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1. CONCEPTS OF GROWTH AND
DEVELOPMENT IN
ORTHODONTICS
INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education
www.indiandentalacademy.com

2. CONTENTS
• INTRODUCTION
• DEFINITION
• PHYSIOLOGY OF GROWTH
• FACTORS AFFECTING GROWTH AND
DEVELOPMENT
• PATTERN OF GROWTH
• VARIABILITY OF GROWTH
• TIMING OF GROWTH

3. CONTENTS
• MODES OF GROWTH
• CHARACTERISTICS OF GROWTH
• SITES AND TYPES OF GROWTH
• THEORIES OF GROWTH CONTROL
• METHODS OF STUDYING GROWTH
• METHODS OF COLLECTING DATA
• BIBILOGRAPHY

4. THE MOBILE MASK IN FRONT OF
HUMAN BRAIN BEGAN TO ATTRACT
OUR ATTENTION WHEN WE WERE
BABIES AND CONTINUES TO FASCINATE
US AS LONG AS WE LIVE
W. K. GREGORY,
OUR FACE FROM FISH TO MAN

5. WITHIN THE TEXT OF THE CRANIOFACIAL
EMBRYOLOGY,WE COME ACROSS TWO TERMS
GROWTH & DEVELOPMENT.
WHAT DOES THE TERM GROWTH IMPLIES TO US ?
CHANGE IN MAGNITUDE.
DOES IT EXPLAIN TO HOW FAR IT HAPPENS ?
WHY SHOULD IT HAPPEN IN A PREDETEMINED
DIRECTION ?

6. TO UNDERSTAND THIS ,THE MORE
DESCRIPTIVE & EXPLANATORY TERM
DEVELOPMENT IS ADDED.
DEVELOPMENT CONNOTES A
MATURATIONAL PROCESS INVOLVING
PROGRESSIVE DIFFERENTATION AT THE
CELLULAR & TISSUE LEVELS,THERE BY
FOCUSING ON THE ACTUAL BIOLOGICAL
MECHANISM THAT ACCOUNTS FOR
OVERALL GROWTH.

7. DEFNITION:
GROWTH DEVELOPMENT

8. DEFINITION
GROWTH
• GROWTH IS AN INCREASE IN SIZE
-“TODD”
• THE SELF MULTIPLICATION OF LIVING
SUBSTANCE
-“HUXLEY”
• THE INCREASE IN SIZE,CHANGE IN
PROPORTION AND PROGRESSIVE COMPLEXITY
-“KROGMAN”

9. • ENTIRE SERIES OF SEQUENTIAL ANATOMIC
AND PHYSIOLOGICAL CHANGES TAKING
PLACE FROM THE BEGINNING OF PRENATAL
LIFE TO SENILITY
“MERIDTH”
• QUANTATIVE ASPECT OF BIOLOGIC
DEVELOPMENT PER UNIT OF TIME.
“MOYERS”
• CHANGE IN ANY MORPHOLOGICAL
PARAMETER WHICH IS MEASUREBLE
“MOSS”

10. DEFNITION:
DEVLOPMENT
• DEVELOPMENT MEANS PROGRESS TOWARDS
MATURITY.
“TODD”
• ALL THE NATURALLY OCCURING
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.
“MOYERS”

11. DEFINITIONS OF
DEVELOPMENT
ACC TO PROFITT
INCREASE
IN COMPLEXITY

12. • ACC TO CARLSON:
DEVELOMENT IS A LIFE LONG
PROCESS THAT ENCOMPASSES
ALL OF THE STRUCTURAL AND
FUNTIONAL CHANGES THAT
TAKES PLACE FROM
CONCEPTION THROUGH
MATURITY.

13. NEGATIVE GROWTH
• GENERALLY WE EQUATE GROWTH
WITH ENLARGEMENT BUT THERE
ARE INSTANCE IN WHICH GROWTH
RESULTS IN DECREASE IN SIZE.
• EXAMPLE: THYMUS GLANDS AFTER
PUBERTY. THEREFORE GROWTH
MAY RESULT IN INCREASE OR
DECREASE IN SIZE, CHANGE IN
FORM OR PROPORTION,
COMPLEXITY , TEXTURE.

14. Husband
To
wife

15. HOW DO WE GROW?
(AN OVER VIEW ON
PHYSIOLOGY)
• CONTINOUS INTER ACTION BETWEEN
ENDOCRINE AND SKELETAL SYSTEMS
• MOST OF THE HARMONES INVOLVED
• KEY FACTOR IN ENDOCRINE GROWTH ACCESS IS
HUMAN GROWTH HARMONE (HGH) BY
SOMATOTROPIC CELLS IN Ant.PITUTARY.
• RELEASE OF (HGH ) REGULATED BY
HYPOTHALAMIC HARMONES HGH-RELEASING
AND HGH- INHIBITORY HARMONES.

