Cranial
Component

Functional Skeletal
Matrix Unit

1. Periosteal Matrix -----------> 1. Microskeletal


2. Capsular Matrix -----------> 2. Macroskeletal
a. Masses
b. Functioning spaces
Functional Matrix Hypothesis
– The periosteal – The capsular
matrix matrix
• corresponds to the • defined as the organs
immediate local and spaces that
environment occupy a broader
• E.g. muscles, blood anatomical complex.
vessels, and nerves. • E.g. brain, oral cavity
• Active growth • Passive growth
• Deposition and • No deposition
resorption • No resorption
• Affect size and/or • Affect location
shape
Functional Matrix Hypothesis
Growth Craniofacial Growth
Active growth process
Active growth 1) Sutural growth
(Periosteal) 2) Bone remodeling
3) Cephalic cartilage growth
+
Passive growth Passive growth process
1) The growth of neural,
(Capsular) orbital, CSF, and other
= masses and real substances
Total growth 2) The expansion of oro-naso-
pharygeal and other
functioning spaces
Use of the “Functional Matrix” in the therapy of
orthodontics, dentofacial orthopedics, and
orthognathic and craniofacial surgery

1. Orthodontics
Periosteal Matrix ------------> Skeletal Unit
[Teeth] [Alveolar Bone]
2. Dentofacial Orthopedics and Orthognathic Surgery
Capsular Matrix -------------> Multiple Skeletal Units
[Functional Appliances] [Jaw Bones]
Capsular Matrix -------------> Multiple Skeletal Units
[Distraction osteogensis:
e.g., hemifacial microsomia] [Jaw Bones]
3. Craniofacial surgery
Capsular Matrix -------------> Multiple Skeletal Units
[Craniotomy: e.g. Crouzon Syndrome] [cranial bones]
[Distraction osteogensis:
e.g., Treacher Collin Syndrome] [facial & jaw bones]
Functional Matrix Hypothesis

Schematic representation of the functional matrix hypothesis of


craniofacial growth.
Primary growth of the capsular matrix (brain) results in a stimulus for
secondary growth of the sutures and synchondroses, leading to overall
enlargement of the neurocranium (macroskeletal unit). Function of the
temporalis muscle exerts pull on the periosteal matrix and bone growth of
the temporal line (microskeletal unit).
SERVOSYSTEM THEORY
• Popularized by Alexandre Petrovic in 1970s which
stated that craniofacial growth happened because of
growth signals and feedback mechanisms.
• Petrovich theorized a Cybernetic Model for the
Servosystem Theory.
• This theory states that occlusion provides a
constantly changing input which influences the
horizontally regulated growth of the midface and
anterior cranial base.
• This midface growth then serves as a rate limiting
factor for the growth of the mandible.
SERVOSYSTEM THEORY
SERVOSYSTEM THEORY
• According to this concept, the influence of the STH—
somatomedin complex on growth of the
– Primary cartilages (epiphyseal cartilages of the long
bones, cartilages of the nasal septum and sphenooccipital
synchondrosis, lateral cartilaginous masses of ethmoid,
cartilage between the body and the greater wings of the
sphenoid, etc.) has the cybernetic form of a ‘command’ (i.e.,
does not include any so far detected local feedback loops)
– Secondary cartilages (condylar, coronoid, and angular
cartilages of the mandible, cartilages of the mid palatal suture,
some other craniofacial sutures, and the provisional callus
during bone fracture repair, and (to some extent) rib growth
cartilages) comprise not only direct but also some indirect
effects on the cell multiplication.
SERVOSYSTEM THEORY
Components of a servosystem
SERVOSYSTEM THEORY
The face as a servosystem
VAN LIMBORGH’S THEORY
Van Limborgh suggested the following five
factors that he believed controls growth.
• Intrinsic genetic factor: They are the genetic control of the
skeletal unit themselves.
• Local epigenetic factor: Bone growth is determined by
genetic control originating from adjacent structures like
brain, eyes etc.
• General epigenetic factor: They are genetic factors
determining growth from distant structures. Eg: Sex
hormones, growth hormones.
• Local environmental factor: They are non genetic factors
from local external environment. Eg: habits, muscle force
• General environmental factor: They are general non
genetic influences such as nutrition, oxygen etc
VAN LIMBORGH’S THEORY
The views expressed by Van Limborgh can be
summarized in the following points:
• Chondrocranial growth is controlled mainly by intrinsic
genetic factors.
• Desmocranial growth is controlled by Epigenetic &
environment
• The cartilageneous part of the skull must be considered as
the growth centres.
• Sutural growth is controlled mainly by influences originating
from the skull cartilages and from other adjacent skull
structures.
• Periosteal growth largely depends upon growth of the
adjacent structures.
• Sutural and periosteal growth are additionally governed by
local non genetic environmental influences.
ENLOW’S EXPANDING
‘V’ PRINCIPLE
• Many facial bones or part of bone
have a V shaped pattern of growth.
• The growth movements and
enlargement of these bones occur
towards the wide ends of the V as a
result of differential deposition &
selective resorption of bone.
ENLOW’S EXPANDING
‘V’ PRINCIPLE
• Bone deposition occurs on the
inner side of the wide ends of the V
and bone resorption on the outer
surface.
• The V pattern of growth occurs in a
number of regions such as base of
the mandible, ends of long bones,
mandibular body, palate etc.
ENLOW’S EXPANDING
‘V’ PRINCIPLE
• Maxilla: Vertical growth of the maxillary complex is due to
continued apposition of alveolar bone on the free borders of
the alveolar process as the teeth erupt. Transversely,
additive growth on the free ends increases the distance
between them. The buccal segments move downward and
outward as the maxilla itself is moving downward and
forward, following the principle of expanding V.
• Mandible: Transverse dimensions, after first year of life are
mainly due to the growth at the posterior border in an
expanding v pattern. The two ramus also diverge outward
from below to above so that additive growth at the coronoid
notch, coronoid process and condyle also increases the
superior inter-ramal dimension.
ENLOW’S EXPANDING
‘V’ PRINCIPLE
ENLOW’S COUNTERPART
PRINCIPLE
The counterpart principle of craniofacial
growth states that the growth of any
given facial and cranial part relates
specifically to other structural and
geometric counterparts in the face and
cranium.
There are regional relationships
throughout the whole face and cranium.
ENLOW’S COUNTERPART
PRINCIPLE
• It explains: growth of one bone has influence on its
adjuvant bone which is called counter part, & this
controls the growth & proportional relationship with
its counterpart.
– Nasomaxillary complex relates to the anterior cranial
fossa
– Horizontal dimension of the pharyngeal space relates to
the middle cranial fossa.
– Middle cranial fossa & breadth of the ramus
– Maxillary & mandibular dental arch
– Bony maxilla & corpus of the mandible.
– Maxillary tuberosity & the lingual tuberosity.
NEUROTROPHIC PROCESS
IN ORO-FACIAL GROWTH
• The neurotropic factor involves the
network of nerves (all kinds, motor as
well as sensory) as links for feedback
interrelationships among all the soft
tissues and bone.
• The nerves are believed to provide
pathways for stimuli that can trigger
certain bone and soft tissue remodeling
responses.
THEORIES ON MAXILLARY GROWTH

