Role of hormones n vitamins in craniofacial growth n develpoment

Role of
Hormones and Vitamins
in
Craniofacial Growth and
Development
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HORMONES
 Definition:
“A hormone is a chemical substance that is
secreted into the body fluids by one cell or a
group of cells and has a physiological
control effect on other cells of the body.”
- Arthur C. Guyton
Textbook of Medical Physiology

 Hormones exert an important influence on:
• the chemical and functional processes,
• modify course of fundamental enzymatic reactions,
• regulate metabolic processes throughout the body and
• control the actions of specific organs.
 They also react strongly on the nervous system,
upon behavior and psychological processes and
contribute to the reactions of the organism
when an emergency arises.

Classification of Endocrine Glands
 Pituitary – cranuim (sella
turcica of sphenoid)
 Thyroid, Parathyroid and
Thymus - upper part of trunk
 Adrenals and Pancreas
- abdominal cavity
 Gonads (Testis and Ovaries)

Anterior Lobe
PITUITARY GLAND
Posterior Lobe

ANTERIOR PITUITARY GLAND

POSTERIOR PITUITARY GLAND

ANTERIOR LOBE OF PITUITARY
 Controls and stimulates Growth and Development of the
body in general.
 Exerts considerable control over function of metabolic
processes of other endocrine organs like the thyroid,
adrenals and sex hormones.
 Builds body resistance to infections.
 Influences the Oral and Facial structures.

GROWTH HORMONE
 Also called Somatotrophic hormone (STH) or
Somatotropin.
 Causes growth of almost all tissues of the body by
increasing mitosis and specific differentiation of cells.
 Causes increased growth of the skeletal frame:
 Increased deposition of protein by the
chondrocytic and osteogenic cells.
 Increased multiplication of these cells and
conversion of chondrocytes to osteogenic cells.

 It has been postulated that most if not nearly all of the
growth effects of GH, result from somatomedin.
 It has been found that GH causes liver to form several
small proteins called Somatomedins, that in turn have
very potent effect of increasing all aspects of bone growth.
When GH is supplied directly to cartilage condrocytes cultured
outside the body, proliferation and enlargement fail to occur.
 Atleast 4 different types of somatomedins have been
isolated and of this somatomedin-C is most important for
functioning of GH.
The pygmies of Africa have a congenital inability to synthesize
significant amount of somatomedin-C and therefore even though they
have normal levels of GH in plasma, they are people of short stature.

 Growth hormone and somatomedin as well as testosterone
and estrogen are seen to play a primary role in extrinsic
control of postnatal growth of upper jaw - and their effect
is by direct and indirect stimulating action
- Stutzmann and Petrovic 1976.
Direct Effect:
Stimulates the growth of spheno occipital
synchondrosis, nasal septal cartilage, lateral mass of
ethmoid bone and the cartilage between the body and
greater wing of sphenoid.
A small effect on the growth of cranial and facial
sutures in these areas.

Indirect Effect:
 Forward growth of nasal septal cartilage
• Produces a forward thrust effect of premaxillary bone
which leads to increase in growth of
premaxillomaxillary suture.
• Results in forward traction of septopremaxillary
ligament and labionarinary muscles, resulting in
forward growth of the premaxilla.
 Outward growth
• Outward growth of lateral cartilagenous masses of the
ethmoid and cartilages between body and greater
wings of sphenoid and therefore produces a
lateralization of the alveolar ridges on both the sides,
which turn stimulates growth of the mid palatal suture.www.indiandentalacademy.com

Control of Maxillary Growth by STH

STH
Forward growth
of septal cartilage
Forward traction of
septomaxillary lig.&
labionarinary musc.
Growth in length
Increase in
tongue vol.
Posteroanterior
shift of
premaxillary bones
Protrusion of
upper anteriors

STH
Outward growth
of lateral ethmoid
Outward growth
by apposition
Growth in width
Increase in
tongue vol.
Growth of
Midpalatal
suture
Outward shift of
alveolar bone
Cartilage growth b/w
greater wing & body
of sphenoid

Control of Mandibular Growth by STH
 Stimulates growth of condylar cartilage, coronoid and
angular cartilage of the mandible.
 Growth of the condylar cartilage has an effect on the
mandibular angle.
The mandibular angle along with the appositional growth
of posterior border of ramus, controls the forward growth
of the mandible and therefore helps maintain the condyle-
dental arch distance.
 The condyle- dental arch distance along with the tongue,
maintains the sagittal position of the mandible.

