1

SECTION II

Growth & Development

Chapter 2

General Principles & Concepts of Growth

Introduction
Definitions related to growth and development
Methods of studying growth
Methods of gathering data
Types of growth data
Factors influencing growth and maturation
Basic tenets of growth—Pattern, variability, timing
Clinical implications of growth
The nature of skeletal growth—osteogeneis
Endochondral bone growth
Intramembranous bone growth
Mechanisms of bone growth—Remodelling, drift, displacement
Wolf’s law of transformation of bone
Theories of growth
Remodeling theory
Genetic theory
Sutural dominance theory
Cartilaginous theory
Functional matrix theory
Van Limborgh theory
Enlow’s “V” principle
Enlow’s “counterpart” principle
Neurotropism theory
Servosystem theory

INTRODUCTION
The growth of the face is characterized by a number of changes that occur from birth to adult. One
should have a Good knowledge of about how where and when this normal changes occur in the normal
facial complex. The growth pattern of an individual has a strong influence on dentition.This helps dental
surgeon to identify and diagnose any existing abnormalities so that better treatment can be provided to
the patient..

DEFINITIONS RELATED TO GROWTH AND DEVELOPMENT

Growth
There is no universally accepted definition of growth. Various clinicians have defined growth in different
ways.

JS Huxley “The self multiplication of living

substance.”
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Krogman “Increase in size, change in proportion

and progressive complexity.”

Todd “An increase in size.”

Moyers “Quantitative aspect of biologic

development per unit of time.”

Moss “Change in any morphological

parameter, which is measurable.”

Profitt “Growth refers to an increase in size/

number.”

Meridith “Entire series of sequential anatomic

and physiologic changes taking place
from the beginning of prenatal life to
senility.”

Generally, growth is irreversible. It is partially true as in the case of increase in the length of the body.
Growth may be reversible as seen in the case of increase in weight of the body. Growth is generally
associated with an increase in size and is unidirectional. There are some conditions, which involve
regression or negative growth. The best example is the atrophy of the thymus gland that occurs after
puberty. Another example is senile regression that occurs during old age.

Development
Growth is often used as a synonymous for development. Biologically, development is a process of
continuous changes occurring in a predetermined direction. Various authors have given following
definitions.

Todd “Development is progress towards

maturity.”

Profitt “Development is in complexity.”

Moyers “Development refers to all the naturally

occurring unidirectional changes
in the life of an individual from its
existence as a single cell to its
elaboration as a multifunctional unit
terminating in death.”

Thus, it encompasses the normal sequential events between fertilization and death.

Growth
Increase in the size or change
in proportions
It is an anatomical
phenomenon
It is quantitative in nature
It includes the dimensional
Development
Increase in complexity and progress
towards maturity
It is physiological and Psychological
(Behavioral) phenomenon
It is qualitative in nature
It includes all the sequential events from
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changes occurring over a fertilization till death

particular period of time
It is Bidirectional. Usually it is Usually it is unidirectional
progressive and can become
regressive some times

Differentiation
Differentiation is the change from a generalized cell or tissue to one that is more specialized. Thus,
differentiation is a change in quality or kind.

Development = Growth + Differentiation Maturation

METHODS OF STUDYING GROWTH

According to Profitt, there are two main approaches to studying physical growth. The datum is collected
for the evaluation of physical growth, which is done in two ways.

Measurement approach Experimental approach

This is based on the techniques for measuring living This approach uses experiments in which
growth is
animals (including humans). The measurement itself manipulated in some way. These are destructive
techniques
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will do no harm as the animal will be available for where the animal that is under observation is
killed.
additional measurements at another time. Animal Experimental approaches are usually not carried
out on
will not be killed for experimental purpose. humans for this reason; such experimental
studies are
restricted to non-human species.
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Methods of
Studying Growth

Measurement Experimental
Approach Approach

Vital staining
Craniometry

Autoradiography
Anthropometry
Radioisotopes

Cephalometry
Implant Radiography

Natural markers
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1. Measurement Approach:
a) Craniometry 2. Involves measurement of skulls found among human skeletal remains.
3. Advantage: Exact measurements can be made directly on dry skulls
4. Disadvantage: such a growth study can only be cross sectional.

b) Anthropometry 1. Involves measuring skeletal dimensions on living individuals.

2. Various bony landmarks identified on the dried skulls are transferred on to the
living individuals the by using corresponding soft tissue points.
3. Advantage is that the longitudinal studies can be conducted with repeated
measurement without any harm to the subject.

c) Cephalometry 1. It is a standardized radiographic technique of the craniofacial region

introduced by Broadbent in 1931. He designed a cephalostat for correct
orientation of the head.
2. combines the advantages of both craniometry and anthropometry
3. Direct bony measurements as seen on the radiograph can be made over a
period of time for the same individual.
4. Serial radiographs can be taken to predict and assess the growth of the
Individuals under study.
Experimental Approach:
a. Vital Staining Originated by John Hunter in 18th century.
Growth is studied by observing the pattern of stained mineralized tissues after the
injection of the dyes into the animal. These dyes remain in the bones and the
teeth, and can be detected later after killing the animal.
1. It is possible to study the manner and type of bone laid down.
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2. It also helps us to study the site of growth, the direction, duration and
amount of growth at these different sites in the bone.
Such studies are, however, not possible in the humans as the experimental
animal has to be killed. The dyes used for this purpose are listed further.

Stains used : 1. Alizarin red 2.Acid Alisarin blue 3.Trypon blue

4. Tetracycline and 5. Lead acetate

In 1936, Belchier accidentally noted that bones of animals, which had eaten
madder plants were stained red. Subsequently, the dye in the madder plant,
Alizarin was identified and used for bone research.
It was discovered too late that tetracycline is an excellent vital stain that binds
to calcium at growth sites in the same way as Alizarin.

1. Autoradiography is a technique in which a film emulsion is placed over a thin

b. section of tissue containing radioactive isotope.
Autoradiography 2. This tissue section is exposed in the dark by the radiation. After the film is
developed, the location of the radiation indicates where growth is occurring in
the given tissue section

c. Radioisotopes 1. Radioisotopes of certain elements or compounds act as in-vivo markers.

2. When injected into body they get incorporated in the developing bone or other
structures. They can be detected by means of a Geiger counter by tracking
down the radioactivity they emit, e.g., 99mTc, Ca-45 labeled component of
protein, e.g., proline.
3. The gamma-emitting isotope 99mTc can be used to detect areas of rapid
bone growth in humans, but these images are more useful in the diagnosis of
localized growth problems than for studying growth patterns.

d. Implant Implant radiography, the use of implants to study bone growth was first
Radiography introduced by Bjork in 1969.
This technique can also be used in human subjects.
1. The metallic implants used for studying growth are usually very tiny and
biologically inert alloys (generally made of titanium) into growing bone.
He placed the implant pins in certain areas of the mandible (symphysis,
corpus and lateral aspect of the ramus) and the maxilla (on the
zygomatic bone ridges, hard palate, below the anterior nasal spine).
2. These serve as radiographic reference points for serial radiographic
analysis. These implants serve as reference points to study the amount,
direction and manner of bone growth.
3. Superimposing radiographs (cephalograms in case of face) on the
implants allow precise observation of both changes in the position of one
bone relative to another and changes in external contour of the individual
bone.

C. Others
e. Natural Markers 1. Normal bone has certain histological features such as nutrient canals
and nutrient foramina, transverse lines to apportion, lines of arrested
growth and certain prominent trabeculae.
2. These successive development features of a bone can be used as
natural markers to study growth by means of serial radiographs.

3. Natural markers can be used to study bone remodelling including bone

deposition and resorption.
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f. Molecular 1. Rapid advances in molecular genetics are providing new information

genetics about growth and its control.
2. The family of transforming growth factor-beta( TGF-β) genes now are
known to be important in regulating cell growth and organ development.

g. Twin studies To study the comparative influences of Genetic and Environmental influences on
the Growth

METHODS OF GATHERING DATA

The various growth studies can be broadly grouped as:
a) Longitudinal studies
b) Cross section studies
c) Semi-longitudinal studies

1. Longitudinal Studies 2. Cross-sectional Method

 As the name implies these studies extend
over a long period of time(months to years).
 The observation and measurements are
made on the same person/group at regular
intervals repeatedly over a prolonged
period.
Thus it is basically a follow-up examination
Example: To assess the change is height of the
individuals, an initial examination is done at 10
years and the same group( same individuals) is
reexamined at 12 years of age.
Advantages
1. Best to study the Growth pattern and timing.
2. It is more accurate
2. The individual variations within the group can
be identified easily.
Disadvantages
1. Time consumption is more as the follow-up
period may extend to years together.
2. Sample size is restricted
2. Specific laboratory research tool and data
storage are expensive.
3. The attrition (reduction) in selected samples
is a common problem in this method because
this study is conducted for many years. For
example, if 50 children are chosen as sample
for the longitudinal study, few may die and
few may migrate to other places or lose
interest during the course of study.
Here different individuals in different groups are
examined at a single point of time. It is a quick
process.
For example, in a school survey measuring the
change in height --- two different groups of 10-
year-old and 12-year-old girls, on the same day
are examined . The change in heights later
determined from the data obtained..
Advantages
 It is quicker as studies are short duration.
 It is possible to get a large sample as the
duration of study is short
 statistical analysis can be conducted
easily.
 Study can be repeated if there is any
flaw. This may not be possible in a
longitudinal study.
 They are less expensive than
longitudinal studies as they are
completed in a shorter span of time.
Disadvantages
Comparison of different groups to obtain the end
result is difficult sometimes.
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3. Overlapping/Semi-longitudinal Method

This method is a combination of both longitudinal and cross-sectional methods and derives the
advantages of both the methods in gathering growth data.

TYPES OF GROWTH DATA

Various methods of studying growth are:
1. Opinion
2. Observations
3. Ratings and rankings
4. Quantitative measurements
5. Experimental approach
6. Measurement approach
The physical growth can be studied by a number of ways.

1. Opinion
Opinion is the crudest means of studying growth. This is expression of a person’s opinion on simple
observations. It is not very scientific and should be avoided when better methods are available. For
example, father expresses his opinion to mother that their daughter is going to be taller than her
(mother).

2. Observation
Observations are useful for studying all-or-none phenomena, e.g., absence of caries, periodontal
disease, presence or absence of a class II molar relation, etc..

3. Rating and Rankings

Certain data are difficult to quantify. In such cases we may use ratings and comparison. 54 Ranking is
the method of arranging the data in a sequential order according to its value. For example, the ranks of
the students are determined on their performance in the sports.

4. Quantitative Measurements
A scientific approach to study growth is one that is based on accurate measurements. The
measurements taken can be of three types:
n Direct data: Direct data are obtained from measurements that are taken directly on living persons or
cadavers by means of scales, measuring tapes or calipers.
n Indirect data: The growth measurements can also be taken from images or reproduction of the
person such as photographs, radiographs or dental casts.
n Derived data: These are data that are derived after comparing two measurements. These two sets of
measurements can be of different periods or of two different samples. For example, mandible grows 2
mm when measured at 7 and 8 years of age.

FACTORS INFLUENCING GROWTH AND MATURATION

A number of factors affect the rate, timing and character of growth. They include:
1. Genetic factors: There seems to be a considerable genetic influence on the size of parts, rate of
growth and the onset of growth. A genetic control influences the size of the organism and the rate of
the growth depends on the interaction between the genetic and environmental factors.
For example, in male–female growth differences, the genetic factors play a major role. Females attain
puberty earlier than males due to delaying ‘Y’ chromosome action in males. Thus, the genes play a
major role in the overall growth of a person.
2. Nutrition: Sufficient intake of nutritional food is necessary for normal growth. Malnutrition tends to
cause deficient growth. Minerals such as calcium, phosphorus, fluorides, etc are essential for teeth
and bone growth. In addition, vitamins A, D and C participate in the skeletal growth. Deficiency of
such minerals, vitamins, etc in food leads to defects in the growth of bone/teeth. For example, vitamin
D deficiency - Rickets; vitamin C deficiency - scurvy.
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3. Illness: Chronic and debilitating illness can affect malocclusion either as direct cause or as a result of
its treatment. The effect of disease is similar to that of malnutrition. After an illness, a catch-up growth
is possible to bring back the child to normal growth when the illness is treated. For example,
poliomyelitis – paralysis of orofacial muscle results in malocclusion.
4. Hormones: Hormone imbalances show effect on the physical growth. For example, growth hormone
(pituitary) deficiency leads to retarded growth of skeletal tissue and excess leads to acromegaly,
which causes mandibular prognathism.

5. Race: Different races exhibit various growth and development. This is again influenced by climate,
nutrition and socioeconomical status. For example, the timing of calcification and eruption of teeth
occurs almost a year earlier in Black population compared to their White counterparts.
6. Socioeconomic factors: This includes some growth factors mentioned previously (e.g., nutrition).
Children in favourable socioeconomic conditions tend to put on weight and grow in height more when
compared with unfavourable children.
7. Family size and birth order: There are differences in the sizes of individuals in their maturation and
their intelligence, which can be correlated with the size of the family. Studies have shown that the first
born babies in the family weigh less at birth and have smaller stature but higher IQ. The smaller size
families have better advantage in terms of nutrition and other basic needs compared to a bigger
family.
8. Exercise: Adequate exercise may be essential for the development of motor skills for increase in the
muscle mass, for fitness and for general health conditions.
9. Secular trends: Changes in the size and maturational status are notably advancing between
generations. The puberty age for the current generation girls is much earlier compared to the
previous generation. This is called as secular trends in growth.
10.Climate and seasonal effects: The cold climate residents have a greater proportion of adipose
tissue. The climate influences the variations in the growth rates of children and in the weights of
newborn babies. Climate changes are believed to have a minute direct effect on the rate of growth.
11.Psychological factors: When children experience stressful conditions, it retards the growth due to
deficiency of growth hormone secretion. Removal of stressful condition tends to normal secretion and
“catch-up” growth is seen.

BASIC TENETS OF GROWTH—PATTERN, VARIABILITY, TIMING

Concept of Normality
To know the abnormality, one should have the knowledge of normality. ‘Normal’ refers to something
which is usually expected, is ordinarily seen or is typical. An important aspect of craniofacial growth is
that normality changes with age. Thus, what is normally seen or is expected for one age group may not
be necessarily normal for a different age group.

1. Pattern
The first important feature of growth corresponds to pattern. ‘Pattern’ refers to “A set of proportional
relationships at a given point of time and also refers to the change in these proportional relationships
over time.”. Under pattern, we will study cephalocaudal gradient of growth, rhythm of growth and
Scammons growth curves.

i. Cephalocaudal Gradient of Growth—Scammon

Cephalocaudal gradient of growth simply means that there is an axis of increased growth extending from
head (cephalic) towards the feet (caudal region). .

There is difference in the growth rate between different regions or structures in the body when compared
prenatally and postnatally. During growth and development, a gradual change in the overall body
proportions is noted.
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This is because that the postnatal growth of regions or parts of the body that are away from the
hypophysis grow more rapidly and at a faster rate than the structures that are nearer to it.

In fetal life, about the third month of intrauterine development (IUD), head occupies 50% of the total body
length and within the head the cranium is large relative to the face. The trunk and limbs are rudimentary.
By the time of birth, the head is proportionately decreased to 30–40%. Gradually, the limbs occupy 50%
of the vertical length and the head proportionately reduced to 1/8 or 12% of total body length of a
normally grown adult (Fig. 2.1). This is referred popularly as ‘cephalocaudal gradient of growth.’ The
word ‘gradient’ refers to “changes or increase and decrease between one region and another.” Cepha’
means “head” and ‘caudal’ refers to “elongated extremity of an organ/body.” In this case, it points to the
lower limbs.
‘

At birth In adults

Head 39% of the total 12% of the body

body length length

Legs 1/3rd of total body ½ of total body length length

Changes from birth to adulthood

Head 2 x Birth size

Trunk 3 x Birth size
Arms 4 x Birth size
Legs 5 x Birth size

Thus, we can see that during post natal growth, trunk and limbs grow faster than head and face. Again
within head also, cephalocaudal gradient of growth is evident as the face (viscero cranium) grows
proportionately at a higher rate compared to cranium ( neuro cranium). The neurocranium or cranium,
which occupies more than 50% of the skull at birth is relatively decreased to 30% the vertical length of
the skull in adults due to increased growth of the face or viscerocranium (Fig 2.2).

Once again within the face, the cephalocaudal gradient of growth is reflected postnatally with
mandible growing at a faster rate compared to maxilla, as it is situated relatively farther away from sella
turcica compared to maxilla.

ii. Differential Growth—Growth Characteristics of Different Tissue Systems

The human body does not grow at the same rate throughout life. Different organs grow of different rates,
to different amount and at different times. This is termed differential growth.

Scammon’s Curve of Growth (Fig. 2.3)

Different tissues and organs exhibit different patterns of growth. Richard Scammon has given classical
curves to explain the growth patterns of different tissues in the body. These curves cover the postnatal
period right from the birth to 20 years of age.
The body tissues can be broadly classified into four types. They are lymphoid tissue, neural tissue,
general tissue or somatic and genital tissue. Each of these tissues grow at different times and rates.
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ii. Rhythm of Growth

According to Hooton, “Human growth is not a steady and uniform process”. Not all the parts of the body
enlarge at the same rate and the increments of 1 year equal to that of the preceding or succeeding
year.” However, there seems to be a rhythm during the growth process. This growth rhythm is most
clearly seen in stature or body height.
The first ‘wave’ of growth is seen in both sexes from birth to the 5 th or 6th year. It is most intense and
rapid during the first 2 years. There follows a slower increase terminating in boys about the 10–12th year
and in girls no later than the 10th year. Then both sexes enter upon another period of accelerated
growth corresponding to adolescence, which is completed in girls between the 14 th and 16th year, but
extends in boys through the 16th or 18th year. Following this, a final period of slow growth is seen, which
ends between the 18th and 20th years in females, but goes on in boys until about the 25th year.

iv. Growth Spurts (Fig. 2.4)

Growth does not take place in a steady manner in the growing individual. There are certain periods
where a sudden acceleration of growth occurs. These periods are called growth spurts.
Growth spurts are believed to be due to the physiological changes in hormonal secretion. For
example, during puberty, secondary sexual characteristics appear due to secretion of sex hormones
(males’ testosterone and females’ estrogen).
The timing of growth spurts varies in males and females. The growth spurts occur earlier in girls
compared to boys.
In general, three ‘L’s should be remembered in boys. Growth spurts start late in boys and extends
longer, thereby giving larger growth compared to females.