A. Functional matrix theory (Moss)


– Any given bone grows in response to functional
relationships established by the sum of all the
soft tissues operating in association with that
bone, i.e., the functional soft tissue matrix is the
actual governing determinant of the skeletal
growth process.
• In the Maxilla:
– The major determinant of growth in the maxilla is the
enlargement of the nasal and oral cavities, including the
sinuses which grow in response to functional needs. This
is called the orofacial capsular matrix.
THEORIES ON MAXILLARY GROWTH

B. Cartilage growth (Scott)


– The cartilage as a determinant of
maxillary growth.
– Although there is no cartilage in the
maxilla itself, there is cartilage in the
nasal septum which provides a
thrusting force which carries the
maxilla forward and downward during
growth.
THEORIES ON MAXILLARY GROWTH

C. Sutural growth theory (Enlow)


– The sutures of the maxilla are sites not
centers of growth; they allow downward &
forward positioning of the maxilla
– As growth of surrounding soft tissues
translates the maxilla downward and
forward, new bone is added on both sides
of the superior and posterior sutures.
MAXILLARY GROWTH
A. The maxilla is displaced downward and forward, but is
remodeled upward & backward.

B. Growth of the maxilla & its associated structures occurs


from a combination of growth at sutures & direct remodeling
of the bone.

C. The maxilla is translated downward and forward as the


face grows and new bone fills in at the sutures.

D. The surrounding soft tissues playing a role of a functional


matrix contribute to the growth of the maxilla.

E. Growth of the cartilage of the nasal septum plays a role in


the translation of the maxilla.
MANDIBLE GROWTH
MECHANISMS & THEORIES
A. Growth mechanisms of the mandible
• a. Cartilaginous contribution (condylar,
coronoid and angular)
▫ Exits which is more easily modulable & more
subject to local control systems
• b. Periosteal contribution
▫ Exists which is subordinated both to orders
affecting the whole organism & to local control
factors represented chiefly by muscular
contraction
MANDIBLE GROWTH
MECHANISMS & THEORIES
B. Skeletal subunits of the mandible
• The basal bone of the body forms one unit, to which
are attached the alveolar, coronoid, angular &
condylar processes and the chin.
• Functional matrix theory (Moss):
▫ a. Teeth act as a functional matrix for alveolar unit.
▫ b. Action of temporalis muscle influences the coronoid process.
▫ c. Masseter and medial pterygoid muscles act upon mandibular
angle and ramus.
▫ d. Lateral pterygoid has some influence on condylar process.
▫ e. Functioning of related tongue and perioral muscles and
expansion of the oral and pharyngeal cavities provide stimuli for
mandibular growth to reach its full potential.
MANDIBLE GROWTH
MECHANISMS & THEORIES
C. Condylar cartilage
• a. Periosteal growth processes involved in ramal, corpal and
alveolar growth were viewed as secondary to the condylar changes.
• b. With time, the periosteal contributions were further diminished
conceptually.
• c. The proliferative zone of the mandibular condyle in a non-
functional environment.
• d. The influence of extrinsic factors upon the mandibular condyle
is on cellular differentiation rather than on the proliferative
activity that is linked to some intrinsic programmer of a genetic
nature.
• e. Differentiation between primary cartilages (such as epiphyseal
plate) and secondary cartilages (do not develop ontogenetically
and phylogenetically from the primary cartilaginous skeleton).

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