Supporting studies
 Effects of growth hormone on craniofacial growth.
Study was done on 57 GH deficient pts. aged between 4-
17yrs.
Conclusion – Long term GH therapy resulted in larger
upper facial heights, maxillary length and ramus height,
with increased growth of the cranio facial skeleton.
– Funatsu M, Sato K, Mitani H
Angle Orthod. 2006 Nov.

 Differential growth and maturation in idiopathic
growth-hormone-deficient children.
Study describes and compares the growth and maturation
of idiopathic growth hormone deficiency (IGHD) and
evaluates the potential effects of growth hormone therapy
in 40 idiopathic growth-hormone-deficient children.
Conclusion – Catch-up growth with hormonal therapy was
established for height , facial height, skeletal age and
posterior cranial base length.
-Cantu G, Buschang PH, Gonzalez JL
Eur J Orthod. 1997 Apr

Supporting studies
 Influence of growth hormone on the craniofacial
complex of transgenic mice.
Study investigated the effect of GH on the size of the
craniofacial structures and their angular relationship. Three
different models of mice with a genetically altered GH axis
were use.
Conclusion - GH plays a major role in the growth and
development of the craniofacial complex by directly and
indirectly modulating the size and the angular relationships
of the craniofacial structures, including the incisor teeth.
- Ramirez – Yanez GO, Smid JR, Young WG, Waters MJ
Eur J Orthod. 2005 Oct

Hypofunction of the pituitary gland
 Dwarfism – Retards the growth and development of the
maxilla and mandible and all facial structures.
 Retardation of tooth eruption – maybe due to reduction of
the vascularity of the periodontal tissues.
 Reduction in growth of paranasal sinuses, especially
frontal sinus.
 Teeth have short roots, wide pulp chamber and wide apical
foramina.

Hypofunction of the pituitary gland
 Reduction in arch length, with crowding and submersion
of teeth.
 Rate of bone growth is decreased and therefore bodies of
maxilla and mandible are reduced in length and height,
resulting in lessened vertical dimensions.
Since the reduction in vertical dimension of rami is
greater than loss of alveolar height, the mandible ends up
in a distal relationship with maxilla.

Hyperfunction of the pituitary gland
 Produces Gigantism in early life and Acromegaly in adult
life.
Class III - In acromegaly excessive growth of mandible
may occur, creating a skeletal Class III malocclusion.

Hyperfunction of the pituitary gland
 Overgrowth of alveolar process in height and breadth, with
spacing between teeth.
 Vertical height of face increased and paranasal sinuses
overdeveloped.
 Enlargement of tongue.
 Acceleration of tooth eruption and increase in occlusal
height.

THYROID GLAND
 Highly vascular, bilateral lobed, U-shaped gland located
on the trachea, below the larynx and inferior to the thyroid
cartilage

Thyroid Hormones

Hypothyroidism
 Congenital hypothyroidism affects primarily –
 bone of cartilaginous origin
 bone of endocondral origin – cranial base
 bone of intermembranous origin - cranial vault.
 Cranial vault is disturbed and arrested in growth more
than the facial bones and the length of the cranial base
is shortened more than the cranial vault and face.
 There is retardation in normal rate of deposition of
calcium in bones and development of tooth buds in
embryo.

Hypothyroidism
 Irregularities of tooth arrangement and open bite may
be present as a result of tongue enlargement and the
habit of holding the tongue between the maxillary and
mandibular dental arches may result in mandibular
prognathism.

Hypothyroidism
 In early childhood hypothyroidism –
 Teeth develop slowly and show structural defects.
 Resorption of roots of deciduous dentition is delayed, resulting in
delayed eruption of permanent dentition as well.
 Growth takes place, but these is delayed ossification and retention
of infantile characteristics.
 Pituitary cretinism – caused by anterior pituitary
thyrotrophic hormone
 Sphenoid bone is stunted, especially at the spheno-occipital suture.
 Nose is short, root of nose is depressed and nasal bridge broad and
flat.
 Ossification of cartilaginous centers is delayed.