17. BASIC CONCEPTS OF GROWTH
PHYSIOLOGY OF GROWTH
PITUITARY GLAND OR HYPOPHYSIS – 1CM
DIAMETER, 0.5 – 1gm IN WEIGHT
LIES IN SELLA TURSICA AND IS CONNECTED TO
HYPOTHALAMUS BY PITUITARY STALK
PITIUTARY GLAND ANTERIOR PITUITARY OR ADENOHYPOPHYSIS
POSTERIOR PITUITARY OR NEUROHYPOPHYSIS
ANTERIOR PITUITARY RELEASES 6 IMPORTANT
PEPTIDE HARMONES-GH, ACTH, FSH, LH, PROLACTIN

18. GROWTH HARMONE :
 PROTEIN IN NATURE WITH MOL WT 21500
FUNCTIONS
METABOLIC: INCREASES SYNTHESIS OF PROTEINS, INCREASES MOBILIZATION OF
LIPIDS, CONSERVATION OF CARBOHYDRATES
BONE : DIFFERENTIATION AND DEVELOPMENT OF BONE CELLS
INCREASES GROWTH OF SKELETON( LENGTH AND THICKNESS)
PARTICULARLY MEMBRANOUS BONES SUCH AS JAW BONES AND SKULL BONES
BECOME THICKER
GH HAS INDIRECT EFFECT ON BONES
LIVER SOMATOMEDIN
GH EFFECT ON
BONES
IGF-1
SOMATOMEDIN C
IGF-2
ACTS ON BONE
AND CAUSES
GROWTH

19. HYPOTHALAMUS
GHRH , GHIH SOMATOSTATIN
ALSO SECRETED BY DELTA CELLS OF
ISLETS OF LANGERHANS (PANCREAS)
INHIBITION
STIMULATION OF
ANTERIOR PITUITARY
GH WHICH ACTS
ON LIVER,
TISSUES
SOMATOMEDIN
FEED BACK INHIBITION

20. PHYSICAL GROWTH
AND DEVELOPMENT
PRENATAL POSTNATAL
PRENATAL GROWTH:
MOST CRUCIAL IN DETERMINING A CHILDS GROWTH AND
FUTURE WELL BEING SINCE GROWTH IS AT ITS FASTEST DURING
THIS TIME
PRENATAL PERIOD – 18 TO 22 WEEKS OF GESTATION (BODY
LENGTH)
PEAK VELOCITY FOR HEIGHT – 34 WEEKS GESTATION
GREAT RATE OF GROWTH OF FETUS COMPARED WITH THAT OF
A CHILD IS LARGELY DUE TO CELLULAR PROLIFERATION .

21. Physiology of growth
(an over view)
• HGH ACTS ON LIVER AND PRODUCES
SOMATOMEDIN (SMD) WHICH
STIMULATES CARTILAGE TO DIVIDE AND
SYNTHESIZE CARTILAGE MATRIX
• DESPITE EPISODIC SWINGS IN HGH
LEVELS, SMD ACTIVITY TENDS TO REMAIN
CONSTANT AS ITS HALF-LIFE IS LONGER
THAN HGH

22. Physiology of growth
(an over view)
• SMD ACTIVITY IS LOW IN PROTIEN-
CALORIE MALNUTRITION
• EXESSIVE GLUCOCORTICOIDS
SUPRESS SMD GENERATION AND
REDUCED SMD ACTIVITY IS
ASSOCIATED WITH ESTROGEN
ADMISTRATION

23. Physiology of growth
(an over view)
• SKELETAL MATURATION IS
CONTROLLED BY:
-THYROXINE
-ADRENAL STERIODS
-GONADAL STEROIDS
• EXCESS OF THESE ACCLERATES
MATURATION AND DEFACIENCY
CAUSES DELAY
• DURING PUBERTY SEX STEROIDS
AND HGH PRODUCE PUBERTAL
GROWTH SPURT.

24. Principles of growth and development
1. Bone grows by adding new bone on
one side of bony cortex and taking it
away from the other side, due to
which bone drift occurs.
2. The inner and outer surface of the
bone are covered with mosaic type
appearance of growth fields, which
can be resorbtive or depository. If it
is resorbtive on one side it will be
depository on other.

25. 3. Bone has periosteal and endosteal
layer if one is resorbtive then other
will be depository.
4. The control of growth is done by the
soft tissue matrix present around the
bone. The blueprint of the design
construction and growth of the bone
lies in the composite of muscles,
tongue, lips, connective tissue, nerves,
blood vessels, airways etc.

26. 5. The various sites of growth do
not show a same rate of growth
activity.
6. Remodeling is a basic part of
growth process.
7. Growth process leads to primary
or secondary displacement.

27. FACTORS AFFECTING
GROWTH AND DEVELOPMENT
• 1. HEREDITY.
• 2. NUTRITION.
• 3. ILLNESS.
• 4. RACE.
• 5. SOCIO ECONOMIC FACTOR.
• 6. FAMLY SIZE AND BIRTH ORDER.
• 7. EXCERSIZE.
• 8. ADULT PHYSIQUE.
• 9. CLIMATE AND SEASONAL
FACTORS.
• 10. PSYCOLOICAL DISTURBANCES
• 11. ENDOCRINE FACTORS

28. HEREDITY: (genetic control)
- Genetic control on size of parts, rate of growth and onset of growth
events.
E.g.: teeth eruption, ossification of bones, adolescent growth spurt.
NUTRITION:
-Malnutrition delays growth and affect size of body parts. i.e. body
proportions, body chemistry, quality and texture of tissues.
E.g. teeth, bones.
During short periods of mal nutrition growth slows and with return of
good nutrition growth takes place fast.
ILLNESS:
Minor childhood illness does not have much effect. Prolonged serious
illness have marked effect on growth.

29. Race :
• Most of the differences are due to climatic, nutritional
or socioeconomic
• North American blacks are ahead of whites in skeletal
maturity at birth up to 2 yrs of age and is associated
with advanced motor behavior. Calcification & eruption
is 1 yr earlier in blacks.
Socio Economic factors:
•Is directly related to size of the baby
•Child living in favorable condition tend to be
larger, display different types of growth & show
variation in timing of growth when compared with
disadvantaged children.

