factors effecting growth & development /certified fixed orthodontic courses by Indian dental academy

Factors affecting growth and
development.
theories of growth.
Sutural and cartilagenous
theories.

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FACTORS AFFECTING
GROWTH AND DEVELOPMENT
“ As thou knowest not the way of the spirit, nor how
the bones do grow in the womb of her that is with the
child, even so thou knowest not the works of God who
maketh all.”
- Ecclesiastes(11:5)


Classification of factors
 1. Intrinsic factors
2. Extrinsic factors
 VAN LIMBORGH’S CLASSIFICATION:
1. Intrinsic factors
Local
2. Epigenetic factors
General
Local
3. Environmental factors
General

 INTRINSIC FACTORS – genetic, inherent.
 EPIGENETIC FACTORS –
- Indirect genetic control (Proffit)
- Genetically determined but manifest influence
indirectly on associated structures (Graber)
- The sum total of all biochemical, biomechanical
and biophysical events produced by the
functioning of cells, tissues and organs – (Rakosi
and Petrovic)
Ex. Eye, Brain etc.

EPIGENETIC FACTORS
act on products of genome
regulate all developmental processes
produce, regulate & maintain biologic structural complexity

LOCAL EPIGENETIC FACTORS –ex Muscles
GENERAL EPIGENETIC FACTORS-ex Hormones

VARIOUS FACTORS AFFECTING
GROWTH AND DEVELOPMENTpre-natal factors
Causing INTRAUTERINE GROWTH RETARDATION
(IUGR)1. Chromosomal abnormalities
2. Teratogens – a. Infectious agents
b. Physical agents
c. Chemical agents
d. Hormones
‘ MALE – MEDIATED TERATOGENESIS’

3. Congenital infections- a. Rubella
b. CMV
c. Toxoplasmosis
d. Syphilis
e. HSV, HIV
4. Poor Maternal health- hypertension, renal & cardiac
disease
5. Mother’s nutritional status/ Socioeconomic status
6. Mother’s use of alcohol, cigarettes, drugs etc
7. Placental insufficiency
8. Multiple births

Developmental anomalies
 CLEFT LIP & CLEFT PALATE
 CLEIDOCRANIAL DYSOSTOSIS
 CRANIOFACIAL DYSOSTOSIS (Crouzon’s
disease)
 MANDIBULOFACIAL DYSOSTOSIS
(Treacher-Collins Syndrome)
 PIERRE ROBIN SYNDROME
 FACIAL HEMIHYPERTROPHY
 ECTODERMAL DYSPLASIA

Natal causes
Growth can be affected by injuries during birth1. Intrauterine moulding
 Arm pressed against the face
-maxillary deficiency
 Head flexed against the chestmandibular deficiency.
2. Trauma to mandible during birth process –
forceps delivery

Post-natal factors
 GENETICS/HEREDITY:
 GENERAL EPIGENETIC FACTORS:
a. Hormonal factors
b. Neural control
c. General body growth
 LOCAL EPIGENETIC FACTORS:
a. Neurotrophism
b. Function
c. Muscles

 GENERAL ENVIRONMENTAL FACTORS:
a. Nutrition
b. Illness
c. Race
d. Climate and seasonal effects
e. Exercise
f. Family size & birth order
g. Psychological disturbance
h. Socioeconomic factors
i. Secular trends
 LOCAL ENVIRONMENTAL FACTORS:
a. Habits

Genetic / hereditary factors
 Potential for growth is genetic.
 Actual outcome of growth = Genetic potential
+
Environmental influences
 Advanced rate of maturity in females than males –
delaying action of ‘Y’- chromosome.
 Ex. Klinefelter’s syndrome (XXY)
Individuals with XYY
Turner’s syndrome (XO)

 Genetic control seen ina. body size, shape, deposition of fat
b. patterns & rate of growth
c. onset of growth events-menarche,
-eruption of teeth,
-ossification of bones,
-beginning of adolescent growth spurt


 Genetic studies of physical growth done using1.TWIN STUDIES
Sir Francis Galton – first scientific analysis of twins &
concluded that it is possible to separate ‘Nurture’
from ‘Nature’.