Hypothyroidism
 Juvenile myxedema –
 Retardation in rate of deposition of calcium in bones and tooth
buds.
 Delayed carpal and epiphyseal calcification.
 Disharmonies in eruption of teeth.
 Incomplete unfolding of nasal area and inadequate development of
maxilla.
 Prolonged retention of deciduous dentition – as late as third
decade.
 Permanent teeth are slow to erupt.
 Mesio- or distoclusion and crowding of teeth.
 Malposed maxillary and mandibular incisors and canines with loss
of proximal contact.
 Abnormal dental calcification and root resorption.
 Disturbances of periodontium – osteoporotic condition of alveolar
bone.

Hyperthyroidism
 Produces an increase in the rate of maturation, an increase
in the metabolic rate and exophthalmic goiter.
 Premature eruption and disturbed resorption of roots of
deciduous teeth, in association with early eruption of
permanent teeth.
 Bones become fragile.
 Secretion of saliva is increased.
 Acceleration of skeletal ossification.

Hyperthyroidism
 Hyperthyroidism is rare in children but when it does occur
eruption of teeth is accelerated; occasionally some of teeth
may be present at birth.
 Acceleration of eruption of permanent by as much as 2
years or more ahead of their normal time.
 Teeth may show bluish white coloring.
 Osteoporosis may be present.

Supporting studies
 Baume et al. found thyroidectomy in rats to reduce the rate of canine
size and rate of eruption. Differentiation of tooth structures was
retarded as well.
 Role of thyroid hormone in craniofacial and eye development
using a rat model.
Analysed the craniofacial and eyeball developmental characteristics in
a rat model of congenital-neonatal hypothyroidism (HG), induced by
combined chemical-surgical thyroidectomy.
Conclusion – Essential for somatic and neural development. TH plays
a pivotal role in the development of face and eye and loss of TH action
results in defects of anterior – posterior development of head and
face.
- Gamborino MJ, Sevilla-Romero E
Dept. of Cellular Biology, RCU Hosp.,Spain

PARATHYROID GLAND
 Parathyroids usually consist of 4
small glandular bodies about 8 mm
long, embedded on the dorsal
surface of the thyroid.
 Regulate normal level of diffusible
calcium and phosphorus in the blood
plasma
 Regulate calcium metabolism and
play leading role in calcification of
teeth and bones.
 They have little or no direct effect
on growth or eruption.www.indiandentalacademy.com

Parathyroid Hormone

Hypoparathyroidism
 If present when teeth are developing, there is delayed eruption and
resorption of the roots of the deciduous teeth and retarded eruption of
permanent teeth.
 Enamel defects – teeth have a white appearance but later turn brown
through staining. They are brittle, pitted, show opaque areas and are
fractured easily because of poor calcification.
 Teeth show large pulp chambers and irregularities in occlusion.
 If hypocalcemia present before teeth have erupted, it may show itself
in enamel of teeth in the form of aplasia and hypoplasia.
 Hypothyroidism in adults (thyroidectomy) does not affect teeth.

Hyperparathyroidism
 Calcium is withdrawn from bones and is deposited in blood, resulting
in teeth becoming loose from lack of alveolar support.
 Bone shows abnormal increase in osteoclasts and a fibrous change of
the bone marrow – Osteitis fibrosa Cystica. Alveolar bone will be
markedly reduced.
 In growing children there may be interruption in tooth development,
producing marked effect on dentin formation in the form of deeply
stained contour lines.
 Formation of osteodentin and osteocementum also may take place.
 Early distortion of trabecular patterns, demineralization and
disappearance of lamina dura may be seen.

ADRENAL GLAND
 Adrenals or suprarenals are 2
small yellowish masses above or
near the kidney consisting of an
outer layer (cortical) and an inner
layer (medullary)
 Glands maintain the potassium –
sodium balance.
 Increased activity of cortex
increases rapidity of skeletal
maturation.
 Tumors of adrenals at the time of
tooth development may produce
premature eruption of permanent
teeth.

Adrenal Hormones

Adrenocortic hyperfunction
 Brings about decrease in protein body mass including the bony matrix
into which calcium is deposited when bone is formed, interfering with
bone formation
 There is premature development with early closure of the epiphyses
and hence dwarfism.
 Height age, bone age and tooth eruption are also accelerated
Adrenocortic insufficiency
 A reduction in adrenaline effects utilization of proteins for formation
body tissue resulting in diminished muscular strength and inhibition of
growth

GONADS
 Gonad hormones are evolved by
the ovaries and testes and exert
a marked influence upon
somatic growth.
 Hypofunction retards closure of
the epiphyseal growth centres
and hence tend to increase body
stature.
There is also an increased rate
of endomembraneous bone
formation, resulting in larger
bodies of jaw with short rami.
 Hyperfunction causes premature
closure and reduction in body
height.