Clinical Implication of Growth Spurts

Knowledge of growth spurts is essential for successful treatment planning in orthodontics. This helps us
to decide the timing of orthodontic treatment, i.e., whether to start the treatment at the time of peak
growth or after the active growth is completed.
1. Interceptive orthodontic procedures are performed during the growth spurt period. Correction of
skeletal malocclusions during this period is the best choice avoiding surgical corrections in the future.
Skeletal malocclusions are corrected by functional appliances and orthopaedic appliances. For
example, for class II skeletal correction, functional appliances like activator, Bionator, etc are used
during the pubertal growth spurt period.
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2. Malocclusions needed to be corrected surgically can be carried out after the completion of active
growth.
3. Arch expansion (skeletal expansion) can be undertaken during these growth spurts.
4. To differentiate the growth: Whether normal or pathologic can be determined. Puberty and the
adolescent growth spurt occur on the average nearly 2 years earlier in girls than in boys. Thus the
growth modulation procedures by functional appliance therapy must be done earlier in girls than in
boys to take advantage of the adolescent growth spurt. In girls, it should be done in late mixed
dentition stage and in boys in early permanent dentition stage.
5. Onset of menarche in females and change to male voice in boys indicates that they have crossed the
peak height velocity of pubertal growth spurt.

2. Variability
Deviations from the usual pattern are called as variability. All the individuals do not show a similar way of
growth. Thus, it is important for a clinician to assess whether the patient falls under normal, extremes of
normal or abnormal. One of the methods of assessing is to evaluate a patient (child) based on the
standard growth chart. Variability in growth may be due to external influence (illness/trauma) or from
timing effects.

3. Timing
Variation in timing arises because the same biological event that happens for different individuals at
different times. Such a variation in timing is evident in onset of adolescence. In a given population, some
may be rapid growers and some are slow growers. For example, the time of onset of menarche in girls,
which is a good indicator of arrival of sexual maturation need not necessarily be same for two girls of
same age or height or weight. This is the reason why biologic age is more relied on than chronologic age
to evaluate a child’s growth status.

THE NATURE OF SKELETAL/ SOFT TISSUE GROWTH

I. CELLULAR LEVEL

At the cellular level of growth in the body, three mechanisms are involved.
1. Hyperplasia/ Multiplicative Growth – Increase in the number of the cells.
2. Hypertrophy/Auxetic Growth – Increase in the size of cell.
3. Accretionary Growth; Secretion of extracellular (intercellular) matrix.

II. TISSUE LEVEL

a. Interstitial Growth: It is the growth process involving within the whole body of the tissue. Each and
every point with in the tissue grows.
 There is growth from a number of different centers within an area
 Either combined or separately all the three mechanisms –Hyperplasia, Hypertrophy and
secretion of the inter cellular matrix are involved.

 It is the characteristic method of growth when non rigid tissues are involved. Soft tissues and
cartilages (other than teeth and mineralized bone) all undergo interstitial growth.

 Soft tissues primarily grows by hyperplasia and matures by hypertrophy finally resulting in interstitial
growth. Growth by extracellular matrix secretion is secondary

 Cartilage behaves like a soft tissue until it is calcified . Interstitial growth is an important aspect of
overall skeletal growth because a major portion of the skeletal system is originally modeled
in cartilage. This includes the basal part of the skull as well as the trunk and Iimbs.
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 If the extracellular matrix is NOT mineralized, interstitial growth may continue in soft tissues
and cartilages.

 Due to Interstitial growth lengthening of growing bone occurs . Interstitial

growth only occurs as long as hyaline is present, cannot occur after epiphyseal plate
closes.

b. Appositional growth

 There is growth from the centers that are located on the surface
 It is the characteristic method of growth when non rigid tissues are involved. Soft tissues and
cartilages (other than teeth and mineralized bone) all undergo interstitial growth.
 In case of hard tissue (bone and teeth), interstitial growth takes place first for the initial tissue
growth. Later, the extracellular matrix mineralizes to form hard tissue; the interstitial growth is not
possible when once the matrix is mineralized tissue.
 In such a case- Hyperplasia, hypertrophy and extracellular matrix secretion all occur only on the surface
of the bone
 The mineralized bone is covered on its surface by a non-mineralized soft tissue membrane called
as periosteum. This is very active and formation of new cells ( osteoblasts) occur in the layer
and they secrete a layer of extracellular matrix on the surface of the existing bone, which then
mineralizes to form a new layer of fresh bone.
 Addition of layers or increments to the surface of existing bone is called appositional bone
growth. This is also called direct or surface apposition
 Appositional growth occurs at endosteal and periosteal surfaces, increases width
of growing bones.

Skeletal Tissue Formation

The craniofacial skeleton is derived from three processes:

Chondrogenesis

Endochondral ossification
Intramembranous
ossification

1. Chondrogenesis: Formation of cartilage is called chondrogenesis. The cartilage is a firm, non-

calcified connective tissue that serves as a skeletal tissue in the body. Cartilage forms the temporary
skeleton of the embryo and supports for certain soft tissues after birth. Cartilage is also present at
articular surface of all joints such as TMJ.
2. Osteogenesis – Mechanism of bone formation:
 Bone is a hard tissue, which forms the framework of the body.
 Bone is a specialized tissue; its origin is from the mesoderm layer.
 It contains 65–70% of inorganic matter and 32–35% of organic matter
 All over the body, bones are invested by soft tissues (muscles, blood vessels, nerves, etc),
which have direct influence on their growth.

Osteogenesis is the process of bone formation. This bone formation takes place by two basic modes,
which are:
a) Endochondral ossification
b) Intramembranous ossification
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a) Endochondral bone formation (Figs. 2.5, 2.6):

 As the name implies this type of the bone formation is from a cartilage model. Initially
formed cartilage is slowly replaced by bone.
 This type of bone formation is seen in the areas of zones under compression.
 This type of bone is pressure adaptive and seen at/with movable joints and some parts of
cranial base.

The following steps are involved in this type of bone formation.

n Mesenchymal cells condensed and differentiated into chondrocytes. These chondrocytes
initially lay down a hyaline cartilage, which is enclosed by perichondrium. This perichondrium is
rich in blood vessels and contains osteogenic cells (Fig. 2.5 A-D).
n The cells of the cartilage are at first small and irregularly arranged. However, in the area where
bone formation is to begin, the cells enlarge considerably and intercellular matrix is formed (Fig.
2.5 E).
n As the cartilage grows rapidly, the intercellular substance surrounding the cartilage cells,
undergoes calcification by the activity of enzyme alkaline phosphatase, which is released from
cartilaginous cells.
n Due to the calcification, the cartilage cells are under-nourished leading to cell death, thereby
leaving empty spaces that are named as primary areole (Fig 2.5 F).
n From the perichondrium, the blood vessels invade the calcified cartilaginous matrix. They are
accompanied by osteogenic cells. These blood vessels along with the osteogenic cells is called
as perio-steal bud and eat up the calcified matrix. Thus, primary areolas are fused, thereby
leaving large empty places called secondary areole or medullary spaces (Fig. 2.5 G, H).
n The osteogenic cells that are carried from the perichondrium transforms into osteoblasts .
These osteoblasts secrete osteoid on the remnants of the calcified cartilage matrix (Fig 2.5 I).
n The osteoid tissue laid by osteoblasts mineralizes to form a lamella of bone. Above this, layer
by layer osteoid secretion proceeds to form a bone. This is similar to intramembranous bone
formation discussed below (Fig. 2.5 J, K).
n Thus, the cartilage precursor is necessary in endochondrial bone formation. Please note
however the bone is not directly formed from the cartilage but slowly replaces it.

Importance of endochondral ossification:

 The hyaline cartilage from which endochondral bone is formed behaves like a soft tissue. It can
develop in size by interstitial growth (hypertrophy and hyperplasia) and bone grows initially
interstitially and later by appositional growth (surface deposition).
 Cartilage unlike bone can withstand pressures during growth, e.g., cranial base and mandibular
condyle (in case of mandibular condyle, remember it is fibrous cartilage).
 Endochondral bone formation is not unidirectional.
 It is the main type of bone formed during fracture healing
 The entire process of endochondral ossification is continuous and repetitive, one zone
transferring into the next.

b) Intramembranous bone formation (Fig. 2.7): In this type of bone formation, there is no cartilage
precursor; there is directly laying down of the fibrous membrane. Bones of calvaria, facial skeleton
(maxilla and mandible) are few examples of intramembranous bone formation. Following steps are
involved:
n Initially, the mesenchymal condensation takes place. In these, few cells lay down bundles of
collagen fibres and other cells enlarge and differentiate into osteoblasts.
n These osteoblasts secrete osteoid around the collagen fibres. The osteoid is a gelatinous
matrix, which flows in and around the collagen fibres.
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n This osteoid calcifies to form bone lamella; few osteoblasts become entrapped in their own
matrix and become osteocytes. Remaining osteoblasts move away from the lamellae and a
new layer of osteoid is secreted and calcifies to form one more layer. Thus, in intra
membranous bone formation there is no cartilaginous precursor. Addition of layers to the
surface of existing bone is called appositional bone growth.

Importance of membranous ossification:

1. Intramembranous ossification or growth is seen in the areas of tension.
2. Growth takes place outward externally.

Face Cranial Cranial

base vault

Purely intra- Maxillary Parietal

membranous and nasal and frontal bones

Both endo- Mandible Occipital,

chondrial temporal,
and intra- sphenoid
membranous bone

Purely Ethmoid endochondrial bone

Characteristics Cartilage Bone

Calcification Non-calcified Calcified

Blood supply Nonvascular Vascular

Rigidity Flexible Inflexible

Pressure Tolerant of Sensitive to

resistance pressure pressure

VARIOUS MECHANISMS OF BONE GROWTH

Various mechanisms of bone growth are (Fig. 2.8):
1. Remodelling
2. Growth fields, growth sites, growth centres
3. Growth movements
a) Cortical drift
b) Displacement

1. Remodelling
16

Before going to remodelling, we should know about bone apposition and bone resorption.

Bone Deposition and Resorption

Bone changes in shape and size by two basic mechanisms, bone deposition and bone resorption. The
process of bone deposition and resorption together is called bone remodelling. Addition of new bone to
the bony surfaces by osteoblastic activity is called apposition (deposition) usually represented by “+”
sign. The removal of bone by osteoclastic activity is called resorption usually represented by “-ve” sign.
The progressive sequential change in the position of the bone as a result of remodelling is called as
relocation.

Remodelling is the differential growth activity involving simultaneous deposition and resorption on all
the inner and outer surfaces of the bone, e.g., ramus moves posteriorly by a combination of resorption
and deposition (Fig. 2.9).

The changes that bone deposition and resorption can produce are
n Change in size
n Change in shape
n Change in proportion
n Change in relationship of the bone with adjacent structures

2. Growth Fields
The outside and inside surfaces of a bone are blanketed by a mosaic-like pattern of soft tissues,
cartilage or osteogenic membrane called as growth fields. These when altered are capable of
producing an alteration in the growth of the particular bone. For example, take brain as a “growth field.”
The growth of the brain is adapted to the calvaria (cranial base and vault), causes the growth of the
calvaria by resorption at inner side (endosteum) of the calvaria and deposition at outer side of the
calvaria, thereby calvaria grows accordingly (periosteum) with the growth of the brain. These growth
fields may be “growth sites” and “growth centres,” which were coined by Baume.

i. Growth sites ii. Growth centres

Growth sites are growth fields, which is a
location or place that have a special
significance in the growth of a particular point of
the bone, e.g., mandibular condyle in the
mandible, maxillary tuberosity in the maxilla.
Growth centres are special growth sites, which
control the overall growth of the bone, e.g.,
epiphyseal plates of long bones.

The growth sites may possess less intrinsic They are genetically controlled and have the
potential to grow. They do not have inherent inherent capacity to grow on its own when
potential and cease to grow when transplanted transplanted at another place.
at other sites.

They control the localized areas and most of the They control overall growth of the bone. They
times they are under the control of external are less effected by external factors,but respond
factors. to functional demands.

All growth centres are growth sites. But all the All growth centres are growth sites. But all the
growth sites are not growth centres. growth sites are not growth centres.
17

3. Growth Movements
Growth movements are primarily of two types:
a) Displacement
b) Drift (cortical drift)

a) Displacement (Fig. 2.10)

It is the movement of the whole bones as a unit. Displacement can be of two types:
n Primary displacement or translation: This is the displacement of the bone as a result of its own
growth. For example, growth of the maxilla grows with deposition of bone at the tuberosity region.
The formation of new bone at its post-erior end results in pushing of the maxilla against the cranial
base, which results in the displacement of the maxilla in a forward and downward direction.
n Secondary displacement or translocation: This is the dislacement of the bone resulting from the
pull or push of the growth of the peripheral structures or an adjacent bone. For example, the growth of
the cranial base pushes the entire maxilla in forward and downward direction. This displacement is
passive in nature.

b) Cortical Drift (Fig. 2.11)

All bone structures have one growth principle in common, which was termed as drift by DH Enlow.
Cortical drift is a type of growth movement occurring towards the depository surface by a combination of
resorption and deposition (Fig. 2.11A).
Drift of the bone may occur in the same direction as displacement, e.g., palate, both in downward
direction. Drift of the bone may occur in opposite direction of displacement, e.g., condylar growth and
maxillary growth. Bone deposition takes place in posterior and superior direction of the maxilla and
mandible where they are displaced anteriorly and inferiorly, i.e., forward and downward.
If bone deposition and resorption on either side of a bone are equal, then the thickness of the bone
remains constant (Fig. 2.11B). A best example is cranial vault. As the brain grows, the diameter or size
of the cranial vault also increases; but the thickness is maintained. Herein the drift mechanism occurs by
apposition or deposition at the outside (periosteum) and resorption at the inner side (endosteum) occurs
in same rate; but the direction of growth (relocation of the cranial vault bone) is determined by brain
enlargement.
If in case more bone is deposited on one side and less bone resorbed on the opposite side, then the
thickness of the bone increases (Fig. 2.11C).
On the other hand, if resorption dominates deposition, it may result in decreased dimensions.

THEORIES OF GROWTH
1. Remodeling Theory of Craniofacial Growth (Brash)
The research by Brash on bone provided the foundation for the development of the first general theory of
craniofacial growth – the remodeling theory. The remodeling theory postulated that all of craniofacial
skeletal growth occurs exclusively by bone remodeling – selective addition and resor-ption of bone at its
surface sutures and the cartilages of the craniofacial skeleton have little or no role in the growth of the
craniofacial skeleton.

2. Genetic Theory (Brodie)

This is one of the earliest theories put forward by Brodie. According to this theory, the entire growth
process is under the influence of genetic control and is pre-programmed. The role of ‘genetic’ tissues in
growth is controlled by epigenetic influences from other tissue groups and their functional, structural and
developmental input signals.

3. Sutural Dominance Theory (Weinmann and Sicher)

 The sutural theory is put forward by Weinmann and Sicher, two prominent anatomists.
 According to Sicher’s view, all bone-forming elements are growth centres (cartilage, suture and
periosteum).
18

 These growth centres are primarily under the control of heredity and this theory is also based on
the genetic control of growth.
 Sicher believed that craniofacial growth occurs at the sutures.
 The facial areas are attached to the skull and the cranial base region by paired parallel sutures.
 These sutures push the nasomaxillary complex forwards to pace its growth with that of the
mandible
 However, this theory is referred to as the sutural dominance theory with proliferation of
connective tissue and its replacement by bone in the sutures being a primary consideration.

Points Unfavourable to this Theory

 The sutures between two facial bones when transplanted to another location (to a pouch in the
abdomen), the tissue does not continue to grow. This indicates a lack of innate growth potential
in the sutures.
 Microcephaly (small head) – if the cranial sutures are primary growth centres, this condition
cannot be explained.
 In the cleft palate, growth continues in absence of sutures.

4. The Cartilaginous Theory/ Nasal septal theory (Scott)

 This is put forward by the Irish anatomist, James H Scott.

 According to him, the cartilaginous sites throughout the skull as primary centres of growth.
 According to this theory, sutures play little or no direct role in the growth of the craniofacial
skeleton, but cartilage and periosteum play primary role in the craniofacial growth.
 According to him, intrinsic growth-controlling factors are present in cartilage and periosteum with
sutures being only secondary.
 Scott concludes that various craniofacial regions are dependent primarily on the cartilage and
secondarily on the sutures. He explained his theory with following examples.

1. Mandible: The mandible can be viewed as a diaphysis of long bone, bent into a horse-shoe shape
with epiphysis removed so that the cartilage constituting half an epiphyseal plate at the ends are
represented by the condyles. He explained the mandibular condylar cartilages are growth centres for
the growth of the mandible as its “pushes” the mandible downward and forward.
2. Calvaria (base and vault): “Synchondrosis” in the cranial base is the primary cartilage for the
calvaria growth and sutures of cranial vault are secondary. These two factors are involved in the
calvarian growth.
3. Mid face (nasomaxillary complex): He explained that the “nasal septal cartilage” is responsible for
mid face growth in the prenatal and postnatal period up to 4 years of age in humans. The nasal septal
cartilage situated against the cranial base “drives” the midface downwards and forward.

Latham elaborated on Scott’s idea and emphasized the role of septopremaxillary ligament in the
growth of face in the beginning of later part of fetal period.

Points Justifying Scott’s Theory

 Transplantation of the nasal septal cartilage and epiphyseal cartilage of long bones shows
significant growth. This indicates the innate growth potential of the cartilage.
 Many bones are formed by endochondral bone formation (i.e., cartilage forms first merely
replaced by bone later).
 Injuries to the nasal septum in children results in deficient growth of the midface.
 Removal of nasal septal cartilage in rabbits leads to deficient growth of the nasomaxillary
complex (mid face).

5. The Functional Matrix Theory of “Moss”

The Functional Matrix Concept
 Melvin Moss introduced the functional matrix hypothesis to the orthodontic world in
1962. It was developed complimentary to the original concept of functional cranial component by
Van der Klaauw (1952).
19

 At present, this is the widely accepted growth theory.

 According to the functional matrix theory of Melvin Moss, bone growth within the craniofacial
skeleton is not genetically determined but is primarily . is influenced primarily by functional
demands.

 .The functional matrix concept attempts to establish the relationship between form and function.

 It stressed the dominance of non-osseous structures of the craniofacial complex over the
skeletal components.

 According to the functional matrix hypothesis, the origin, form, position, growth and maintenance
of all skeletal tissues and organs is always secondary, compensatory and mechanically
obligatory necessary response to chronologically and morphologically prior events or process
that occur in specifically related non-skeletal tissues, organs or functioning spaces. In this view,
the soft tissues grow and both bone and cartilage react and are grown is response to the growth
of soft tissue. This he stated as “Bones do not grow; bones are grown.”

What is functional cranial component?

This is clearly explained by taking the head as an example. Head is a composite structure; number of
relatively independent functions are operating in the craniofacial region. These include respiration,
olfaction, vision, hearing, balance, chewing, digestion, swallowing, speech and neural integration. Each
of these functions is accomplished by certain tissues and spaces in the head.

All tissues, organ spaces and skeletal parts necessary to carry out a given single function have been
termed as “functional cranial component” (FCC).

Each FCC is composed of two elements (Figs 2.12–2.15):

I. A skeletal unit
II. A functional matrix

All the tissues, organs and functioning spaces taken as a whole comprise the functional matrix (soft
tissue component), while the corresponding skeletal tissues, which support and protect this related
specific functional matrix comprise the skeletal unit.

