Hormones

ROLE OF HORMONES IN ORTHODONTICS
BY: DR. ABDULWAHAB. MDwww.indiandentalacademy.com

CONTENTS
• Introduction
• What is a hormone
• Discovery of hormone
• Exocrine and endocrine glands.
• Embryology of endocrine glands
• Classification
• Mode of action
• Role of hormones in the body
• Problems related to increased or decreased hormonal
secretions.
• Role of hormones in orthodontics
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Introduction

• ENDOCRINOLOGY
e n d o n = inside.
k r i n w = secretion.
l o g o s = study, or
discussion.

• HORMONE
o r m a w = urge into
activity.

WHAT IS A HORMONE ?

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.

DISCOVERY 0F HORMONES
• Bayliss and Starling (1902)
were studying digestion and
absorption in an isolated loop
of duodenum
• Since the duodenal loop had a
blood supply, but no nerve
supply they concluded that it
could communicate with the
pancreas only via some blood-
borne substance, which they
called "secretin".
• When more of these blood-
borne messengers were
discovered they were given the
generic term "hormones".

Exocrine and endocrine glands.

EMBRYOLOGY OF ENDOCRINEGLANDS

• ECTODERM - pitutary (anterior)
• MESODERM- cortex of suprarenal glands
• ENDODERM – thyroid
                            parathyroid
                            liver
                            pancreas

Development of pitutary gland

Suprarenal glands

THYROID GLAND

Classification

ACCORDING TO ANATOMICAL SOURCE OF THE
HORMONE:
Hypothalamus:
• SomatostatinGrowth
hormone releasing
hormone (GHRH)
• Thyrotropin releasing
releasing hormone
(GnRH)
• Corticotropin releasing
hormone (CRH)
• Prolactin releasing
hormone(PRH)

Anterior pituitary gland

   Growth hormone (hGH)

   Thyroid stimulating hormone (TSH)

   Gonadotropins (FSH and LH)

   Adrenocorticotropic hormone (ACTH)

   Prolactin

   Melanocyte stimulating
   hormone (MSH)
AP
G
PP
G

Posterior pituitary
gland:
• Antidiuretic hormone
(ADH, or vasopressin)
• Oxytocin

• Thyroid gland :
•     Thyroid hormones (T3

         and T4)
•     Calcitonin

•Parathyroid glands :
Parathyroid hormone
        (PTH)


Liver:
Insulin-like growth factor (IGF I)
or: somatomedin
Adrenal cortex
Cortisol
Aldosterone
Adrenal medulla :
Adrenalin (or: epinephrine)
Noradrenalin (or: norepinephrine)

Pancreas:
   Insulin
   Glucagon
Gonads:
   Sex hormones: Oestrogen,                    females
                            progesterone,
                            testosterone.                  males

CLASSIFICATION OF HORMONES
ACCORDING TO CHEMICAL
COMPOSITION:
PEPTIDE HORMONES

Polypeptide hormones:
• All the hormones from the anterior pituitary gland.
• The anterior pituitary-like hormones from the pancreas and liver.
• Parathyroid hormone (PTH) and
• calcitonin.
• Erythropoietin.


• Oligopeptide hormones:
All the hormones from the posterior
pituitary gland.
All the hormones from the hypothalamus
(except dopamine).
Angiotensin I and II.

AMINE HORMONES (all derived from the
amino acid: tyrosine):
• Thyroid hormones (T3 and T4).
• Adrenalin.
• Noradrenalin.
• Dopamine

STEROID HORMONES (all derived
from cholesterol)
• Sex hormones from the gonads and
placenta.
• All the adrenal cortex hormones.
• 1,25 dihydroxycholecalciferol - Vit D3.

Role of hormones
in the
body

Hormones are chemical messengers that
travel throughout the body coordinating
complex processes like growth,
metabolism, and fertility.

They can influence the function of the
immune system, and even alter
behavior.
Before birth, they guide development of
the brain and reproductive system.

Hormones are the reason
• why your arms are the same length,
• why you can turn food into fuel, and
• why you changed from head to toe at
puberty.


It is thanks to these chemicals that distant
   parts of the body communicate with one
   another during elaborate, and important,
   events.

FUNCTIONS
OFENDOCRINEGLANDS
ANDITS
HORMONES

•Hypothalamus makes up the third
ventricle of the brain. Among its multitude
of functions the hypothalamus controls
temperature and vascular changes, the
emotions and certain visceral changes.
It provides neurogenic controls of the
pituitary gland, which controls the target
glands, i.e., the thyroid, adrenals and
gonads.

HYPOTHALAMUS
PITUTARY
TROPHIC HORMONE
TARGET GLAND
TARGET GLAND
HORMONE
BODY CELLS

• Pituitary The master gland, secretes hormones that
influence many other glands and organs, affecting
growth and reproduction.
Anterior pituitary gland
Posterior pituitary gland:


Anteriorpituitary gland is chiefly
concerned with:
1. Stimulation of growth and development of the body in general
2. Hyperfunction at an early age produces gigantism; at a later age
    acromegaly results.
3. Control of function of metabolism of other endocrine organs,
    especially the thyroid, adrenals and sex organs.
4. In hypofunction there is retardation of tooth development and
    eruption. When there is hyperfunction during the developmental
    period, eruption of the dentition is accelerated.
6. Hypofunction   produces   emaciation,   retarded   growth,   and
    hypogonadism.

Functions of Growth Hormone
It has effects:
1) On growth of skeleton, skeletal muscle
      and viscera.
2)  On metabolism of a) carbohydrate b)
     protein c) fat d) electrolytes.
3)  On milk production - lactogenic effect.
4)  On erythropoisis.

Action On Growth :
a) G.H. stimulates the growth of skeleton. It has
     specific action on the epiphysis, cartilages and
     promote chondrgenesis,  consequent
     mineralization causes linear growth of bones.
b) Growth hormone stimulate growth of viscera
e.g. Liver, Kidney, Thymus and alimentary
canal.
c) Growth hormones increase skeletal muscle
mass.

