SEMINAR

ON
Nutrition and Hormones
 Nutrition:

Food is the basic requirement for all organisms to survive. It is essential not only
from growth and development point of view but also for producing energy to carry
out various body functions.

Nutrition in simple terms can be defined as a science of nourishing the body

properly or analysis of the effect of food on the living organisms.

Yudkin defined it as the relationship between man and his food and implies the
psychological and social as well as the physiological and biochemical aspect .

Others called it as the science devoted to the determination of requirements of the

body for food constituents both qualitatively and quantitatively and to the selection
of food in kinds and in quantity to meet these requirements.

Council of food and nutrition of the American Medical Association

Defines nutrition as-

“The science of food, the nutrients and other substances therein ,their
action ,interaction and balance in relation to health and diseases and the processes by
which the organism ingest, digest, absorbs, transports, utilizes and excretes food
substances”

Four basic functions of the nutrients are –

-To supply energy

-To promote growth.

-Repair of the body tissues.

-Regulate body processes.

Nutrients can be broadly classified as-

-Carbohydrates

-Fat\lipid

-Proteins

-Minerals

-Vitamins

-Water

Carbohydrates:

Energy yielding nutrients, is the largest single component, aside from water, of most
diets

Almost nothing is known of the effect of carbohydrate deficient diet on the oral
cavity.
Composed of carbon, hydrogen and oxygen. The ratio of hydrogen to oxygen in all
carbohydrates is 2:1, which is similar to water, and hence they are called
carbohydrates.

Sources of carbohydrates includes

- Rice - sweet potato

-Wheat - honey

-Bajra - jaggery

-Pulses -vegetables

Functions of carbohydrate-

It is the main source of energy. On oxidation one gram of carbohydrate gives rise to
four kilocalories of energy. All this is used up by the body for carrying out various
functions.

Classified as-

 Monosaccharides- these are the simplest structural unit of carbohydrates.

They form the chemical building blocks from which one or more complex
carbohydrates are built –eg glucose, fructose, and galactose.

 Disaccharides-They are composed of two or more monosaccharide units-and

form about 35% of the dietary carbohydrates eg sucrose(cane sugar) ,
lactose(milk sugar) ,maltose
  Polysaccharides-these are the more complex structures and are composed of
many molecules of monosaccharide eg –starch, glycogen ,cellulose

Digestion-

Digestion of carbohydrates starts in the mouth; this is brought about by the enzyme
called salivary amylase. The action of this enzyme continues as the food passes from
the mouth to the stomach and finally reaches the small intestines, which is the main
site of carbohydrate digestion

Mouth – salivary amylase

Stomach

Small Intestine

In the small intestine disaccharides are broken down into monosaccharides by

specific enzymes-

Sucrose is acted upon by Invertase to give rise to - glucose and fructose.

Maltose is acted upon by Maltase to give rise to - glucose and glucose.

Lactose is acted upon by Lactase to give rise to - glucose and galactose

Hence the overall product of digestion of carbohydrates is glucose.

Absorption-

All the carbohydrates are reduces to there basic structure that is monosaccharides
and it is mainly absorbed in the small intestines.

Storage

End product of carbohydrate metabolism is glucose and this I is converted into

glycogen and is stored in the liver and the muscles. When carbohydrates is supplied
in the diet and monosaccharides are absorbed beyond the bodies immediate need for
energy and its capacity to store glycogen, they are converted into fats as human body
has unlimited capacity to store fat.

Summary of carbohydrate metabolism-

-It is metabolized and oxidized immediately as a source of energy.

-Converted into glycogen and stored in liver and muscles

-When in excess it is converted into fat and stored in regular body cells and as
adipose tissue.