The Skeletal Unit (Fig. 2.12, 2.14, 2.15; Table 2.7)

 All the skeletal tissues associated with a single function is called the ‘skeletal unit.’
 The skeletal unit may be comprised of bone, suture, cartilage, synchondrosis and tendinous
tissue, etc. The skeletal unit (bone) is made up of several small contiguous skeletal units
(microskeletal unit).
 When adjoining portions of a number of microskeletal units work in tandem to carry out a single
cranial component, we term this a macro-skeletal unit. Thus, macroskeleton is composed of
small micro skeletal units.
 Macroskeleton does not necessarily mean same anatomical bone and consists of microskeleton
units situated on different anatomical bones performing same function. Exam-ple is cranial vault.
Cranial vault is a macroskeleton with numerous microskeletons of anatomically different bones.
20

Microskeletal units Macroskeletal units

Condylar process
Coronoid process
Angular process
Corpus
Alveolar process
Chin

Orbital, maxilla,
pneumatic,
palatal basal
microskeletal units

Parietal, temporal,
frontal, occipital,
synchondrosis

Functional Matrix (Fig. 2.13–2.15)

The functional matrix refers to all soft tissues and spaces (muscles, glands, nerves, vessels, fat, teeth
and the functioning spaces) that perform a given function. There are two types of functional matrices:
a) Periosteal matrix
b) Capsular matrix
21

The periosteal matrix (Fig. 2.14, 2.15) The capsular matrix (Figs 2.13–2.15)

 Corresponds to the immediate local  The capsular matrix is defined as the

environment. functional matrix that encloses
functioning cavities/spaces/organs.

 Periosteal matrices include the muscles,  Examples are neurocranial and

blood vessels, nerves, glands, teeth, etc.
These matrices act directly and actively on
adjacent skeletal units. With the direct action, the
skeletal tissue undergoes transformatory
changes by deposition and resorption process.
 The net effect of periosteal matrix is to
alter the form and relative position of that
particular microskeletal unit.
orofacial capsule. Neurocranial
capsule encloses brain. Orofacial
capsule encloses oral, nasal and
pharyngeal spaces. Other examples
are orbital capsule, otic capsule, etc.
The capsular matrix unlike periosteal matrix
acts indirectly and passively on
macroskelteton (in total on all these
microskeletal units) producing a secondary
translation of whole macroskeleton in space
 Capsular matrices do not act by the
processes of resorption and
deposition.

 All orofacial microskeletal units, together with their periosteal matrices exist within orofacial
capsules (oral, nasal, pharyngeal), which surround and protect the functioning spaces of the oral,
nasal and pharyngeal cavities.
22

 As the volume of the functioning spaces increases due to increasing demands, the
surrounding capsule expands and the embedded macroskeletal units are passively translated
in space.
 Since periosteal matrices simultaneously are translated, they in turn produce simultaneous
transformations of their respective microskeletal units (Fig. 2.14).

Thus, the growth of periosteal matrices brings about active transformation of microskeleton, whereas
growth of capsular matrices brings about passive transformation of macroskeleton, which in turn
again stimulates periosteal matrices to bring about transformation of individual microskeletal units.

Neurocranial capsule and orocranial capsule are good examples for capsular matrix present in the
head region. Each of these capsules is an envelop, which contains a series of functional cranial
components (skeletal units and related functional matrix), which as a whole are sandwiched in between
two covering layers (Fig. 2.15).
Neurocranial capsule – Comprises brain and covering layers, aponeurosis, dura mater, skin, etc. In the
neurocranial capsule, the covers consist of the skin and dura mater. Orocranial capsule matrix
comprises spaces like oropharynx, nasopharynx, which arise within the facial bones, grow and are
maintained. In the orofacial capsule, the skin and mucosa form the covering.

Briefly, functional matrix theory is explained by the growth of the cranium. The brain grows primarily and
skeletal unit grows secondarily. Here, primary growth of the capsular matrix (brain) results in a stimulus
for secondary growth of the sutures and syndhondrosis, leading to the overall enlargement of the
neurocranium (macroskeletal). Function of the temporalis muscle exerts pull on the periosteal matrix and
bone growth of the temporal bone (microskeletal unit).
Mandibular growth can be taken for the demonstration of the integrated activity of periosteal and
capsular matrices in facial growth. It is a combination of the morphologic effects of both capsular and
periosteal matrices. Capsular growth causes an expansion of the capsule as a whole. The enclosed
macroskeletal unit is passively and secondarily translated in space to successively new positions. The
periosteal matrices related to these mandibular microskeletal units also respond to this volumetric
expansion (Fig. 2.14).
In essence, all skeletal tissues originate, grow and function completely embedded in their several
matrices. Thus, changes in the size, shape and spatial position of all skeletal units including their very
maintenance is due to the operational activity of their related functional matrices.

Growth Growth process

Active growth - Sutural growth

- Bone remodelling
+ - Cephalic cartilage
growth

Passive growth - Growth of neural, orbital, CSF

and
other masses

Total growth - The expansion of the

oronasopharyngeal
and other functional
spaces
23

6. Van Limborgh’s Multifactorial Theory of Craniofacial Growth

A multifactorial theory, which has given a new view to the morphogenesis of skull was put forward by
Van Limborgh in 1970. This synthesis is essentially from the three basic theories of craniofacial growth.
His theory is conceptual, taking only the positive aspects of Scott’s cartilaginous theory, sutural
dominance theory by Sicher and Moss’ functional

matrix theory. The drawbacks of the above theories were left unanswered to a large extent. Thus, in
essential, it is a logical interpretation of the existing theories. Van Limborgh has suggested the following
six factors that control growth. Van Limborgh lists the essentials of all the three hypothesis.
1. Growth of synchondrosis and endochondrial growth (chondrocranium) is exclusively under the control
of intrinsic genetic factors.
2. The intrinsic factors controlling intramembranous growth, i.e., growth at sutures, perisosteum
(desmocranium) growth to a large extent are general in nature.
3. The cartilaginous parts of the skull must be considered as growth centres.
4. Sutural growth is controlled by both cartilaginous growth and growth of the adjacent structures in the
head.
5. Periosteal growth to a large extent depends on growth of adjacent structures.
6. Intramembranous bone formation is additionally influenced by local non-genetic environmental factors
inclusive of muscle forces.

Definition Factor

Intrinsic genetic Genetic factor inherent to the

factor skull tissues.

Local epigenetic Genetically determined influ-

factor (capsular ence originating from adjacent
functional matrix) structures and spaces (brain,
eye, etc). Bone growth is
determined by genetic control
originating from adjacent
structures like brain, eyes, etc.
General epigenetic Genetically determined
factor influence originating from
distant structure (sex
hormone, growth hormone).

Local environ- Local non-genetic influence

mental factors originating from the external.
(periosteal func- environment, e.g., habits,
tional matrix) muscle force, etc.

General General non-genetic influence

environmental originating from the external
factors environment (nutrition and
oxygen supply, etc).

OTHER THEORIES RELATED TO CRANIOFACIAL GROWTH

1. Enlow’s ‘V’ Principle of Growth (Area Relocation Theory)
Most of the facial bones have ‘V’ shaped configuration. Bone deposition occurs on the inner sides of the
‘V’ and resorption
24

occurs on the opposite outer surface of the ‘V.’ Due to this, the bone moves in the direction towards the
wide end of ‘V.’ Simultaneously deposition takes place at the ends of the two arms of the ‘V,’ resulting in
its widening.
These growth shifts and changes involve corresponding and sequential remodelling adjustments to
maintain the same shape of that particular bone, e.g., base of the mandibular body, coronoid, condylar
process, palate, etc follow the growth of ‘V principle (Figs. 2.16, 2.17, 2.18).

2. Enlow’s Counterpart Principle (Fig. 2.19)

 The counterpart principle of craniofacial growth states that events (growth) in any one region of
the skull necessarily influence the growth in others. Consequently, a functional equilibrium is
maintained

 The growth of certain skeletal parts of the craniofacial region are related specifically to other
structural and geometric counterparts in the face and cranium.

 These various components of the craniofacial structures grow simultaneously.

 A balanced growth occurs if the regional part and its counterpart enlarge to the same extent.

 However, if the counterpart shows variation in growth, it may result in misfit both of the different
anatomical structures of the skull.

This ‘counterpart principle’ suggests that imbalances in the regional relationships are produced due to
variation in:
a. Magnitude of growth between the counterparts.
b. Timing of growth between the counterparts.
c. Directions of growth between the counterparts.

There are number of counterparts, which are situated in the craniofacial region. Few of them are:
n Nasomaxillary complex v/s anterior cranial fossa (Fig. 2.19 B).
n Middle cranial fossa and breadth of ramus are coun- terparts (Fig. 2.19 C).
n Maxillary arch v/s mandibular arch.
n Bony maxilla and corpus of mandible are mutual counterparts.
n Maxillary tuberosity vs lingual tuberosity.

3. Neurotrophism
This was proposed by Behrents in 1970. This theory states that the nerve impulse involving
axoplasmic transport has direct growth potential. It also has an indirect effect on the osteogenic growth
by influencing soft tissue growth.
The different types of neurotrophic mechanisms are:
1. Neuroepithelial trophism
25

2. Neurovisceral trophism
3. Neuromuscular trophism

Neuroepithelial Trophism
Epithelial growth is normally controlled by the release of certain neurotrophic substances by the nerve
synapses. Lack of this neurotrophic process causes abnormal epithelial growth, orofacial hypoplasia and
malformation, etc, i.e., the tissues and epithelium become atrophic when they are deinnervated since the
nerves have a neurotrophic effect in sustaining healthy growth.

Neuromuscular Trophism
At the myoblast stage of differentiation, the embryonic myoblasts establishes neural innervation without
which further myogenesis usually cannot continue.

Neurovisceral Trophism
The periosteal matrices genetically determine the apparent localized neurotrophically controlled
genomes. The attributing factors that form the basis of the neuro-visceral tropism, e.g., the salivary
glands, fat tissue and other organ, regulate the embedded passive position of the skeletal units.
The degree to which neurovisceral control has altered the casual change indicates the dominance of
the homeostatic control of genome.

10. Servo System Theory

This theory was postulated by Alexander G Petrovic. To understand the concept of this theory, it is
important to know few key differences between primary and secondary cartilage (Table 2.10).

The servo system theory is explained in a cybernetic language (Fig. 2.20). According to this theory, the
growth of primary cartilage (maxilla) is controlled by somatomedin hormone (STH) complex through a
cybernetic command. There are no local feedback loops. Whereas the growth of secondary cartilage
(mandible) by STH complex is by direct or indirect effect on cell multiplication and not by a command.
The indirect effect is by the influence of local factors multiplication. With condylar, coronoid and angular
cartilages these indirect effects correspond to regional and local factors invol-ving primarily
neuromuscular mechanisms relative to postural adjustment.
From Table 2.10, it is understood that maxilla and cranium comprise primary cartilages, and
mandible arises from secon-dary cartilages.
Local factors cannot influence primary cartilage as the cells are protected by cartilaginous matrix,
which is not the case in secondary cartilage.

PREVIOUS YEARS UNIVERSITY QUESTIONS

Essay Type Questions
1. Define growth and development. Enumerate the different methods of studying growth.
2. What are growth spurts and their implications in orthodontics?
3. Name the different theories of growth and explain functional matrix theory in detail.

Short Answer Questions

1. Factors influencing growth
2. Limborgh multifactorial theory of growth
3. Enlow ’V” principle
4. Scammon’s growth curve
5. Growth spurts
6. Cephalocaudal gradient of growth
7. Wolf’s law of transformation of bones
8. Functional matrix
9. Servosystem
10. Neurotropism
11. Scott’s hypothesis
12.Servosystem theory
26

Very Short Answers

1. Implant studies
2. Involution
3. Remodelling
4. Cortical drift
5. Displacement

REFERENCES
1. Proffit’s Contemporary Orthodontics, Elsevier India. 3/E; 2000 (permission).
2. Graber TM. Orthodontics: Principles and Practice, 3rd ed., WB Saunders; 1988.
3. Moyers E. Handbook of Orthodontics, 4th ed. Year Book Medical Publishers, Inc.; 1988.
4. Limborgh J Van. A new view on the control of the morphogenesis of the skull. Acta Morph Need
Scand 1970;8:143–60.
5. Enlow OH, Hans MG. Essentials of Facial Growth, Philadelphia, Saunders; 1996.
6. Moss M, Salentijn L. The Primary role of functional matrices in facial growth. Am J Ortho 1969;5:566–
77.
7. Moss ML. Neurotrophic processes in orofacial growth. J Dent Res 1971;50:1492–1494.
8. Moss ML. Twenty years of functional cranial analysis. Am J Orthod 1972;61:479–485.
9. Moss ML, Salentijn L. The capsular matrix. Am J Orthod 1969;56:474–490.
10. Donald H Enlow, W Stuart Hunter. A differential analysis of sutural and remodeling growth in the
human face, American Journal of Orthodontics 1966;52 (11): 8–11 (permissions-Elsevier).
11. Donald H Enlow, Robert E Moyers, W Stuart Hunter, James A McNamara. A procedure for the
analysis of intrinsic facial form and growth: an equivalent-balance concept. American Journal of
Orthodontics July 1969;56 (permissions-Elsevier).
12. Donald H Enlow, Seong Bang. Growth and remodeling of the human maxilla. American Journal
of Orthodontics (permissions-Elsevier).
13. Donald H Enlow, et al. An evaluation of the morphogenic and anatomic effects of the functional
regulator utilizing the counterpart analysis. The European Journal of Orthodontics 1988;10(1)
(permissions-Oxford University Press).

Chapter 3.
Prenatal Growth of the Craniofacial
Skeleton
Introduction
Prenatal periods of growth
- Period of ovum
- Period of embryo
- Period of fetus
Primordia of craniofacial complex
- Fertilization, morula
- Bilamellar disk
- Gastrulation
- Trilamellar disk
- Formation of notochord
- Formation of neural crest cells
- Differentiation of mesoderm
- Folding of embryo
- Pharyngeal arches and pouches
27

Prenatal development of craniofacial skeleton

- Neurocranium – Chondrocranium, desmocranium
- Viscerocranium
- Prenatal development of neurocranium
- Capsules and formation of basal cartilages
- Bones of cranial base
- Flexure of cranial base
- Development of cranial vault
- Development of face
- Different processes
- Prenatal growth of maxilla
- Formation of palate – Cleft lip and palate
- Prenatal growth of mandible
- Meckel’s cartilage
- Formation of tongue
- Development of TMJ

INTRODUCTION
Knowledge of basic embryology is essential for under-standing normal postnatal growth as well as the
development of various craniofacial abnormalities.

EMBRYOLOGY OF OROFACIAL STRUCTURES

The life of an individual begins from the single-celled structure “zygote” formed from the fusion of sperm
and ova. This prenatal development from zygote is divided into three successive phases. The forming
individual is described as an embryo or fetus depending on its developmental stage (Fig. 3.1).

PRIMORDIA OF CRANIOFACIAL COMPLEX

After fertilization, mammalian development involves a phase of rapid proliferation. The daughter cells
formed from cleavage of the zygote are known as blastomeres. This proliferative phase lasts until three
germ layers of a ball of cells called the morula is formed. Sixteen-cell stage is called as morula. Note
that the number of blastomeres usually varies from 12 to 16 (Fig. 3.2).

Morula undergoes changes in succession producing blastocyst from which embryo proper, yolk sac and
placenta are formed by cell differentiation (Figs. 3.3, 3.4). During this process of embryo-genesis, a
bilaminar disk and trilaminar disk stage are formed (Figs. 3.4, 3.5 & 3.6). During 4th week, in the
trilaminar disk stage the embryo is called trophoblast. Major tissues and organs differentiate from the
trophoblastic embryo. These include the head and face and the tissues contributed to the development
of the teeth. The term gastrulation means the formation of gut (Greek, gastrula = belly), but has now a
more broad sense to to describe the formation of the trilaminar embryo.The embryonic body wall is
made of three layers: ectoderm (ecto = outside, derm = skin), mesoderm (middle) and endoderm (inner)
layer derived from the totipotent cells of the epiblast layer. Collectively these layers are called primary
germ layers or primary embryonic layers, and each is destined to form certain organs/parts of the body.

In the trophoblastic stage, following important events takes place.

n The differentiation of nervous system and neural crest tissue from ectoderm.
n The differentiation of mesoderm.
n The folding of embryo in two planes along the rostro caudal (head-tail) and lateral plane and the
formation of Notochord (Fig. 3.7).

Formation of Neural Crest Cells (Figs. 3.8, 3.9, 3.10)

28

 The nervous system develops as a thickening within the ectodermal layer at the rostral end
towards head side) of the embryo. This thickening constitutes the neural plate, which rapidly
forms raised margins (the neural folds). A deepening midline depression called as neural
groove is noted at this stage.
 The neural folds eventually fuse so that a neural tube separates from the ectoderm to form the
floor of the amniotic cavity with mesoderm intervening in between.

 As the neural tube forms, a group of cells separate from the neuroectoderm. These cells have
the capacity to migrate and differentiate extensively within the developing embryo. In the avian
embryo, these cells can be distinguished as differentiating and separating at the crest of the
neural folds, hence the name neural crest cell. In the mammalian embryo, these cells separate
from the lateral aspect of the neural plate rather than from its crest; even so, the term neural
crest is retained.
 Neural crest cells have an important role in the head region,. In addition to assisting in the
formation of the cranial sensory ganglia, they also differentiate to form most of the connective
tissue of the head.
 ln Embryonic connective tissue elsewhere is derived from mesoderm and is known as
mesenchyme, whereas in the head it is known as ectomesenchyme because it is formed from
neuroectoderm.

 Neural crest cells leave neuroectoderm and enter mesoderm neural crest cells; gives rise to
heterogeneous array of tissues in the craniofacial region.

1. Ectomesenchyme of facial prominences and brachial arches

2. Membrane bones of face (maxilla, large portion of mandible)
3. Chondrocranium rostral (head) part
4. Dermal tissue of face and neck
5. Odontoblasts – Dental papillae and hence dentin
7. Melanocytes
8. Arachnoid and pia mater (leptomeninges)
9. Cranial nerve ganglia, spinal ganglia, sympathetic chain and preaortic ganglion
10.Schwann cells, glial cells

Improper formation, improper migration of neural crest cells causes various deficient developments of
craniofacial structures. Among these, few important deformities are given in Table 3.2.

Differentiation of Mesoderm (Fig. 3.11)

As the neural tube is formed, the mesoderm present either side of the tube forms paraxial mesoderm.
Along the trunk of the embryo, this paraxial mesoderm breaks up into segmented blocks called somites.
Each somite has ‘three’ components.
n Sclerotome – Gives rise to the adjacent vertebrae and disk.
n Myotome – Gives rise to adjacent muscles.
n Dermatome – Gives rise to the connective tissue of the skin overlying the somite.

In the head region, the mesoderm only partially segments to form a series of somatomeres, which give
rise to the head musculature.