30. Family size and birth order :
• Size of individuals, maturation levels and
intelligence can be correlated with the size of
family.
• First born children tend to weigh less at birth,
ultimately achieve less stature and higher IQ.
Exercise:
Favors development of motor skills, increase in
muscle mass and fitness.
Adult physique:
correlates with developmental events.
Taller women tend to mature late.

31. Climate & seasonal factors:
• There is general tendency for those living in cold
climate have greater proportion of adipose tissue.
• Skeletal variations are associated with the climatic
conditions
Psychological disturbances :
Children experiencing stressful conditions display
an inhibition of Growth Hormone.
Catch up growth is seen when the stress on them
is removed.

32. Endocrine Factors :
• Males exhibit a more rapid growth for 3 –
6 months after birth.
• This is due to presence of testosterone in
serum of male infants in first few post-
natal months.
• This acceleration is again found after
puberty that is during adolescence.

33. PATTERN OF GROWTH
Proportionality of growth at a point of time and also changes in
this proportionality over a period of time.
At 3rd month of intra uterine life:
Head: 50%of total body length.
At birth:
Head: 39% of total body length
Legs: 30% of total body length
Adults:
“Cephalo Caudal gradient of growth” Head: 12% of total body length
“Scammon” Legs: 50% of total body length.

34. SCAMMON’S GROWTH
CURVE
1) NEURAL TISSUE :
90% BY 6 YRS
96%BY 10 YRS
2) LYMPHOID TISSUE :
100% BY 7 YRS
3)SOMATIC TISSUES :
Slow during child hood
&
accelerates at puberty
4)GENITAL TISSUES :
• Accelerates rapidly
-on Set of puberty

35. VARIABILITY OF GROWTH
• Indicates the degree of difference
between two growing individuals, in all
planes of space including the all
important time.
• Everyone is not alike in the way that they
grow.
• Difficult but clinically important to decide
an individual is normal or away from the
normal range.
• Evaluate deviation from usual pattern and
express variability quantitatively.

36. VARIABILITY OF GROWTH
Charts to assess Height and Weight:
Boys: Girls:
1. To evaluate the present growth status of individuals
2. To follow the growth over a period of time

37. Variability in growth occurs in
several ways
From normal variation
From influences out side the normal experience
E.g.: Serious illness
From Timing effects

38. TIMING OF GROWTH
•Timing of Developmental events is largely under
genetic control yet altered by environment.
•Sex related differences in timing of growth
phenomena.
•Physique related difference.
e.g. taller one’s mature late.
• BIOLOGICAL CLOCK SET DIFFERENTLY FOR
DIFFRENT INDIVIDUALS

39. TIMING OF GROWTH
Growth is not a steady and uniform process.
• There are four growth spurts :
1. At birth.
2.1 yr. after birth.
3.Pre pubertal growth spurt.
• 6-7 yrs. in females.
• 7-9 yrs. in males.
1. Adolescent growth spurt.
• 11-13 yrs. in females.
• 14-16 yrs. in males.

40. Pre pubertal Growth Spurt
• Occurs due to production of sex hormones from
adrenal gland at the age of around 6 yrs. In the
form of a weak androgen
(Dihydroepiendosterone).
• This activation is therefore also referred to as
adrenarche.
• In girls more amount of hormones are released
hence is more prominent than in boys.

41. Adolescent Growth Spurt
• Initiation occurs in the brain.
Hypothalamus releases releasing factor
from neuroendocrine glands.
Via cytoplasmic transport
Base of the hypothalamus near pituitary
Via capillaries
pituitary
Ant.. pituitary releases
pituitary gonadotropins
Stimulates endocrine cells in adrenal gland and
sex glands to produce sex hormones

42. IN MALES:
In testes :
- Sertoli cells produce testosterone
- Leydig cells produce estrogen
In adrenal cortex:
-Male and female sex hormones are produced.
IN FEMALES:
In ovaries:
-Estrogen is produced initially and then
progesterone.
In adrenal cortex:
-Male and female sex hormones are produced.

43. sex hormones
blood stream
development of GENERAL BODY decrease in
secondary GROWTH lymphoid
sexual tissue
characteristics
growth of genitals

44. Timing of puberty makes a difference
in ultimate body size. The earlier
the puberty the smaller will be the body
size.

45. sex hormones
cartilage to grow Increases the rate at which
cartilage is
transformed into bone
increase in skeletal
maturation
adolescentcomplete
Growth growth spurt
This maturation occurs faster in females
hence
they have a shorter stature.

46. Clinical significance of
growth spurts
• Differentiate normal or pathologic growth changes
• Treatment of skeletal discrepancies is advantageous
if carried out in mixed dentition
• Pubertal growth spurt offers the best time for
treatment direction and management
• Orthoganthic surgery should be performed after
growth ceases.
• Arch expansion is carried out during maximum
growth period.