Deficiency of carbohydrates-

Almost nothing is known of the effect of carbohydrate deficient diet on the oral
cavity.
There is a group of disease, which represents a primary genetically determined
disturbance of the mucopolysaccharide metabolism. Rare disorder and is
characterized by the following features-

Hurler syndrome-

-Head appears large with prominent forehead and puffy eyelids

-Nasal congestion with noisy breathing

-Shortening and broadening of the mandible with wide intergonial distance

- Increased arch length from ramus to ramus

- Dentition-small and misshaped teeth.

-Soft tissue –gingival hyperplasia.

Lipids

Like carbohydrates, lipids are also composed of 3 elements that are carbon hydrogen
and oxygen. It differs from carbohydrate, that they have lower ratio of oxygen to
carbon and hydrogen. This means that less of carbon and hydrogen is oxidized in the
fat molecule and therefore there is a greater potential for the release of energy when
these elements are oxidized within the body cell.

Basic structure of a fat –consists of molecule of glycerol to 1 to 3 fatty acids

molecules are attached.
They are Classified depending on the degree of saturation of the fatty acid present
into two types –

-Saturated fatty acids

-Unsaturated fatty acids

Sources –

-Fruits -egg yolk

-Vegetables -butter

- Milk - ghee

-Meat -cereals

-fish

Physical properties –

-Insoluble in water and soluble in organic solvents like ether and chloroform.

- Less dense than water and will rise to the surface of any aqueous mixture.

-Not affected by temperature unless they are heated to a very high temperature.
Digestion-

Unlike carbohydrates digestion of the fats begins in the stomach. Whereas some
naturally occurring emulsified fat such as egg yolk may be broken into fatty acids
and glycerol .However larger particles of the unemulsified fat which are found in
meat, butter are not digested here.

Stomach- naturally occurring emulsified fat

Small intestine-bile is secreted emulsification.

In the small intestines bile is secreted by the gall bladder which acts on the
larger fat molecule to break them into smaller fat particles –this process is
called as emulsification.

This result in-

-Decrease in the surface tension.

-Increase in the surface area.

-Decrease distance through which the enzyme must penetrate

-Decrease coalescing of the fat molecules.

Once they are in a finely divided form they are acted upon by pancreatic lipase and
intestinal lipase. Fat molecules are splitted by the enzyme by the process of
hydrolysis.

Pancreatic lipase and intestinal lipase act on the fat molecules -

Triglycerides

Diglycerides

Monoglycerides

Complete separation –fatty acids and glycerol

Absorption

Digested and divided molecules are taken up from the GIT as separate molecules of
fatty acids and glycerol.

30%-free fatty combine with bile salts which facilitate their release into intestinal
cells from which they are inturn released into the lymph and the portal system.

70%-of the absorbed fat is resynthesised immediately to form triglycerides which

are released into the lymph and they are transported as microscopic fat particles
called as chylomicrons which in turn are transported in through blood because they
are more soluble.
Both fatty acids and glycerol are metabolized immediately as a source of
energy .glycerol and fatty acids combine to form fat which is stored as a reserve of
energy. Glycerol is converted into glucose and then is metabolized in the same way
as the source of energy.

Functions of lipids-

-Act as a source of energy –one gram of fat gives rise to nine kilo calories of energy,
which is two and a half more times than that of carbohydrates.

-Satiety value-fats tend to leave the stomach relatively slow, being released
approximately three and a half hour after ingestion. This delay in emptying time of
the stomach helps to delay the onset of hunger and contributes to feeling of satiety
after meals.

-They act as the carrier of the fat soluble vitamins-Vit A, D, E, K .elimination of fats
from diet leads to a reduces intake of these nutrients.

-They also act as the sources of essential fatty acids-which can not be produced in
the body.

Disturbances in the lipid metabolism

These are very rare disorders, but they do occur as autosomal recessive traits -
Gauchers disease, Neimann Pick disease

Proteins

The term protein means “to take first place”. Mudler ,a Dutch Chemist in 1883
attributed it to a nitrogen containing constituent of the food that he believed to be of
prime importance in the functioning of the body and without which life is
impossible.