Folding of the Embryo (Figs. 3.12, 3.13)

n The folding of the embryo is initiated at 24th day. The anterior neural plate carries the developing
forebrain up and over the primordial of the oral cavity and heart.
29

n Due to the cephalocaudal folding, the heart, which was in line with the foregut rotates backwards
(dorsally) and downwards and becomes the floor of the pharynx.
n The head fold is critical to the formation of a primitive stomadeum or oral cavity; through this fold
ectoderm comes to line the stomatodeum, with the stomatodeum being separated from the gut by
the buccopharyngeal membrane.
n Thus, the buccopharyngeal membrane is formed around 4th week of IU life with ectodermal lining
towards stomodeum or future oral cavity and on the other side endoderm as lining facing the gut.
n Buccopharyngeal membrane ruptures at the end of 4th week (27th day).

The Pharyngeal Apparatus (Figs. 3.14, 3.15, 3.16)

 Many structures of the head and neck develop from the branchial (pharyngeal) apparatus.
 The apparatus consists of pharyngeal arches, pouches and grooves.
 The grooves are composed of ectoderm, the pouches are composed of endoderm and the
arches are composed of mesoderm and neural crest cells.

 Branchial arches/pharyngeal arches are rod-like thickenings of mesoderm present in the wall of
foregut.

 Five pharyngeal/branchial arches are formed below the stomatodeum in the region of future
head, which are invaginated by ectomesenchymal cells giving rise to bones and cartilages of the
head and dentin and cementum of teeth.
 Initially, there are six pharyngeal arches. They are named from Ist to VIth, except Vth, which
degenerates leaving only five. They are separated by four branchial grooves.

 The first arch is called the mandibular arch and the second arch, hyoid arch. The other arches
do not have any specific names. Each of these five arches contains:
n A central cartilaginous part – Skeletal derivative
n A muscular part – Bronchomere
n A vascular component
n The neural component

Each arch contains all three germ layers. The muscular component of each arch carries its own nerve. In
an orthodontic context, the proper migration of neural crest cells is essential for the development of the
face and the teeth.

Pouches Derivatives

1st pouch n Pharayngotympanic tube

n Middle ear cavity
n Tympanic antrum

2nd pouch n Tonsil

n Tubotympanic recess

3rd pouch n Inferior parathyroid glands

n Thymus

4th pouch Superior parathyroid glands

5th pouch (ultimo Parafollicular cells of thyroid branchial pouch)
30

Groove 1 External auditory meatus

Grooves 2–4 Cervical sinus

Membrane 1 Tympanic membrane

PRENATAL DEVELOPMENT OF CRANIOFACIAL SKELETON

(Skull – Cranial base, Vault, Mandible and Maxilla)
Introduction
The skull forms from mesenchymal connective tissue around the developing brain.

The prenatal development of the skull is considered in two components (Figs. 3.17, 3.18).

1. Neurocranial Thus, neurocranium refers to that portion immediately to the brain

elements or and special sensory organs.The cartilages and bones
neurocranium: developing around the brain are called neuro-cranial elements
(i.e., above cranial vault and below cranial base). These are
derived from occipital somities and somitomeres.
n Cranial base: The neurocranial elements of the cranial
base are mainly derived from cartilages. The endochondral
ossification occurs principally, so it is called cartilaginous
neurocranium or chondrocranium.

n Cranial vault: The neurocranial elements of the cranial

vault are formed from intramembranous ossification (no
cartilage precursors), so it is called membranous
neurocranium or desmocranium.

2. Viscerocranial Those bones supporting the face and associated structures (i.e.,
elements mainly maxilla and mandible) are called viscerocranial elements
.

PRENATAL NEUROCRANIUM
(Cranial Base and Cranial Vault)
Growth of Cranial Base/ cartilaginous neurocranium / chondrocranium.

Initially, the cranial base in prenatal period is by the fusion of several cartilages. Later, these cartilages
undergo endochondral ossification to form the base of the skull/cranial base (Table 3.5).

n Formation of a capsule around the brain called as ectomenix or ectomeningeal capsule.

n The ectomeningeal is slowly converted into cartilage from the end of second week. The mesenchymal
condensation into cartilage is noticed occurs at four regions.
n Thus, the earliest evidence of formation of the cranial base is seen in the post or late somitic period
(4–8th week of intrauterine life).
n In the 18th week, the cranial base cartilages begin to ossify by endochondral bone formation. This
process will continue throughout prenatal and early postnatal life.
n The early establishment of the various nerves, blood vessels, etc, from and to the brain results in
numerous perforations or foramina in the developing cranial base.
31

n Both cartilage and membranous centres support the enlarging bone. The ossifying chondrocranium
meets the ossifying desmocranium (cranial vault) to form the neurocranium.

The series of cartilaginous band consists of following cartilages extending anteriorly to posteriorly (Fig.
3.20):

Synchondrosis
n After endochondral bones are formed, sutures appear gradually in the cranial base between the
ethmoid and sphenoid, and the sphenoid and occipital bones.
These cartilaginous sutures are called “synchondrosis.” The bones are united by a plate of hyaline
cartilage, so that the joint is immovable and strong.
. Their function starts in the postnatal life from birth till 25 years, which are going to be discussed in detail
in the postnatal growth (Fig. 3.21).

The cranial base or chondrocranium acts as a junction between the cranial vault and the facial skeleton,
being shared by both.
The cranial base is relatively stable during growth compared to the cranial vault and the face. Thus, the
cranial base can be taken as a base against which the cranial vault and facial skeleton can be
compared.

Flexure of the Cranial Base (Fig. 3.22)

n Initially cranial base grows linearly.
n During the embryonic and early fetal period, the linearly growing cranial base exhibits bend or flexure
along the transverse axis in the body of the sphenoid.
n The cranial base flexes backwards and downwards to accommodate downward growth of the
increased capacity of brain tissue.
n This flexure of the cranial base is an adaptive mechanism in increasing the neurocranial capacity.
n Now the face, which was in line with cranium descends under the cranium.
n Due to this, the spinal cord and the foramen magnum, which during the early stages of development
were directed backwards, now become directed downwards.
n The cranial growth is flexed in the fetal period. At around the 10th week of intrauterine life, the flexion
of the base is about 65o. This flattens out at the time of birth to 135°.

Uneven Nature of Growth of Cranial Base

The cranial base is characterized by uneven nature of the growth. This is mainly attributed to difference
in the nature of growth seen in the different regions of the brain. The anterior cranial base increases in
length and width by 7 times while the posterior cranial base exhi-bits only 5-fold increase between the
10th and the 40th weeks of intrauterine life.

Growth of Cranial Vault

The sites of intramembranous ossification that appear in the mesenchyme covering the brain is termed
as membranous neurocranium or desmocranium. The cranial vault is formed by intramembranous
bone formation without any cartilage precursor.
n These sites first appear at the 8th week of IUL, the beginning of fetal period, as ossification centres.
The membranous neurocranium gives rise to the flat bones of the calvaria including the superior
portion of the frontal, parietal and occipital bones.
n The calvarial bones are separated by dense connective tissue sutures and six large fibrous areas
called “fontanelles.” These fontanelles enables the skull to undergo shaping during birth, which is
called molding.
32

PRENATAL VISCEROCRANIUM/ DEVELOPMENT OF FACE

The beginning of facial development is seen in the human embryo during the 4 th week of IUL. The face
is formed from the three processes (Fig. 3.23). They are the frontonasal process, maxillary and
mandibular process of the mandibular or first pharyngeal arch (Fig. 3.24).
n The face develops from three promordia or processes resulting in five swellings or structures around
stomadeum (oral cavity). They are frontonasal process (unpaired), a pair of mandibular prominence
and a pair of maxillary prominence (pair or 2). Thus, five structures contribute to the development of
face.
n The frontonasal prominence arises from the growing forebrain and arises from neural crest. It
proliferates and forms a downward projection that overlaps the upper part of stomodeum.
n Maxillary and mandibular prominences are derived from the 1st branchial arch (mandibular arch). The
maxillary prominence arises as an offshoot from the mandibular arch (1st phrayngeal arch).
n First pharyngeal arch consists of dorsal portion called the maxillary process and ventral portion called
mandibular process, which contains Meckel’s cartilage.
n The mandibular prominence is derived directly from the 1st phrayngeal arch. Maxillary process arises
as a offshoot from mandibular process.

1. Frontonasal process: Frontonasal prominence forms the forehead and the dorsum and apex of
the nose. Parts arising from frontal process:
n Upper part of the face (forehead region)
n The nasal septum
n The premaxilla (primitive palate) and philtrum of upper lip

2. Mandibular arch processes (Fig. 3.24): The first arch is called as mandibular arch, which
contributes major share to the development of the face. The mandibular arches of both the sides form
the lateral walls of the stomodeum.
n The mandibular arch gives off a bud from its dorsal end called the maxillary process
The two mandibular processes grow medially and fuse to form the lower lip and lower jaw.
n The mandibular process gives rise to the lower part of cheeks, the lower lip, the lower jaw and part
of the tongue.
3. Maxillary prominences: This arises as a bud from the mandibular arch. It forms upper cheek region
and most of the upper lip, except in midline, which is contributed by frontonasal process. It also
contributes to the secondary palate. The primary and secondary palate fuse to form the definite
palate.
n

The connective membrane between the stomodeum and primitive digestive tract (primitive pharynx) is
called bucco-pharyngeal membrane. By the end of IV week of IUL, this membrane ruptures and forms
continuity with the digestive tract.

Prenatal Development of the Maxilla

Maxilla is purely intramembranous bone. It has a large pyramidical body and four processes –
zygomatic, frontal, alveolar and palatine. It houses the largest air sinuses, the maxillary air sinus within
its body.
n Maxilla develops from the first brachial arch.
n The maxilla is a pure intramembranous bone and there is no arch cartilage or primary cartilage
existing in the maxillary process. However, primary ossification centre of maxilla is closely associated
with the nasal cartilage.
n By around the 4th week of intrauterine life, five branchial arches form in the region of the future head
and region.
n The first branchial arch is called the mandibular arch and plays an important role in the development
of the nasomaxi-llary region.
n The mandibular arch gives off maxillary process from which the maxilla develops.
33

n Maxilla ossifies in membrane from three primary centres of ossification, one for the maxilla proper
and two for premaxilla.
n The maxilla proper develops from a single centre of ossification on each in the mesenchyme of the
maxillary process of the 1st arch. The centre for maxilla proper appears above the canine fossa
during 6th week of intrauterine life on each side.
n The promordia of this mesenchymal tissue is situated in the neural crest cells.
n Around 6th week of IUL, the centre of ossification appears at the termination of infraorbital nerve just
above the canine tooth dental lamina (junction of anterior superior alveolar nerve and infra-orbital
nerve).

n Of the two premaxillary centres, the main centre appears above the incisive fossa during 7th week of
intrauterine life. The second centre – paraseptal or prevomerine appears at the ventral margin of
nasal septum during 10th week and soon fuses with the palatal process of maxilla.

From these primary ossification centres, formation of bone spreads in three dimensions and five
directions.

Posteriorly Below the orbit and lateral sides

of nasal capsule towards the
zygoma.

Superiorly Towards nasal capsule to from

frontal process.

Anteriorly On the outer aspects of anterior

superior alveolar nerve till
incisor region.

Downwards Towards the lateral aspect of

dental lamina and tooth germs as
alveolar plate to accommodate
tooth germs.

Medially The ossification also spreads into

palatine process to form the hard
palate (later discussed in detail).

At around the 8th week of IUL, three secondary ossification centres appears named as zygomatic,
orbitonasal and naso-palatine. Out of these, the zygomatic/molar cartilage mainly contributes to the
zygomatic process development and also for a short time in the general development of the maxilla.
The ventral portion of the first branchial arch, the ‘mandibular’ process, contains Meckel’s cartilage.
Mesenchyme around Meckel’s cartilage condenses and ossifies by membranous ossification and gives
rise to mandible. Meckel’s cartilage disappears, except in the sphenomandibular ligament. Meckel’s
cartilage acts as a scaffold for mesenchymal condensation and does not contribute directly to the
formation of mandible.

PRENATAL GROWTH AND DEVELOPMENT OF THE MAXILLA

The bony structure that forms the upper face is maxilla and the lower face is mandible. The bony
elements, which are supporting these facial skeleton arises from the pharyngeal arches are called
viscerocranial elements.
A secondary cartilage, i.e., zygomatic cartilage or malar cartilage that forms in developing zygoma
contributes much to the growth of the maxilla. There is controversy regarding this.
34

The viscerocranial elements are also of two types.

Cartilaginous Includes the middle ear ossi-

viscerocranium cles, the styloid process, the
hyoid bone and the larger car-
tilage. The bones are formed
by endochondral ossification.

Membranous Includes the maxilla, zygo-

viscerocranium matic bones, squamous part
of temporal bones, the mand- ible &
the midline of the chin.
Development of Maxillary Sinus
Maxillary sinus is the first air sinus to develop. The maxillary sinus forms around the 4th month of IUL.
According to some authors, it develops as early as 9th week (3rd month). It develops on the medial
surface of maxilla as a small invagination of the nasal mucous membrane into the maxillary bone. Later
the sinus enlarges by resorption of the internal wall of maxilla. It develops by invasions and expansion of
the nasal mucous membrane into the maxillary bone.

Development of the Palate (Fig. 3.25)

n The growth and development of the palate is very important because this is a more common area
associated with the developmental failure – cleft palate, which may or may not be associated with the
cleft lip.
n The palate begins to develop around 6th week of IUL and proceeds until 12th week of IUL.
n As described earlier, the frontonasal process gives rise to the premaxillary region or primary
palate, while the palatal shelves from the maxillary proper form the rest of the palate or secondary
palate.
n Thus, the palate is developed from three processes; they are listed further.

n The two A medial growth of two palatal palatine shelves each from the
bilateral
processes maxillary process
(secondary (Fig. 3.25 A,B).
palate)

n The primitive Which harbours the incisors is

palate formed from frontonasal process
(premaxilla/ (Fig. 3.25 A,B).
primary
palate)

n Initially, the palatal shelves grow medially. Their union is prevented by the presence of the tongue.
Due to this inter-vening posture of the tongue, the developing palatal shelves then grow vertically
downwards towards the floor of the mouth (Fig. 3.25C).
n However, during the 8 weeks of intrauterine life, again a transformation in the position of the palatal
shelves occurs. Now they change back from a vertical to a horizontal growth (Fig. 3.25D). This
transformation is thought to be for the following reasons:
- Alteration in biochemical and physical consistency of the connective tissue of the palatal shelves.
- Alteration in vasculature and blood supply to the palatal shelves.
- Intrinsic shelf force within the growing palatal shelves.
- Rapid differential mitotic activity.
35

-
Muscular movements.
-
Descent and withdrawal of the tongue from between the palatal shelves aids in the elevation of the
palatal shelves from a vertical to a horizontal position.
n By 8½ weeks of intrauterine life, the actively growing two palatal shelves are in close approximation
with each other. The connective tissue of the palatal shelves interdigitate with each other resulting in
their fusion. A thin epithelial lining covering the two palatal shelves in the initial stages degenerates as
the fusion is completed.
n This fusions starts by fusing of two palatal shelves ante-riorly with primitive palate; later both palatal
shelves fuse in the midline. The lower free edge of the nasal septum fuses with the midline along with
the fusion of palatine processes. This separates the two nasal cavities from each other and also
separates from the mouth (Fig. 3.25E,F).
n The definitive palate is formed by the fusion of these three processes with each other. The entire
palate does not contact and fuse at the same time. Initially, contact occurs in the central region of the
secondary palate posterior to the premaxilla (Fig. 3.25G).

Ossification of Palate
n Ossification of the palate occurs from the 8th week of intra-uterine life. The palate ossifies from a
single centre derived from the maxilla. The mesoderm in the palate and primitive palate undergoes
intramembranous ossification to form the hard palate and premaxilla (which carries the incisor teeth).
n The posterior most portion of the palate does not undergo ossification, which remains as soft palate.
The most posterior part of the palate does not ossify. This forms the soft palate. The mid-palatal
suture ossifies by 12–14 years.

Cleft Lip and Palate Formation (Fig. 3.27)

n Complete non-fusion of premaxilla (primitive palate) with the both palatal shelves, giving rise to a “Y”-
shaped cleft extending into lips both sides – bilateral cleft lip and palate (BLCLP).
n One side of the palatine process fuses with the premaxilla (primitive palate), but non-fusion on the
other side exten-ding into the lip – unilateral cleft lip and palate (ULCLP).
n Midline cleft extending into the hard palate here; soft palate and hard palate are involved partly.
n Cleft of soft palate only.

PRENATAL GROWTH AND DEVELOPMENT OF THE MANDIBLE

Development of the Mandible Proper (Fig. 3.28)

n The mandible is the second bone next to the clavicle to ossify in the body. It is also the only mobile
bone of the skull besides the ear ossicles. It also contains main core of the body and different
processes like condylar, coronoid, angular, etc.
n Mandible is a mixed bone, i.e., it develops both by intra-membranous and endochondrial ossification.
Its greater part ossifies in membrane bone. The parts ossifying in cartilage include the incisive part
below the incisor teeth, the coronoid and condyloid processes and the upper half of the ramus above
the level of the mandibular foramen.
n The first pharyngeal or the mandibular arch forms the lateral wall of the stomodeum. It gives off a bud
from its dorsal end. This bud is called the maxillary process. It grows ventromedially, cranial to the
main part of the arch.
n When once the maxillary process is formed, now the main arch is called as the mandibular process.
n The mandibular process of both sides grow towards each other and fuse in the midline. They now
form the lower border of the stomodeum, i.e., the lower lip and the lower jaw.
n The cartilage of the first arch is called as Meckel’s cartilage. At about 6th week (41st–45th day of
intrauterine life) of IUL, this Meckel’s cartilage derived from the first branchial arch extends bilaterally
from the ear region (otic capsule) and joins in the midline by a thin band of mesenchyme (Fig. 3.28).
n The cartilage of the first arch (Meckel’s cartilage) in human beings has no contribution towards
mandible formation. It acts as a mere template/guide to the developing
mandible around which mesenchymal condensation occurs.
36

n The first structure to develop in the primordium of the lower jaw is the mandibular division of the
trigeminal nerve. This is followed by the mesenchymal condensation forming first branchial arch.
n The mandibular branch of the trigeminal nerve (the nerve of the first arch) appears first at about 2/3 rd
length (from down upwards) of the Meckel’s cartilage level. This nerve bifurcates into medially lingual
nerve and laterally inferior alveolar branches. Further, inferior alveolar branch bifurcates into incisive
and mental branches more anteriorly. Neurotrophic factors produced by the nerve induce osteo-
genesis in the ossification centres.

Ossification of Mandible
1. Intramembranous ossification
n A single ossification centre for each half is formed around the 6th week of IUL in the mesenchymal
sheath of Meckel’s cartilage near the future mental foramen.
n Mesenchymal sheath is mesenchymal condensation that occurs adjacent to the Meckel’s
cartilage. These are called primary ossification centers.
n Intramembranous ossification mainly starts in the region of bifurcation of lingual and inferior
alveolar branches and again at the point of division of inferior alveolar into incisive and mental
branches, i.e., around the mental foramen area.