48. CATCH UP GROWTH
Growth in man is very carefully regulated
process
Children are meant to achieve a certain height
determined in large part by genetic factors
If growth is interrupted by acute
malnutrition/illness and this is then corrected
then child catches up his/her original growth.
This increased velocity of growth following
correction of adverse circumstances is
termed catch up growth

49. CRITICAL PERIODS
- SMITH.D.W, BIERMAN.E.L
The biologic ages of man
• The stage that an individual has reached at a
particular time may be referred to as Biologic or
Maturational age
• During these periods of rapid change and
differentiation, developing tissues and organs are
most susceptible to humoral and environmental
insults leading to growth deficiency and resultant
malformations, referred to as Critical periods

50. CRITICAL PERIODS
Brain cells have been formed by 6 months of age and so it is
highly susceptible to produce growth deficiency disorders during
fetal and early infancy life.
Bone and cartilage cells continue to divide till 15-20 years of age.
Hence skeletal system is susceptible during prenatal and
throughout childhood and adolescence

51. MODES OF GROWTH
At the cellular level there are only
three possibilities of growth
• HYPERTROPHY
• HYPERPLASIA
• EXTRA CELLUAR MATERIAL
SECRETION

52. NATURE OF THE
SKELETAL GROWTH
• INTERSTITIAL GROWTH:
Combination of hyperplasia and hypertrophy and
secretion of extra cellular material can also accompany.
e.g.: ALL SOFT TISSUES & UNCALCIFIED CARTILAGES
• DIRECT (OR) SURFACE OPPOSITION:
formation of new cells in periosteum, extra cellular
material secreted, get mineralized and new bone
formed.
e.g.: BASAL PART OF THE SKULL,TRUNK & LIMBS

53. CHARECTERISTICS OF
BONE GROWTH
• INTRAMEMBRANIOUS OSSIFICATION
Transformation of mesenchymal connective tissue into
membranous sheets to osseous tissue
EX: CALVARIUM,
CLAVICLES
BODY OF MANDIBLE
SPINAL PROCESS OF VERTEBRA
PART OF PELVIS
• ENDOCHONDRAL OSSIFICATION
Conversion of hyaline cartilage prototype into bone
EX: TUBULAR BONE
CUBOID BONES
BASE OF SKULL
VERTEBRAL BODIES
PART OF PELVIS

54. GROWTH MOVEMENTS
(Bone
remodeling)
CORTICAL DRIFT:
Growth movement towards the depository surface by a
combination of resorption and deposition
DISPLACEMENT:
Movement of the whole bone as a unit
- PRIMARY
Displacement in conjunction with its own growth
- SECONDARY
Displacement of bone as result of growth and enlargement of
adjacent bone.

55. SITES & TYPES OF GROWTH IN
THE CRANIOFACIAL COMPLEX
CRANIO FACIAL COMPLEX IS
DIVIDED INTO FOUR AREAS
1)CRANIAL VAULT
2)CRANIAL BASE
3)NASOMAXILLARY COMPLEX
4)MANDIBLE

56. CRANIAL VAULT
FLAT BONES FORMED BY INTRA
MEMBRANEOUS OSSIFICATION
GROWTH PROCESS IS ENTIRELY THE
RESULT OF PERIOSTEAL ACTIVITY AT
THE SURFACES OF BONE
REMODELLING AND GROWTH AT
SUTURES
CONTOUR IS BY REMODELLING IN
INNER AND OUTER SURFACES
FONTANELLAE FUSE IN ADULT LIFE

57. CRANIAL BASE
INITIALLY BY CARTILAGE
TRANSFORMED LATER BY
ENDOCHONDRAL OSSIFICATION
CENTERS OF OSSIFICATION:
BASI OCCIPITAL
SPHENOID
ETHMOID
CARTILAGE IN BETWEEN CENTERS
IS SYNCHONDROSIS

58. NASO MAXILLARY COMPLEX
ENTIRELY BY
INTRAMEMBRANEOUS
OSSIFICATION
BY APPOSITION OF BONE AT
THE SUTURES MAXILLA
MOVES DOWN WARDS AND
FORWARDS RELATIVE TO
CRANIUM.

59. NASOMAXILLARY COMPLEX
BY SURFACE REMODELLING
BONE RESORBTION ANTERIORLY

60. “ENLOW’S” CARTOON REPRESENTATION
SURFACE REMODELLING OF BONE IN OPPOSITE
DIRECTION TO THAT IN WHICH IT IS BEING
TRANSLATED BY GROWTH OF ADJACENT STRUCTURES

61. NASOMAXILLARY COMPLEX
REMODELLING OF
PALATAL VAULT
BONE REMOVED FROM
NASAL FLOOR AND ADDED
IN THE ROOF OF MOUTH
RESULTING DOWNWARD
AND FORWARD MOVEMENT
AND ALSO WIDENING

62. MANDIBLE
ENDO CHONDRAL AND PERIOSTEAL
ACTIVITY
CONDYLE AS AN EXCEPTION, THE REST IS
BY SURFACE APPOSITION AND
REMODELLING.
PRINCIPLE SITES ARE POSTERIOR SURFACE
OF RAMUS,CONDYLAR AND CORONOID
PROCESSES

63. MANDIBLE
The height of the mandible is by
endochondral ossification at the condyle
accompanied by surface remodeling.
The chin moves downwards and
forwards but as a growth site chin is
almost in active.
Grows longer by apposition of new bone
on the posterior surface of ramus and
large quantities of bone resorbed from
anterior surface of ramus.