2. FAMILIAL STUDIES.

a. Parent child study.
b. Sibling studies.

TWIN STUDIES
 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 summarized a number of twin
studies - concluded that 40% of the dental and
skeletal variations can be attributed to hereditary
factors.


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

Assessment of the transmission of craniofacial
characteristics from a study of twins and their
siblings when compared to their parents.

Aims:

1.To analyse from the local population the factors
affecting the heritability of craniofacial structures.
2.To test the various parameters related to
cephalometric & study model analysis to evaluate
the amount of heritability of various components
of craniofacial structures.
3.To explore the possible application of the findings
to clinical situations.

 10 pairs of monozygotic twins
 Zygosity of the samples were determined.
 2 pairs of dizygotic twins were analysed separately.
 Analysis was done based on cephalometrics &
study models.
 Direct comparison of the variations was done


RESULTS
1.The twins - similar in large linear measurements &
ratios; differ slightly in other measurements in the
cephalometric reading,
-good co-relation in the study models.
2.Large differences between twins and parents
indicating the ultimate size of the craniofacial
components is difficult to predict.
3.No definite pattern of inheritance could be
discerned.

Assessment of the transmission of the craniofacial
characteristics from a study of monozygotic twins,
their parents & their siblings using conventional
cephalometry, FEM cephalometry & model analysis.

• Aim:
To test and evaluate the heritability of craniofacial
and dental characteristics using FEM analysis in 20
pairs of monozygotic twins, their parents and 5
siblings.


results
1. Anterior vertical dimensions are under strong
environmental control as compared to horizontal
parameters.
2. Twins inherit their genetic pattern more from
mother than from father.


Comparison of the soft tissue similarities
between children and their parents and
between children and their older siblings.

Aims :
1.To study the degree of correlation of facial soft
tissue structures in a profile perspective
between parents and offspring and the control
group.
2.To asses the degree of similarity between young
children in an age group at which orthodontic
treatment is usually started with their older
siblings who have completed growth.

 The study comprised of 30 families,11families had
2 daughters and 11 families had 2 sons for
comparison.
 Comparison based on- cephalometric tracing,
profile photographs.
RESULTS:
1.Strong genetic control in the transmission of soft
tissue facial characteristics.
2.Forecasting of the child’s nose, lips and position of
chin can be done by comparing with that of the
adult sibling. www.indiandentalacademy.com

Experimental study
Van Limborgh’s study on chick embryo –
 Intrinsic genetic information necessary for
tissue differentiation.
 Primary Genetic control – Initial features.
 Secondarily- inductive local feedback & inner
communication mechanisms between cells &
tissues.

Review article -ajo-do june 2004
Growth & Development : Heredity & Mechanical
Modulations – Jeremy Mao, Hyun-Duck Nah
Goals:
1. Synthesize current knowledge of bone & cartilage of
craniofacial skeletal lineage
2. Explore effective means of mechanical stresses to
communicate with bone & cartilage cells.


discussion
 3 cell lineages primarily involved – osteogenic,
chondrogenic, fibrogenic – common progenitor of
mesenchymal cells.
 Behaviour of all cells controlled by genes.
 Genes regulated by environmental cues including
mechanical stimuli.
 Combined approaches of genetics, bioengineering &
quantitative biology.
 “Bottom-up” approach instead of “top-down” approach.

summary
 Facial dimension inheritance – POLYGENIC, not
Mendelian


If Mendelian inheritance
numerous environmental influences
great change in underlying genetic features
inherited features undetectable

 Face not under rigid genetic control – impossible
to predict features of children from cephalometric
data of parents.

 If both parents are alike with respect to a
particular trait, the chances of sibiling showing that
particular trait are more.

 If one parent is unlike the other with respect to a
particular trait the chances of the sibling showing
either trait vary.