The extension of intramembranous ossification

n Intramembranous ossification spreads in both (i) dorsal (backwards or posteriorly) and (ii) ventral
(forwards or anteriorly).
n The ossifying membrane is located lateral to the Meckel’s cartilage and its accompanying
neurovascular bundle. Spread of the intramembranous ossification dorsally (posteriorly) extends
till the bifurcation of the mandibular nerve. This posterior spread of ossification forms the body of
the mandible.
n Further extension away from the Meckel’s cartilage forms the ramus. Intramembranous
ossification spreads ventrally (anteriorly) till the symphysis region (midline).
n Ossification surrounding the inferior alveolar nerve forms a gutter (future inferior alveolar canal).
Now the ossification forms a trough-like structure above this developing nerve canal to
accommodate the developing tooth buds.
n Thus by 10th week of IUL, the rudimentary mandible is formed almost entirely by
intramembranous ossification by using the Meckel’s cartilage only as template.
2. Endochondral bone formation: The further growth of the mandible until birth is influenced strongly
by the appearance of three secondary (growth) cartilages and the deve-lopment of muscular
attachments. These three cartilages are:
n The condylar cartilage
n The coronoid cartilage

n The symphyseal cartilage

- The condylar cartilage: At about 5th week of IUL, the condylar cartilage develops initially as a
separate area of condensation just above the ventral part and close to the body of the mandible
(Fig. 3.29).
• Later at 12th week of IUL, it rapidly takes shape of cone/carrot, migrates inferiorly and
merges with the developing ramus by about 4th month. This mass of cone-shaped cartilage
undergoes endochondral bone formation and takes shape of the condyle.
• At 20th week of IUL much of the cone-shaped cartilage is replaced by bone. Finally, a thin
layer of cartilage remnant is seen capping the condylar head. This cartilage remnant persists
until 20 years of life, providing mechanism of growth and as an articular cartilage.
• Note that condylar cartilage is fibrous in nature in contrast to other articular surfaces, which
is hyaline in nature.
- The coronoid cartilage: This secondary accessory cartilage appears at about 4 months of IUL
(10–14 weeks of intrauterine life), the anterior border and top of the coronoid process, which is
believed to grow as a response to the developing temporalis. Coronoid cartilage is a transient
37

growth cartilage, becomes incorporated into the expanding intramembranous bone of the
ramus and disappears long before birth.
- The symphyseal cartilage: These are two in number, appear in the symphyseal region at the
junction of two Meckel’s cartilage in the midline. At about 7th month of IUL, these undergo
ossification and form mental ossicles; later, these ossicles merge in the symphysis region along
with the ossification of symphysis, which will be completed by the end of 1st year after birth (in
some individuals 18 months).

Fate of Meckel’s Cartilage (Fig. 3.30)

 The Meckel’s cartilage acts as a mere template around which the intramembranous bone
formation for mandible occurs. It does not contribute anything anatomically to the mandible
formation.

 With the increase in ossification, the Meckel’s cartilage becomes surrounded by the bone.
Ossification terminates at the point of future mandibular lingula.
 From this point, the Meckel’s cartilage continues into the middle ear and forms the auditory
ossicles, i.e., malleus and incus.
 The sphenomandibular ligament, which is extending between the lingula of mandible and the
sphenoid bone is also a remnant of the Meckel’s cartilage.
Thus, a major portion of the Meckel’s cartilage disappears during growth and the remnants of
Meckel’s cartilage gives rise to the following structures:
n The incus and malleus of the inner ear
n The sphenomandibular ligament
n The lingula as bony spicule at the entrance of inferior alveolar canal
n Anterior ligament of malleus
n The mental ossicles
n Spine of sphenoid bone

Development of the Temporomandibular Joint (Fig. 3.30)

n Meckel’s cartilage extends from the midIine backward and dorsally and terminates as the malleus. It
articulates with the incal cartilage. Early minor movements of jaw occur between these two cartilages.
n This primary jaw joint exists for about 4 months until the cartilages ossify and become incorporated in
the middle ear.
n At 3 months of gestation, the secondary jaw joint, the TMJ begins to form.
n The first evidence of its development is the appearance of two distinct regions of mesenchymal
condensation, the temporal and condylar blastemas.

n The temporal blastema appears before the condylar, and initially both are positioned some distance
from each other. The condylar blastema grows rapidly in a dorsolateral direction to close the gap.
n Ossification begins first in the temporal blastema.
n While the condylar blastema is still condensed mesenchyme, a cleft appears immediately above it
that becomes the inferior joint cavity.
n The condylar blastema differentiates into cartilage (condylar cartilage), and then a second cleft
appears in relation to the temporal ossification that becomes the upper joint cavity.
n With the appearance of this cleft, the primitive articular disk is formed.

Development of Tongue (Fig. 3.31)

 The tongue is formed from 1st, 3rd, 4th branchial arches.
 It develops from the two lingual swellings – tuberculum impar and cranial part of hypobranchial
eminence.
 The two lingual swellings and one tuberculum impar are formed from the first branchial arch and
contribute to the formation of anterior 1/3rd of tongue.
38

 The posterior 2/3rd is formed from the cranial half of hypo branchial eminence, which shoots off
from the third arch.
 The posterior most part is developed from the fourth arch. The different parts of the tongue are
supplied by different nerves reflecting the origin of nerve from the respective branchial arches.
 The anterior part is supplied by lingual nerve and chorda tympani. Posterior 1/3 rd is supplied by
glossopharyngeal nerve and the post most part developed from the fourth brachial arch and
hence supplied by vagus nerve.
 Second arch does not contribute to the development of tongue. Thus, only 1, 3 and 4 arches
contribute to the formation of tongue.
 The intrinsic muscles of tongue develop from occipital myotomes, which are supplied by the
hypoglossal nerve.

Essay Questions
1. Discuss the prenatal development of viscerocranium (face) in detail.
2. Discuss the development of palate in detail and add a note on the development of clefts.
3. What are the various process that contribute for the formation of face and write in detail about
prenatal development of mandible.

Short Answer Questions

1. Pharyngeal arches and pouches
2. Derivatives of mandibular arch
3. Neural crest cells
4. Buccopharyngeal membrane
5. Fontonelles
6. Sutures
7. Synchondrosis
8. Development of TMJ
9. Development of tongue
10. Neurocranium
11. Flexure of cranial base
12. Meckel’s cartilage

REFERENCES
1. Graber TM. Orthodontics: Principles and Practice, 3rd ed. WB Saunders; 1988.
2. E Moyers, Handbook of Orthodontics, 4th ed. Year Book Medical Publishers, Inc.; 1988.
3. Profitt. Contemporary Orthodontics, Elsevier India, 3rd ed.; 2000 (permissions).
4. TW Sadler. Langman’s Medical Embryology, 9th ed., Chapter 15: Head and neck.

Chapter 4
Postnatal Growth of the Craniofacial
Skeleton
Introduction
Postnatal development of cranial vault
Sutures and fontanella
Postnatal growth of cranial base
Synchondroses
Cortical drift and remodelling
Sutural growth
Postnatal growth of maxilla
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Displacement
Growth at sutures
Surface remodelling
Dimensional changes–height, width and depth
Introduction
Postnatal development of cranial vault
Sutures and fontanella
Postnatal growth of cranial base
Synchondroses
Cortical drift and remodelling
Sutural growth
Postnatal growth of maxilla
Displacement
Growth at sutures
Surface remodelling
Dimensional changes–height, width and depth
Postnatal growth of mandible
Dimensional changes–height, width and depth
Rotation of jaw bases

INTRODUCTION
The growth of the face is an enormously complex interaction of skeletal, dental and soft tissues with
genetic and environmental factors both playing important role in the ultimate facial form. Postnatal
growth is defined as the first 20 years of life growth after birth. It is composed of three periods.

Infancy Birth to 1 year

Childhood 1 year to 14 years; this is subdivided

into early, middle and late childhood.
Puberty occurs in the late childhood,
i.e., 13–14 years in males & 12–13
years in females.

Adolescence 14–20 years

A knowledge of the the normal changes of the craniofacial complex is essential to detect any deviations
from normality (abnormality) and to provide optimal treatment to the patient. The craniofacial region can
be conveniently divided into thirds for the description purpose.

Upper third Mainly made up of neurocranium

Middle third Made up of the nasomaxillary

complex - maxillary bone

Lower third Is mainly composed of mandible

Neurocranium is the first to achieve its maximum growth potential before the age of 10 years and ceases
to grow significantly after 12 years of age.
In contrast, the middle and lower thirds grow more slowly over a prolonged period extending until late
adolescence.
Completion of the masticatory apparatus by eruption of the third molars (at 18–25 years of age) marks
the cessation of growth of the lower two-third of the face.

The postnatal growth of the craniofacial region is studied under following categories:
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1–5 5–10 10–20

years years years

Cranium 85% 11% 4%

Maxilla 45% 20% 35%

Mandible 40% 25% 35%

The number of bones in adult skull is 22. Out of 22 bones (8+14); the calvaria or brain case is
composed of 8 bones. The facial skeleton is composed of 14 bones.

Calvaria bones—8 bones

Paired Unpaired

- Parietal - Frontal
- Temporal - Occipital
- Sphenoid
- Ethmoid

The facial skeleton—14 bones

Paired Unpaired

- Maxilla - Mandible
- Zygomatic - Vomer
- Nasal
- Lacrimal
- Palatine
- Inferior nasal concha bones

POSTNATAL GROWTH OF THE CRANIAL VAULT

 The cranial vault is made up of a number of flat bones that are formed directly by
intramembranous bone formation, without cartilaginous precursors.
 To accommodate the rapidly expanding brain, the cranial vault should also expand.
 By the end of 5–6 years of postnatal life, about 90% of cranial vault completes its growth
 Sutures are joints that are peculiar to skull, and are immovable. (Fig. 4.1). At birth, the flat
bones of the skull are widely separated by loose connective tissue. These are called fontanella
(Fig. 4.2 and Table 4.3).
These fontanelles allow the maximum deformation of the skull during the birth. The fontanelles are
slowly filled by bone apposition within first 2 years and the edges of the corresponding bones form
sutures.

Sagittal suture It is placed in the median plane

between the two parietal bones.

Coronal suture The suture between the parietal

and frontal bones.
41

Lambdoid The suture between the parietal

suture and occipital bones.

Frontal or This is occasionally present in some

metopoic individuals. It lies in the median
suture plane and separates the two halves
of the frontal bone.

Wormian or Sutural Bones

These are small irregular bones found in the region of the fontanelles and are formed by additional
ossification centres.

Mechanism of Growth of Cranial Vault

n Apposition (deposition) of new bone at the sutures plays a major role to expand the cranial bone.
The intramembranous calvarial bones are interdigitated with sutures. These bones grow with the
addition of bone at sutures. This is apposition of bone and is also called as sutural growth.
n Surface remodeling – Inner side resorption and outer side deposition allows the vault to grow into
convex shape. The intramembranous bones of the calvaria also increase in thickness due to
appositional growth by outer covering periosteum. This is also called as periosteal growth.

Timing of Growth in Width, Length and Height

Cranium grows quite rapidly and approaches adult size, considerably before the face. This is because it
is under the influence of growing brain, which is a neurological tissue. From Scammon’s differential
growth, we know that neural growth attains maximum growth at any early age.
All cranial dimensions do not show the same percentage of growth pattern; growth in cranial depth is
rapid, with growth in width and height following in that order. Height of the cranium is closest to adult size
at birth. It means that the depth of the cranium postnatally is more and last to complete. Height of the
cranium is completed first followed by width and depth to be completed in the last.

POSTNATAL GROWTH OF THE CRANIAL BASE

The cranial base not only supports and protects the brain, but also articulates the skull to the facial
skeleton (i.e., maxilla and mandible). The maxilla is attached to the cranial base by means of a number
of sutures. The mandible is also related to the cranial base by the temporomandibular joint. Thus, the
growth processes occurring at the cranial base can concurrently affect the growth of maxilla and the
mandible.

Mechanism of Growth
The cranial base grows postnatally by following three growth processes:
1. Elongation at synchondrosis
2. Extensive cortical drift and remodeling
3. Sutural growth

1. Synchondrosis
n Synchondroses are basically temporary cartilaginous joints between the bones of the cranial base. It
acts as a growth centre.
n They are basically remnants of primary cartilages seen in postnatal life situated in between the bones
of the cranial bones. They are equivalent to sutures seen in the intramembranous cranial vault.
n In prenatal life, the bones of the cranial base develops from the primary cartilage and its subsequent
replacement by endochondral bone formation (chondrocranium).
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n In the postnatal life, these cartilaginous bands are located inside and in between the bones of cranial
base. These cartilaginous bands are called synchondroses.
n They are important growth sites of the cranial base postnatally.
n Cranial base by cartilaginous growth at synchondrosis and its subsequent replacement by
endochondral bone formation.
n Histology of synchondrosis – The structure of a synchondrosis looks like a double-sided
epiphyseal plate positioned back to back. The area between the two bones consists of growing zone
of reserve cartilage. It consists of cellular hyperplasia in the centre with band of maturing cells
extending in the both sides, which will eventually be replaced by bone (Fig. 4.4).
n The important synchondroses are of four types that are found in the cranial base (Fig. 4.3).

2. Cortical Drift and Remodeling

n Remodeling refers to a net result of the process where bone deposition and resorption occur so as to
bring about change in the size, shape and oriental relationship of the individual bones.
n Cortical drift is the direction of growth by resorption on one side and apposition on other side of the
same bone. Most of the inner surface of the cranial fossa undergoes resorption and the other or
below surface undergoes deposition.
n The cranium is divided into a number of compartments by bony elevations and ridges present in the
cranial base.
n In the cranial floor, bony elevations (e.g., pituitary fossa) and ridges are formed by deposition while
the predominant part of the floor, fossae and grooves are formed by resorption.
n This intracranial bone resorption helps in increasing the intracranial volume to accommodate the
growing brain.
n The cranial base is also characterized by perforations formed due to foramina, which provide a
passage for a number of blood vessels and nerves communicating with the brain. The foramina that
transmit these nerves and blood vessels undergo continuous drifting by bone deposition and
resorption so as to constantly maintain their proper relationship with the growing brain.

3. Sutural Growth
The cranial base has a number of bones that are joined to one another by means of sutures. Some of
the sutures that are present include the following:
n Sphenofrontal
n Frontotemporal
n Sphenoethmoidal
n Frontoethmoidal
n Frontozygomatic

Apposition (deposition) takes place in these sutures allowing growth of the cranial base. As the brain
enlarges during growth, bone formation occurs at the ends of the bone (that is at either ends of the
suture) (Fig. 4.5).

Timing of Cranial Base Growth

n Birth: 55–60% of adult size is completed.
n 4–7 years: 94% of adult size is completed.
n 8–13 years: 98% of adult size is attained.

Clinical Significance
1. The cranial base in under the influence of neural growth. The anterior cranial base extending from
nasion to sella completes its growth as early as 10 years. The sella nasion plane can be used as a
comparison for the assessment of other structures.
2. The cranial base by its relationship to maxilla and man-dible largely influences their growth.
3. If the flexure of cranial base remains more obtuse, it may lead to mandibular retrognathism. At the
same time, if it is more acute it may lead to mandibular prognathism.
43

4. The syndromes or disease effecting the cartilaginous growth will also have influence on the cranial
base, e.g., achondroplasia.

POSTNATAL GROWTH OF MAXILLA

Maxilla at birth;-
The body consists of a little more than the alveolar process with the tooth sockets almost all touching the
floor of orbit.
The frontal process is small. The maxillary sinus is a mere furrow on the lateral wall of the nose. Now we
discuss how the maxillary dimensions change postnatally. At birth, the transverse and anteroposterior
dimensions are each more than the vertical diameter.

The growth of the maxilla is purely by intramembranous ossification since there is no cartilage
replacement. The growth of the nasomaxillary complex is produced by the following mechanisms:
1. Displacement
2. Growth at sutures
3. Surface remodeling

1. Displacement
Maxilla is attached to the cranial base by means of a number of sutures. Thus, the growth of the cranial
base has a direct bearing on the nasomaxillary growth. Thus, the displacement of maxilla can be further
divided into two types as given in Table 4.4.

2. Growth at Sutures
The maxilla is connected to the cranium and cranial base by a number of sutures. These sutures
include:
a) Frontonasal suture
b) Frontomaxillary suture
c) Zygomaticotemporal suture
d) Zygomaticomaxillary suture
e) Pterygopalatine suture

These sutures are all oblique and more or less parallel to each other and directed downwards. The
growth at these sutures allows the downward and forward repositioning of the maxilla. Another important
phenomenon is that the growth of the

surrounding soft tissue capsule carries the maxilla in downwards and forward direction. This leads to
opening up of space at the sutural attachments and a tension related bone formation occurs at the
sutures. Thus, new bone is now formed on either side of the suture. Thus, the overall size of the bones
on either side increases.

3. Surface Remodeling
In addition to the growth occurring at the sutures, massive remodeling by bone deposition and resorption
occurs to bring about the following:
a) Increase in size
b) Change in shape of bone
c) Change in functional relationship

The selective resorption and deposition takes place in a complex manner in the maxilla to attain its
typical shape to form orbital surface, palatal surface, alveolar surfaces maxillary sinuses, lateral wall of
the nose, etc (Fig. 4.8).
1. Orbit: The lateral surface of the orbital rim undergoes resorption, permitting the lateral movement of
the eyeball. As a compensation, there is bone deposition on the medial rim of the orbit and on the
external surface of the lateral rim.
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Surface deposition occurs in the orbital floor and as a result the floor of the orbit faces superiorly,
laterally and anteriorly (Fg. 4.9A).
2. Maxillary tuberosity: Characteristic bone deposition is seen along the entire posterior margin of the
maxillary tuberosity. This results in lengthening of the dental arch and enlargement of the antero-
posterior dimension of the entire maxillary body. Thus, posteriorly the space for erupting molars is
provided (Fig. 4.9B).
3. Nasal cavity palatal side: The size of the nasal cavity increases with bone resorption on the lateral
wall of the nose. Bone resorption is also seen on the floor of the nasal cavity. There is compensatory
bone deposition on the palatal side. The net result is the downward shift of the palatal vaults leading
to increase in maxillary height. The anterior nasal spine prominence increases due to bone deposition
(Fig. 4.9C).
The anterior nasal spine becomes prominent due to increase in bone deposition. In addition, there is
resorption from the periosteal surface of labial cortex. As a compensatory mechanism, bone
deposition occurs on the endo-steal surface of the labial cortex and periosteal surface of the lingual
cortex (Fig. 4.9D).
4. The zygomatic bone: The zygomatic bone moves in a posterior and lateral direction. The posterior
movement is achieved by resorption on the anterior surface and deposition on the posterior surface.
The face enlarges in width by bone formation on the lateral surface of the zygomatic arch and
resorption on its medial surface (Fig. 4.9E).
5. Alveolar ridges: Deposition occurs as the teeth erupt. As of all permanent teeth, the teeth start
erupting, bone deposition occurs at the alveolar margins. This increases the maxillary height and the
depth of the palate (Fig. 4.8).
6. Maxillary sinus: The entire wall of the sinus except the mesial wall undergoes resorption. This
results in increase in size of the maxillary antrum. It appears as a shallow groove during fourth month
of intrauterine life, grows rapidly during 6–7 years, and reaches full size after the eruption (Fig. 4.8).
The amount and direction of the maxillary growth can be discussed under following headings:
1. Maxillary height
2. Maxillary width
3. Maxillary length

Maxillary Height (Fig. 4.8)

The increase in the maxillary height is by various mechanisms.
n The maxilla is attached by ‘5’ pairs of sutures to the cranium. Sutural growth (except pterygopalatine)
contributes to increase in the height of the maxilla.Height of maxilla is increased by following
mechanisms–Sutural growth in the frontomaxillary and zygomatico maxillary sutures.
n To allow functional demands, there will be resorption on the nasal floor and simultaneously on the
other side (oral side) apposition occurs on the palatal shelves of the maxillary bone. This apposition
on the palatal shelves increases the palatal depth.
n Apposition in the alveolar process to accommodate the eruption of the succeeding teeth adds to the
height of the maxilla.
n The nasal cartilage is a primary cartilage, which has innate growth potential, i.e., it has genetic
determined growth. Thus, the growth of the nasal cartilage (nasal septum) pushes the maxilla
downward.
n The maximum amount of vertical growth takes place in the maxilla between the ages of 5 and 15
years. The growth of the alveolar process in downward direction—eruptive mechanism of the teeth
contributes mainly for it.