Half of the dry weight of the body and 20% of the total adult weight is made up of
proteins.

In the absence of proteins there is a failure in the body growth, followed by a loss of
already established body fluid. Proteins are the part of every enzyme, and many more
hormones vital in regulation of the body processes.

If energy intake is adequate when the needs for growth and repair of tissues have
been met any remaining protein is used as a source of energy.

Chemical composition

Proteins are extremely complex substances made up of many amino acids together in
along chain, there are 20 different naturally occurring amino acid that have been
identified as the building blocks for body protein.

Sources

-Wheat - peanut butter

-Milk - peas

-Egg white -cottage cheese

-Legume -rice

-Boiled ham -oatmeal

They are Classified depending on functional point of view-

Essential amino acids-non dispensable

Non essential amino acids-dispensable

Based on the amino acids content-

Complete –that contain all essential amino acids in proportions which are promoting
growth .When they are the sole source of promoting growth. They are made up of
33%of essential and 66% of non essential amino acids.

Incomplete/poor quality/proteins with low biologic value-these proteins lack one

or more essential amino acids and hence are unable to provide all amino acids for
synthesis of body proteins. They constitute 25% of essential amino acids .when they
are the sole source of proteins in the diet, no new tissues can be formed nor can worn
out tissues be replaced.

Digestion

With the exception of egg white, most protein of the food occurs attached to another
substance or surrounded by fat or carbohydrate from which it must be separated
before it can be digested.

Like all the other nutrients, before it is absorbed it must be broken down into
simplest structural blocks i.e. constituents of the amino acids.

No proteins splitting enzyme is present in the saliva, so first attack on the proteins
occurs in the stomach.
In the stomach, in the presence of the acidic medium gastric peptase (pepsin) acts on
to the specific linkage and the chains are reduced to shorter units of amino acids i.e.
peptones and peptides.

As the food passes from the stomach to the small intestines acid is neutralized and
the mixture becomes slightly alkaline. Pancreatic enzymes then become active in this
medium.

30 % of the proteins are released as amino acids which are-absorbed directly 70%-
consist of chain of two or three amino acids i.e. carboxy peptidase and amino
peptidase. These are acted upon by dipeptidase which converts them into amino
acids.

Absorption

The end product of protein digestion is amino acid which enters the blood stream
from where it goes into the portal circulation and finally reaches the tissues and the
cells of the body.

Functions of proteins

-Essential for growth-for growth to occur, amino acids must be present in

amounts over and above the body requirements i.e. hair ,skin ,nails. Some amino
acids are needed for replacing for the tissues such as lining of the intestines
which are renewed everyday.

-Formation of essential body compounds-like hormones such as insulin

adrenaline, thyroxine. All the enzymes are made up of proteins.
 -Regulation of the water balance-they act as buffers molecule and help in
maintaining the PH of the plasma, and water balance in the CSF and interstitial
secretions.

-Transport of nutrients in the form of lipoproteins.

-Protective role- brings about stimulation of the antibodies which have the ability
to combact infections.

Deficiency of proteins

The inadequate consumption of protein and energy as a result of primary dietary

deficiency conditioned deficiency may cause loss of body mass and adipose
tissue, resulting in protein energy malnutrition-

- Kwashiorkor

- Marasmus

Kwashiorkor –

Definition - protein deficiency with sufficient calorie intake.

Age-6 months and 3yrs

Features -growth failure

-wasting of muscles

- Edema
 -enlarged fatty liver

-serum protein low

- Flag sign

Marasmus-

Definition –starvation in infants with an overall lack of calorie.

Age-infants under 1 yr of age

Features- wasting of all tissues

-no edema

-no hepatic enlargement

 -monkey like face

Vitamins

Defined as organic substances not made by the body, which is soluble in either
fat or water and ordinarily is needed in only minute quantities to act in a variety
of metabolic reactions.