Hormonal factors
HORMONES
LOCAL

GENERAL(ENDOCRINE)

Ex. Acetyl choline

NON-SPECIFIC

Secretin

(all body cells)
ex. Growth hormone
Thyroid hormones
Insulin

SPECIFIC
(target organs)
ex. ACTH
LH, FSH

Endocrine glands


Hormones affecting growth
1. Growth Hormone
2. Thyroid Hormones
3. Parathyroid Hormone
4. Calcitonin
5. Insulin
6. Adrenocortical hormones

Growth hormone/ somatotropin


Secreted by-



ACTIONS
INDIRECT






DIRECT

Protein synthesis
synthesis & secretion
Lipolysis
of IGF
Protein breakdown
Use of glucose for ATP production

 Increases size & number of cells
 Converts chondrocytes into osteogenic cells
 Deposition of proteins by chondrocytic and osteogenic

IGF- INSULIN-LIKE GROWTH
FACTORS
 Small protein hormones
 Previously called ‘ Somatomedins’
 Structure & function – similar to insulin; growthpromoting effects more potent
 GH- release of IGF by cells of liver, muscle, cartilage,
bone etc
 Act through blood (endocrine) or locally (autocrine /
paracrine)
 Increased amino acid entry in cells, prevent protein
breakdown - increased cell growth & multiplication

Pituitary gigantism, dwarfism &
acromegaly


Thyroid hormones
(t3 and t4)
 Regulate –
1. O2 & BMR
2. Cellular metabolism
3.GROWTH & DEVELOPMENT- G & D of brain
- No. & size of neurons
- Myelinization of axons

 Hypothyroid- retarded growth
 CRETINISM

 Hyperthyroid- excessive

growth, early maturity of bones,
short height eventually.


Parathyroid hormone
 Increases serum Ca1. Rapid phase – Ca & PO4 absorption from bone matrix
around osteocytes & osteoblasts- Osteolysis
2. Slow phase- activation & formation of new
osteoclasts
3. Promotes formation of – 1,25 dihydroxycholecalciferol in
kidneys
 Increases Ca absorption & reabsorption

calcitonin
 Secreted by C-cells / parafollicular cells of thyroid.
 Antithesis of PTH.
Decreases serum Ca1. Immediate effect - decreases osteolytic effect of
osteocytic membrane
2. Prolonged effect - decreases new osteoclast
formation
 Effect negated by PTH - except in
- children

- Paget’s disease

insulin

 First isolated from pancreas by Banting & Best in 1922
 Hormone associated with ‘Energy Abundance’
 Peripheral uptake of glucose by cells
 Glycogenesis
 Lipogenesis
 Protein synthesis
 Glycogenolysis, neoglucogenesis

SYNERGISTIC ACTION WITH GROWTH HORMONE ON
GROWTH


Adrenocortical hormonesGLUCOCORTICOIDS
 Stimulate Gluconeogenesis
 Decreased glucose utilization by cells
 Decreased cellular protein
 Increased liver & plasma proteins
 Mobilization of fatty acids
 Anti-allergic, anti-inflammatory
 Decreased immunity

Cushing’s syndrome


Role in growth
 Physiological levels (10-9 M) –
-promote DNA synthesis,
-mesenchymal cell growth
-with other hormones/ growth factors- controls stages of
palatogenesis
 Increased levels – Cleft palate
-inhibition of mesenchymal cell proliferation
-interference with protein production

Adrenal androgens
 Weak male sex hormone, converted to testosterone
 Development of male sex organs in fetal life & early
childhood
 Mild effect in females throughout life


Growth
factors


Neural control
 Neural growth centre – in Hypothalamus
 Keeps children on genetically determined growth
curves
 At birth- body size limited to accommodate birth
process.
 After birth- children destined to become large
experience burst of early growth during first 2
years.

General body growth
 Co-relation exists between adult physique &
developmental events
 Variations in rate of growth of different somatotypes
 Ex. tall women mature later
 Facial dimensions spurt at
about the same time as stature
 Period of growth modification


neurotrophism
Definition:
“Interaction between nerves and other cells which initiate
or control molecular modifications in other cells.”
- Guth (1969)
“Nervous control of skeletal growth, assumedly by
transmission of a substance through the axons of the
nerves.”
- Moyers
DIRECT
INDIRECT

Neurotrophic substances pass, utilising the processes of
axoplasmic transport, from their sites of synthesis in the
neural cell body to the innervated tissues.