Maxillary Width
Growth in the median suture (the suture joining the two maxillary bones in the middle) plays a very
important role in the growth of maxillary width. Growth increase at median suture will be maximum at the
time of puberty.

Secondarily, surface apposition (deposition) on the zygomatic process will contribute to increased
maxillary width.
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Maxillary Length (Depth)

The length is increased by apposition in the maxillary tuberosity and also accelerated by sutural growth
in the pterygopalatine sutures.

Important Growth Theories Applicable to the Maxillary Growth

1. Sicher’s sutural theory states that growth occurs at the sutures due to the proliferation of sutural
connective tissue. Since, the nasomaxillary complex is attached to the cranium by various sutures,
this theory can be applicable to the maxillary growth.
2 Scott’s cartilaginous theory: Scott has divided the growth of nasomaxillary complex into two
phases (Fig. 4.10):
a) Birth to 7 years: The size of nasomaxillary complex is mainly due to nasal septal cartilage growth.
The nasal septal growth drives the nasomaxillary complex downward as a unit. The growth of
synchondrosis of cranial base pushes the nasomaxillary complex forwards. Here, cartilaginous
growth is dominated and surface apposition makes only minor contribution.
b) 7–16 years: The growth of the nasomaxillary complex is mainly due to surface remodeling
(deposition and resorption). The suture growth, the nasal cartilage activity gradually ceases.
3. Moss’s functional matrix theory: The growth of bone is secondary and passive. It does not have
any primary growth potential. The nasomaxillary responds to the functional matrices in a passive
manner pertaining to such functions like breathing, mastication, vision, etc, which are located within
the maxillary bone. To adapt these functional matrices, the nasomaxillary complex grows accordingly
and attains its shape and size.
4. Enlow’s ‘V’ principle: Especially the growth of the palate follows the ‘V’ principle, i.e., apposition on
the inner aspect and resorption on the outer aspect (also refer Fig. 2.14).

Clinical Significance
n The maxilla is formed from the first branchial arch and ecto-mesenchyma of neural crest cells. Any
aetiological factors, which interfere with the formation of this structure may give rise to
underdeveloped maxilla, e.g., craniofacial dyostosis (Crouzon disease), cleidocranial dysplasia,
achondroplasia, cleft lip and palate, congenital syphilis, Down syndrome, etc.
n The maxilla forms the middle one-third of the face. The underdevelopment of maxilla leads to midface
deficiency particularly if nasal septum is involved.
n The maxilla is the major site of cleft formation, particularly the cleft lip and palate. This not only
causes the disfigurement, but also affects the normal functioning capacity. The maxilla becomes
narrow with high-arched palate. There is tendency for posterior and anterior crossbites. Some of the
teeth may be missing. Speech, mastication and hearing are also impaired.
n The maxilla is surrounded by envelope of facial muscles. Restricted growth of this muscular envelope
will retard the growth of the maxilla. This muscular coverage is effected by scarring that results from
surgery as seen in cleft lip repair. In this case, the scarred lip restricts the normal anterior
development of maxilla leading to anterior crossbites and dish face deformities. The scarring of the
muscles also results from trauma and burns.
n The vertical lengthening of the maxilla is equal in both anterior and posterior regions. If anterior
vertical height is in excess, it may result in anterior deep bite and gummy smiles. Similarly, decreased
anterior vertical height may result in open bite.
n The normal formation and development of dentition is a must for proper development of alveolar
bone. Anything that interferes with the development of the teeth may affect the alveolar bone and
hence the vertical height of the maxilla, either of the whole arch or at particular segments. This may
give rise to open bite or deep bite depending on the segment and the teeth affected.
n The maxilla is related to cranial base by an angle of 82 o (angle SNA—to be discussed in detail in
cephalometrics). The values less than 82o results in retrognathic maxilla and class III conditions. The
values greater than 82o gives rise to prognathic maxilla and class II conditions.
n The maxilla follows the general somatic growth pattern. The growth spurts are utilized for both
restricting the overgrowth of maxilla or increasing the rate of growth in underdeveloped maxilla. This
is done by utilizing the headgear for restricting the maxillary growth and reverse pull headgear or
46

facemask with class III functional appliances for correction of retrognathic maxilla. Both have their
effect on the maxillary sutures.
n The orthognathic surgical correction for maxillary skeletal deficiencies or excess is usually taken
when the active growth is completed.

POSTNATAL GROWTH OF THE MANDIBLE

 Mandibular bone is one of the bones, which exhibit a wide variation in their morphology because
it undergoes the largest amount of growth postnatally.
 Although the mandible appears in the adult morphologically as a single bone, it is
developmentally and functionally divisible into several skeletal subunits.
 The basal bone or the body of the mandible a horizontally curved portion that forms the basal
unit. It is also called as Corpus.
 The rami are two vertical processes located on either side of the body and joins the body at the
angle
 The subunits, get attached to this basal bone and Ramal Bone.

After the first year of life, the mandibular growth becomes more selective. For our discussion, it is handy
to know the growth of the mandible in terms of its various anatomical sub units (Fig. 4.11):
n The condylar portion
n The ramus
n The corpus
n Coronoid process
n Angle of the mandible
n The alveolar process
n The chin

 In the process of mandibular formation only a small amount of “endochondral bone formation”
and greater amount of “intramembranous bone formation” occur.
 Cartilaginous portion of the condylar cap undergoes endochondral bone formation and rest of
the entire portion undergoes intramembranous bone formation.
 Further, the growth changes are determined by its muscle attachment, teeth eruption and
growth of surrounding tissue.

Mandible at Birth

At the time of birth, the mandible is little more than a curved base of bone, the coronoid, angular and
alveolar processes are under developed. At birth, the two halves of the mandible are connected by a thin
fibro-cartilaginous tissue. The two halves are united by bony replacement of symphyseal cartilage by 18
months of age (Fig. 4.12).

1. The condyle (Fig. 4.13A)

n The mandibular condyle has been recognized as an important growth site.
n Condylar is peculiar in that it shows both surface apposition (by endochondral bone formation) and
interstitial growth (hypertrophy and hyperplasia) occurs in it.
n The head of the condyle is covered by a thin layer of cartilage called the condylar cartilage.
n This condylar cartilage (fibrous cartilage) is not like the cartilage of an epiphyseal plate or a
synchondrosis. Another peculiar feature is that it is a fibrous cartilage, but usually it is within the
hyaline cartilage the endochondral bone formation is initiated.
n It is a secondary cartilage indicating that it does not develop from the primary embryonic
structures. Although it is secondary cartilage, it is believed to have growth potential.
47

n The presence of the condylar cartilage is an adaptation during growth periods to withstand the
compression that occurs at the joint.
n Intramembranous bone is not pressure adoptive so a thin layer of cartilage and endochondrial
bone formation occurs as a surface phenomenon at condylar head.
n The head of the condyle grows in posterior direction with proliferation of cartilage and its
subsequent replacement by endochondral ossification.

n The condylar cartilage is responsible for the condylar growth, thereby increasing mandibular
length.
n The condyle grows upwards and backwards resulting in downwards and forward translocation of
the mandible (remember likewise the growth at the maxillary tuberosity is in backward direction,
whereas the maxilla is displaced in forward direction).
n Simultaneously selective remodelling of the condyle (apposition and resorption) follows Enlow’s ‘V’
principle (resorption outside and deposition inner side as ‘V’ pattern) to achieve typical shape of
the condyle (condylar neck and head).
n The condylar growth reaches peak at pubertal growth spurt (12–15 years) and ceases by 20 years
of age.
However, the role of the condyle in the mandibular growth is still controversial in two ways. There are
two schools of thought regarding the role of the condyle.

The condyle According to one school of

determines thought, the condylar cartilage the mandibular is considered as the primary

growth “growth centre,” which controls the entire mandibular growth by

bone deposition in the mandibu lar condyles.

The rest of According to second school, the

the mandible entire mandible is displaced
determines anteriorly and inferiorly into its
the condylar functional position (carry away growth phenomenon) due to the growth
of soft tissues and muscles
surrounding the mandible. Bone
growth follows secondarily at the
condylar articulating surface to maintain constant contact with
the cranial base.

2. Ramus (Fig. 4.13B)

n After first year of postnatal life, the corpus and ramus are not well differentiated.
n The ramus moves progressively in posterior direction by a combination of deposition and
resorption.
n The ramus grows posteriorly by resorption at the anterior border and deposition at the posterior
border; with this the ramus drifts posteriorly. But note the mandible translates anteriorly.
n The functions of remodelling of the ramus are:
- To accommodate the increasing functional mass of muscles of mastication inserted into it.
- To accommodate the enlarged breadth of the pharyngeal space.
- Facilitates the lengthening of the mandibular body to accommodate the increasing dental arch
length and the erupting molars.
3. Corpus or the body of mandible (Fig. 4.13C)
n The corpus or body of the mandible is formed at the expense of ramus repositioning in posterior
direction.
48

n The resorption occurs at the anterior end and deposition at the posterior end of ramus. This
causes displacement of the ramus in posterior direction and also increases the length of the
corpus or body of the mandible.
n Thus, additional space made available by means of resorption of the anterior border of the ramus
is made use of to accommodate the erupting permanent molar tooth buds.
4. The coronoid process (Fig. 4.13D)
n It has a propeller-like twist mechanism of growth. It increases in height (superiorly), widens
(laterally) and at the same time grows posteriorly.
n When the bone deposition is added to the lingual side of the coronoid process, this brings about a
posterior growth movement so that its lingual side faces three general directions all at once, i.e.,
posteriorly, superiorly and laterally.
n The ramus and coronoid follows ‘V’ principle of growth pattern, i.e., resorption outer side and
deposition inner side. This is best appreciable in the coronal section. In this way, the coronal
section grows in height with sharp border.
n In the infants, the coronoid is at the level as the lingual tuberosity of adult mandible. With the
increase in height of the coronoid process, their terminal part grows apart following the ‘V’ principle
of growth. Viewing it from the occlusal aspect, the deposition on the lingual of the coronoid
process brings about a posterior growth movement in the ‘V’ pattern.

5. Angle of the mandible (Fig. 4.13E)

n The region of the angle of the mandible is augmented by deposition in the posterior border of the
ramus.
n On the buccal side, resorption occurs on the anterio-superior portion while deposition takes place
on the postero-inferior part.
n On the lingual side of the angle of mandible, resorption takes place on the postero-inferior aspect
while deposition occurs on the antero-superior aspect.
n Thus, angle of the mandible is decreased from about 175° at birth to 115° in the adult. As a result
gonial angle moves downwards, backwards and outwards.
6. The lingual tuberosity (Fig. 4.13F)
n The lingual tuberosity is counter equivalent of the maxillary tuberosity in mandible.
n It forms the boundary between the ramus and the body and is a major site of growth for the lower
bony arch.
n In the lingual side of the mandible, the border between the ramus and the corpus is elevated by
deposition called as lingual tuberosity.
n It can be seen that the lingual tuberosity protrudes prominently in a lingual direction and that it lies
well extending towards the midline of the ramus. The prominence of the tuberosity further
increases by the presence of a large resorption field just below it.
n Below the lingual tuberosity a large amount of resorption takes place to form lingual fossa. The
lingual tuberosity moves posteriorly by deposition on its posteriorly facing surface.
7. The alveolar process (Fig. 4.13B)
n Alveolar process develops in response to the presence of tooth buds. The alveolar process grows
upwards by the apposition (deposition) of bone on its occlusal border in response to the tooth
buds.
n Due to the growth of alveolar process, the height of the mandibular process increases. The
ascending ramus slopes (before the coronoid process) upwards and backwards, the alveolar
border increases in length to accommodate posterior most teeth.
n In case of absence of teeth, the alveolar bone fails to develop and it resorbs in the event of tooth
extraction.
8. The chin (Fig. 4.13C)
n The chin is the anterior inferior most part of the mandible, which influences the profile of the
patient.
n The chin develops as a separate subunit of the mandible.
n It is poorly developed in the infancy period. Gradually, deposition (apposition) occurs in the
anterior inferior most part of the mandible and accelerates during pubertal growth to attain chin
prominence.
49

n The deepest point in this concavity is known as point B in cephalometric terminology.

n Chin prominence is influenced by sexual and specific genetic factors.
n Chin prominence is more in males than females.

Growth Theories as Applicable to Mandible

n Scott’s cartilaginous theory: The cartilage growth at the mandibular condyles was thought to be
primary growth centres previously, but recent studies have proven that the growth at the condyle is
mostly reactive and not of primary nature. Another thing to note is that the condylar cartilages are
secondary cartilages.
n Moss’s functional theory: This theory states that bone responds to the matrices in a passive
manner and does not have any primary growth potential.
In the mandibular growth, functional matrices, i.e., periosteal matrix (muscles, vessels, nerves,
glands, etc) and capsular matrix (oro-capsule – oral cavity) have the primary growth control on
skeletal matrix, i.e., microskeletal units (ramus, body, condyle, etc) and macroskeletal units of the
mandible to attain its size and shape.
n Enlow’s ‘V’ principle: The bone growth in the ‘V’ manner by apposition in the inner side and
resorption on the outer aspect. Growth of the condyle, coronoid process, lower border of the corpus,
etc follows ‘V’ principle of growth.

Timing of Growth in Width, Length and Height

For the three planes of space in both the maxilla and mandible, there is a definite sequence in which
growth is “completed” (i.e., declines to the slow rate that characterizes normal adults). Growth of the face
in width is completed first, then growth in length, and finally growth in height takes place.

Rotations of the Jaw Bases (Fig. 4.14)

Bjork in 1960s conducted implant studies of jaw rotation. The rotation that occurs in the core of each jaw
is called internal rotation. Core is that portion of the mandible that surrounds the inferior alveolar nerve.
The surface changes produce external rotation. The overall change in the orientation of each jaw results
from the net changes of internal and external rotation as judged by the palatal plane and mandibular
plane.

Total rotation = Internal rotation – External rotation

= IR–ER= 15–12= 3–4o approximately

By convention, the rotation of either jaw is considered “forward” and given a negative sign if there is
more growth posteriorly than anteriorly. The mandible rotates in anti-clockwise direction and growth is
said to be in horizontal pattern and has deep bite tendency.
The rotation is “backward” and given a positive direction if it lengthens in anterior dimensions more
than posterior ones, bringing the chin downward and backward. The mandible rotates in clockwise
direction. The growth is said to be vertical pattern and have open bite tendency.

Clinical Significance
n The hereditary effects are more pronounced on mandible, e.g., prognathic mandible as seen in
Hapsburg jaw of German royal family.
n Mandible is formed from the first branchial arch and ecto-mesenchyma of neural crest cells. Any
aetiological factors, which interfere with the formation of these structures may give rise to
underdeveloped mandible, e.g., Pierre Robin syndrome, mandibulofacial dysostosis (Treachear
Collins syndrome), etc.
n The condylar cartilage is the main growth site in the mandible. Any interference with this cartilage
either during prenatally or postnatally during growing periods hampers the proper development of
mandible, e.g., forceps trauma during birth, arthritis, accidents, etc. If the problem is unilateral, it gives
rise to facial asymmetry.
50

n The effects of growth hormone are more pronounced on secondary cartilage such as condylar
cartilage, leading to prognathic mandible as seen in class III conditions, e.g., acromegaly or
gigantism.
n Anything that interferes with the development of the teeth may affect the alveolar bone and hence the
vertical height of the mandible either of the whole arch or at particular segments. This may give rise to
open bite or deep bite depending on the segment affected and the teeth affected.
n Mandible usually follows somatic growth pattern. The growth of the mandible proceeds the growth of
cranium and maxilla implying the cephalocaudal gradient of growth.
n The mandible is related to cranial base by an angle of 80o (angle SNB–to be discussed in detail in
cepahlometrics). The values less than 80o result in retrognathic mandible and class II conditions. The
values greater than 80o result in prognathic mandible and class III conditions.
n The downward and backward rotation of the mandible results in retrognathic mandible with long face
patterns and open bite tendency.
At the same time, the forward and upward rotation of the mandible results in short faces with deep bite.
Class II conditions with this type of growth pattern have good prognosis if corrected with
myofunctional appliances.
n The growth spurts are utilized for both restricting the overgrowth of mandible. This is done by utilizing
the chin cap for restricting the mandibular growth in class III conditions.
n The growth spurts are utilized for increasing the rate of growth in underdeveloped mandible This is
done by utilizing the chin cap for restricting the mandibular growth in class III conditions. This is done
by class II functional appliances for correction of retrognathic mandible. .
n The mandible situated caudally to maxilla grows at a faster rate postnatally compared to maxilla. This
is particularly borne is mind when treating the class II and class III malocclusion during growth spurts.
n The orthognathic surgical correction for mandibular skeletal deficiencies or excess is usually taken
when the active growth is completed.

PREVIOUS YEARS UNIVERSITY QUESTIONS

Essay Type Questions
1. Discuss in detail the postnatal development of cranial base.
2. Discuss the dimensional changes that occur postnatally in maxilla.
3. Discuss in detail the postnatal growth of maxilla and add a note on its relevance to orthodontics.
4. Discuss the postnatal growth of mandible in particular relation to the Enlow’s “V” principle of growth.
5. Discuss the prenatal and postnatal growth of mandible and its clinical significance in orthodontics.