Action On Metabolism :
a) On proteins : Growth hormone is a protein anabolic
      hormone it produces a positive nitrogen and
      phosphorus balance.
b)   It decreases blood urea nitrogen and aminoacid levels.
c)   It increases the transport of neutral and basic
      aminoacids into the cells.
d)   It stimulates R.N.A synthesis. It exerts its effects at
      ribosomal level and increases protein synthesis.

Carbohydrate Metabolism:
• Growth hormone is diabetogenic that is it
   increases blood glucose level. This is achieved
   by stimulating hepatic glycogenolysis and by
   opposing the action of insulin in muscle.  It
   stimulates gluconeogenesis.
• Growth hormones prevents entry of glucose into
the cells. It inhibits
   phosphorylation of glucose so rise in blood
   glucose occurs.

On Fat Metabolism:
• Growth hormone causes lipolysis of
adipose tissue at the same time promoting
lipogenesis in liver.

Action On Milk Production:
   Growth hormone has lactogenic and
   mammogenic activity. It helps in the
   maintenance of milk secretion along with
   the thyroxine and prolactin. It has prolactin like
activity.
Action On Erythropoisis :
   Stimulate erythropoisis. It increases erythropoisis
production from kidney.

Thyroid Stimulating Hormone
(TSH)
Actions On Thyroid Gland :
• T.S.H is responsible for normal size weight structure and vascularity
     of the glands.
• It is responsible for the normal production and secretion of thyroid
     hormones (T4 and T3) it stimulates all the steps in the biosynthesis
     of the thyroid hormones.
On Orbital Tissue :
• In graves disease (a form of hyper thyroidism) exopthalmus
     (protrusion of eye balls) is present.  This is due to a
accumulation of fatty tissue in the retro orbital space combined
withweakness of external occular muscles

Adreno Carticotrophic Hormone
• ACTH is responsible for the normal size, structure and
vascularity of adrenal cortex.
• It stimulates synthesis, and secretion of glucocorticoid
hormones.
• ACTH mainly acts on zone fasciculata and zona reticularis.
• ACTH can stimulate pigment production by the melanocytes
• ACTH can mobilize fat from depots seen in cushing syndrome.

Follicular stimulating hormone(F.S.H)
• In females:
• development and growth
of graffian follicle. Along
with LH it helps in
maturation of graffian
follicle.
• Stimulate the secretion of
oestrogen from ovary.
• has role in oogenesis.
• In males :
• it stimulates
spermatogenesis

Luteinizing Hormone (L.H)
• in female
• it stimulates ovulation
• It helps in the
formation of corpus
luteum
• Stimulates secretion
of progesterone from
corpus luteum.
• In male :-
• it acts on laydig cells
and stimulate
production of
testosterone..
• Through testosterone
it stimulates
spermatogenesis and
growth of accessory
sex organs

Melanocyte Stimulating Hormone:
• acts on meloncytes and cause dispersal of
   pigment. This darkens the skin. When MSH is
   not present pigment aggregate and lighten the
   skin.
• Function: It may play a role in the response of
   skin to sun light.
• It may have role in pathological pigmentation as
   in addison's disease. In hypopituitarism skin is
   pale due to lack of M.S.H.

The Hormones Of The Posterior
Pituitary (Neurohypophysis)
Its hormones are two in number
• 1) Antidiuretic hormone (ADH)
• Function of ADH is to conserve body
water, when the body is
threatened with dehydration, it also has
some vasoconstrictor action.

2) Oxytocin:
To cause contraction of the uterine
muscle, to cause contraction of the
myoepithelial cells of the matured female
breast, so that milk ejection occurs.

• Regarding uterine contraction oxytocine
causes uterine contraction during labor,
this helps in the delivery of the fetus.

Thyroid gland
• Regulates metabolism and blood calcium
   levels.
• On skeletal system. Thyroxine is
required
   for the growth and maturation of
   epiphyseal cartilage so that in the absence
   of this hormone, linear skeletal growth
   does not occur.

• Excess thyroxine causes osteoporosis
because of calcium drainage from the
bone.

Parathormone
• Regulates the use of calcium and phosphorus.
• They act as a check on thyroid gland.
• These glands are important organs in calcium
metabolism and play a leading role in the
calcification of teeth.
• The parathyroids are important in regulating the
blood calcium level but have little or no direct
effect on growth or tooth eruption.

•Adrenal cortex secretes androgens
("male" hormones), and aldosterone,
which helps maintain the body's salt and
potassium balances.
• Adrenal medulla
epinephrine (adrenaline) and
norepinephrine (noradrenaline) which are
involved in "fight or flight" responses.

Pancreas
• Secretes insulin and glucagon,
• Islets of langerhans in the pancreas are
the structure which secrete hormones.
These are collections of cells present
through out the gland


• Four type of cells are present in the gland.
• 1) Alpha cells Alpha cells secrete
glucagon which mobilizes glucose, fatty
acid and aminoacids and is called
catabolic hormones.

• Beta cells secrete insulin which increases
the storage of glucose, fatty acids and
aminoacids and is called anabolic
hormones.

• D' cells create somatostatin which may
play a role in regulation of secretions of
insulin and glucogen.

The classified hormones of pancreas as :
1. Insulin.
2. Glucogon.
3. Gastrin.
4. Pancreatic.

Fucntion of Glucagon
1. It is largely viewed as an anti insulin
hormone.
2. Its major action is to raise blood sugar
level.
3. Glucagon enhances liver glycogenolysis
(glycogen of the liver is converted into
glucose and released into the blood).

4. It enhances gluconeogenesis.
5. It is also known has hyperglycaemic
glycogenolytic factor.
6. Glucagon is also involved in lipid
metabolism.