TYPES OF NEUROTROPHISM
1. Neuromuscular Trophism
2. Neuroepithelial Trophism
3. Neurovisceral Trophism
Effects of NEUROMUSCULAR TROPHISM :
a. Muscle development
b. Muscle denervation-reinnervation
c. Cross-innervation
d. Control of genetic activity

MUSCLE DEVELOPMENT:
 Embryonic myogenesis – independent of neural
innervation
 Neural innervation – Myoblast stage of differentiation
 i.e. until then – Neurotrophic control (Studitsky et al ’62)

MUSCLE DENERVATION-REINNERVATION
 Autotransplanted minced muscle fragments – reform
into a functional muscle if supplied by a motor nerve

CROSS-INNERVATION:
 Respective nerves of fast-slow muscle pair cut
 Free ends implanted in the other muscle – fast muscles
become slow & vice-versa
 “Changes in speed resulting from nerve cross-union are
brought about by a neural influence which has a direct
effect on the contractile material itself, thereby
determining intrinsic speed of contraction.” Close(1969)


CONTROL OF GENETIC ACTIVITY:
 Regenerating nerves may exert direct control on
synthesis of DNA, RNA & protein in regenerating
tissues (Dresden, Thornton).
 Qualitatively different myosin in cross-innervated
muscle- new species of protein produced by nerve
influence of gene expression in muscle cell.


Neuroepithelial trophism
 In regions of sensory loss- skin lacks usual ability
to withstand trauma…. Healing slow unless
regeneration of nerve occurs.
 In amphibians- subepidermal grafts of neural
tissue stimulate epidermal mitosis (Overton).
 LIMB REGENERATION- epithelial activity
must occur first for limb regeneration – requires
neural innervation (Singer & Craven).
 Maxillary & Mandibular hypoplasia – intra-oral &
intra-nasal sensory deficits (Henkin).

Presence of taste bud depends on intact innervation
(Jeppsson)
Gustatory nerve section- degeneration of taste buds &
adjacent epithelium.


Evidence against neurotrophic
theory
 Gutmann – complete differentiation of some
myotubes to muscle fibres can occur without
neural innervation; though very slowly &
occasionally
 In vitro- aneurogenic limb with fully developed
muscles experimentally produced in amphibiansperipheral tissues may produce & utilize their own
trophic substances.
 If motorneurons sectioned & related muscles
reinnervated – muscle tissue reforms & grows
before recovery of neuronal conductive function.

Function
 Role of function is the primary factor in control of
craniofacial growth- Moss’ Functional Matrix Theory
 Absence of normal function – gross distortion of bony
morphology ex. TMJ ankylosis, aglossia, NM disorders
etc.
 Malfunctions cause compensatory abnormal growth
 Ex. Altered nasorespiratory function, tongue-thrusting.
 Wolff’s Law- internal architecture of bone represents
external stresses.

muscles
 Formation of bone at the point of muscle
attachment depends on muscle activity
 Musculature – imp. part of total soft-tissue matrix
whose growth carries jaws downwards & forwards.
 Loss of part of musculature – underdevelopment of
that part of face

 Excessive muscle contraction – restricts growth ex.
Torticollis.

Functional equilibrium
 There should be a balance between the forces of the
tongue and compensating action of lips & cheeks
musculature to allow the jaws & dentition normally.
 Deleterious patterns of muscles behavior produce1. Perverted osseous growth.
2. Tooth malpositions.
3. Disturbed breathing.
4. Difficulty in speech.
5. Upset balance of facial musculature.
6. Psychological problems.


nutrition
 Proteins ( 9 essential amino acids), carbohydrates, fats.
 Ca, PO4, Mg, Mn, F, Vit D – bone & tooth
 Fe- Hb formation
 Vit A- activities of osteoblasts & osteoclasts
 Vit B complex- DNA formation & cell maturation
 Vit C- collagen formation
 Oxygen – cardiac anomalies – stunted growth
 Undernutrition- accentuates normal differential growth
of body tissues
 Teeth- bone- soft tissues

Effects of malnutrition
 Delays growth, adolescent spurt
 Affects size of body parts, proportions & chemistry
 Quality & texture of tissues – bone & teeth
 If period of malnutrition short – “catch-up growth”
 Girls better buffered against malnutriton & illness.


illness
 Minor childhood illnesses – not much effect
 Serious, prolonged, debilitating illnesses – marked effect
 Disease

increased cortisone

decreased GH.