Classified as-

Water soluble-vit B and C

Fat soluble-vit A, D, E and K

Their presence in food is in very low concentration and hence they were easily
overlooked .There concentration varies from few micrograms to as high as
30milligrams.The smallest amount are as important as those needed at the hundred or
thousand times.

Vitamin A

It occurs in three forms

Acidic- retenoic acid

Alcoholic- retinol

Aldehyde- retinaldhyde

Sources –Spinach

- Carrot broccoli
 -Peas cabbage

- Milk cheese

-butter meat, fish

-egg beef

Functions-

-Vision –plays an important role in dark adaptation and vision in dim light. The first
sign of vit A deficiency id night blindness. Growth studies have shown that animals
deprived of vita A cease to grow once the reserves are depleted. This growth failure
may bean indirect result of loss appetite which inturn results in vit A deficiency.

Retenoic acid is in the form in which vit A exerts its effects on growth. bone fails to
grow in length and remodeling process is poorly controlled. defect in growth is
thought to be the result of failure to convert osteoclasts which are cells responsible
for the remodeling process.

Deficiency-night blindness

-keratinzation of cornea

-bitots spots

- xerosis conjunctiva

- xeropthalmia

- complete blindness
 -loss of sense of taste

Effect on the epithelial cells-vit A is concentrated in the differentiating epithelial

cells and in the deficiency state cells fail to differentiate resulting in the sloughing of
the epithelial cells.

Effect on to the dentition-

- Disturbances in differentiation and growth of developing teeth

-Calcification of teeth

-Retardation of eruption

- Disturbances in periodontal tissues.

-Failure to form tooth enamel.

Hypervitamosis –

Administration of high doses of vit A in early pregnancy causes a variety of

malformations in the offsprings.Exact nature of the defect depends on the time of
administration and the dose.

Congenital malformations have recently been associated with the use of retenoic
acid, during pregnancy-

-Malformed ear

-Flat nasal bridge

-Mandibular hypoplasia

-Cranial defects

Vitamin D

Group of compounds collectively called as cholicalceferol.

Source –

Endogenous synthesis-sunlight

Exogenous synthesis-deep sea fish, fish oil, butter, milk.

Since it is produced in the body technically it is a hormone, but if insufficient

amounts are produced in the body it has to be supplied in the diet, in which case it
can called as a vitamin.
It is necessary for all animals with a bony skeleton, since it facilitates absorption and
utilization of calcium and phosphorous for bone formation.

Function-

Maintain normal plasma level of calcium and phosphorus.

It is necessary for all animals with a bony skeleton, since it facilitates absorption and
utilization calcium and phosphorus for bone formation
Deficiency

1. Rickets in growing child

-Craniotabes

-Harrisons sulcus

-Rickets rosary

-Pigeon chest

-Bow legs

-Knock knees

Features of Rickets
2. Osteomalacia –in adults

-osteoid matrix which is laid down fails to mineralize

-vague bony pain

-muscular weakness

-frequent fractures

Effect on to the dentition –

Delayed eruption

Malalignment

Weakening of jaws

Fractures are common.

Vitamin E-

It is also called the anti sterility factor. It is required for normal reproduction in
animals

Sources –

Vegetable oils yellow cornmeal

Wheat bread

Egg butter
Role in human nutrition is poorly understood.

Vitamin K

Basic structures consist of a group called as quinones

Sources-green vegetables

-fruits

Function-it is necessary for the synthesis of prothrombin

Vitamin C

Vitamin C (ascorbic acid)

This cannot be synthesized endogenously and hence human beings are dependent on
its uptake from food

Sources-

Citrus fruits –orange, lemon, grape,

-certain vegetables.

Function-

-Formation of the collagen.-it is required for the hydroxylation of praline into

hydroxyproline
 -Normal formation of dentin-it is one the important constituents of the ground
substance of the dentin.