Supporting Studies
 Effect of low-dose testosterone treatment on
craniofacial growth in boys with delayed puberty.
Craniofacial growth was investigated in boys treated with low-dose
testosterone for delayed puberty and compared with controls. At the
beginning of the study, statural height, mandibular ramus length,
upper anterior face height, and total cranial base length were
significantly shorter in the delayed puberty boys.
After 1 year, the growth rate of the statural height, total mandibular
length, ramus length, and upper and total anterior face height was
significantly higher in the treated boys.
Conclusion: Low doses of testosterone accelerate statural and craniofacial
growth, particularly in the delayed components, thus leading towards a
normalization of facial dimensions.
- Verdonck A etal
Eur J Orthod. 1999 Apr

Adolescence and Growth
 This period is important in orthodontic treatment, because the physical
change at this stage significantly affects face and dentition.
 The increasing level of sex hormones cause physiologic changes
including the acceleration in general body growth and shrinkage of
lymphoid tissues.
 Sex hormones stimulate cartilage to grow faster and this produces
adolescent growth spurt.
 There is an adolescent growth spurt in the length of the mandible
which produces an acceleration in mandibular growth relative to the
maxilla. Therefore the maturing face becomes less convex as the
mandible and chin become more prominent.
 Although jaw growth follows the curve for general body growth, the
correlation is not perfect. There is a juvenile acceleration in jaw
growth, especially in girls that occurs 1-2 years before this adolescent
growth spurt.
 And therefore this a major reason for the careful assessment of
physiological age in planning orthodontic treatment and avoiding
delays in the opportunity to the utilize growth spurt.

VITAMINS
 Definition:
“ Vitamins are naturally occurring organic
nutrients which are required in minute
amounts to maintain normal health of the
organism and which have to be supplied in
food as they cannot be synthesized by the
organism. ”

Classification
Vitamins
Fat Soluble
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Water Soluble
Vitamin B complexVitamin C
B1-Thiamine Folic Acid
B2-Riboflavin B12
B3-Niacin
B6-Pyridoxine
B7-Biotin
Pantothenic Acid

Vitamin A
 Source: Cod liver oil, animal liver, milk and milk
products and egg.
Carotenoid pigments (precursors) – carrots, sweet potato
and spinach.
 Function: Vision, proper growth and differentiation,
reproduction, maintenance of epithelial cells.
Carotenoids function as antioxidants and reduce the risk
of cancers initiated by the free radicals and strong
oxidants.

 Dietary requirements:
 Adults-750ug
 Infants and young children- 300ug
 Women during pregnancy and lactation- 1200ug.
 Deficiency manifestations:
 Effect on eyes: night blindness, xeropthalmia,
keratomalacia.
 On growth: retardation due to impairment in skeletal
formation
 On reproduction: degeneration of germinal epithelium
leads to : sterility in males, termination of pregnancy
due to fetal death
 On skin and epithelial cells: keratinization of epithelial
cells. www.indiandentalacademy.com

 Hypervitaminosis:
Can lead to toxicity.
Acts as a teratogen – Cleft lip and palate

Vitamin D
 Source: fish liver oils, egg yolk, by irradiating foods
(yeast) that contains precursors of vitamin D, and natural
sunlight.
 Functions: Ergocalciferol and Cholecalciferol are the
sources of vitamin D activity and are referred to as
provitamins. The biologically active form is Calcitriol.
Calcitriol regulates the plasma calcium levels of calcium
and phosphate. It acts on intestine, bone and kidney to
maintain calcium levels.

 Dietary requirements:
 Infants: 400 to 800 IU daily.
 Children and adolescents: 400 IU daily.
 During pregnancy and lactation: 400 to 800 IU daily.
 Deficiency manifestations:
 Results in demineralization of bone . The result is
rickets in children and osteomalacia in adults.
 Rickets in children is characterized by bone deformities
due to incomplete mineralization resulting in soft and
pliable bones and delay in teeth formation. In
osteomalacia demineralization of bone occurs making
them susceptible to fracture.