Short Answer Questions

1. Spheno-occipital synchondrosis (SOS)
2. Fontanella
3. Sutures
4. Condylar cartilage and mandibular growth
5. Rotation of jaw bases

REFERENCES
1. Donald H Enlow, David B Harris. A study of the postnatal growth of the human mandible. American
Journal of Orthodontics 1964;50(1):26.
2. DH Enlow. The “V” principle. American Journal of Ortho-dontics 1984;85(1):1.
3. Donald H Enlow, W Stuart Hunter. A differential analysis of sutural and remodeling growth in the
human face. American Journal of Orthodontics 1966;52 (11): 8–11 (permissions-Elsevier).
4. Donald H Enlow, Robert E Moyers, W Stuart Hunter, James A McNamara. A procedure for the
analysis of intrinsic facial form and growth: an equivalent-balance concept. American Journal of
Orthodontics July 1969;56 (permissions-Elsevier).
5. Donald H Enlow, Seong Bang. Growth and remodeling of the human maxilla. American Journal of
Orthodontics (permissions-Elsevier).
6. Samir E Bishara. Textbook of Orthodontics; 2001.
7. Sperber. Craniofacial development, ISBN-1-55009-127-1.
51

8. Graber TM. Orthodontics: Principles and Practice, 3rd ed., WB Saunders; 1988.
9. E Moyers Handbook of Orthodontics, 4th ed., Year Book Medical Publishers, Inc.; 1988.
10. Profitt. Contemporary Orthodontics, Elsevier India, 3rd ed., 2000 (permissions-Elsevier).

CHAPTER 5
Development of Dentition and Occlusion
Introduction
Prenatal development of teeth
Dental lamina
Bud, cap and bell stages
Root formation
Postnatal development of dentition
Predental stage
Gum pads
Natal and neonatal teeth
The deciduous dentition stage
52

Sequence and timing of eruption

General physiological spacing, anthropoid spaces
Flush terminal plane
The mixed dentition stage
Eruption of first molar
Molar relation—FTP, distal step, mesial step
Early mesial shift, late mesial shift
Incisal liability
Leeway space of Nancy
Ugly duckling stage
Transient deep bite
Dimensional changes of the arch
The permanent dentition stage

INTRODUCTION
The main aim of this chapter is to discuss the normal development of human dentition. Human dentition
undergoes a number of changes from primary dentition to permanent dentition. Understanding what is
normal at particular stage of dentition is essential for proper orthodontic diagnosis and treatment plan.

PRENATAL DEVELOPMENT OF TEETH

Dental Lamina – Initiation of Tooth Formation
Oral ectoderm is the stratified squamous epithelium that lines the stomodeum. This oral ectoderm
contacts the endoderm of the foregut to form the buccopharyngeal membrane, which ruptures at the
27th day of gestation. A continuous band of thickened epithelium forms around the mouth in the
presumptive upper and lower jaws around 4th week IUL from the fusion of separate plates of thickened
epithelium. These bands are roughly horseshoe shaped and correspond in position to the future dental
arches of the upper and lower jaws (Fig. 5.1).
Each band of epithelium, called as the primary epithelial band gives rise to two subdivisions: the
vestibular lamina and the dental lamina. The vestibular lamina (lip furrow band) develops labial and
buccal to dental lamina. The cells rapidly enlarge and degenerate to form a cleft that becomes the
vestibule (Fig. 5.2).
Dental lamina forms at 6th week intrauterine of life; thus, initiation of tooth starts at 6th week of
intrauterine life, when fetus is 18–22 cm in length. The dental lamina plays an important role in the
development of the dentition. It serves as a primordium for the developing teeth.
The deciduous teeth are formed by direct proliferation of the dental lamina. The permanent
successors (incisors, canines, premolars) develop from the lingual extension of this primary dental
lamina (successional lamina). The permanent molars develop as a result of its direct distal proliferation.
Thus, all teeth originate from the dental lamina.
Within the dental lamina, continued and localized proliferative activity leads to the formation of a
series of epithelial ingrowths into the ectomesenchyme at sites corresponding to the positions of the
future deciduous teeth and it is called the enamel organ.
The enamel organ passes through a number of stages ultimately forming the teeth. On the basis of
the shape of the enamel organ, the development of teeth can be divided into three stages. They are the
bud, cap and the bell stage.
In the human, 20 primary and 32 permanent teeth develop from the interaction of the oral epithelial
cells and the underlying mesenchymal cells. Each developing tooth grows as an anatomically distinct
unit, but the basic development process is similar for all teeth.

Morphological Stages of Tooth Development

The morphological stages are explained based on shape of the enamel organ. They are named after the
shape of the epithelial part of the tooth germ and are called the bud, cap and bell stages.
53

Root Formation (Fig. 5.7)

Root development is initiated after the enamel and dentin formation reaches the cementoenamel
junction. The IEE and OEE fuse to form an epithelial structure called as “Epithelial sheath of Hertwig,”
which determines the number and shape of the roots.
n The entire primary dentition is initiated between 6–8 weeks of IUL.
n Successional permanent teeth – 20th week IUL to 10 months after birth.
n Permanent molars – 20th week IUL to 5 years of life.

POSTNATAL DEVELOPMENT OF DENTITION

Development of dentition/occlusion from birth to adult can be divided into four periods (Fig. 5.8).

Predental Stage (Birth – 6 months)

The mouth of a neonate from birth to 6 months is described in this category. There will be no teeth seen
in this phase. The alveolar arches at the time of birth are called gum pads.

Gum Pads (Fig. 5.9)

 The gum pads are pink, firm and are covered by a dense layer of fibrous periosteum. The basic
form of gum pads is determined by 4th month of IUL.
 The upper gum pad is horseshoe shaped and the lower is ‘U’ shaped. They develop in two parts.
First the gum pads differentiate into a labiobuccal portion and later lingual portion.
 The lingual portion is separated from labial–buccal portion by dental groove, which is the site of
origin of dental lamina. It starts from incisive papilla, runs backward and extends laterally up to
molar region. It merges with gingival groove in the canine region

 The labial–buccal portion is divided into ten transverse grooves, each corresponding to one
developing deciduous tooth sac.
 The gingival groove separates the gum pad from the palate in the upper jaw and from the floor
of the mouth in the lower jaw.
 The transverse groove between canine and deciduous molar is referred to as lateral sulcus. The
lateral sulci are useful in judging the inter-arch relationship at a very early stage.

Relationship of Gum Pads (Fig. 5.10)

 The upper gum pad is both wider as well as longer than the mandibular gum pad.
 When the upper and lower gum pads are approximated, there is a complete overlap (overjet) all
around.
 The lateral sulcus or the transverse groove of the canine in the mandibular arch is normally more
distal or retropositioned in relation to that of the maxillary arch. In other words, the neonate
exhibits class II or post normal relation
54

 When gum pads are in contact, they occlude only in the molar region. Thus, anterior open bite
exists, the tongue protrudes anteriorly through this space. This transient open bite/infantile open
bite is considered normal and it helps in suckling. This is a self-correcting anomaly, which closes
by eruption of primary teeth.

Growth of Gum Pads

At birth, gum pads are long enough only to accommodate all primary teeth if they were to erupt at the
same time. However, the width of the gum is just adequate to accommodate the incisors. In the first few
months after birth, the growth of gum pads is rapid. Transverse dimensions of the gum pads increase
with the growth of the jaws.
With the development of the deciduous tooth, the segments of each gum pad become prominent. The
eruption of deciduous teeth commences at 6 months of age.

Natal and Neonatal Teeth (Fig. 5.11)

Occasionally, a child is born with teeth usually lower incisors called natal teeth. The teeth that erupts
within first 30 days after birth are called neonatal teeth. This causes difficulty in feeding. This may
cause ulcers on the breast of the feeding mother.
Riga-Fede disease: Early eruption of teeth (natal or neonatal teeth) causes ulceration on the ventral
surface of the tongue by the sharp edges of the tooth. This may interfere with the infant’s feeding and
suckling, which may in turn affect nutrition.

The Deciduous Dentition Stage (6 months to 6 years)

n The stage starts from eruption of first deciduous mandibular central incisors (around 4–6 months) and
ends with the eruption of first permanent molar (6 years).
n The deciduous dentition is initiated during the first 6 weeks of intrauterine life. The primary teeth begin
to erupt at the age of about 6 months.
n By 12–18 months, the first molars erupt, resulting in a vertically supported occlusal contact between
the two arches.
n The eruption of all primary teeth is completed by 2½–3½ years of age when the second deciduous
molars reach into occlusion.
n The mandibular central incisors are the first teeth to erupt into the oral cavity. The mandibular
eruption precedes maxillary dentition (Table 5.1).

Sequence of Eruption of Deciduous Teeth

Timing of Eruption

Central incisors 6–7 months

Lateral incisors 8–9 months

55

First molar 12–16 months

Canines 16–20 months

Second molar 24–30 months

The timing of tooth eruption may vary up to 3 months from the mean age of accepted eruption.

Normal Features of Primary Dentition

Features of Normal Primary Dentition

n Spaced anteriors
n Primate spaces
n Shallow overbite and overjet
n Straight terminal plane or mesial step
n Class I molar and cuspid relation
n Shallow cuspal interdigitation
n Almost vertical inclination of anterior teeth
n Ovoid arch form
n Flat occlusal plane or almost no curve of Spee is present

I. Spacing in deciduous dentition (Fig. 5.12)

a) Physiological spacing
n Generalized spacing is very common in deciduous teeth. These spaces are called physiological
spaces or developmental spaces.
n Physiological generalized spacing is common and is usual and desirable in deciduous dentition
to accommodate large succeeding permanent teeth.
n It is average 4 mm in the upper arch and 3 mm in the lower arch.
n It is possible to use spacing between lower deciduous teeth for predicting the degree of
crowding. Absence of spaces in the primary dentition is an indication that crowding of teeth may
occur in permanent dentition (Table. 5.2). Baume has described spaced and unspaced primary
dentitions and the effect on future permanent incisor eruption.

b) Primate/Simian/Anthropoid space/Baume spaces (Fig. 5.13)

n This type of spacing is seen mesial to the maxillary canines and distal the mandibular canines.

n These physiological spaces are similar to the dentition of the primates, so called
anthropoid/simian/primate spaces.
n These spaces are utilized during early mesial shift of molars from end on to class I relation.

II. Shallow overjet and Deep overbite: There is increased overbite and shallow overjet seen in the
initial phase of deciduous dentition. The deep bite is accentuated by the fact that the deciduous
incisors are more upright than their successors. The lower incisal edges often contact the cingulum
area of the maxillary incisors. Gradually, reduction of overbite takes place and attains edge-to-edge
bite due to:
n Eruption of posterior deciduous teeth
n Attrition of anteriors
n Growth tendency of the mandible (downward and forward growth)
56

III.Primary molar relationship (Flush terminal plane or FTP)

Mesial step: In majority of the cases, however, in primary dentition the mandibular cusp will be
ahead of corresponding maxillary cusp in a mesial direction giving a mesial step. This is the most
favourable relation for class I molar relation in permanent dentition. Some of them may convert
into class III molar relation in permanent dentition.
Flush terminal plane: When upper primary second molar occludes with the lower second primary
molar, a tangent line drawn vertically touches the distal surface of both upper and lower primary
molars. This line is called flush terminal plane (FTP). The straight FTP is considered as normal
molar relationship in the primary dentition to guide the permanent molars (Fig. 5.14) to a class I
relationship.
Distal step: In some other cases, the maxillary cusp will be ahead of mandibular cusp in mesial
direction giving distal step relation. This is unfavorable relation. In otherwise normal occlusal
pattern, a distal step of primary molars indicates developing class II malocclusion.
- 49% cases seen are mesial step
- 37% cases seen are flush terminal
- 14% cases seen are distal step

The Mixed Dentition Period (6–12 years) (Fig. 5.15)

n This is the period where both deciduous and permanent teeth are present in the oral cavity. This is
also the most watchful period of development of normal dentition and occlusion.
n During the course of this period, various malocclusions are encountered. Alveolar process is most
actively adaptable (areas of bone growth) during this period and thus ideal time for most orthodontic
interventions.
n This is also important because the growth spurts of maxilla and mandible coincides with the mixed
dentition stage.

The mixed dentition period can be divided into two stages:

n Early mixed dentition – 6–9 years
n Late mixed dentition – 9–12 years

Further, the mixed dentition can also be subdivided into following stages.
I. First Transitional Phase (6–9 years)
It is characterized by the emergence of the first permanent molars and the exchange of the deciduous
incisors with the permanent incisors.

Features
1. Eruption of permanent molars—The mandibular first molar is the first permanent tooth to erupt at
around 6 years of age. It is also called ‘key to normal occlusion’ by Angle as they play an important
role in establishment and function of occlusion.
a) Molar relation (Table 5.5 and Fig. 5.16): The type of molar relationship in the permanent
dentition is dictated by the skeletal jaw bases and the relationship of the distal surfaces of upper
and deciduous second molars.
The mesiodistal relation between the distal surfaces of the upper and lower second deciduous
molars can be of three types (see Table 5.5).
About 4 mm forward movement of lower molar relative to upper molars is required for smooth
transition to class I molar relation in permanent dentition.
Space for this provided by:
1. By differential growth of lower jaw: The mandible grows at a faster rate carrying the mandibular
molars ahead of maxillary molars.
57

2. By physiological and leeway spaces. Apart the shift in lower molar from a flush terminal plane
to class I relation can by occur either by utilizing of the physiologic spaces or leeway space in
the lower arch. Accordingly they are designated as the early and the late shift.

i) Early mesial shift: The erupting first permanent molar exerts a mesial force on the deciduous
dentition anterior to it. The primate spaces are closed and transformation into class I relation
occurs from end-on relation. Since this occurs early in the mixed dentition period it is called early
shift.

ii) Late mesial shift: In some dentitions there is lack of primate spaces. In these cases, when the
deciduous second molars exfoliate, the permanent first molars drift mesially utilizing the leeway
space. This occurs in the late mixed dentition period and is thus called late shift.

2. Incisal liability (Figs 5.17, 5.18)

 The erupting upper permanent incisors are considerably larger than the deciduous incisors they
succeed.
 The difference in the mesiodistal dimensions of the deciduous incisors and their succedaneous
permanent incisors is called as incisor liability.
 Warren Mayne stated that the total amount of mesiodistal width of succeeding permanent
incisors are larger than exfoliating primary incisors by 7.6 mm in the maxilla, 6 mm in the
mandible.

Compensation of Incisal liability

Then how do the permanent incisors align so well in the arch. The incisal liability is compensated
by the following three mechanisms.

Incisal liability = interdental spaces + increase in Intercanine width+ Incisor inclination

a) Utilization of interdental spaces:. This is compensated by interdental physiological spacing in

the deciduous dentition. It is on average 4 mm in the maxillary arch and 3 mm in the
mandibular arch.
.
b) Increase in intercanine width (Fig. 5.17)
- It is one of the main mechanisms of compensating the incisal liability.
- This is the increase in transverse dimensions in the canine region. This increase occurs due
to the lateral thrust created by the erupting permanent incisors (Baume and van der Linden).
- There is difference in maxillary and mandibular arch and also between males and females in
relation to the increase in intercanine width.
- Intercanine width increase is more in closed arches than in spaced arches.

c) Change in incisor inclination: Permanent incisors erupt labially inclined to the primary incisors by
2–3 mm. The primary incisors are more upright than the permanent incisors. There is decrease in the
inter-incisal angle of 150 degrees in exfoliating primary incisors to 123 degrees in erupting
permanent incisors. This is due to change in the inclination; this increases the arch perimeter (Fig.
5.19).
58

3. Lingual eruption of permanent lower incisors (Fig. 5.20)

 Usually the permanent lower incisors erupt lingually to the corresponding primary teeth even
before they are exfoliated.
 This is a common phenomenon and most of the parents are concerned with the look of
crowding. This is a self-correcting anomaly. The primary teeth are shed by the eruptive forces
from the permanent teeth. Then the lingually erupted permanent teeth are pushed labially into
the arch into their normal position by the tongue pressure. This is so in the case of spaced
primary dentition.
 However, in some cases even after the complete eruption of permanent incisors the primary
teeth are not shed off. The preventive measures are taken to maintain the normal shedding
and eruption timetable and accordingly the primary teeth are extracted.
 In some crowded primary dentitions, the permanent incisors cannot be pushed by tongue
pressure into the arch. In such cases, selective extraction of primary canines or serial
extractions has to be planned.

II. The Intertransitional Phase (8–10 years)

This is the most stable period of mixed dentition. This stage is marked by the presence of both the
permanent and primary dentition in both the arches. The deciduous canines and molars are present in
between the newly erupted permanent incisors and fist molars. This stage is stable and persists for an
average of 1.5–2 years.
n Teeth present are:
6EDC21 12CDE6
6EDC21 12CDE6
n Relatively stable period.
n No changes occur.

Ugly Duckling Stage (8–11 years) (Fig. 5.21)

(Broadbent Phenomenon)
n This is a transient or self-correcting malocclusion and is seen in the maxillary incisor region between
8–10 years of age in late mixed dentition stage.
n This is particularly seen during the eruption of the permanent canines.
n Children in the elementary schools tend to look unusual during the time of exchange of their incisors,
especially in the upper arch when permanent incisors are about to erupt.
n The permanent incisors appear to be much too large compared with the primary teeth and distal
divergence of the crowns (flaring) takes place resembling like inverted ‘V.’
n The children exhibit midline diastema along with the distal flaring of the incisors.
n But, this is self-correcting anomaly (transient malocclu-sion), which gets corrected by itself with the
eruption of the canine.
n This situation has been described by Broadbent as the ugly duckling stage as children tend to look
ugly during this phase of development. The erupting flared incisors tend to look like the walking of a
duckling.
n During this phase, it is usually misinterpreted by the parents and they will rush to the dentist.
The period from the eruption of incisors to appearance of canine into the arch is known as the ugly
duckling stage.
Features include
- Maxillary midline diastema.
- Distal tilting and flaring of incisor crowns.

Dynamics of Ugly Duckling Stage (Figs. 5.22, 5.23)

 Crowns of cuspids impinge on developing roots of lateral incisors causing the
crowns to flare laterally. This force is transmitted to the roots of central incisors
causing distal divergence of crowns and midline diastema.
59

 As the canines descend, the force is transmitted from the roots of lateral incisor on
to the crown portion and the crown divergence is corrected with closure of midline
diastema.
 If path of eruption of cuspids exceeds normal range there is impingement of incisor
roots leading to resorption of roots and insufficient growth and intercuspid arch
width.

Transitional Anterior Deep Bite

 In early mixed dentition, the permanent central incisors appear relatively larger and there is
anterior deep bite
 The maxilla and mandible has not reached the pubertal growth spurt and there is decreased
posterior vertical dimension as the cervico-occlusal height of primary molars is relatively less
compared to the permanent central incisors.
 This is self corrective. Anterior bite is relieved with the catch-up growth of jaws during pubertal
growth spurt in vertical direction and the correct proportion between the permanent central
incisors and the face is achieved. The permanent molars erupt and the premolars replace the
primary molars, thus the vertical height in the posterior segment is increased. This relieves the
anterior deep bite (Table 5.8).

III. The Second Transitional Phase (10–12 years)

The second transitional period is characterized by the replacement exchange of primary canines and
premolar to permanent canines and molars (i.e., exchange of C,D,E to 3,4,5). Since permanent molars
and incisors are already erupted into the arch, later 3,4,5 should erupt in exchange to C,D,E for proper
establishment of occlusion.
a) Leeway space of Nance (Fig. 5.24, Table 5.6)
n The term “leeway” means “a margin of freedom,” or “more room.”
n An important portion of the dental arch in the deve-lopment of occlusion of the permanent dentition
is the premolar segment.
n In this zone, the erupting premolars are significantly smaller in mesiodistal dimension than the
primary molars, which they replace.
n The combined mesiodistal width of the permanent canine and premolars (i.e., 3, 4, 5) is lesser
than the combined width of deciduous canine, first molar and second molar (i.e., C, D, E). Simply it
is C+D+E > 3+4+5.
- In maxilla—1.8 mm per arch (both sides) or 0.9 per quadrant (one side).
- In mandible—3.4 mm per arch (both sides) or 1.7 mm per quadrant (one side).

