Factors affecting growth and development /certified fixed orthodontic courses by Indian dental academy

FACTORS AFFECTING
GROWTH AND
DEVELOPMENT

www.indiandentalacademy.com

INDIAN DENTAL ACADEMY
Leader in continuing dental education


“ WHAT IS THE MOST RIGOROUS LAW OF
OUR BEING? GROWTH . NO SMALLEST
ATOM OF OUR MORAL, MENTAL, OR
PHYSICAL STRUCTURE CAN STILL A
YEAR. IT GROWS/IT MUST GROW,
NOTHING CAN PREVENT IT”
--- MARK TWAIN


Contents
1.
2.
3.
4.
5.

Definition
Classification
Prenatal factors
Natal factors
Postnatal factors


GROWTH






It is the quantitative aspect of biologic
development and is measured in units of
increase per units of time.--- MOYERS
Change in any morphological parameter which
is measurable– MOSS
Increase in size, change in proportion and
progressive complexity-- KROGMAN


DEVELOPMENT







Progress towards maturity– TODD
All 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– MOYERS
Characterized by changes in complexity, a shift to
fixation of function, and more independence, all of
which is under genetic control, yet modified by the
environment.
DEVELOPMENT=GROWTH+DIFFERENTIATIO
N+TRANSLOCATION

Why to assess growth of an
individual?
1.

2.

3.
4.

Identification of grossly abnormal pathologic
growth.
Recognition and diagnosis of significant
deviations from normal growth.
Planning of therapy.
Determination of the efficacy of therapy.


MOYER’S CLASSIFICATION
NATURAL

DISRUPTIVE FACTORS

GENETICS

ORTHODONTIC FORCES

NEUROTROPISM

SURGERY

FUNCTION

MALNUTRITION
GENERAL BODY GROWTH

GROSS CRANIOFACIAL ANOMALIES
MALFUNCTION


VAN LIMBORGH’S
CLASSIFICATION
1.

2.

3.

INTRINSIC FACTORS
EPIGENITIC FACTORS
a) Local
b) General
ENVIRONMENTAL FACTORS
a) Local
b) General





Pre natal
Natal
Post natal


Pre-natal factors
1.
2.
3.
4.
5.
6.
7.

Developmental anomalies.
Teratogens.
Congenital infections.
Maternal health.
Socioeconomic status of parents.
Multiple births.
Congenital defects.

Natal causes
1.
2.

Trauma during birth. e.g. forceps delivery
Intrauterine moulding.


Post natal factors
1.
2.
3.

Hereditary
Epigenitic
Environmental


PRENATAL FACTORS


DEVELOPMENTAL ANOMALIES
1.
2.
3.
4.
5.
6.
7.

PIERRIE ROBIN SYNDROME
TREACHER COLLINS SYNDROME
CLEFT LIP AND PALATE
CROUZON’S SYNDROME
ECTODERMAL DYSPLASIA
APERT SYNDROME
HEMIFACIAL HYPERTROPHY

Pierrie robin syndrome






Retrognathia or micrognathia
Glossoptosis
Airway obstruction
Crying child
Management- prone position, relief of airway,
mandibular lengthening process


Treacher collins syndrome










Autosomal dominantmutation in tracheal gene
Diminished neural crest cell
migration
Avian like faces with
colobamata of lower
eyelids, slanting palpebral
fissures, malar defficiencies,
microstomia, auricular
defects.
Severe conditions show
malformed ears, cleft palate.
Enlarged antigonial notch.

Crouzon syndrome








Maxilary hypoplasia with
reduced dental arches and
crowding
Prenatal fusion of superior
and posterior sutures of
maxilla
Short upper lip, widely
spaced eyes, protruding
eyeballs
Unilateral or bilateral
crossbite

Apert syndrome






Premature fusion of skull bonesmalformed head shape
protruding eyes, fused fingers and toes,
cleft palate, airway problems, ear
infections and hearing loss, etc
Management- multidisciplinary
approach.. Orthodontist play a role in
correction of facial form.


Hereditary ectodermal dysplasia









X linked recessive disorder…
Hypohydrosis , hypotrichosis and
hypodontia
Decreased vertical dimension of
face, protruding lips, thin sparse
hair over the head.
Very few teeth, malshaped or peg
shaped teeth, caries
Severe cases may be associated
with cleft of lip or palate

Hemifacial hypertrophy







One half of face
enlarged
F>M
Unilateral teeth size,
tongue increased
Eruption of teeth on
affected side is hastened


Cleft lip and palate






1 in 700
Most common congenital anomaly
Due to nonfusion of medial nasal, lateral nasal
and maxillary process
Oronasal communication, facial deformity,
malposition of teeth, speech problems,
breathing problems, frequent infections

TERATOGENS


Agents which are capable of producing
embryological defects in critical doses.