 Hypervitaminosis:
 Demineralization of bone (resorption) and increased
calcium absorption from the intestine, leading to
hypercalcemia.
 Prolonged hypercalcemia leads to deposition of
calcium in the soft tissues such as kidneys, blood
vessels, forming renal calculi.

Vitamin K
 Source: Cabbage, cauliflower, tomatoes, Alfa alfa,
spinach, egg yolk, meat, liver, cheese and dairy products.
 Functions:
 Concerned with the blood clotting process.
 It brings about post-translational modification of
certain blood clotting factors.
 Deficiency manifestation: Leads to the lack of active
prothrombin in the circulation, adversely affecting the
blood coagulation.
The blood clotting time is increased.

Hypervitaminosis:
 Administration of large doses produces hemolytic anemia
and jaundice particularly in infants.
 The toxic effect is due to increased breakdown of RBC.
 Supporting studies:
Vitamin K--its essential role in craniofacial
development - A review of the literature regarding
vitamin K and craniofacial development.
Conclusion: First trimester deficiency results in maxillonasal
hypoplasia in the neonate with subsequent facial and orthodontic
implications. Maternal dietary deficiency or use of a number of
therapeutic drugs during pregnancy, may result in frank vitamin K
deficiency in the embryo.
- Howe AM, Webster WS
Aust Dent J 1994 Apr.

Vitamin C (Ascorbic acid)
 Source: Abundantly seen in citrus fruits, berries,
melons, sprouting seeds, leafy vegetables, spinach,
cauliflower, cabbage, tomatoes, drumstick and guava. In
animals present in liver, kidneys and adrenal cortex.
 Functions:
 plays an important role in collagen formation, acting as
a coenzyme, thereby facilitating cross linkage of
collagen fibers and increases its strength.
 Helps in bone formation, plays a role in iron and
hemoglobin metabolism, takes part in the metabolic
reactions of tryptophan, tyrosine, folic acid and
cholesterol, enhances the synthesis of immunoglobulin.

 Deficiency manifestation: Leads to scurvy,
characterized by spongy and sore gums, loose teeth,
swollen joints, anemia, fragile blood vessels, delayed
wound healing, hemorrhage and osteoporosis etc.
 Hypervitaminosis: Ascorbic acid, as such, is not toxic,
but, dehydroascorbic acid (oxidized form of ascorbic acid)
is toxic.
Oxalate which is a major metabolite of vitamin C, have
been implicated in the formation of kidney stones.

B-COMPLEX VITAMINS
VITAMIN SOURCE FUNCTION DIETARY
REQ.
DEFICIENCY
Thiamine
B1
Cereals,
pulses, oil
seeds, nut,
yeast
pork, liver
heart,
kidney
and milk
Energy releasing
reactions in the
carbohydrate
metabolism
1.5mg per
day
Wet beriberi –
Breathlessness,
palpitations.
Dry beriberi –
Peripheral
neuritis,
weakening of
muscles.
Riboflavin
B2
Milk,meat,
eggs,liver,
kidney,
cereals,
fruits &
vegetables
Cellular Oxidation
Reduction
reactions.
Adults-
1.5-1.8 mg.
Pregnant/
lactating
women/
children -
2.0-2.5 mg
Cheilosis,
Glossitis, and
Dermatitis.

REQ.
DEFICIENCY
Niacin
Liver,
yeast
grains,
pulses,
peanuts,
milk, fish
and eggs
Cellular
Oxidation
Reduction
reactions.
17-21mg
per day
Pellagra –
Skin, GIT &
CNS.
3D’s –
Dermatits,
Dementia &
Diarrhea.
Pyridoxine
B6
Egg yolk,
fish, milk,
meat,
wheat,
corn and
cabbage
Transamination,
Decarboxylation,
Deamination,
Transsulfuration
and condensation.
Synthesizes -
Serotonin,
histamine.
Adults-
2-2.2 mg.
Pregnant/
lactating
women/ old
age - 2.5
mg
CNS –
Depression,
irritability,
nervousness
and mental
confusion.