64. “ALTHOUGH WE APPEAR TO HAVE A
FAIRLY CLEAR IDEA OF HOW THE
FACES GROWS. AND OF WHERE IT
GROWS, WE HAVE LITTLE IDEA OF
WHY IT GROWS… WE DO NOT FULLY
UNDERSTAND THE FACTORS WHICH
CONTROL THE AMOUNT AND
DIRECTION OF GROWTH”.
MILLER - 1982

65. THEORIES OF GROWTH
CONTROL
• 1) GENITIC THEORY
• 2)SUTURAL DOMINANCE THEORY
- SICHER
• 3)CARTILAGENOUS THEORY
- JAMES SCOTT (1950)
• 4)THE FUNCTIONAL MATRIX THEORY
- MELVIN MOSS (1962)
• 5)VAN LIMBORGH’S THEORY
- VAN LIMBORGH (1970)

66. THEORIES OF GROWTH
CONTROL
• ENLOW’S EXPANDING “V” PRINCIPLE
• ENLOWS COUNTER PART PRINCIPLE
-ENLOW
• SERVO SYSTEM THEORY
-CHARLIER & PETROVIC(1967)
-STUTZMANN &PETROVIC (1970)

67. SUTURAL DOMINANCE THEORY
SICHER -1952
CARTILAGE SUTURES AND PERIOSTIUM PLAY A
SIGNIFICANT ROLE IN CONTROL OF THE GROWTH
OF SKULL.
POINTS OPPOSING :
- EXTIRPATION OF FACIAL SUTURES HAS NO APPRECIABLE EFFECT ON
DIMENSION
- SUTURAL GROWTH HALTED BY MECHANICAL FORCES EVIDENCING
THAT SUTURE DOES NOT HAVE INDEPENDENT GROWTH POTENTIAL
( KOSKI, 1968)
- MICROCEPHALAY AND HYDROCEPHALAY RAISED DOUBTS ON
INTRENSIC GENETIC STIMULUS OF SUTURES

68. CARTILAGENOUS THEORY
JAMES SCOTT-1950
INTRNSIC GROWTH CONTROLLING FACTORS WERE
PRESENT ONLY IN THE CARTILAGE AND PERIOSTEUM
AND THE SUTURES BEING SECONDARY.
NASAL SEPTAL CARTILAGE
IS PACEMAKER IN
NASOMAXILLARY
COMPLEX

69. CARTILAGENOUS THEORY….
• Mandible considered as
diaphysis of a long bone, bent
into horse shoe shape with a
cartilage constituting, half an
epiphyseal plate at the ends
represented by condyles.

70. EXPERIMENTAL STUDIES
FOVOURING THE THEORY
TO TEST THE IDEA THAT CARTILAGE SERVE AS
TRUE GROWTH CENTER.
1. TRANSPLANTATION OF CARTILAGE IN A NEW
LOCATION OR IN CULTURE
2. EVALUATION OF THE EFFECT ON GROWTH BY
REMOVING CARTILAGE AT EARLY STAGE OF LIFE.
TRANSPLANTATION RESULTS:
•NOT ALL SKELETAL CARTILAGE ACTS THE SAME
•EPIPHYSEAL PLATE OF LONG BONES, CARTILAGE FROM
SPHENOID AND CARTILAGE FROM NASAL SEPTUM
APPEARED CAPABLE OF ACTING AS GROWTH CENTERS.
•ALMOST NO GROWTH WAS OBSERVED ON CONDYLAR
CARTILAGE TRANSPLANTATION.

71. EXPERIMENTAL STUDIES
FOVOURING THE THEORY
THE IDEA IS THAT IF REMOVING A CARTILAGENOUS AREA STOPS OR
DIMINISHES GROWTH, PERHAPS IT REALLY WAS AN IMPORTANT
CENTRE FOR GROWTH.
SEPTAL CARTILAGE
SEGMENT OF NASAL CARTILAGE
REMOVED AT 8YRS OF AGE
REMOVED IN A GROWING RABBIT.
DUE TO TRAUMA
MOST OBSERVERERS CONCLUDED THAT THE SEPTAL CARTILAGE
DOES HAVE SOME INNATE GROWTH POTENTIAL.

72. POINTS IN FAVOUR OF THE
THEORY:
1. IN MANY BONES CARTILAGE GROWTH OCCURS,
WHILE BONE MERELY REPLACES IT.
2. TRANSPLANTED EPIPHYSEAL PLATE CONTINUES
TO GROW IN NEW LOCATION INDICATES THE
INNATE GROWTH POTENTIAL OF THE CARTILAGE.
3. NASAL SEPTAL CARTILAGE ALSO SHOWED INNATE
GROWTH POTENTIAL ON BEING TRANSPLANTED
TO ANOTHER SITE.
4. EXPERIMENTS ON RABBITS INVOLVING REMOVAL
OF NASAL SEPTAL CARTILAGE DEMONSTRATED
RETARDED MID-FACE DEVLOPMENT.
BUT…..

73. SOME AUTHORS ARGUE THAT SURGERY ITSELF
AND THE ACCOMPANYING INTERFERENCE WITH
BLOOD SUPPLY TO THE AREA, NOT THE LOSS OF
THE CARTILAGE, CAUSE FOR THE GROWTH
DEFICIENCY.
AS RECENTLY AS THE 1960s
IT WAS STATED THAT CONDYLAR
FRACTURES, AT AN EARLY AGE LEAD TO
SEVERE GROWTH DISTRUBANCES.
THIS MAY BE DUE TO , THE CONDYLAR
FRAGMENT IS PULLED AWAY FORM ITS
ORIGINAL LOCATION BY THE LATERAL
PTERIGOID MUSCLE AND GET RESORBED
OVER A PERIOD OF TIME.
AND SO THE GROWTH DISTURBANCE.
BUT….

74. “Gillhums-moe and Lund” in their studies conducted
scandinavian children, only 15 to 20% suffered from
reduction of growth after condylar #s.
“THEY DEMONSTRATED THAT AFTER THE #
OF MANDIBULAR CONDYLE IN A CHILD ,
THERE WAS AN EXCELLENT CHANCE THAT
THE CONDYLAR PROCESS WOULD
REGENERATE TO OPPROXIMATELY ITS
ORIGINAL SIZE”.
“THEY ALSO EXPLAINED THAT A NEW CONDYLE
REGENERATES DIRECTLY FROM THE PERIOSTEUM
AT THE SITE OF FRACTURE”.