7. It cause a reduction both in volume of
gastric juice and its hydrochloric acid in
contents.
8. Glucagon degradation takes place in liver
and kidney.

Insulin
Insulin is hypoglycemic antidiabetic factor and
the protein hormone which regulates
the blood glucose.
• Function
1. On cell membrane permeability.
2. Action on metabolism (carbohydrate, protein,
fat, mineral and nuclieic acids).

• Actions On Cells Membrane Permeability
• Insulin promotes the entry of glucose into all
cells of the body except the cells of liver, brain
and RBC.
• It is much more important in skeletal muscle and
in adipose tissue.
• It also promotes entry of aminoacids and fatty
acids into the cells.
• Entry of potassium inside the cell is facilitated
by insulin.

• Insulin inhibits neoglycogensis (synthesis
of glucose from sources other than
carbohydrate) this action causes reduction
of blood sugar level.
• Insulin promotes glycogenesis, the two
major sides of glycogenesis are liver and
the muscles.

• Blood sugar level falls as a result.
• It enhances peripheral utilization of
glucose causing blood sugar level to fall.

Fat
• Insulin promotes lipogenesis.
• may inhibits lipolysis thus a diabetic
patients on receiving insulin begins to put
on fat in his adipose tissue.
• Insulin inhibits formation of ketone bodies.

• Protein
Insulin promotes protein synthesis.
It also facilitates action of several
enzymes e.g. hexokinase.
• Nucleic acids
• Insulin promotes synthesis ofDNA and
RNA.

Suprarenal Glands (Adrenal
glands)
• Consists of two glands :
• 1 Outer suprarenal or (adrenal) cortex.
• 2 Inner supra renal medulla.
• Cortex secrets steroid hormones called
adreno cortico steroids or corticoids.
• While medulla secrets catecholamines.

• The hormones of the adrenal cortex are
divided into 3 groups.
• 1 ) Minerals cortico steroids (eg)
aldosterone.
• 2 ) Glucocorticosteroids (eg) adrenal
corticoids
• 3 ) Sex hormones (eg) progesterone
oestrogen.

• Minerals cortico steroids (eg) aldosterone.
keeps body fluids in balance
• Glucocorticosteroids (eg) adrenal corticoids
Regulates metabolism and carbohydrates
• Sex hormones
Regulate devolopment of sexual traits.

Hormonesof adrenal medulla
• Epinephrine increases heart rate and
blood sugar
• Nor epinephrineraises raises blood
pressure

• Ovaries release estrogen which makes hips
widens and breast enlarge and progestrone
which prepares the body for pregnancy.
• Testicles secrete hormones that influence
male characteristics, respectively.

From this overview of the endocrine
system, it is clear that most of the
metabolic functions of the body are
controlled one way or another by the
endocrine glands.

For instance,
• without growth hormone, the person remains a dwarf.
• Without thyroxine and triidothyronine from the thyroid
gland, almost all the chemical reactions of the body
become sluggish, and the person becomes sluggish as
well.
• Without insulin from the pancreas, the body's cells can
utilize very little of the food carbohydrates for energy.
• And without the sex hormones, sexual development and
sexual functions are absent

• the increasing level of the sex hormones
also causes other physiologic changes
including the acceleration in general body
growth and shrinkage of lymphoid tissues
seen in the classic growth curves.

MODE OF ACTION
(where & how they act)

• If we liken a hormone to a radio signal,
then a receptor is the antenna. Without
the antenna, no signal would be received
and no music would exit the radio.

TYPES OF ENDOCRINE DISORDERS

TYPES OF ENDOCRINE DISORDERS
HORMONE DEFICIENCY
HORMONE EXCESS
DECREASED RESPOSIVENESS OF RECEPTORS

• Disturbances of endocrine function can
usually be divided into
1. hyperfunction and hypofunction
2. primary or
secondary dysfunction.

• Hypofunction can be caused by:
• Congenital defects
• Destruction of a gland,
• Aging,
• Inactive hormones:

• Hyperfunction can be caused by:
• Excessive stimulation of a gland,
• Hyperplasia of a gland;
• Hormone producing tumours of the gland
– sometimes ectopic tumours will produce
hormones.

PITUTARY MALFUNCTIONS
The two extremes of
human stature are
giantism and
dwarfism.

Gigantism:-
• It is due to hyper
secretion of G.H
before the epiphyseal
plates as fused.
The cause is mainly
an acidophil tumour.

• Features:-
1. Stature of the subject will be between 7
to 8 feet this is mainly due to ncrease in
length of lower limbs.
2. Disproportionate growth of long bones.
3. Visceral enlargement is not much.

4. Hyper glycemia is present as G.H is
diabetogenic
a Growth hormone prevents glucose up take.
b Opposes the action of insulin.
c Cause glycogenalysis and gluconeogeneisis,
hence increase in blood
glucose level.
5 .The teeth in gigantism or proportional to the size
of jaws, the roots may be longer than normal.

ACROMEGALY
• There is enlargement of
the soft tissues of the
face, the nose and
puffiness of the lips and
cheeks.
• It is due to hyper
secretion of growth
hormone after the
epiphyseal plates
are fused .

DWARFISM

ACHONDROPLASTIC
DWARF
• Achondroplastic
dwarfism is due to
ab-normal
osteogenesis which
begins early in
intrauterine life as
disturbance of
chondrification and
later of ossification.
• It has no endocrine
basis.

HYPOTHYROIDISM
OR
CRETINISM
• When the condition originates
in fetal life or in early infancy, it
is known as cretinism and has
specific facies.
• Physical growth in cretins is
markedly stunted. The upper
and the lower body segments
show an infantile ratio: upper
1.7 to lower 1.
There is a marked retardation
in appearance of ossification,
and epiphyseal closure is
retarded.

Myxedema
• This is due to deficiency
of thyroid hormones in
adults.
• Cause : Primary
hypothyroidism is adults it
may be due to
• a. Iodine deficiency
• b Secondary
hypothyroidism due to
pituitary failure.