 Cartilage cell growth stopped temporarily
 Lines of arrested growth- on X-rays, teeth.
 Catch up growth – brings child back on predetermined
genetic curve


race
 Racial differences-climatic, nutritional or socioeconomic.
 Gene pool differences – North American blacks ahead
of whites in skeletal maturity at birth & for at least first 2
yrs of life.
 Calcification & eruption of teeth 1 yr earlier than whites.


Climate & seasonal effects
 Cold climates- increased adipose tissue.
 Increased height – in spring than autumn.
 Increased weight - in autumn than spring.
 Growth in height & eruption of teeth – more at
night than day.
 Fluctuations in hormone release.


Family size & birth order
 First-born children – weigh less at birth, ultimately
less stature ; higher I.Q.
 Sizes, maturation, intelligence of individuals- no
correlation with size of family.

EXERCISE
 Effects on linear growth not proved.
 Development of motor skills, in muscle mass,
fitness, general well-being.

Psychological disturbances
 Psychological abuse adversly affects growth- accidental
discovery in 1948 by German physician.
 Ht. & wt. gain of children in 2 German orphanages for 1
yr.
 Orphanage governed by harsh headmistress – grew less
in ht. & wt. though 20% extra calories.
 Inhibition of growth hormone.
 Catch-up growth.

Socioeconomic factors
 Favorable socioeconomic status-larger
-different type of growth
-variation in timing of growth
 Positive relationship associated with socioeconomic
“class” ; not family income.
 As our society becomes more affluent, how long will we
get bigger & mature earlier ?

Secular trends
 15 yr-old boys now are approximately
5 inches taller than 15 yr-old boys
were 50 yrs ago.
 Children grow at a faster rate but stop
growing sooner.
 Adolescent growth spurt earlier
but not accentuated.
 Earlier total ht. reached at 25 yrs of age ; now at 20.
 i.e. secular trend more marked in children than in total
adult ht.
 Progressive advancement in timing of menarche.

habits
 Habits are learned patterns of muscle contraction
of a very complex nature.
1. Thumb-sucking
2. Tongue-thrusting
3. Mouth-breathing


Thumb-sucking

Begins

at birth and outgrown by 3-4 years.
Through sucking child obtains- nutrients,
feelings of euphoria, sense of security and
feeling of warmth.
Maxillary constriction- not due to negative
pressure.


 Mandible positioned in a
downward manner to
accommodate the interposed
thumb- causing increased eruption
of posterior teeth.
 Tongue is lowered which decreases
the pressure on the upper posterior
teeth.
 Imbalance between tongue &
cheek pressures.
 Cheek pressure increased as
buccinator muscle contracts during
suckling

Tongue-thrusting
 Tongue thrust is forward placement of
the tongue between the
anterior teeth
& against the
lower lip during
swallowingSchneider (1982).
 Tongue thrusting results due to lack of anterior seal.
 Skeletal openbite
 Steep mandibular plane.
 Increased anterior facial height.

Mouth-breathing
 Breathing through the
mouth alters equilibrium
of the jaws & teeth.
 Lowering of the mandible
& tongue & extension of
the head is seen.


 ‘Adenoid facies’-separated lips, small
nose, nostrils poorly developed, pout in
the lower lip, vacant facial expression.
 James Mcnamara- caused complete nasal
obstruction in primates using silicon plugs.
 Found downward & backward rotation of
mandible & increased lower facial height.
 Linder- Aronson studied 41 children who
underwent adenoidectomies- 5 years.
 34 children who switched to oral
respiration compared with 54 normal
children.

 Greatest change occurred in the
dentition and the sagittal depth
of the nasopharynx in the first
year.
 Mandibular plane angle
diminished by 4 degrees
(gradual change).
 Results were statistically
significant but no large
measurement differences –
facial height only 3 mm larger
in adenoidectomy group.