-Utilization of iron and calcium

Deficiency of Vit C

-Scurvy- Haemorrhagic diasthesis-

This results from the defective collagen synthesis which causes an inadequate
support of the walls of the capillaries and venules resulting in purpura and
ecchymoses of the skin and the mucosa.

There is also loose attachment of the periosteum to the bone resulting in

subperiosteal heamatomas and bleeding in the joint spaces.

Skeletal lesions-includes disturbances in the formation of the osteoid matrix and

not in the metabolism. The epiphyseal end of the growing bone have cartilage cells
which normally undergo periosteal mineralization due to lack of vit C deficiency.
Laying down of the matrix by the ostoeblast is poor and results in the failure of
resorption of the cartilage.

Delayed wound healing-this occurs because of deranged collagen fibres and also
because of localization of the infection.

Teeth and gums.-defect in the tooth mineralization mainly in the dentin and swollen
and red gums which are profusely bleeding
 Vitamin C deficiency

B complex

These consist of a group of essential compounds which are Biochemically

unrelated but occur together in some foods
 Sources-

Green leafy vegetables

Cereals

Yeast,

Liver,

Milk.

Thaimine(B1)

Function- carbohydrate metabolism.

Deficiency-results in group of disorder called as Beri Beri, this is of two types-

Dry beri beri-neuromuscular symptoms weakness,

paresthesia, sensory loss, polyneuritis.

Wet beri beri-cardio vascular involvement

Riboflavin(B2)

Function- required for cellular respiration.

Deficiency- results in

-Ocular lesions

-Cheilosis ,angular stomatitis

 -Glossitis.

-Dermatitis.

Niacin

Function-it is required for the metabolism of fat

Deficiency-Pellagra this is characterized by a triad of –

-Dermatitis

-Diarrhoea.

- Dementia.

Pyridoxine (B6)

Function-exact function not known

Suppose to play a role in fat and protein metabolism

-transmission of neural impulse

Deficiency-dermatitis

-glossitis

-angular stomatitis
 Minerals

These are the group of nutrients which can be divided into two group depending
on the amount they are required by the body-

Macronutrient elements-these include

Calcium and Phosphorus

Potassium and Sodium

Micronutrient elements

Calcium

Inert inorganic element which is associated with bone and tooth formation.It
constitutes 1.5-2.5 wt –of the adult body and 99% of the hard tissue.

Source- Milk and milk products

Green leafy vegetables

Legumes

Citrus fruits

Function –

1. Bone formation –one of the most important constituents of the bone. it is

required for the overall lengthening of the bone by both increase in the size
and diameter and is also required for continuous repair .
 2. Tooth formation-major constituent of the inorganic matrix. It is required for
then normal formation of the dentin and enamel i.e. by hydroxyapatite
crystals. Once then teeth erupt there is no further need for dietary source of
calcium to maintain it.

3. Essential for growth-required for normal growth and development

4. Blood clotting-act as in important factor for the conversion of prothrombin

into thrombin.

Abnormalities of Ca Metabolism –

Osteoporosis-

-Normally seen in middle aged women

- There is decreased density of bone but bony mass is of normal composition

- Shortening stature because of calcium deficiency

- Bone fractures are very common along with low backaches.

Osteomalacia

–Decrease in the mineral content of the calcium but not in the total amount

-Lack of Vit D due to exposure of sunlight and decrease in the calcium content in
the diet
Diagrammatic representation of bone morphology in Calcium deficiency.

Phosphorus

-It constitutes 1% of the total body weight and is major constituent of bone and teeth.

- Regulates the release of energy in the form of ATP and also controlled release of
energy from combustion and oxidation of fat, carbohydrates and proteins.

Clinical Implications

Role of various nutrition deficiencies and its role in dentofacial growth

Nutrition and Skeletal Maturation

Various studies have shown that “prolonged nutritive failure in growing child
result in retardation of bone growth centers in the hand and wrist radiographs”.
Malformations and prenatal deficiencies-

Dietary intake of the expectant mother is directly related to the condition of the
infant at birth.