Features:
• 1. Obesity weight gain with
solid non-pittmg oedema,
accumulation of myxomatous
tissue in the skin.
• 2. Puffy face tongue large with
typical periorbital puffmess.
This is also due to infiltration of
these structures with
myxomatous tissue.
• 3. Hoarse ness of voice : due
to infiltration of vocal cords
with myxomatous tissue.

Hyperthyroidism: -
• In this there is increased secretion of
thyroid hormones
• hyper thyroidism may be due to
1. Hyper activity of the gland.
2. Increased secretion ofT.S.H from
pituitary.
3. Follicular carcinoma.
4. Long acting thyroid stimulator (LATS).

• Produces an increase in
the rate of maturation an
increase in the metabolic
rate, and exopthalmic
goiter.
• There is premature
eruption and disturbed
resorption of the roots of
the deciduous teeth in
associated with early
eruption of permanent
teeth.

Hypoparathyroidism
• Hypofunction produces changes in
calcium metabolism. blood calcium may
fall to as low as 7 mg per 100 ml (9 - 11
mg per 100ml is normal).
• Hypoparathyroidism can manifest itself in
the mouth at any stage during tooth
development.

• It can cause delay in tooth eruption and
can effect the morphology of teeth.
• It present when the teeth are developing,
there is delayed eruption and resorption of
the roots of the deciduous teeth and
retarded eruption of the permanent teeth.

• Enamel defects usually follow tetany due
to hypoparthyroidism the teeth have a
white appearance but, later turn
brown through staining.

hyperparathyroidism:
• The parathyroids are concerned with
shifting calcium from the bones to the
blood stream and to excretion.
Hyperparathyroidism produces an
increase in blood calcium which is with
drawn from the bones, while the latter in
turn undergo decalcification.

• There is demineralization of bone in the
form osteitis fibrosa cystica.
• The diaphysis of the bones are involved,
but not the epiphysis as in rickets.

ABNORMALITIES OF
ADRENOCORTICAL SECRETION

hypoadrenalism
• Basically, the disturbances in Addison's
disease are as follows:
• Mineralocorticoid Deficiency.
• Glucocorticoid Deficiency.
• Melanin Pigmentation.

• Lack of aldosterone secretion greatly
decreases sodium reabsorption and
consequently allows sodium ions, chloride
ions, and water to be lost into urine in
great profusion.
• The net result is a greatly decreased
extracellular fluid volume.

• As the extracellular fluid becomes
depleted, the plasma volume falls, the red
blood cell concentration rises markedly,
the cardiac output decreases, and the
patient dies in shock,

• death usually occurring in the untreated
patient 4 days to 2 weeks after complete
cessation of mineralocorticoid secretion.

Glucocorticoid Deficiency.
• Loss of cortisol secretion makes it
impossible for the person with Addison's
disease to maintain normal blood glucose
concentration between meals because he
cannot synthesize significant quantities of
glucose by gluconeogenesis..

• Furthermore, lack of cortisol reduces the
mobilization of both proteins and fats from
the tissues, thereby depressing many
other metabolic functions of the body.
• This sluggishness of energy mobilization
when cortisol is not available is one of the
major detrimental effects of glucocorticoid
lack

• However, even when excess quantities of
glucose and other nutrients are available,
the person's muscles are still weak,
indicating that glucocorticoids are needed
to maintain other metabolic functions of
the tissues in addition to energy
metabolism.

Melanin Pigmentation.
• Another characteristic of most persons
with Addison's disease is melanin
pigmentation of the mucous membranes
and skin

The cause of the melanin deposition is believed to
be the following:
• When cortisol secretion is depressed, the
normal negative feedback to the
hypothalamus and anterior pituitary is also
depressed, therefore allowing tremendous
rates of ACTH secretion as well as
simultaneous secretion of increased
amounts of MSH.

• Probably the tremendous amounts of
ACTH cause most of the pigmenting effect
because these can stimulate formation of
melanin by the melanocytes in the same
way that MSH does.

HYPERADRENALISM
• Hypersecretion of cortisol by the adrenal
cortex causes a complex of hormonal
effects called Cushing's disease,
• this results from either a cortisol-secreting
tumor of one adrenal cortex or general
hyperplasia of both adrenal cortices.

• The hyperplasia in turn is usually caused
by increase secretion of ACTH by the
anterior pituitary
• A special characteristic of Cushing's
disease is mobilization of fat from the
lower part of the body, with concomitant
extra deposition of fat in the thoracic and
upper abdoiminal regions, giving rise to a
so-called "buffalo" torso

edematous appearance
of the face, and the
androgenic potency The
total appearance of the
face is described as a
"moon face,"

Diabetes Mellitus
• Diabetes mellitus is a disorders of
metabolism characterized by high blood
sugar level and excretion of sugar in urine.

– In diabetes a large volume of urine is passed.
– Hyperglycemia,glycosuria,ketosis,acidosis,dia
betic coma, polyuria, weight loss in spite of
polyphagia (increased appetite) and
polydypsia (increased thirst) are the abnormal
characteristics of diabetes.

• Causes Of Diabetes Mellitus
– 1. Due to insulin lack.
• a. Juvenile diabetes has its onset in childhood or
adolescence
• frequently complicated by ketoacidosis. In this beta cell
pathology is common and insulin content of the pancreas is
low.
• b. Maturity onset diabetes is mild, develops late in life and
occurs
– much more frequently in obese persons. Ketoacidosis is
uncommon
– reduction of weight improves glucose tolerance. In this, beta-
cell
– morphology and pancreatic insulin content are normal.

2. Hyperpituitarism - gigantism and acromegaly
(due to hyper secretion of GH).
3. Hyperthyroidism - graves diseases.
4. due to hypersection of adrenal
glucocorticoids.