75. It appears that epiphyseal cartilages,
nasal septal cartilage (to a lesser
extent) and cranial base synchondroses
probably act as independently growing
centers.
Transplantation experiments nor
experiments in which condyle is removed
lend any support to the idea that the
condylar cartilage is an important growth
centre.

76. Functional Matrix Hypothesis
(Moss’ Hypothesis-1968)
“The functional matrix is primary and the
presence, size, shape, spatial position, and
growth of any skeletal unit is secondary,
compensatory, and mechanically obligated to
changes in the size, shape, spatial position of
its related functional matrix”
PROFESSOR MEVLIN L MOSS

77. Functional Matrix Hypothesis
(Moss’ Hypothesis)
“The origin, development and maintenance of
all skeletal units are secondary, compensatory
and mechanically obligatory responses to
temporally and operationally prior demands of
related functional matrices.”

78. The functional cranial component is
divided into two:
• Functional Matrix
• Skeletal Unit.
•All the tissues, organs and spaces comprise the
functional matrix
•Skeletal matrix comprises the skeletal unit.

79. Skeletal unit:
• All skeletal tissues associated with a
single function are called “skeletal unit”.
E.g. bone, cartilage and tendinious tissue.
When a bone is comprised of several contiguous skeletal units,
they are termed as “micro- skeletal units”.
Maxilla and Mandible are comprised of number of such Micro-
Skeletal Units.
e.g. Mandible: alveolar,angular,condylar,gonial,mental,coronoid
and Basal skeletal units.
Maxilla: Orbit, Pneumatic,, palatal micro skeletal units.

80. Types of Functional Matrix
1. Periosteal matrix 2. Capsular matrix
(e.g., muscles, blood vessels, (e.g., brain, oral cavity)
nerves and glands) Passive growth
Act directly on skeletal units No deposition
Deposition and resorption No resorption
Affect size and/or shape Affect location

81. Craniofacial Growth
Active growth process
1) Sutural growth
Growth
2) Bone remodeling
3) Cephalic cartilage growth
Active growth (Periosteal)
+
Passive growth (Capsular) Passive growth process
= 1) The growth of neural,
Total growth orbital, CSF, and other
masses and real substances
2) The expansion of oro- naso-
pharyngeal and other functioning
spaces

82. He theorizes that growth of face
occurs as response to functional needs
and neurotrophic influences, and is
mediated by the soft tissue in which
the jaws are embedded.
The soft tissues grow, and both bone and
cartilage react.

83. • The growth of cranium is a
direct response to the growth
of the brain.
• Pressure exerted by the
growing brain separates the
bones at sutures, and new
bone passively fills in at these
sites .
e.g. Microcephaly &
Hydrocephaly are
explanatory.

84. • Enlarged eye or small eye causes a
corresponding change in the orbital cavity.
• Moss theorizes that major determinant of
growth of maxilla and mandible is
enlargement of nasal and oral cavities,
which grow in response to functional needs.
• Absence of normal function would have
wide-ranging effects.

85. • Resulting loss of condyle in condylar #
does not impede mandibular growth.
• Children in whom a growth deficit occurs,
may be due to interference with normal
function.
• Mandibular Ankylosis.
• Infection or trauma in the TMJ, leading
to scarring causes mechanical restriction,
thus impeding the growth .

86. Illizarow: 1950
• Demonstrated that bone can be induced
to grow at surgically created sites by a
method called Distraction osteogenesis.
“If cuts were made through
the cortex of any bone, they
could be lengthened by
applying graduated traction
(.5-1.5mm/day) after initial
callus formation (7 days).
Large amounts of new bone
can be formed in between the
cut segments”.

87. Distraction osteogenesis is now a days
widely used in lengthening Arms or
legs by several centimeters.
In 1992, McCarthy et al, reported the first
clinical cases of mandibular lengthening
by gradual distraction.
Molina et al, reported mandibular
elongation by distraction as a farewell to
major osteotomies.
Reconstruction of mandibular and
maxillary defects, treating patients
with “hemi facial microsomia” is
done now a days by distraction
osteogenesis.

88. Mouth breathing children tend to have
higher mandibular inclination and more
vertical growth. These findings support
the influence of the breathing mode in
craniofacial development.
Fernanda Campos Rosetti Lessa,etal
Otorrinolaringol.
V.71, n.2, 156-60, mar./apr. 2005

89. Obliterative osteogenesis occurred in the
inter nasal suture (synostosis) in the group of rats
with reduced masticatory function. Thus,
it seems that masticatory function may influence
suture closure.
Christer Engström, Stavros Kiliaridis and etal
The European Journal of Orthodontics 1986 8(4):271-279;
doi:10.1093/ejo/8.4.271
© 1986 by European Orthodontic Society

90. Van limborgh’s theory: 1970
He explained the process of growth and
development in a view that combines all the
three theories.
He suggested five factors which controls growth.
1. Intrinsic genetic factor
2. Local epigenetic factor
3. General epigenetic factor
4. Local environmental factor
5. General environmental factor

91. Intrinsic genetic factor :
They are genetic control of the skeletal units themselves
Local epigenetic factor :
Bone growth is determined by genetic control originating from adjacent
structures like brain, eyes etc
General epigenetic factor:
They are genetic factors determining growth from distant structures. E.g.
sex harmones, growth harmones. Etc.
Local environmental factors:
They are non-genetic factors from local external environment. e.g. habits,
muscle force. etc.
General environmental factors: They are general non-genetic
influences such as nutrition, oxygen. Etc.