REQ.
DEFICIENCY
Biotin
Liver,
kidney,
egg yolk,
milk,
tomatoes,
grains
Carries CO2 in
carboxylation
reactions.
100-300
mg per day
Anemia, loss of
appetite,
nausea,
dermatitis,
glossitis
Pantothenic
Acid
Egg, liver,
meat,
yeast, milk
Co enzyme A –
Acts as a carrier of
acyl groups
Adults-
5-10mg
None

REQ.
DEFICIENCY
Folic
Acid
Green
leafy
vegetable,
cereals,
liver,
kidney,
yeast &
eggs.
Required for
synthesis for
amino acid,
purine and
pyrimidine -
thymine
Adults-
100 ug.
Pregnant/
lactating
women
150-300
ug
Macrocytic
anemia.
Cobalamine
B12
Egg,
liver,
meat,
milk &
kidney
Synthesis of
nuclei acids and
along with folic
acid –
hemopoeisis
Pernicious
anemia. Low Hb
level, decreased
number of RBCs.

Nurition Imbalance
 Growth and Development:
 Deficiency of essential nutrients during hyperplastic growth phase
may result in permanent, irreversible damage to the tissue.
 Deficiency of essential nutrients during hypertrophic growth –
organs may temporarily stop growing but usually “catch up”
occurs when adequate amounts of missing nutrients become
available and may become normal in size, contents and function.
 A number of oral tissues are particularly sensitive to nutritional
stress during critical periods in their development, including
maxillary and mandibular bones, tooth, salivary glands, oral
epithelium and other craniofacial strcutures such as the lip
and palate.

 Developing Oral tissues:
 Deficiency of folic acid, riboflavin and zinc are known to induce
clefting.
 Suboptimal levels of nutrients may potentiate other teratogenic
agents.
 Iodine deficiency in the mother’s diet causes cretinism in the
offspring.
Supporting Studies:
 Evans, Nelson and Asling found that deficiencies of folic acid
and biotin in the expectant mothers caused cleft palate and
general growth retardation.
 Van Creveld associated cleft palate, micrognathia and other
congenital malformations to extremely deficient maternal diet
during pregnancy.www.indiandentalacademy.com

 Wakarny, experimenting on animals, repeatedly induced cleft
palate, congenital abnormalities of dentofacial development and
occlusion, shortening of the mandible when maternal diet was
deficient of riboflavin.
 Teeth and Salivary Glands: Teeth and salivary glands enter into
hypertrophic and hyperplastic growth phases and critical periods
do exist in the development of the teeth salivary glands during
which time, imposed stress (nutritional imbalance) will lead to
irreversible changes in these tissues.
Therefore a variety of amino acids, vitamin A, D and C, calcium
and phosphorus must be present to insure optimal calcification
during the teeth formation and calcifying periods.

 Skeletal Tissues: Optimal growth and development of maxillary
and mandibular bone is necessary to maintain a harmonious dental
arch. Nutritional factors can adversely affect tooth eruption,
alignment and alveolar bone integrity.
Guilford advanced that dietary deficiencies cause dentofacial
irregularities. Wolbach and Howe indicated that lack of vitamins
C and D, may be causative factors in malocclusion by arresting
growth of the maxilla and mandible.
 Protein caloric malnutrition, vitamin A, D, E and C deficiencies,
along with deficiency of mineral calcium and phosphorus may
result in-inadequate bone growth patterns with malalignment
and malocclusion.

Conclusion
 Hormones and Vitamins play a major role in Growth and
Development of Craniofacial Complex.
 Quantity of vitamins can be controlled through diet intake
and therefore should be supplemented in appropriate
proportions during growth and development.
 Whereas hormones, since they are controlled by the
endocrine system, it is important for us to be able to
identify a potential hormone deficiency through their
various clinical manifestations and be able to treat the
particular patient appropriately.

References
 Textbook of Medical Physiology – Guyton. 8th
Edition.
 Human Physiology – Vander, Sherman, Luciano. 6th
Edition.
 Principles of Anatomy and Physiology – Tortora. 8th
Edition.
 Essentials of Biochemistry – Harper
 Textbook of Medical Physiology – Rama Rao. 6th
Edition.
 Medical Problems in Dentistry – Scully & Cawson. 5th
Edition.
 Contemporary Orthodontics – William Profitt. 3rd
Edition.
 Dentofacial Orthopedics with Functional Appliances – Graber, Rakosi,
Petrovic. 2nd
Edition.
 Textbook of Orthodontia – RWH Strang. 4th
Edition.
 Orthodontics – Practice and Technics – JA Salzmann .
 Angles Orthodontia - Nov 2006.
 European Journal of Orthodontics – Apr 1997, Oct 2005 & Apr 1999.
 Australian Dental Journal – Apr 1994.

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