Warkany –showed riboflavin deficiency may act as one of the predisposing factor in
the development of cleft palate, shortening of mandible

Evans ,Nelson-showed acute folic acid deficiency results in more chances of

developing a cleft palate.

Role of fluorides-

Anticariogenic factor- helps by forming fluorapatite crystals which are resistant to

bacterial attack and hence help in the prevention of caries.

Long continued exposure to excessive amounts may result

–Dental fluorosis-which may be localized to few teeth or the entire dentition and
varies in severity depending upon the amount and the time of fluoride intake.

- Skeletal fluorosis-it a more severe form which is seen with very high levels of
fluoride intake usually because of endemic areas with high fluoride concentration in
water. There is a generalized deformity in all the bones which are very weak and
prone to fracture.

-Increased density of various bones.

-Increased calcification of ligaments, tendons and vague pain in small joints of

the hands and feet
 -In the most severest form –stiffening of the spine virtually making the patient
immobile.

Nutrition and malocclusion-

This results from various nutrient deficiencies, which have been already covered

-Abnormal bone growth

-Loss of teeth.

-Severe caries.

-Periodontal breakdown.

Vitamins in relation to growth and dentition-

Vitamin A-

-Causes disturbances in differentiation and positional growth of the developing

teeth.

-Defective calcification.

-Retardation of eruption.

-disturbances of periodontal tissues

Vitamin B-

-Loss of apatite.

-Disturbed digestion.

-Retardation of growth

Vitamin C

-Disturbed calcification of teeth.

-Retarded eruption.

-Thickened jawbones.

-Narrow maxilla.

-Short mandible.

-High vault palate.

Role of nutrition on the periodontium-response to tooth movement

Physical nature of the food-

Experiments on various animals have shown that soft diet results in the increase
incidence of plaque and calculus formation, all of which act as a local factor for
periodontal disease.
In contrast to this fibrous food stimulates the salivary flow which aids in the oral
clearance of the food debris. It also helps in maintaining the integrity of the
periodontal apparatus by keeping it intact by stimulating effect of under the forces of
mastication.

Vitamin deficiency

Vitamin C deficiency as described earlier results in scurvy, which is characterized

by bleeding and swollen gums. All this result in poor periodontal support.

Vitamin A deficiency predisposes to periodontal diseases. There is disturbance in

the keratinization of the epithelium and gingival hyperplasia and inflammation.

Vitamin B deficiency causes gingivitis, glossitis, glossodynia and inflammation of

the oral mucosa.

Vitamin D deficiency results in the osteoporosis of the alveolar bone and cemental
resorption.

Increased blood sugar levels

This also affects the periodontal support to the teeth.

Role of Nutrition in Root Resorption

It is one of the most common iatrogenic problems associated with orthodontic

treatment.

Marshall et.al- showed that greater degree of resorption is seen in patients with
deficient diets though it is of mulitfactorial origin.
Beck –stated that patients with calcium deficiency were more susceptible to root
resorption than normal patients.

Effects of consistency of food

Throughout its various stages of growth mouth is affected by complex system of

forces.

Diet that does not supply food of a sufficient hard consistency does not supply
adequate stimulus for proper mastication resulting in a narrow maxillary arch poor
periodontal support as discussed earlier.

Similar observations have been made in humans –arch collapse syndrome.