92. Views expressed by van limborgh
summsrised as:
• Chondro cranial growth is mainly
controlled by intrinsic genetic factors.
• Desmocranial growth is controlled by any
few intrinsic factors
• Cartilagenous parts of the skull must be
growth centers.

93. Views expressed by van limborgh
summsrised as:
• Sutural growth is controlled by influences
originating from skull cartilages and from
other adjacent skull structures.
• Periosteal growth largely depend upon
growth of adjacent structures.
• Sutural and periosteal growth are
additionally governed by local non-genetic
environmental influence.

94. ENLOWS’S “V” PRINCIPLE:
Many facial bones or parts of bones have a
“V” shaped pattern of bone growth.
“V” pattern of growth occurs in:
- Base of the mandible
- Ends of long bones
- Mandibular body
- Palate. etc.
Bone deposition occurs on the inside of the wide end
V and resorption on the outer side

95. Enlow’s counter part
principle:
• Growth of any given facial or cranial part
relates to other structural and geometric
counter parts in the face and cranium.
• There are regional relationships
throughout the whole face and cranium.
• If each regional part and its counter part
enlarge to the same extent balanced
growth occurs

96. Enlow’s counter part
principle:
• Imbalances in the regional relationships
are produced by differences in:
- Amounts of growth between counterparts
- Directions of growth between them
- Time of growth between them.

97. Different parts and their counter
parts:
• NASOMAXILLARY COMPLEX – ANTERIOR CRANIALFOSSA
• HORIZONTAL DIMENSION OF – MIDDLECRANIAL
FOSSA
• PHARYNGEAL SPACE
• MIDDLE CRANIAL FOSSA – BREADTH OF RAMUS
• MAXILLA – MANDIBLE
• BONY MAXILLA – CORPUS OF MANDIBLE
• MAXILLARY TUBEROSITY – LINGUAL TUBEROSITY

98. SERVO SYSTEM THEORY :
Charlier and Petrovic 1967, stutzmann and petrovic-1970
• The influence of the Somatomedin complex
(STH) on growth of primary cartilages like:
- Epiphyseal cartilage of long bones
- Cartilage of nasal septum
- Spheno occipital synchondrosis
- Lateral cartilagenous mass of ethamoid
- Cartilage between body and greater wing of
sphenoid
has a cybernetic form of command.

99. SERVO SYSTEM THEORY :
The influence of the
somatomedin complex on the
growth of secondary cartilages
like condylar, coronoid, angular
cartilage of mandible, cartilage
of mid-palatal suture, some
other cranio facial sutures and
provisional callus during bone
fracture repair comprises not
only direct but also some
indirect effects on the cell
multiplication.
With condylar , coronoid & angular cartilages, these indirect
effects corresponds to regional and local factors involving
primarily neuro muscular mechanisms relative to postural
adjustment.

100. Methods of studying growth:
• 1) MEASUREMENT APPROACH : Technique for
measuring living animals including Humans, so that measurement itself
does not harm the animal, and it is available for additional measurements
another time.
CRANIOMETRY
ANTHROPOMETRY
CEPHALOMETRIC RADIOGRAPHY
• 2)EXPERIMENTAL APPROACH: This approach
manipulates in the some way. The subject is available for a detailed study
that may be destructive. And so done in only in Non- Human species.
VITAL STAINING (JOHN HUNTER)
AUTO RADIOGRAPHY
RADIO ISOTOPES
IMPLANT RADIOGRAPHY
(VJORK&COWORKERS)

101. OTHER METHODS:
• 1)NATURAL MARKERS
- NUTRIENT CANALS
- TUBERCULAE
• 2)COMPARITIVE ANATOMY
• 3)GENETIC STUDIES

102. Craniometry:
• Involves measurement of skull
found among human skeletal
remains.
• Can be made on dry skulls.
• Such a growth study can only be
cross sectional.
Anthropometry :
•Involves measuring skeletal dimensions on living individuals
by using soft tissue points overlying these bony landmarks.
•Measurements can be made on both dry skull as well as living
individuals, where the thickening of soft tissue is also
considered.
•Study is longitudinal, where in the growth of an individual can
be followed directly over a period of time with repeated
measurement without damaging subject.

103. Cephalometric Radiography :
• This technique depends on placement
of an individual in a cephalostat so that
the head can be precisely oriented and
controlled magnification can be made.
• Combines the advantage of both cranio
and anthropometry
• Bony measurements as seen on the
radiograph can be made over a period
of time for the same individual.
• Dis-advantage: produces only two
dimensional representation of two
dimensional structure making it
impossible to make all measurements

104. Vital staining: originated by John hunter in 18 th
centuary
• Growth is studied by observing the pattern of
stained mineralized tissues after the injection of
the dyes into the animal. E.g. Alazarin was used
for vital staining studies in animals.
• The gamma emitting isotope can be used to
detect areas of rapid bone growth in humans.

105. Auto radiography:
• Technique in which film emulsion is placed over
a thin section of tissue containing radio active
isotope and then is exposed in dark by radiation.
• After the film is developed, the location of the
radiation that indicates where growth is
occurring can be observed by looking at the
tissue section through the film.

106. Radio isotopes:
• These elements were injected into tissues which
get incorporated in the developing bone and act
as in vivo marker.
• These can be later detected by tracing down the
radioactivity they emit. The radio isotopes used
are:
• Technetium – 33
• Calcium – 45
• Potassium – 32.