BREAK

ROLE OF HORMONES IN
ORTHODONTICS
CONTENTS
Growth hormone
Hormones and growth
Bone remodelling
Puberty
Timing of Puberty
Problems related to increased or decreased
hormonal secretions in orthodontics

ZONA GLOMERULOSA
‘Glomerulus’ is in the
kidney
ZONA FASCICULATA
Muscles have ‘Fascicles’
ZONA RETICULARIS
ALDOSTERONE
CORTISOL
ANDROGENS

• Adrenal medulla is a derivative of the
neural crest cell, and secretes adrenalin.
• One of the other derivatives of the neural
crest cells is the autonomic ganglia (ANS).

• It should be noted that this is one of the
very few hormones that act on neural
tissues.
• It is probably related to the fact that the
hormone acts on the cells that are derived
from similar origin.

Enzymes:
• Enzymes: a protein produced by living
cells that catalyses chemical reactions in
organic matter. Most enzymes are
produced in minute quantities and
catalyze reactions that take place within
the cells.
• Some enzymes are produced in large
quantities and their area of action is
outside the cell. For example: digestive
enzymes.

Hormones:
• Hormones: a complex chemical substance
produced in one part or organ of the body
that initiates or regulates the activity of an
organ or a group of cells in another part of
the body.

“SECOND MESSENGER”
SYSTEM
• All cells have signalling systems that
convert the external stimuli such as
hormones or mechanical forces into
internal signals known as second
messengers.
• cAMP as the second messenger is well
known and widely accepted.

Calcium Ions and ‘Calmodulin’
• Another second messenger operates in
response to the entry of calcium ions into
the cell.
• The calcium entry may be initiated by
 Change in membrane electric potential
 Hormones interacting with membrane
receptors

• On entering the cell the calcium binds with
calmodulin.
• This brings about a cascade of events
within the cell similar to the cAMP

Membrane Phospholipid Breakdown
Products
• Some hormones activate transmembrane
receptors that they become activated
enzyme phospholipase c.
• This enzyme causes some of the
phospholipids in the cell membrane itself
to split into smaller substances that have
widespread ‘second messenger’
intracellular effect.

• The type of hormones that bring about this
effect are the ‘local hormones’, most
notably the hormonal factors.
• The most important products that serve as
second messengers are
 inositol triphosphate (IP3) and
 diacyglycerol

• The IP3 especially mobilizes the calcium
from the mitochondria and the
endoplasmic reticulum , and the calcium
ions bring about their own second
messenger effect.

• The diacylglycerol activates the enzyme
protein kinase C.
• This activation is further enhanced by the
increased calcium ions that have been
released in response to the IP3.
• The activated protein kinase C has an
especially important role in promoting cell
division proliferation.

BONE REMODELLING
• Bone is a highly dynamic connective
tissue with a capacity for continuous
remodelling.
• It is composed of a variety of cell types
and and extracellular organic matrix that
has become mineralised.

• The two principal cell types ,
• the osteoblast and the osteoclast, are the
major effectors of bone turnover or
remodelling i.e. resorption and deposition.

Bone resorbing factors
Systemic factors
• Parathyroid hormone
• Parathyroid related peptide
• Vitamin D,
(1,25 dihydroxycholecalciferol)
• Thyroid hormone

Local factors
Prostanoids
Lipoxygenase metabolites
Cytokines:
Interleukin-1 alpha
Interleukin-1 beta
Tumour necrosis factor alpha
(cachectin)
Tumour necrosis factor beta C
(lymphotoxin)
Interleukin 6

Growth factors
• Epidermal growth factor
• Transforming growth factor alpha
• Transforming growth factor beta
• Platelet-derived growth factor

Bacterial factors
• Lipopo Saccharide
• MuramyI dipeptides
• Capsular material
• Peptidoglycans
• Lipoteichoic acids

The mediators of bone remodelling
• Parathyroid hormone secreted by the four
parathyroid glands.
• Physiological concentrations appear to
promote bone formation and increase the
distal tubular reabsorption of calcium by
the kidney,

• Increased concentrations promote
osteoclastic bone resorption.
• PTH can also indirectly increase the
absorption of calcium by the gut, through
the stimulation of 1,25-dihydroxyvitamin
D3 synthesis in the kidneys-)

The vitamin D metabolites
• The vitamin D metaboliies,are steroid like
compounds which are derived from the
plant ergosterol, fish oils and ingested in
the diet, or synthesised in the skin by
exposure of epidermal cells to ultraviolet
light.

• It's effect on bone resorption appears to
be by the differentiation of committed
progenitor cells into mature cells.

• Cytokines are defined as short range
soluble mediators,released from cells
which modulate the activity of other cells.
• The first ones identified were non-antibody
mediators of cellular immunity produced
by lymphocytes and called lymphokines

• It was thought that lymphocytes were the
only cells that could produce such factors,
hence the term lymphokines. It is now
known that many different cell types can
produce these molecules, and the term
cytokine is more appropriate.

• Several of these cytokines are potent mediators
of bone metabolism
Interleukin-1 alpha
Interleukin-1 beta
Tumour necrosis factor alpha
(cachectin)
Tumour necrosis factor beta C
(lymphotoxin)
Interleukin 6

IL-1.does not have a direct action on the
osteoclast, but like PTH acts via the
osteoblast.

Eicosanoids
• The products of the lipoxygenase and
cyclooxygenase pathways are colletively
referred to as eicosanoids.

Prostaglandins
• They were first discovered by Von Euler
in 1934.The compound was isolated from
human semen and it was believed at the
time that the prostate gland was the major
source.

Prostaglandins
• It is now known that prostaglandins are
produced by nearly all tissues, but the
name has been retained. Similarly,
leukotrienes which are also metabolites of
arachidonic acid, were originally
demonstrated in leukocytes and were
called leukotrienes.