Can be physical , chemical or biological
agents.


Other prenatal factors
1.
2.
3.
4.
5.
6.

Poor maternal health
Mother’s nutritional status
Placental insufficiency
Multiple births
Socioeconomic conditions
Congenital infections


Poor maternal health






E.g systemic diseases like renal failure, cardiac
failure, diabetes, hypertension
Affects fetus due to altered blood flow, altered
diet of mother, drugs
Also complications during delivery


Mother nutritional status






Balance diet
Alcohol and cicarettes
Depends on financial
condition, culture, society,
emotional status of mother
Fetal alcohol syndrome- due
to defficiency of midline
tissue of neural plate



Placental insufficiency- may occur due to poor
nutrition of mother, maternal health, etc



Multiple births- 1st child is less in weight and
more in I.Q when compared to subsequent
children. Too many children- difficult to
concentrate




Socioeconomic conditions- children with
unfavorable conditions lag in growth and
development when compared to children with
favorable conditions



Congenital infections- CMV, Rubella,
toxoplasmosis, syphilis, HSV, HIV


NATAL FACTORS


Intrauterine moulding
1.

2.

3.

Pressure of arm against
face– maxillary
defficiency.

Flexion of head against
chest– mandibular
deffiency.
Forceps delivery

4.

Sometimes head distortion during passage
through the birth canal


Childhood fractures





# of condyle is most common
Reduced development on the affected side
Jaw deviated to affected side.
Management- early mobilisation and
symptomatic treatment


GENETIC FACTORS







Actual outcome of growth= genetic potential+
environmental influences.
Mutations- inherited by offspring
Genetic studies make use of twin and family
data.
N.b:- difference between growth before and
during adolescence.


a)
b)
c)

Genes control:Size of body parts
Rate of growth
Onset of growth events e.g menarche,
calcification of teeth, eruption of teeth,
ossification of bones and start of adolescent
growth spurt.

Genetic influences on malocclusion






Malocclusion runs in families– e.g Hapsburg
jaw
Primitive humans– genetic isolation– uniform
malocclusion
Urban population– e.g U.S.A c/a Genetic
melting point have highest rate of
malocclusion.


Stockard study





Crossbreeding of boston terrier with collie
Results showed malocclusions due to jaw
discrepancies than from tooth size- jaw
imbalances.
Results were misleading as malocclusions
were due to the extent to which achondroplasia
was expressed.


Twin study by Lundstorm(1963)







100 pair of twins
50 monozygotic & 50 dizygotic
Skeletal and dental overjets measured
More variations in dizygotic
Skeletal problems were more variable
Disadv– environmental and climatic
conditions may not be the same for both the
twins

Epigenetic factors




Genetically determined but manifest influence
on associated structures– GRABER
Sum total of all biochemical, biomechanical
and biophysical events produced by the
functioning of cells, tissues and the organs–
RAKOSI AND PETROVIC








Primary genetic control determines certain
initial features like tooth buds calcify in
jaws,etc.
But there are inductive local feedback and
inner communication mechanisms between
cells and tissues- e.g teeth talk to bone.
If face is under genetic control then it should
be possible to predict 100% features of
children from cephalometric data of parents.



1.
2.

Hence from investigations so far, two
conclusions are inescapable:Inheritance of facial dimensions is polygenic
Not more than 25% of any variability of any
dimension in children can be explained by
consideration of that dimension in parents.



1.

2.
3.


1.
2.

Local epigenetic factors–
Muscles
“ what is environment to bone is genetic to
muscles and teeth”
Neurotropism
Function
General epigenetic factors–
Hormonal
General body growth

Muscles


Influences both initiation and formation of
bone



Decreased contraction– underdevelopment of
that part of face



Excessive contraction– restricts the growth e.g
torticollis or wry neck.

Neurotropism


It is the nervous control of skeletal growth by
transmission of a substance through the
axons



TypesNeuromuscular
Neuroepithelial
Neurovisceral

1.
2.
3.


Axoplasmic transport
Efferent- muscle
Afferent-epithelial cell

Neuromuscular trophic relationships
1.
2.
3.
4.
5.

Muscle development
Muscle denervation- reinnervation
Cross- innervation
Hyperneuralization
Control of genetic activity


Muscle development


Myoblast stage of differentiation- neural
innervation is established



If muscle is not efferently innervated- motor
end plates will never develop.



Also muscle spindles, receptors and tendon
organs require afferent innervation.

Muscle denervation and
reinnervation


Ventral root section- muscle degeneration



Denervation atrophy or disuse atrophy of
innervated but inactive muscles?



Studitsky et al(’62)—
Autotransplanted mince muscle fragments–
if supplied by motor nerve– reform to
functioning muscle

Cross innervation


Demonstrates neurotrophic relationship
between neuron and uninnervated tissue.