107. Implant Radiography
used by : Bjork and co-workers
• Inert pins made of titanium are inserted in bone
anywhere in the skeleton including face and
jaw.
• These pins are biocompatible super-imposing
radiographs (cephalograms in case of face) on
the implants allow precise observation of both
changes in position of bone relative to another
and changes in external contour of the
individual bone.

108. METHODS OF COLLECTING
GROWTH DATA
• LONGITUDINAL STUDIES
INVOLVES GATHERING DATA OF GIVEN INDIVIDUAL OVER A
PERIOD OF TIME AT REGULAR INTERVALS
* ADVANTAGES AND DISADVANTAGES
• CROSS SECTIONAL STUDIES
OBSERVATIONS AND MEASUREMENTS MADE OF DIFFERENT
SAMPLES STUDIED AT DIFFERENT PERIODS
* ADVANTAGES

109. TYPES OF GROWTH DATA
• 1)OPINION
From experienced person, but not reliable scientifically when
better sources available.
• 2)OBSERVATION
all or none phenomenon
• 3)RATINGS AND RANKINGS
a standard conventionally accepted scale for classification.
• 4)QUANTITATIVE MEASURMENTS
- DIRECT DATA
- INDIRECT DATA
- DERIVED DATA

111. Genes in growth and
development
 Hox genes: {homeobox genes}:they are
an excellent example of molecular studies
as applied to craniofacial embryogenesis
is homeoboxgenes
 These were first discovered in fruitfly
[drosophila} research and subsequent
similar genes were aslo discovered in
other organisms

112.  This high similarity of genes in which more than
400 have been indentified in human ,fly
underlines the universality of basic biologic
templates from which developmental
mechanisms evolve
 A recentlu developed hox genes 7 8 9 is
expressed in range of neural crest derived
tissues and areas of putataive epithelial
mesenchymal interactions during
embryogenesis

113. Growth factors in growth and
development
 They are mitigenic polypeptides tht
influence cell differntiation and
morphogenesis
 Three imp growth fators are
 TGF-BETA
 EGF
 FGF

114. TGF-BETA
 IT IS IMP GROWTH FACTOR IN
EMBRYOGENESIS
 IT IS MAINLY USEFUL IN
 CHEMOTACTIC PROLIFERATION
 APOPTOSIS
 CONTROL THE EDEVELOPMENT AND
MAINTANENCE OF MOST TISSUES

115.  TGF BETA SIGNALLING PATHWAY ACTS
MAINLY BY PHOSPORELATION OG SMAD
PROTIENSBY SERINE AND THREONINE
KINASE
 THEY REGULATE SPECIFICATION OF
CRANIAL NEURAL CREST CELLS
 THEY PLAY MAJOR ROLE IN DEVELOPMENT
AND MAINTANENCE AFFECTING BOTH
CARTILAGE AND BONE METABOLISM IT
AFFECTS BOTH OSTEOBLATS AND
OSTEOCLASTS

116. The FGF signalling pathway plays crucial
role in development of craniofacial
skeletogenesis, synchondrosis regulation,
lacrimal and salivary gland formation,
myogenesis and even tooth formation
X Nie,K Luukko, P Kettunen
Oral Diseases(2006) 12,102-111

117. FGF PATHWAY
 FGF CONSTITUTE LARGE FAMILY OF
POLYPEPTIDE GROWTH FACTORS
 THERE SIGNALLING PATHWAY IS THROUGH
RECEPTOR TYROSINE KINASE
 THEY HELP IN
 APOTOSIS
 CELL SURVIVAL
 CHEMOTAXIS
 CELL ADHESION
 CELL MIGRATION
 CELL DIFFERNTIATION
 AND PROLIFERATION

118. REFERENCES
 INTRODUCTION TO CRANIOFACIAL BIOLOGY BY
DAVID S CARLSON
 ESSENTIALS OF MEDICAL PHYSIOLOGY BY
DICKSON AND TORTORA
 ESSENTIAL PEDIATRICS BY GHAI
 DENTISTRY FOR CHILD AND ADOLESCENT BY MC
DONALD EIGHTH EDITION
 CONTEPORARY ORTHODONTICS 3RD EDITION BY
WILLIAM R PROFITT
 MOYERS TEXT OF ORTHODONTICS 3 EDITION
 STEWARTS TEXT OF PEDIATRIC DENTISTRY

120. CONCLUSION
JUST AS THE CLINICIAN NEEDS THE
MEDICAL HISTORY TO MAKE A LOGICAL
DIAGNOSIS,
SO TO THE GROWTH AND DEVELOPMENT
OF FACE IS ESSENTIAL FOR A LOGICAL
EXPLANATION OF ANY STRUCTURAL AND

121. REFERENCES:
• PEDIATRIC DENTISTRY
• -REY E STEWART
CONTEMPORARY ORTHODONTICS
• -WILLIAM R PROFIT –3 rd
EDITION
• ORTHODONTICS PRINCIPLES AND PRACTICE
• -GRABER T.M –3 rd EDITION
• HAND BOOK OF ORTHODONTICS
• -ROBERT E MOYERS-4 th
EDITION

122. REFERENCES:
Christer Engström, Stavros Kiliaridis and etal
The European Journal of Orthodontics 1986 8(4):271-279
Fernanda Campos Rosetti Lessa,etal
Otorrinolaringol.
V.71, n.2, 156-60, mar./apr. 2005
X Nie,K Luukko, P Kettunen
Oral Diseases(2006) 12,102-111

123. THANK YOU