Growth&development /certified fixed orthodontic courses by Indian dental academy

FACTORS AFFECTING AND
THEORIES
OF
GROWTH AND
DEVELOPMENT
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com

Factors affecting growth and
development.
VAN LIMBORGHIntrinsic Genetic-Heredity
Local-Muscle, Function,
Neurotrophism
Epigenetic
GeneralHormones,Neural

Local- Habits
Environmental
General- Secular trends


Miscellaneous –
Nutrition,Illness,Race,Climate and
Season,Exercise,Family size & Birth
order, Socioeconomic status,
Psychological disturbances.
•Prenatal
•Natal
•Postnatal

PRENATAL FACTORS
Chromosomal abnormalities(Klinefelters
syndrome,Turners syndrome)
Teratogens
Congenital infectionsRubella,CMV,HSV,HIV,Syphillis
Nutritional status of mother
Multiple birth
Congenital defects- Cleft lip &palate

NATAL FACTORS
Birth trauma
Intrauterine moulding
Forcep delivery


POSTNATAL FACTORS
Heredity
Epigenetic factors
Environment
Miscellaneous


GENETIC FACTORS
Body size,shape,fat deposition,growth
pattern
Male – female growth differences
Advancement of girl over boy
Y
chromosome
Actual outcome = Genetic
potential+Environmental influences.


STOCKARD STUDY


Methodically crossbred dogs
Inheritance of facial characteristics –
major cause malocclusion.
Dog carry gene for achondroplasia.


Investigations in Hawaii – Chung
et al


TWIN STUDY


Lundstrom(1963) conducted
a study on 100 pair of twins,
half of which were
monozygotic and half were
dizygotic.
Both skeletal and dental
overjets were measured.
More variations in the
dizygotic than monozygotic.
Larger genetic variations for
skeletal pattern than dental
overjet.

Lauweryns et al - concluded that 40% of
the dental and skeletal variations can be
attributed to hereditary factors.


FAMILIAL STUDY


PARENT-CHILD CORRELATION
COEFFICIENTS:
Facial skeletal dimensions-0.5
Dental characteristics
-max for overjet-0.5
-min for overbite-0.15
Suzuki(1961) - studied 243 Japanese
families.
-1 parent had anomaly- 20% children
affected.
-Both parents had anomaly- 40% children
affected.

Cephalometric analysis of siblings
participated in BOLTON-BRUSH
STUDY


Heritability for - craniofacial growth, high.
- dental growth , low.
Dental variation – influenced by
environment.
Inheritance for mandibular prognathism is
strong.


TERATOGENS
Chemicals & other agents capable of
producing embryological defects if given at
critical time.
Low level – Specific defects
High level – Lethal defects


TRAUMA DURING BIRTH
Major impact

Unlikely to produce
long term deformity.


Forcep delivery -


EPIGENETIC FACTORS
Indirect genetic control (MOSS)
Genetically determined but manifest
influence indirectly on associated
structures(GRABER)


Muscles1.Important part –
functional matrix
2.Formation & Growth –
bones
3.Loss underdevelopment


Function –
1.Primary factor – CF
Growth (MOSS)
2.Absence – distortion of
bone morphology
3.EX – NM disorders,
TMJ ankylosis
4.Malfunction – abnormal
growth
5.EX – Tongue thrust


NeurotrophismNervous control of skeletal growth
assumedly by transmission of
substance through axon of nerves
(MOYERS)
Interaction btw nerves & other cells
which initiate or control molecular
modifications in other cells (GUTH)


Neuroepithelial,Neuroviseceral,
Neuromuscular.
Axioplasmic transport -


NEUROMUSCULAR TROPHIC RELATION


NEUROEPITHELIAL TROPHIC RELATION


Neurotrophic control of genetic activity• Interferes – Genomic potential to final
functional differences.
• Protein & specific enzyme synthesis.
•Synthesis of DNA,RNA.