Motor nerve to fast and slow muscles cut- fast
nerve + slow muscle and vice versa



Results- fast muscle becomes slow and vice
versa.

Hyperneuralisation


It is seen when neurotrophic substance were
released in quantal amounts.



Nerve crushed and 2nd nerve implanted- will
form new end plate but if implanted


Neurotrophic control of genetic
activity


Protein synthesis in oral epithelial cells



Specific enzymes synthesis in epithelium



Mechanism- direct control on the synthesis of
DNA, RNA and Protein synthesis


General body growth


Rate, pattern, timing of peak growth is
different for different individual



Affected by many factors like genetic,
hormonal, climate, racial, nutritional



Height– 2 spurts
6-7 yrs- small but inconsistent
Pubertal spurt- 12 yrs in girls and 14 in boys

1.
2.


Hormones


I excite or arouse



Specific stimulus– endocrine glands release
hormones into circulation in small amounts--acts on target cells



2nd great controlling system of our body after
nervous system



Most mysterious and elegant of all systems of
the body.

Hormones responsible for growth
1.

2.

3.

Group I- responsible for influencing skeletal
growth .e.g GH, Insulin, Thyrotrophic
hormones
Group II- responsible for ossification of long
bones. E.g Parathormone
Group III- responsible for pubertal growth
spurts .e.g Androgens, Progesterone,
Estrogen

4.

Group IV- prolactin


Growth hormone


Infancy- growth due to thyroid hormone and
GH.



Permissive action



Excess GH- Gigantism and Acromegaly



Decrease GH- Dwarfism

Summary of effects of growth hormones
Ant pitutary
GH

Negative
feedback
mechanism
Indirect growth promoting action

Direct anti insulin action

cortisol

Liver and other organs
somatomedians
Skeletal
chondrogenesis
Skeletal growth

extraskeletal
Protein synthesis

fat
lipolysis

Cell proliferation

carbohydrate
Blood sugar

GIGANTISM


Increased production of GH before the closure of
the epiphyseal plate- grows at rapid pace .



Clinical features
Extreme height (7 ft tall)



Oral changes
Enlargement of facial soft tissues
Enlargement of the mandible
True generalized macrodontia

ACROMEGALY
•Excess GH after the closure of the epiphyseal
plate.
•Clinical features
Increased size of hands and feet
coarse facial features
•Oral changes
cause or accentuate sleep apnea
Mandibular prognathism -- Apertognathia
(anterior open bite), spacing, macroglossia

Acromegaly

PITUITARY DWARFISM
• Decreased production of GH
Clinical features
1. Short stature
2. Face is small
3. skull size is usually normal


Oral changes

Smaller jaws

Size of teeth is reduced with delayed
eruption

Shedding of deciduous teeth is delayed by
several years

Third molars absent

Thyroid hormones


T3 and T4(follicular cells)



Calcitonin (parafollicular cells)



Inc O2 consumption by cells



Key role in development of brain and
nervous system in children.

Hyperthyroidism






Graves disease
Enlarged thyroid
CNS signs
Cardiac signs
Wasting of muscles,
heat intolerance,
osteoporosis (bone
resorption)

Hypothyroidism








Myxoedema , Cretinism
Inc sleep, dec memory, slow
reflexes
Yellowish discolouration of
skin, cold sensitivity, nonpitting oedema
Mental retardation
Decreased sexual development

Parathormone
Chief cells
 Increases serum Ca levels.
 Hypoparathyroidism- Tetany
Tingling and numbness
 Hyperparathyroidism- osteitis
fibrosa cystica
Bone fractures, decreased muscle
tone, mental confusion



Adrenal glands
Adrenal medulla
Adrenaline
Noradrenaline

Adrenal cortex
Zona glomerulasasalt
Zona fasciculatasugar
Zona reticularissex

Glucocorticoids


Cortisol, corticosterone



Must in medical kit



Stimulates gluconeogenesis, protein
catabolism, anti allergic and anti inflammatory


Insufficiency of adrenal cortex
Chronic form

Acute form
Waterhouse friderichen
syndrome

Addison's disease

-Primarily occurs in
children

-Auto immune
destruction of adrenal
glands

-Fulminating septic course
and death in 48-72 hrs

- leathergy, fatigue,
muscular weakness


Hyperfunctioning of adrenal cortex







Cushing syndrome
Moon face, buffalo
hump, muscular
weakness
Children- premature
cessation of
epiphyseal growth
Adults- severe
osteoporosis


Sex hormones


Males- testosterone



Females- estrogen and progesterone



Growth spurts


Girls- I- onset of spurt
II- peak height velocity
III- onset of menstruation

Boys- I-fat spurt (feminine fat distribution)
II- height spurt
III- peak height velocity
IV- end of growth spurt

Environmental factors


Local environmental factors- Habits



General environmental factorsNutrition
Illness
Race

1.
2.
3.