Cell membrane
phospholipids
Mechanical stimuli
Phospholipase A2
Arachidonic acid
Prostaglandins
(PGE2,PGI2,Thromboxane) leukotrines
5 lipoxigenase
5-Lo inhibitors
asprin
cycloxygenase
corticosteroids
ARACHIDONIC ACID METABOLISM

Growth Factors
The TGFs are a family of polypeptides with
biological properties similar to those of
epidermal growth factors (EGF).
Two major classes of TGF have been
identified, TGF alpha and TGF beta.

• The TGFs have been shown to be potent
bone resorbing factors
• TGF alpha is produced by many tumours,
especially solid tumours associated with
hypercalcaemia (squamous cell
carcinoma of lung, oral cavity, kidney and
breast)

Inhibitors of bone resorption
CALCITONIN-
acts directly on osteoclasts
GLUCOCORTICOIDS –
inhibits eiconosoids synthesis
BISPHOSPHONATES-
inhibits osteoclastic bone resorption
probably by making the mineralised surface
inaccessible to the cell by binding to the
hydroxyapatite crystals .

Inhibitors of bone resorption
• TGF –beta –inhibits osteoclast formation
and differentiation
• INTERLEUKIN-1RECEPTOR
ANTAGONIST: Binds to IL1 receptors
effective against TNF as well

calcitonin
• Calcitonin is synthesised by C cells in the
thyroid .
• It inhibits osteoclastic bone resorption
rapidly and effectively.
• However, this effect is only transient.
Showed that calcitonin inhibited
parathyroid hormone mediated bone
resorption only for the first 3 days of
culture.

calcitonin
• Calcitonin has no major effects on bone
formation, vitamin D metabolism or
absorption of calcium from the gut.
• Other factors inhibiting bone resorption
include the corticosteroids, interferon
gamma (IFN gamma) and various
pharmacological inhibitors such as the
bisphosphonates.

BONE REMODELLING (COUPLING)
• The initial events involve the synthesis and release of
matrix metalloproteinases (MMPs) by osteoblasts which
are responsible for degrading the osteoid, exposing the
• "'meralized matrix which maybe chemotactic to the
osteoclast.

BONE REMODELLING (COUPLING)
• The osteoblast also directly stimulates osleoclast activity.
• During the resorption process growth factors are
released released from the matrix which then activate
osleoprogenitor cells. The osteopiogenitor cells mature
into osteoblasts and ultimately replace the resorbed
bone.

BONE REMODELLING (COUPLING
• The mechanism by which osteoblasts are directed to
form bone only in the resorption lacunae may be due to
the presence of molecules such as
• TGF- B & BMPs which are left behind during osteoclastic
activity. Osteocytes communicpte with one another via
intercellular processes.

• What is Growth Hormone?
Growth hormone is a protein hormone
secreted by the pituitary (master gland
which promotes linear growth).

• Why is growth hormone necessary?
Growth hormone is a natural hormone of
the body which is necessary for normal
linear growth. Growth hormone is
therefore indicated for the long- term
therapy of children who have growth
failure due to inadequate growth hormone
secretion.

Hormones and growth

Hormones and growth
• An understanding of endocrinology
enables us to grasp better factors
underlying the changes which occur
during growth and development.
• More specifically we understand the
changes occurring during adolescence,
which is the period when functional
appliances are most commonly used.

• GH causes growth, of the collagenous
tissue, muscles and cartilage.
• As a result-of the GH action, the muscles
grow in bulk as well as the bone formation
is increased,

Stimulation of cartilage and bone
growth
• Although growth hormone stimulates
increased deposition of proteins, and
increased growth in almost all tissues of
the body, its most obvious effect is to
increase growth of the skeletal frame.
• This results from multiple effects of growth
hormone on bone including :

• increased deposition of protein by the
chondrocytic and osteogenic cells that
cause bone growth.
• increased rate of reproduction of these
cells as well as and
• specific effect of converting
chondrocytes into osteogenic cells thus
causing specific deposition of new bone.

• However, before the union of
epiphyseal cartilage , presence of growth
hormone increases the longitudinal length
of the bone.
• after the union of the epiphysis, there
can be no further growth in length. If the
growth hormone is now present in excess
peripheral bone increase in girth

REGULATION OF GROWTH
HORMONE SECRETION
• For many years it was believed that
growth hormone was secreted primarily
during the period of growth but then
disappeared from the blood at
adolescence.

• How ever this has proved not to be true ,
because after adolescence , secretion
decreases only slowly with aging ,finally
falling to about 25 per cent of the
adolescent level in very old age.

INSULIN LIKE GROWTH
FACTOR
IGF I and IGF II, also called somatomedins
are produced in the liver only after growth
hormone (GH) stimulation are necessary for
growth hormone to promote growth.

In cartilages, the mode of
action of GH is as follows :
GH acts on
the cartilage
cells
cartilage cells alter and now
become responsive to the SMs
SMs actsgrowth of
cartilages
(hence growth in
height etc ) results

• termination of normal growth is imperfectly
understood.
but may involve a fall in hormone
production of the sensitivity of
chondroblast to insulin like growth factors
amongst others.

TESTOSTERONE
• interstial cells of leydig in the testis carry
out secretions of testosterone .

Testosterone effect on bone
growth and calcium retention
• Following puberty or following prolonged
secretion of testosterone, the bones
grow considerably in thickness and also
deposit considerable additional calcium
salts.

• Thus, testosterone increases the total
quantity of bone matrix, and it also causes
calcium retention. The increase in bone
matrix is believed to result from the
general protein anabolic function of
testosterone, and the deposition of
calcium salts of result secondarily to the
increased bone matrix

• When great quantities of testosterone (or
any other androgen) are secreted in the
growing child, the rate of bone growth
increases markedly, causing a spurt in
total body height as well.

• However, the testosterone also causes the
epiphyses of the long bones to unite with
the shafts of the bones at an early age in
life.