Intra oral & external epithelium growth in
leaps following sensory nerve contact.
Max & Mand hypoplasia – intra oral & intra
nasal sensory deficits.
Nerves – Soft tissue growth &function –
Skeletal growth & morphology.


NEURAL CONTROL
Centre hypothalamus
Keep children on genetically determined
growth curves.
At birth – size to accommodate birth
process.
After birth – destined to become large.
Growth burst – first 2 years.

Children normally grow very rapidly
during the first two years of life.
Between two years of age and the onset
of puberty, children grow slowly. They
begin to grow rapidly again during the
teen years.

- Growth & Weight: -


HORMONES


1.
2.
3.

GROWTH HORMONE
–
Ant pituatory
General body growth
Regulates metabolism
Gigantism ,
Acromegaly(In
adulthood)

Dwarfism

1.
2.
3.
4.
5.

THYROID HORMONE –
T3 , T4 (Follicular cells)
Calcitonin (Parafollicular
cells)
B.M.R
Growth & Development
Ca homeostasis
Graves disease –
Exopthalmos.

Cretinism , Myxedema.

1.
2.
3.

PTH –
Chief cells
Increases osetoclast –
bone resorption
Increases Ca level –
bone & kidney.
Osteitis fibrosa cystica.

Tetany.

ACTH –
1. Zona glomerulosa –
Mineralocorticoids –
aldosterone – Na & K level
2. Zona fasiculata –
Glucocorticoids –
Cortisol,Corticosterone
Cortisone –
Protein catabolism
Glucogenesis
Lipolysis
Stress resistance.

3. Zona reticularis – Androgen (male sex

hormone)

Addisons disease.
Cushing syndrome.


SEX HORMONES –
1. Estrogen & Progestrone –
Feminine secondary sex characteristics.
2. Testosterone –
Masculine secondary characteristics.


ENVIRONMENTAL
Habits –
1. Thumb sucking , Mouth – breathing ,
Tongue thrusting.
2. Breaks functional equilibrium.


Secular trends –
Size and maturational changes seen in
population occuring with time.

MISCELLANEOUS
1.
2.
3.

Nutrition –
Proper diet.
Malnutrition.
Growth catch up.


IllnessShort term.
Long term.
Reduced GH – Increased cortisone.


RACIAL & ETHINIC DIFFERENCES –


CLIMATE & SEASONAL CHANGES
HT. Spring then in autumn.
WT. Autumn then in spring.
HT. & teeth eruption more in night.
Fluctuation in hormone release.


SOCIO ECONOMIC STATUS –
1. Nutrition.
2. Variation in ht. & wt. ratio.


EXERCISE –
No direct effect on linear growth.
Muscle mass, fitness, general well being.


FAMILY BIRTH ORDER –
First born child weighs less at birth &
higher I.Q.


PSCHYOLOGICAL FACTORS


PARADIGM


PARADIGMS
Normal science – research that members
of specific group of scientist recognize as
central to their field. (KUHN 1970)
Theory – assumption based on certain
evidences but lacking scientific proof.
Hypothesis- assumption not proved by
experiment,conclusion drawn before all
facts are established & tentatively
accepted.

Paradigm –
Conceptual scheme that encompasses
individual theories and is accepted by
scientific community as a model and
foundation for further research.
Define relevant data
Scientist can reject wrong paradigms.


Paradigms in craniofacial biology
Craniofacial biology is a study of
growth,function and adaptation,both
phylogenetically and ontogenetically of the
craniofacial skeleton and related structure.


1920 – 1940 GENOMIC
PARADIGM
CFG – Genetically predetermined.
Classic triad :Sutures-primary growth sites.
Cranial vault growth- periosteal deposition
& endosteal resorption.
Cephalic cartilages – primary growth
centre.

1940-1960 PERIOD OF
SCIENTIFIC REVOLUTION.
Emphasis – Functional factors
Experiments.
Periosteal & Sutural bone growth –
removed.