1. Low level of eruption of the posteriors

2. Maxillary arch are narrower.

3. Mandibles are shorter and condyles are thinner.

4. Less tonicity of temporalis and masseter.

5. Reduced linear dimension of skull.

In humans some authors have proposed-weakening of the temporomandibular

articulation and even resulting in malocclusion. However there is no sufficient
evidence to support it.
 Hormones:

Definition:
A hormone is a chemical substance that is secreted into the internal body fluids by
one cell or a group of cells and has a physiological control effect on other cells of the
body

Hormones may be local hormones or general hormones:

Local hormones are the ones, which have specific local effects on the adjoining
tissues. Examples of local hormones are acetylcholine released at the
parasympathetic and skeletal nerve endings
Most of the general hormones are secreted by specific endocrine glands. These
hormones are transported in the blood to all parts of the body and cause many
different reactions. A few of the general hormones affect all or almost all cells of the
body. Examples are growth hormone, which causes growth in almost all cells of the
body. Others affect only specific tissues called target tissues because only these
tissues have the specific target cell receptors that will bind the hormones to initiate
their actions. For instance, adrenocorticotropin from the anterior pituitary
specifically stimulates the adrenal cortex, causing it to release adrenocortical
hormones.

Overview of the Important Endocrine Glands and their Hormones:

Anterior Pituitary Hormones:

1. Growth Hormone
2. Adrenocorticotropin
3. Thyroid-stimulating hormone
4. Follicle-stimulating hormone
 5. Leutenizing hormone
6. Prolactin

Posterior Pituitary Hormones:

1. Antidiuretic hormone
2. Oxytocin

Adrenal Cortex:
1. Cortisol
2. Aldosterone

Thyroid Hormone:
1. Thyroxine and triidothyronine
2. Calcitonin

Islets Of Langerhans In The Pancreas:

1. Insulin
2. Glucagon

Ovaries:
1. Estrogen
2. Progesterone

Testes:
Testosterone
Parathyroid Gland:
Parathormone
 The Pituitary Hormones:

The pituitary gland, also called the hypophysis or master endocrine gland, is a small
gland that lies in the sella turcica, a bony cavity at the base of the brain. It is
connected to the hypothalamus by the pituitary stalk. The pituitary gland is divisible
into two parts: adenohypophysis or anterior pituitary and neurohypophysis or
posterior pituitary.
The pituitary gland secretes six important hormones that have just been reviewed.

Control of Pituitary Secretions by the Hypothalamus:

Almost all secretions from the pituitary gland are controlled by hormonal or nervous
signals originating from the hypothalamus. Secretion from the posterior pituitary is
controlled by nerve signals that originate in the hypothalamus and terminate in the
posterior pituitary. In contrast, hormones called hypothalamic releasing and
inhibitory hormones, which are secreted within the hypothalamus and then
conducted to the posterior pituitary through the hypothalamic-hypophyseal portal
vessels, control secretion by the anterior pituitary. The hypothalamus, in turn,
receives these signals from all possible sources in the nervous system. For example,
when a person is exposed to pain, a portion of the pain signal is transmitted to the
hypothalamus.

All the major anterior pituitary hormones besides Growth Hormone exert their
principal effects by stimulating target glands. The functions of each of these
hormones are discussed with the respective target glands.
Growth Hormone:
Growth hormone, also called somatotrophic hormone or somatotropin does not
function through a target gland. It causes growth of almost all tissues of the body that
are capable of growing by causing both increase in the size and number of cells and
specific differentiation of certain types of cells such as bone cells and muscle cells.
Although growth hormone causes increased growth in almost tissues of the body, its
most obvious effect is to increase growth of the skeletal frame. This results from: 1)
increased deposition of protein by the chondrocytic and osteogenic cells 2) increased
rate of reproduction of these cells 3) the specific effect of converting chondrocytes
into osteogenic cells
Growth hormone causes an increase in the length of the long bones where the
epiphyses at the ends of the bones are separated from the shafts. However, once the
epiphyses have united with the shafts, growth hormone has no further ability to
lengthen the bones. In intramembranous bone growth, growth hormone strongly
stimulates the osteoblasts. These bones can continue to enlarge throughout life under
the influence of growth hormone. For instance, the jawbones can be stimulated to
grow even after adolescence, causing forward protrusion of the lower jaw.