Therefore, despite the rapidity of growth
this early uniting of the epiphyses prevents
the person from growing as tall as he would
have grown had testosterone not been
secreted at all

Effect of STH , testosterone
on jaws
• if the blood level of STH or testosterone
increases, the supplementary lengthening
of the mandible is relatively greater than
the supplementary lengthening of the
maxilla.

Estrogen
• estrogens cause increased osteoblastic
activity. Therefore,
• at puberty when the female enters her
reproductive years her growth rate
becomes rapid for several years.

• however estrogens have another potent
effect on skeletal growth - that is,
• they cause early uniting of the epiphyses
with the shafts of the long bones. This
effect is much stronger in the female than
is a similar effect of testosterone in the
male.

• After puberty soft tissue growth occurs i.e
we can see the growth of the nose .
• As the soft tissue grows the bone also
grows along with it.

Upper jaw growth control by STH
Apposition
al growth
of
premaxilla
ry
extremitie
s
Gr of
premaxill
omaxillar
y suture
Gr of
maxxilo
palatine
suture
Forward traction of
septomaxillary
ligament
Forward traction of
the labionariary
muscles
Forward
growth of
the septal
cartilage
P.A shift of the
premaxillary
bones
Protru
sion of
incisor
s
incre
asedt
ongue
volum
e
SOMATOMEDINS
Growth in
length of
upper jaw

UPPER JAW GROWTH CONTROL
BY STH
GR in
width
of
upper
jaw
Gr of
interpre
maxillar
y suture
Gr of
mid
palatal
suture
Outw-ard
appositio
nal
growth
TR seperation
of
Pre max
bones
TR separation
Max &of
horizontal
maxillary &
Palitine bones.
Outward
shift of of
upper
border&upp
er molars
Outward shift
of
Alv border
&upper molars
groupsOutward
GR OF 2
max
bones
Outwar
d GR
of later
mass
of
ethmod
GR of
caftilage
between
greater
wing
and
body of
sphenoi
STH

Growth hormone
Septal cartilage
growth
Forward growth of maxilla
Sagital position of the mandible
Growth
of
condylar
cartiage

• Note : there is no negative feed back of
excessive mandibular growth on growth
hormone secretion.
• This has been termed as “OPEN LOOP”
by petrovic.
• This is the reason why even though you
have excessive mandibular growth in
acromegaly GH secretion continues in the
same excessive manner .

CASE OF ACROMEGALY

BASIC SHAPES OF SELLA
TURSICA

Puberty
• Adolescence is a
sexual phenomena.
It can be defined as
the period of life when
sexual maturity is
attained .

• more specifically, it is the transitional period
between the juvenile stage and adult hood
during which the secondary sexual
characteristics appear, the adolescent growth
spurt takes place , fertility is attained and
profound physiologic changes occur .
• All these developments are associated with
accompanying surge in secretion of sex
hormones.

• This period is particularly important in
dental and orthodontic treatment,
because the physical changes at
adolesense significantly affect the face
and dentition.

Major events in dentofacial development
that occur during adolescence include
• the exchange from the mixed to
permanent dentition,
• acceleration in overall rate of facial growth
• Differential growth of the jaws

under the stimulation of the
pituitary ,gonadotropin,
sex hormones from the
testes,ovaries and adrenal
cortex are released into
blood stream in quantities
sufficient to cause
development of secondary
sexual characteristics and
accelerated growth of the
genitalia .
GnRH
TESTIS GONADAL
SEX
HORMONE

• Neural growth is unaffected by the events
of adolescence, since it is essentially
complete by age 6. the changes in growth
curves of jaws, general body, lymphoid
and genital tissues, how ever, can be
considered the result of the hormonal
changes that accompany sexual maturity

TIMING OF PUBERTY
• There is a great deal of individual
variation, but puberty and the adolescent
growth spurt occur on the average nearly
2 years earlier in girls than in boys.
• Why this occurs ?

• but the phenomenon has an important
impact on the timing of orthodontic
treatment, which must be done earlier in
girls than in boys to take advantage of the
adolescent growth spurt..

• Because of the considerable individual
variation, early maturing boys will reach
puberty ahead of slow maturing girls, and
it must be remembered that chronologic
age has very little to do with where an
individual stands developmentally

• The stage of development of secondary
sexual characteristics provides a
physiologic calendar of adolescence that
correlates with the individual's physical
growth status. Not all the secondary
sexual characteristics are readily visible,
of course, but most can be evaluated in a
normal fully clothed examination, such as
would occur in the dental office

• The timing of puberty makes an important
difference in ultimate body size; in a way
seem paradoxical at first: the earlier the
onset of puberty, the smaller the adults
size, and vice versa.

• Growth in height depends
on endochondral bone
growth at the epiphyseal
plates of the long bones,
and the impact of the sex
hormones on
endochondral bone
growth is two fold.
• First, the sex hormones
stimulate the cartilage to
grow faster, and this
produces the adolescent
growth spurt.

• But the sex hormones also increase in
the rate of skeletal maturation, which for
the long bones is the rate at which
cartilage is transformed into bone. The
acceleration in maturation is even greater
than the acceleration in growth. Thus
during the rapid growth at adolescence,
the cartilage is used up faster than it is
replaced.

• Towards the end of adolescence, the last
of the cartilage is transformed into bone,
and the epiphyseal plates close. At that
point, of course, growth potential is lost
and growth stops.

• The stages of adolescent development
described here were correlated with
growth in height.
• Fortunately, growth of the jaws usually
correlates with the physiologic events of
puberty in about the same way as growth
in height.

• There is an adolescent growth spurt in the
length of the mandible, though not nearly
as dramatic a spurt as that in body height
and a modest though discernible increase
in growth at the sutures of the maxilla.

Adolescence in girls
It can be divided into three stages, based
on the extent of sexual development.
• The first stage, which occurs at about the
beginning of the physical growth spurt, is
the appearance of breast buds and early
stages of the development of pubic hair.