ORTHOPEDIC FORCES
MILWAUKEE BRACE THERAPY
 Non dental application of orthopaedic
force
 There are adjustable steel supports
transferring stress directly from the
chin and occiput to the iliac crest.
 Maxilla and mandible may be
deformed by growth guidance
procedures aimed at the endochondral
spine.

“If we could first know where we are & whither we
are tending, we could better judge what to do &
how to do it.”
- Abraham Lincoln


references
1. T.M. Graber – Orthodontics: Principles & Practice, III
Ed.
2. Proffit – Contemporary Orthodontics, III Ed.
3. Moyers – Handbook of Orthodontics, IV Ed.
4. Bishara – Textbook of Orthodontics, I Ed.
5. Enlow – Essentials of Facial Growth, I Ed.
6. Tortora – Principles of Anatomy & Physiology, VIII
Ed.
7. Guyton & Hall – Textbook of Medical Physiology, IX
Ed.

8. Sadler- Langman’s Medical Embryology, VIII, Ed.
9. Craniofacial Growth Series – Monograph 3
(Control Mechanisms in Craniofacial Growth – Edited
by McNamara)
10. Craniofacial Growth Series – Monograph 21
(Craniofacial Morphogenesis & Dysmorphogenesis–
Edited by Vig & Burdi)
11. James A. McNamara jr. –Influence of respiratory pattern
on craniofacial growth. The Angle Orthodontist. 1981;
vol-51, no-4
12. Anders Lundstrom- Nature vs nurture in dentofacial
variation- Eu J www.indiandentalacademy.com
ortho. 1984;

13. Katherine W. L. Vig- Nasal obstruction and facial
growth: The strength of evidence for clinical
assumptions. Am J Orthod. 1998; 113: 603-7.
14. Dr. Chitra Prasad- An assessment of the
transmission of craniofacial characteristics from a
study of twins and their siblings when compared
to their parents. MDS Dissertation Feb-1999.
15. Dr. Mallikarjun Prasad- An assessment of the
transmission of craniofacial characteristics from a
study of monozygotic twins, their parents and
siblings using conventional cephalometry, FEM
cephalometry and model analysis. MDS
Dissertation Sept-2002.

16. Dr. Siju M. George- A comparison of soft tissue
similarity corelation between children and parents
with the same corelation between children and
their older siblings- A profile view photographic
study. MDS Dissertation Mar-2002.


….FACTORS AFFECTING GROWTH
AND DEVELOPMENT

- case reports


Functional appliance therapy in conjunction
with growth hormone treatment. A case
report
-T. I. Davies & P. H. W. Rayner
- Br. J of Orthod 1995;22: 361-5.

Intro:
TURNER’S SYNDROME – 45 XO
Incidence – 1:2000 female births

Features:
1. Low birth weight
2. Oedema of hands & feet in neonatal period.
3. Co-arctation of aorta
4. Short stature
5. Ovarian dysgenesis – Primary amenorrhoea
6. Micrognathia

 Growth-promoting effect of HGH – in children with
retarded growth but normal normal pituitary pituitary
growth hormone secretion also.
 Growth hormone deficient children – 0.5 IU/Kg/week
 Turner’s syndrome- 0.7 – 1.0 IU/Kg/week.
 Theoretical side-effects – diabetes mellitus, neoplasias –
acute leukemia, cerebral tumors.
 Successful functional appliance treatment- rapid rate of
growth associated with pubertal growth spurt.

Purpose of study:
To highlight benefit of using functional appliance in a
patient with retrognathic mandible with a medical need
for GH, thus providing a predictable growth spurt.
Patient (VW) Female – birth wt.- 2.6 kg.
 Diagnosis- oedema, chromosomal analysis
 At age 10.8yrs – Ht.-128.7 cm.
 2nd centile for normal, 75th centile for Turner’s syndrome
 Skeletal age= chronological age.