1960-1980 FUNCTIONAL
PARADIGM.
Melvin Moss


Moss (1981)“Origin ,Growth and Maintenance of all
skeletal tissue and organs are always
secondary,compensatory and obligatory
responses to temporally and operationally
prior events or processes that occur in
specifically related non skeletal tissues ,
organs or functioning spaces(Functional
Matrices).”

CRANIOFACIAL BIOLOGY
Genomic paradigm
- Genetic
predetermination.
- Popular among
clinical orthodontist.

FUNCTIONAL
PARADIGM
- Functional matrix
hypothesis.
- Popular among
scientist &
orthodontics believing
in functions & physical
interrelationship.


EVOLUTION OF THEORIES


EVOLUTION OF THEORIES
Galileo(1638) Monro(1776) – Bone shape.
Meyers(1853) – Mechanics of human
skeleton.


Cullman – stress trajectories.
Meyers 1867 publication – bony trabecular
structures were attributed to specific
trajectories of bone.


Wolff – Internal organization of
femur(1870).
+ interstitial bone growth
_ bone resorption- Wegner & Koelliker
(1872)
Form & Function interaction – Wilhelm
Roux(1881)
Roux argued – Functional stimulus
shaped bone.ex:Fibula & Tibia.


1892 JULIUS WOLFF
Law of bone transformation
“Every change in form & functions of
bones,or of their function alone, is
followed by certain definite changes in
their internal architecture and equally
definite secondary alteration in their
external conformation in accordance with
mathematical laws.”


GENETIC THEORY


GENETIC THEORY
Genetic determination.
Genetic control varied –
Bone
Cartilage, bone responds passively
Soft tissue matrix, others controlled
epigenetically.


SUTURAL THEORY –
(SICHER)


SUTURAL THEORY
Sutures btw membranous bones of
cranium & jaws.
_ Transplanted.
+ Compressed.


CARTILAGENOUS
THEORY(JAMES SCOTT)


CARTILAGENOUS THEORY
Prenatal cartilagenous portions –head,
nasal capsule, mandible, cranial base.
Growth centres.


_ Transplanted
condylar fracture in child –condylar
regeneration
+ Epiphyseal cartilage, nasal septum.


FUNCTIONAL MATRIX
THEORY(MELVIN MOSS)


FUNCTIONAL MATRIX
HYPOTHESIS
1948 – 1951
Studied- Dept. Anatomy,Columbia
university.
Thesis.
The development of vertebrate skullGaven de Beer.
Growth & Form – Thompson

1951 – 1960
Calvarial sutures extripation-no size
reduction of neural skull.
Sutures are not primary growth sites.
No genetically predetermined boundaries
to calvarial bones.
Work of Vander Klaauw – experimentally
verified & expanded by Moss.
1960- Paper published-Functional
approach to craniological problems.

1961 – 1971
Orthodontic field introduced to functional
matrix.
Two types not yet arisen.
Cleared: Conference – 1968
 Sutural tissues & Cartilages.
 Active transformation & passive translation


FUTURE
Neurotrophic regulation – controlled matrix
growth primarily,responsive skeletal tissue
growth.


FMH
Head – Function occurs
Function – FCC
FCC – Functional matrix (Function)
- Skeletal unit (Protect/Support fm)
Growth changes in size,shape,spatial
position are secondary to primary changes
in their specific functional matrices.

SKELETAL UNIT
Bone,Cartilage or
Tendinous tissue
Microskeletal units.

Mandible – condyle
coronoid
ramus
alveolus


Maxilla – nasal
orbital
pneumatic
basal
alveolar


Macroskeletal unit
EX –Endocranial
surface of the
calvaria.


FUNCTIONAL MATRIX
Muscle,Gland,Nerves,Vessels,Fats,Teeth,
Functioning spaces.
FM – Periosteal matrices
Capsular matrices


PERIOSTEAL MATRIX
Temporalis & Coronoid
process.
Fibers – indirectly to
periosteum.
directly into skeletal
tissue.


 Removal / Deinnervation
 Functional hypertrophy / hyperactivity
 Growth changes in coronoid process

(size & shape)
morphogenetically
derived temporalis muscle function.
 Osseous responses
osseous
deposition & resorption.