The peak velocity for physical growth
occurs about 1 year after the initiation of
stage I, and coincides with stage II of
development of sexual characteristics

• The third stage in girls occurs 1 to
1/6years after stage II and is marked by
the onset of menstruation. By this time,
the growth spurt is all but complete. At this
stage, there is noticeable broadening of
the hips with more adult fat distribution,
and development of the breasts is
complete.

The stages of sexual development in boys
are more difficult to specifically define than
in girls. Puberty begins later and extends
over a longer period—about 5 years
compared with 3 ½ years for girls

Fat spurts
In boys, four stages in development can
be correlated with the curve of general
body growth at adolescence.
The initial sign of sexual maturation in
boys usually is the "fat spurt." The
maturing boy gains weight and becomes
almost chubby, with a somewhat feminine
fat distribution.

This probably occurs because estrogen
production by the Leydig cells in the testes
is stimulated before the more abundant
Sertoli cells begin to produce significant
amounts of testosterone.

• During this stage, boys may appear obese
and somewhat awkward physically. At this
time also, the scrotum begins to increase
in size and may show some increase or
change in pigmentation.

• At stage II, about 1 year after stage I, the
spurt in height is just beginning. At this
stage, there is a redistribution and relative
decrease in subcutaneous fat, pubic hair
begins to appear, and growth of the penis
begins.

• The third stage occurs 8 to 12 months
after stage II and coincides with the peak
velocity in gain in height. At this time,
auxiliary hair appears and facial hair
appears on the upper lip only

• A spurt in muscle growth also occurs, along with
a continued decrease in subcutaneous fat and
an obviously harder and more angular body
form. Pubic hair distribution appears more adult
but has not yet spread to the medial of the
thighs. The penis and scrotum are near adult
size.
• Stage FV for boys, which occurs anywhere from
15 to
• 24 months after stage III, is difficult to pinpoint.

• Stage IV for boys, which occurs anywhere
from 15 to 24 months after stage III, is
difficult to pinpoint. At this time, the spurt
of growth in height ends.
• There is facial hair on the chin as well as
the upper lip, adult distribution and color of
pubic and auxiliary hair, and a further
increase in muscular strength.

Timing of growth hormone release
• Growth hormone is released primarily
during the evening time.
• New bone at the epiphyseal plates occur
during the night time.
• We do not know whether facial growth
follows this pattern or not but it is entirely
possible that it does.

• It becomes important to stress to the
patient to wear head gear right from the
evening time rather than waiting for the
bed time.
• It is more likely that the tooth movement
occur more faster at this period of time.

• Sex hormones have profound effects on
bone. Androgens (testosterone and other
anabolic steroids) build and maintain
musculoskeletal mass. The primary
hypertrophic effect of androgens is to
increase muscle mass.

Hypothyrodism is
• characterized by the presence of one or
more of the following features:
• Retardation in rate of calcium deposition
in bones and teeth.
• Marked delay in tooth bud formation and
eruption of teeth
• Delayed carpel and epiphyseal
calcification

• The deciduous teeth are often over
retained and the permanent teeth are
slow to erupt
• Abnormal root resorption.
• Irregularities in tooth arrangement and
crowding of teeth can occur

Hyperthyroidism :
This condition is characterized by increase
in the rate of maturation, and an increase
in metabolic
rate. The patient exhibits premature'
• eruption of deciduous teeth, disturbed root
resorption of deciduous teeth and early
eruption of permanent teeth.
The patient may have osteoporosis which
contraindicates orthodontic treatment.

Radiographic features
• Lamina dura around
the teeth may be lost
• The radiographs of
the jaws show ground
glass appearance
• Well defined
radiolucency may be
present in the maxilla
and the mandible
•
Shortcut to wahab001.jpg.lnk

Hyperparathyroidism :
• This endocrinal disorder is associated with
changes in calcium metabolism.
• It can cause delay in tooth eruption,
altered tooth morphology,delayed eruption
of deciduous and permanent teeth and
hypoplastic teeth.

Hyperparathyroidism:
• Hyper-parathy-roidism produces increase in
blood calcium.
• There is demineralization of bone and disruption
of trabecular pattern.
In growing children, interruption of tooth
development occurs.
• The teeth may become mobile due to loss of
cortical bone and resorption of the alveolar
process.

Role of Estrogens
• Estrogen, on the other hand, has a direct
effect on bone; it conserves skeletal
calcium by suppressing the activation
frequency of bone remodeling.

• At menopause, enhanced remodeling
activation increases turnover. Because a
slight negative calcium balance is
associated with each remodeling event, a
substantial increase in the turnover rate
can result in rapid bone loss, leading to
symptomatic osteoporosis. Even young
women are susceptible to significant bone
loss

• Bone loss is a common problem in women
who have low body fat and who exercise
intensely (e.g., running, gymnastics' and in
women who are anorexic. It is clear that
estrogen protects the female skeleton
from bone loss during the child bearing
years.

Bisphosphonates
• They act as specific inhibitors of
osteoclast-mediated bone resorption, so it
is not surprising that the bone remodeling
necessary for tooth movement is slower in
patients on this medication.

• If orthodontic treatment were necessary in
an older woman taking one of these agents,
it would be worthwhile to explore with her
physician the possibility of switching to
estrogen, at least temporarily.

Diabetes mellitus
• Susceptible to periodontal breakdown
during orthodontic treatment; decreased
resistance to infection; poor wound
healing.

• Hormones can make and break an
individual .
• Hence neither excess nor deficiency is
good for health.

References
• Salzmann
• Proffitt and White
• Proffitt
• Graber and Vanarsdhall
• Shafer
• Guyton physiology

• Life encyclopaedia
• Gray’s anatomy
• Netter’s atlas
• Chaudari physiology
• Graber, Rakosi, Petrovic
• Moyers

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