 Combined Pituitary function test- partial growth hormone
deficiency

 HGH (Gentotropin)- 2 IU subcutaneously- 6 times/wk.
 After 3 mths.- ht.-132.1 (128.7)
 HGH- dose inreased to 3 IU.
 Ethinyloestradiol- 2 µg daily
 After 9 mths.- ht.-139.2 cm ; HGH – 4 units

 Class II Div. 1 – 14 mm overjet
 Class II Skeletal base – Retrognathic mandible.
 No history of habits, well-aligned arches.
 Andresen activator – 8 mths after commencement of
GH therapy – mandibular advancement
 2nd appliance- after 6 mths into treatment – complete
overjet reduction.
 Active treatment completed after 10 mths (12.5 yrs) –
continued in retention phase.
 Avg. daily wear – 18 hrs; Retention phase – 8 hrs.

RESULTS:
 1 yr. 3 mths. of GH – ht. increased by 10.5 cm; ht.
velocity of 8.4 cms/yr.
 Overjet 14 to 2 mm after 10 mths of activator therapy.
 Increase in mandibular length – greater than expected.


Conclusion:
 HGH & etinyloestradiol – needed to induce pubertal
growth spurt in Turner’s syndrome.
 Without hormone administration – successful
orthodontic treatment unlikely, especially in an active
treatment period of 10 mths.


Orthodontic treatment with growth hormone
therapy in a girl of short stature
- Chung-Ju Hwang & Jung-Yul Cha
-AJO-DO July 2004; 126:118-26
SHORT STATURE:
 Ht below 5th percentile for age
 Lower limit of normal for ht. at 3rd or 4th percentile for
age.
 Growth- less than 4cms/yr after 3yrs. of age.
 Skeletal age- 2 yrs behind chronologic age.
 Euthyroid, no GH deficiency, no chronic disease.
 Treatment of short-statured children with GH –
controversial.

 All linear measurements of facial structures – smaller
 Disproportionate growth in cranial base structures & jawsfacial retrognathia.
 Proportionately smaller posterior than anterior facial ht.
 Steep vertical inclination of mandible.
 High incidence of crowding.
Purpose of the study:
To review the characteristics of craniofacial morphology in
children of short stature & the effects of Human Growth
Hormone (HGH) therapy on craniofacial complex.


Case:


Girl- 9yrs, 3mths.



Chief complaint- anterior cross-bite.



Ht.- 120.9 cms. Father- 174 cms, Mother- 150 cms.



GH level –normal.



Normal birth wt., no evidence of non-endocrine causes
of short stature, systemic disease or dysmorphic
features.



Slow post-natal growth, body ht. std. deviation score –
less than -2.



Skeletal age- 7.5yrs.

 High mandibular angle
 Class III dental maloclusion
 Skeletally retrognathic mandible
 Ant. Crossbite (-2 mm overjet), openbite, constricted
maxillary arch- buccal edge bite, incompetent lips, mild
anterior crowding, midline deviation.


Treatment:
 HGH (Eutropin) – 2 IU/m2 s.c. 6 times/week.
 HGH increased to – 3 IU/m2 & then to 5 IU/m2 (4th yr)
 RPE & facemask (8 mths)– crossbite correction.
 Upper plate with anteroposterior screw – for 3 mths.
 After 15 mths – spring-loaded posterior occlusal bite
block appliance on mandibular dentition with chincupvertical discrepancy.
 28th mth- Cl. III molar, anterior- edge-to-edge

 After 3 yrs, 7 mths – fixed appliance.
 Cl III elastics- edge-to-edge
 Vertical elastics on anteriors – overbite.
 Continuous chincup- pt. uncooperative.


Results:
 Increase in ht.10 cms (24 mths); 7.3 cms(3rd yr); 5.2cms(4th yr)
 Intermaxillary elastics –
increased mandibular plane angle,
clockwise rotation of mandible,
extrusion of maxillary molars.
 Dental corrections achieved- poor profile.


Discussion:
 HGH therapy affects growth of mandible more than
growth of maxilla.
 Amount & pattern of growth during HGH
administration unpredictable
 HGH therapy rarely affects dental maturity.
 Further research on effect of HGH- craniofacial growth
& tooth movement during orthodontic therapy.


Thank you
• Leader in continuing dental education
•


factors effecting growth & development /certified fixed orthodontic courses by Indian dental academy

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