CAPSULAR MATRICES
Change in size &shape –
Periosteal matrix
Capsular matrix ???
Neurocranial capsule
<skin + duramater>
Orofacial capsule <skin
+ mucosa>


NCC
Capsule composed – Scalp,Bone,Two layers of
duramater.
NCC =Calvarial bone (microskeletal unit +
periosteal matrix)
Neural mass volume – morphogenetically
significant.
Expansion of this capsular matrix – primary
event.
Translation + periosteal apposition & resorption.

OFC
FCC arise,grow,maintain within OFC
Capsule – Oronasopharyngeal functioning
spaces.
Volumetric growth of these spaces is
primary morphogenetic event.


HEAD
FCC
Skeletal Unit
Microskeletal

-Mandible
-Maxilla

Functional Matrix

Macroskeletal

-Calvaria

Periosteal

-Coronoid
&
Temporalis


Capsular
NCC
OFC

EX- MANDIBULAR GROWTH :-


POINTS IN FAVOUR


FMH – REFLECTIONS IN A
JAUNDICED EYE:JOHNSTON
Not a unitary mechanism.
Physical forces.
Bl. Condylectomy surgery not completed
till OCT.1961 ; Conclusions made in 1962
– Provisional.


Did not specify – capsular growth is
primary/secondary to expanding space.
Initially macroskeletal unit – two or more
adjacent bones,later – set of microskeletal
units.
Genetic control – soft tissue matrix , later
– nervous system.


“All research has no true completion but,
rather is only the beginning of yet another
cycle of work.”
- MELVIN .L.MOSS

References
 T.M. Graber – Orthodontics: Principles &






Practice, III Ed.
Proffit – Contemporary Orthodontics, III
Ed.
Moyers – Handbook of Orthodontics, IV
Ed.
Bishara – Textbook of Orthodontics, I Ed..
Tortora – Principles of Anatomy &
Physiology, VIII Ed.
Guyton & Hall – Textbook of Medical
Physiology, IX Ed.

Moss,Primary role of functional matrix in
facial growth – Am J Orthod, 1969 June
(20-31)
Moss,The capsular matrix – Am J
Orthod,1969 Nov :(56)
Moss,Twenty years of functional cranial
analysis Am J Orthod,1981 Oct:(366-75)
Lysle E Johnston Jr – Factors affecting
the growth of the mid face – The
functional matrix hypothesis:The
Reflections in Jaundiced Eye.

 David S Carlson – Craniofacial biology a

normal science.
 Bone Biodynamics in Orthodontic &
Orthopedic Treatment – David S Carlson
& Steven A Goldstein.
 Control Mechanisms in craniofacial
growth – James Mc Namara Jr.


Contribution of Condylar Growth to
Mandibular Morphogenesis


Condyles – Growth centres / Growth
sites???
Site –
Moss & Salentijin
Centre –
Charles,Brodie,Rushton,Sicher,Symons,
Scott.


Transplantation experiments.
Bernabei & Johnston`76.
200 day old female rats – 45.


Discussion.
Growth after condylectomy(Bl/Unilateral)
Fuller experiment (`74) –
20-30 day old guinea pig – 20
unilateral condylectomy
Control side – Sham operation.


Petrovic et al –
occlusion (maxilla) play imp role as a
regulating mechanism in growth of
condyles.
Stress on local factors
Lateral pterygoid.


Conclusion
Studies add upto our knowledge
By no means conclusive.
May/May not be similar effects in other
mammals,specifically in man.


Reference
Bernabei,R.L. and L.E.Johnston -A cephalometric
investigation of the growth, in situ, of “isolated”
mandibular condyles in adult rats following the
administration of bovine growth hormone. Am.
J. Orthodont. (In press), 1976.
JAMES A. McNAMARA, Jr. - Factors affecting
the growth of midface, C.F.S, 6: 381-391, 1976.


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Growth&development /certified fixed orthodontic courses by Indian dental academy

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