Importance of Leeway space

n The leeway space is the basic factor necessary to carry out the smooth exchange of the C, D, E to
3, 4, 5.
n The leeway space permits the mesial movement of lower molar and shift of the flush terminal
plane (FTP) mesially to establish class I molar relation.
n Presence of leeway space helps to carry out interceptive procedures like serial extractions to
establish normal occlusion.
E–space In the typical eruption pattern, the lower second primary molars (E’s) are the last primary
teeth to be lost in the lower arch, and frequently the permanent canines and premolars (3’s and
4’s) are fully erupted. At this point of time, the only size differential that needs to be taken into
consideration is that between the E’s and 5’s. This is the “E” space (Bishara). Most of the leeway
space is contributed by this ‘E” space. The first permanent premolar and first primary molar are of
similar size, then the leeway space is entirely due to the size differential of the E and its
successor.
60

b) Dimensional changes of the arch (Fig. 5.25): Changes in intercanine width are already discussed.
The other changes are:
n Decrease in arch perimeter
- The arch perimeter of the permanent dentition, as measured from the mesial side of the
mandibular first molars, decreases an average of about 4 mm (Moorrees, 1959) and on
average in maxilla it decreases by 2 mm.
- This change is found to a greater extent in the mandible than in the maxilla and because of the
pronounced tendency for the lower molars to drift mesially, occlusal relationships are in a flux
during the later stages of the mixed dentition.
n Decrease in arch length: The arch length decreases in the mixed and permanent dentition
stages as a result of the uprighting of the incisors and the loss of the leeway space by the mesial
movement of the first permanent molars.
n Increase in intermolar width: The intermolar width as measured from one first permanent molar
to the other increases on an average of 2.2 mm in the maxillary arch between ages 8 and 13
years. The intermolar width in the mandible increases on an average of 1 mm between ages 8 and
13 years. This is despite the fact that there is reduction in arch length.

Permanent Dentition Stage

The final dentition period is the permanent dentition period. This period begins with shedding of the last
primary tooth, usually primary maxillary canine. Thus, this period begins after approximately 12 years of
age and includes eruption of all the permanent teeth, except for teeth that are congenitally missing
or impacted (except the third molars). Growth of the jaw bones slows and stops eventually. Thus, very
little growth of the jaws occurs overall during the period, because puberty has passed. The permanent
molars erupt directly as an extension of the existing deciduous dentition. The permanent incisors
develop lingual or palatal to the deciduous incisors and move labially as they erupt. The premolars
develop below the diverging roots of the deciduous molars.
The sequence of eruption of the permanent dentition (Table 5.7) is more variable than that of the
primary dentition and does not follow the same anterior–posterior pattern. In addition, there are
significant differences in the eruption sequences between the maxillary arch and the mandibular arch
that do not appear in the eruption of the primary dentition (Table. 5.1).

Sequence of Eruption of Permanent Teeth (Table. 5.7)

The frequently seen sequences in the maxillary arch are:

6-1-2-4-5-3-7 (most common) or

6-1-2-4-3-5-7

In case of the mandibular arch the sequence (Knott and Meredith, 1966) is:

6(1)-2-3-4-5-7 or
6(1)-2-4-3-5-7

Overall sequence is: Usually the succedaneous teeth erupt as soon as primary teeth are exfoliated. A
latency period of
6 months between exfoliation of deciduous teeth and eruption of succadaneous permanent tooth.

These are also the most favorable sequences for the prevention of malocclusion. If the second molars
erupt before the premolars are fully erupted, significant shortening of the arch perimeter occurs due to
tilting of permanent first molar mesially. This reduces significantly the space available for the eruption of
the second premolars and may result in malocclusion (Fig. 5.26).
During eruption, the maxillary permanent second molar is situated too palatally. The maxillary 2 nd
molar is tilled distally and buccally and mandibular 2nd molar is tilted mesially and lingually. With the
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emergence of teeth, the occlusal relationship is established by the ‘cone and funnel’ mechanism with
the upper palatal cusp (cone) sliding into the lower occlusal fossa (funnel). When once contact is
established they start to upright.
The variation in eruption of permanent teeth may extend from 2 to 4 years. The most important point
is to watch the bilateral development of dentition rather than specific time of eruption. Usually teeth erupt
5 months ahead in girls compared to boys.
It takes 2–5 years for posterior teeth to reach the alveolar crest after crown formation is completed
and 12–20 months to reach occlusion after eruption.
After reaching occlusion, it takes few months for root formation to be completed. Nolla has given 10
stages of development of teeth. By stage 6, the crown formation is completed. At this stage, most teeth
begin eruptive tooth movements. By stage 8, 2/3rd of root formation is completed at which most teeth
pierce the alveolar crest. The teeth show eruptive movements when crown formation is completed. All
most all the teeth show 1/2–2/3% root formation when they emerge through alveolar crest (Fig. 5.27).

PREVIOUS YEARS UNIVERSITY EXAM QUESTIONS

Essay Type Questions
1. Describe the developing dentition from birth to adolescence.
2. What are the self-correcting anomalies and describe the different self-correcting anomalies during the
period of mixed dentition.
3. What are the various stages of development of dentition and add a note on importance of mixed
dentition period.
Short Answer Questions
1. Flush terminal plane – FTP
2. Sequence of eruption of permanent teeth
3. Permanent first molar
4. Incisal liability
5. Leeway space of the Nance
6. Early mesial shift
7. Late mesial shift
8. Baume spaces
9. Primary molar relationship
10 Intertransitional period
11 Ugly duckling stage/Broadbent phenomenon
12 Nollas stages of calcification of tooth
13 Safety valve mechanism
14. END on relation

REFERENCES
1. Robert G Kroll. Orban’s Oral Histology and Embryology, 5th edition.
2. Major M Ash, Stanley Nelson. Wheeler’s Dental Anatomy, Physiology and Occlusion, 9th ed., WB
Saunders.
3. Graber TM. Orthodontics: Principles and Practice, 3rd ed., WB Saunders; 1988.
4. E Moyers. Handbook of Orthodontics, 4th ed., Year Book Medical Publishers, Inc.; 1988.
5. Profitt. Contemporary Orthodontics, Elsevier India, 3rd ed.; 2000 (permissions-Elsevier).
6. Shoba Tandon. Textbook of Pedodontics, 2nd ed. Paras Medical Publisher.
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CHAPTER 6
Functions of Stomatognathic System
Introduction
Respiration
Deglutition
Infantile swallow
Mature swallow
Mastication
Speech
Passive muscle function – buccinator mechanism
Trajectories of force
Maxilla
Vertical
Horizontal
Mandible
Wolf’s law of transformation of force

INTRODUCTION
Form and function are interrelated as stated in Moss hypo-thesis. The principal physiologic functions of
the oral cavity are respiration, swallowing, mastication and speech. Therefore, normal development of
the orofacial region is dependent on normal function to a large extent.
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The orofacial musculature is relatively the most sophis-ticated in the newborn so that the potency of
airway, breathing and nutritional demands may be met. Tactile sensation is extremely well developed for
the newborn. At birth, mouth is the sole avenue of communication with the outside world and tactile
activity of mouth continues as child brings all objects to his mouth first. Some of the functions of
stomatognathic system are discussed in this chapter.

RESPIRATION
n Respiration is an inherent reflex activity.
n Within few minutes after birth, breathing is evoked spontaneously. Newborn infants are obligatory
nasal breathers and may not survive if the nasal passage is blocked at birth.
n The normal breathing to a large extent influences the normal development of orofacial structures.
n Nasal breathing of 100% may not be possible in patients with nasal obstruction, deviated nasal
septum, enlarged adenoids and chronic respiratory diseases, etc.

n These patients as a compulsion breathe with the mouth. During mouth breathing, the lowering of
mandible and forward positioning of the tongue is exaggerated.
n The normal muscular balance is lost and hence gives rise to abnormal increase in the lower half of
the face. The characteristic features are called as ‘Adenoid facies,’ which is described in detail in the
chapters to follow.

DEGLUTITION / SWALLOWING
n Swallowing reflex occurs during the last months of fetal life and it appears that swallowed amniotic
fluid may be an important stimulus to activation of the infant immune system.
n Swallowing begins around 12½ weeks of intrauterine life.
n Full swallowing and sucking is established around 32–36 weeks IU life.
n The habit of sucking is a reflex occurring in the oral stage of development and disappears during
normal growth between 1–3½ years.
n Deglutition or swallowing is one of the important functions carried out by the stomatognathic system.
There are two main forms of deglutition or swallowing.
n The one which is found in infants is called as ‘infantile swallow’ and that found in normal adults is
called as ‘mature swallow.’

Infantile Swallow (Fig. 6.1)

Once an airway has been established, the newborn infant’s next physiologic priority is to obtain milk and
transfer it into the gastrointestinal system. This is accomplished by two

maneuvers: suckling (not sucking, with which it is frequently confused) and swallowing.
The newborn child has the ability to feed himself from the lactating breast. He cannot suck the milk.
Instead this is done by suckling consisting of small nibbling movements of the lips, a reflex action in
infants. This is called as “Suckling.”
During suckling, the nipple is drawn into the mouth by negative pressure. The tongue protrudes out in
between the lower lip and the nipple. The tongue now encircles around the nipple forming a groove or
channel for free flow of milk posteriorly.
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The lactating breast contains milk ducts. These ducts are surrounded by smooth muscle, which
contracts to force out the milk when stimulated. These muscles are stimulated by the to and fro
peristaltic activity of the infant’s lips, tongue and mylohyoid muscle.
When the breast muscles are stimulated, they squirt the milk into the infant’s mouth. The milk now
freely flows posteriorly and directly into the pharynx and oesophagus by groove formed by the tongue.
.
The characteristic features as described by Moyers include the following:
n The tongue is placed between the upper and lower gum pads in close apposition with lips. The jaws
are apart.
n The normal infantile swallow is characterized by contractions of the facial muscles (seventh cranial
nerve) and tongue and the positioning of the tongue between the gum pads.
n With change to solid food and eruption of teeth, modification of swallowing act occurs. Tongue is not
forced between gum pads, which contact momentarily. The tongue is contained within the dental
arches and the mandible is no longer protruded. Mandibular thrust diminishes—spatula-like portion of
tongue collects the food and forces it posteriorly, signifying the end of infantile swallow.

Mature Swallowing (Somatic Swallow)

The infantile slowly transforms into a mature swallow concomitant with the development of dentition.
This transition starts from the end of the first year. During the transitional period, characteristics of both
infantile and mature swallow can be seen. The infantile swallow gradually disappears with the eruption of
the buccal teeth in the primary dentition. Most children achieve most features of the mature swallow at
12–15 months of age.

Moyers listed the following characteristics:

1. Teeth are together.
2. Mandible is stabilized by contractions of mandibular elevators, i.e., Vth cranial nerve.
3. Tongue tip is held against the palate.
4. Minimal contractions of lips are seen.

Deglutition Cycle
Fletcher divided deglutition cycle into four phases:
1. The preparatory swallow
2. The oral phase
3. The pharyngeal phase
4. The oesophageal phase

Oral phase of swallowing is under voluntary control while pharyngeal phase and oesophageal
phase are involuntary.
The average individual swallows about once a minute between meals and as frequently as 9 times a
minute during eating.

MASTICATION
It is the first movement in the digestive tract. It is a complex process by which coarse food is broken
down into smaller particles.
Fletcher summarizes mastication in adults using the six phases outlined by Murphy.
1. Preparatory phase: Food is ingested and positioned by tongue in the oral cavity and mandible
moved towards the chewing side. Opening of mandible is initiated by Bulbay centre.
2. Food contact: Characterized by momentary hesitation in movement triggered by sensory receptors
concerning the apparent viscosity of food and transarticular pressures probably due to load on the
masticatory apparatus.
3. Crushing phase: Starts with high velocity, then slows as the food is crushed and packed. Food is
crushed by equal and synchronous activity on both sides.
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4. Tooth contact: It is accompanied by a slight change in direction without any delay. Actual contact
with tooth is seen.
5. Grinding phase: It coincides with the transgression of the mandibular molars across their maxillary
counter parts resulting in bilateral muscular discharge becoming unequal and asynchronous
indicating that the person is chewing unilaterally.
6. Centric occlusion: The movement of teeth come to a definitive and distinct stop. Number of
masticatory strokes on an average per minute is 80.

SPEECH
n Speech is largely a learned activity dependent on the maturation of the organism. The muscles of
walls of torso, the respiratory tract, the pharynx, the soft palate, the tongue, the lips, face and nasal
passage are all concerned in the production of speech sounds.
n The lips and tongue undergo maturational changes preparatory to speech. The first sounds actually
make no demands on the lips.
n Articulation is a process by which modification of sounds is done by changing the shape of cavities in
the mouth, nose and throat.

MUSCLE FUNCTION—BUCCINATOR MECHANISM (Figs. 6.6, 6.7)

 Bone is plastic in nature and moulds itself to the muscular forces exerted on it.
 The entire dentition and supporting structures are surrounded by the continuous band of
musculature that encircles and anchored at the pharyngeal tubercle.
 The bands of musculature from anterior to posterior are orbicularis oris, Buccinators and
superior constrictor of pharynx on either sides. These three muscles constitute the buccinator
mechanism.
 Buccinator is a facial muscle, also called as cheek muscle, which extends between modiolus
and pterygomandibular raphae. It flattens cheek against gums and teeth and prevents
accumulation of food in the vestibule.
 All these three muscles exerts inward force on the dentition. To counteract this inward force, the
outward force is exerted by the tongue and gets neutralized; this neutralized zone aids to
maintain the position of the teeth in the arch and stability of the dento alveolar complex.

Applications
n If the tongue force (macroglossia) is more than the buccinator mechanism, the entire dentition flares
facially and buccally.
n The same mechanism plays an important role in the aetiology of tongue thrusting and thumb sucking.
The tongue pressure is not effectively neutralized resulting in flaring of incisors and open bite.
n If the buccinator mechanism is dominated, it results in constriction of arches as seen in class II div I
cases and in some mouth breathers.
n The myofunctional appliances, particularly the Frankel II, eliminate this abnormal buccinator
mechanism and allows the proper growth of dental arches.
n The lip pressure can be taken as anchorage for distal driving of molars.

TRAJECTORIES OF FORCE
Benninghoff in 1925 found that the architecture of the cranial and facial skeleton is built in such a way
so as to resist the functional stresses. These functional stress bearing areas of the bone are known as
Benninghoff’s lines or Trajectories (lines of stress) of bone.
 These trajectories are seen in both spongy and compact bone.
 Trajectories are present both in the maxilla and mandible
 The lines of orientation of these trajectories follow the pathways of maximal pressure and
tension. They indicate the direction of the functional stresses.
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 Benninghoff showed that the stress trajectories obeyed no individual bone limits, but rather the
demands of the functional forces and spread from one bone to another in the skull.

Trajectories of the Maxilla Trajectories of the Mandible (Fig. 6.10)

The maxilla consists of thin bones and plates
along with the support of bony thickenings, these
are called buttresses, which make the maxilla to
be strengthened with minimum bone material. The
buttresses are nothing but stress-bearing areas.
Two types of trajectories are present in the
maxilla:
1. Vertical trajectories
a) Frontonasal buttress
b) Molar zygomatic buttress
c) Pterygoid buttress
2. Horizontal trajectories
Vertical Trajectories (Figs. 6.8, 6.9)
There are three main vertical pillars of trajectories,
all arising from alveolar process and ending in the
base of the skull. These trajectories curve around
the sinuses, and nasal and orbital cavities.
Horizontal Trajectories
The horizontal trajectories of the maxilla include:
1. Hard palate
2. Orbital ridges
3. Zygomatic arches
4. Palatal bones
5. Lesser wings of sphenoid
 The main or common trajectory line or
stress pillar is line of stress extending
from one condyle to the other passing
through the symphysis and along with the
lower border of the mandible.
 A number of vertical trajectories radiate
down below the roots of the mandibular
teeth in the alveolar process and join
together in a common stress pillar
 The mandibular canal with its contents,
the inferior alveolar nerve and vessels, is
protected by this concentrated trabecula,
thus supporting the “unloaded nerve
concept.’
 The thick cortical layer along lower border
of the mandible and the mylohyoid ridges
are the other prominent buttresses of the
mandible.
 The accessory trajectories include the
symphysis, gonial angle, vertical pillar
from coronoid process into the ramus and
body of the mandible.

Wolff’s Law of Transformation of Bone (Fig. 6.11)

 Wolff’s Law of Transformation of Bone is proposed by Julius Wolff, the German physiologist in
1870. This is called as law of orthogonality.

 “Wolff’s law” of the functional adaptation of bone is based on the trajectory hypothesis of
cancellous bone architecture put forward by Meyer, an anatomist, and Culmann, a
mathematician, in 1867.
 Wolff Law states that external morphology and internal architecture of bone are directly
proportional to the functional forces acting upon it.
 Wolff demonstrated that bone trabeculae were arranged in response to the stress lines on the
bone. example:- the internal architecture of the head of the femur and the condylar process of
the mandible.
 These stress trajectories and this can be correlated with its function in a mathematical way.
 Many of the so-called trajectories are not in straight line but are irregular and wavy and they are
angled not at right angles to one another
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 In orthodontic context, when loads are applied, functional remodeling reorients bone
trabeculae so they align with the new principal stress axes.
 Thus, quantity of bone tissue is minimum that would be needed for function requirements. This
minimum amount of bone transforms its structure so as to resist the forces exerted upon it. This
is the basis of Wolff’s law of transformation of bone


PREVIOUS YEARS UNIVERSITY QUESTIONS

Essay Questions
1. Describe the various functions performed by the oro-facial region and add a note on buccinator
mechanism.
2. Describe the different trajectories of force in the maxilla and mandible and add a notes on Wolf’s law
of transformation of force.

Short Answer Questions

1. Infantile swallow
2. Mature swallow
3. Phases of deglutition
4. Mastication
5. Wolf’s law of transformation of force
6. Zygomatic buttress

REFERENCES
1. Samuel Hemley. A text on orthodontics: showing its relationship to every phase of dentistry, Coiner
Publications; 1971.
2. Graber TM. Orthodontics: Principles and Practice, 3rd ed., WB Saunders; 1988.
3. E Moyers, Handbook of Orthodontics, 4th ed., Year Book Medical Publishers, Inc.; 1988.
4. Profitt. Contemporary Orthodontics, 3rd ed., Elsevier India; 2000 (permissions-Elsevier).
5. Shoba Tandon. Textbook of pedodontics, 2nd ed, Paras Medical Publisher.
6. Alfred Benninghoff, Detlev Drenckhahn, Anatomie Bd.1, 17th ed, Urban & Fischer.
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