4.
5.
6.
7.
8.
9.

Climate and seasonal effects
Exercise
Family size and birth order
Psychological disturbances
Socioeconomic conditions
Secular trends


Habits


Eg. Tongue thrusting, mouthbreathing,
thumbsucking



Alter functional equilibrium



Normal growth- abnormal growth


Thumb sucking


Mainly to obtain- nutrients, feelings of
euphoria, sense of security and feeling of
warmth.



Till 3-4 years normal



Management- psychological
Remainder therapies

Tongue thrusting


Tongue between ant teeth and against lower
lip during swallowing



Skeletal open bite



Management- tongue crib


Mouth breathing


Lowering of mandible and tongue with
extension of head



Adenoid faces



Management- Removal of etiology


THE NUTRIENTS

Essential nutrients

Non essential nutrients
Cellulose,

Proteins,
Fats,

Hemicelulose,

Carbohydrates,

Pectins

Vitamins,
Minerals
Water


Proteins




Body building food
Important in infancy and childhood



protein def- reduction in jaw size- new bone
sensitive to protein



Delayed eruption of teeth.

VITAMINS
Water soluble

Fat soluble
Vit A
Vit D

Non B complex

Vit E
Vit K

B-complex

Vitamin C

Energy releasing

Hematopoietic

Thaimin B1,Riboflavi B2

Folic acid

Niacin B3,PyridoxineB6

Vit B12

Biotin B7,Pantothenic acid

Vit A in growth
Malformed enamel
Retardation of eruption
Disturbances in calcification of teeth
Disturbances of periodontal tissues


Vitamin D metabolism

Vitamin D


Rickets and Osteomalacia



Retarded eruption of the deciduous and the
permanent teeth



Jaw bones are thickened and the teeth
irregularly arranged



Narrow maxilla and high arched palate. The
mandible is shortened

Vitamin C


Scurvy



Collagen synthesis



Swollen bleeding gums, periodontal
breakdown- mobile teeth


Minerals
1.
2.

3.

4% human body weight
Macro minerals (require in
>100mg/day).Ca,P,Na,K,Mg
Micro minerals (Trace elements)
Fl,I,Cu,Co,Mn,Se,Cr,Zn.(.004-.00004% of
body weight)


Calcium


Function:-



Rigidity to bone and teeth



Blood coagulation n muscle contraction…



Necessary for release of neurotransmitter


Calcium homeostasis

Phosphorous



FunctionsFormation of bone and tooth



Constituent of nucleotides and nucleic acid



Constituent of lipids



Regulation of acid-base balance

Illness


Minor illness- no effect



Major and prolong illness- marked effect



Catch up growth after recovery


Race


Due to climatic, nutritional or socioeconomic
conditions



Gene pool differences


Climate and seasonal effects


Cold climates- more adipose tissue



Autum- inc height



Spring- inc weight



Growth inc during night

Exercise


Effect on linear growth not made in
quantitative fashion-MOYERS



Exercise- increase in muscle mass


Psychological disturbances


Due to reduction in
GH levels



Catch up growth


Socioeconomic factors


Favourable conditions- children are larger,
display different types of growth, show
variation in timing of growth when compared
with disadvantaged children.



Standard of living more imp than income


Secular trends


15 yr boy 5” taller than boy 50 yrs ago



Onset of growth is earlier but growth also
stops earlier



Menarche achieved earlier in girls when
compared with 50 yrs ago



No satisfactory www.indiandentalacademy.com such trends
explanation for

Summary
Prenatal factors
Developmental
anomalies
Teratogens
Congenital infections
Condition of mother
During pregnancy

Natal factors
Intrauterine moulding
Forceps delivery
Childhood #


Post natal factors
Genetic factors
Epigenetic factors
Environmental factors

References
1.
2.
3.

4.

5.

Hand book of orthodontics- MOYERS
Contemporary orthodontics- PROFFIT
Control mechanisms in craniofacial growthJAMES McNAMARA (monograph 3Craniofacial Growth Series)
Orthodontic principles and practiceT.M.GRABER
Essentials of physiology- A.K.JAIN

6.

7.
8.
9.

10.

Nature vs. nurture in dentofacial variationA. LUNDSTROM (Eu J Ortho, 1984)
Textbook of orthodontics- BISHARA, I Ed
Textbook of Oral Pathology-SHAFER’S
Essentials of Biochemistry- T.N.
PATABHIRAMAN
Textbook of Pedodontics- SHOBHA
TONDON

Thank you
Leader in continuing dental education


Factors affecting growth and development /certified fixed orthodontic courses by Indian dental academy

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