In animal experiments, it is seen that when experimental animals are treated with
growth hormone, new bony trabeculae are formed in a more vertical orientation
causing a closing of the Stutzmann Angle. It us also seen that when blood level of
STH (or testosterone) increases, supplementary lengthening of the mandible is
greater than the maxilla.
Metabolic Effects of Growth Hormone:
Apart from causing growth, GH has many metabolic effects as well, including 1)
increased rate of protein synthesis in all cells of the body 2) increased mobilization
of fatty acids from adipose tissue, increased free fatty acids in the blood, increased
use of the fatty acids for energy 3) decreased rate of glucose utilization throughout
the body

Regulation of Secretion:
The secretion of growth hormone varies depending on a number of factors:
1. Age: The level of growth hormone reaches a peak during adolescence after
which it decreases slowly with aging, finally falling to about 25 percent of
the adolescent level in very old age.
2. Rate: The rate of growth hormone secretion varies in relation to the person’s
state of nutrition or stress such as during (i) starvation especially during
severe protein deficiency (ii) hypoglycemia or low concentration of fatty
acids in the blood (iii) strenuous exercise (iv) excitement (v) trauma. It
characteristically increases during the first two hours of deep sleep

The Somatomedins:
Although growth hormone is generally regarded as the principal hormone regulating
skeletal growth, evidence has accumulated that growth hormone does not itself
stimulate linear growth, but rather induces the formation of a secondary growth-
promoting factor. Although originally designated “sulfation factor” (because it
stimulates the incorporation of radioactive sulfate into glycosaminoglycans of
cartilage), this term has now been replaced by the more generic name
“somatomedin”. The prefix “somato” connotes the hormonal relationship to
somatotropin, whereas the suffix “medin” indicates that somatomedin is an
intermediary in growth hormone action.

Discovery of Somatomedins:
The discovery of somatomedins is attributed to the pioneering work of Salmon and
Daughaday. These researchers drew on the experience of earlier workers who had
shown that radioactive sulfate (35SO 4) preferentially accumulated by cartilage in-
vivo, and that this accumulation is reduced following hypophysectomy and restored
by the administration of growth hormone.
Salmon and Daughaday incubated small costal cartilage segments obtained from
hypophysectomized rats with 35SO 4 in a nutrient medium containing the test sera.
They showed that normal serum stimulated 35SO 4 uptake by cartilage in vitro
whereas serum from hypophysectomized rats or hypopituitary children failed to do
so. When growth hormone was administered to a hypopituitary dwarf, his serum
regained its ability to stimulate 35SO 4 uptake in vitro. Their most provocative
observation, however, was that when serum from hypopituitary children was
enriched by direct addition of growth hormone in vitro, it had no stimulatory effect
on sulfate uptake. Since growth hormone was itself inactive in this assay, it became
apparent that the “sulfation factor activity” of plasma, although induced in vivo by
growth hormone administration, was not growth hormone itself.

Origin of Somatomedins:
So far the mechanism by which growth hormone stimulates somatomedin production
remains unclear. Liver, however, appears to be one site of production. Following
administration of growth hormone labeled with iodine 125, almost none is
concentrated in the skeleton, whereas very high concentrations are found in the liver,
kidney and adrenal cortex.
Since the somatomedin molecule appears to be about one third as large as growth
hormone, it might be reasonable to suspect that it arises from degradation of growth
hormone itself. According to this hypothesis, growth hormone would serve as a
prohormone in a matter analogous to the release of insulin from proinsulin.
Another possibility is that proinsulin might serve as a prohormone for somatomedin
as well as for insulin itself. Evidence has been advanced that somatomedin is not
only insulin-like in its biological actions but that highly specific cellular receptors in
tissues are incapable of distinguishing between insulin and somatomedin.
At least four somatomedins have been identified denoted by the suffixes A, B, C,
D.

Actions of Somatomedins:
Studies were undertaken to determine which of the metabolic effects ascribed to
growth hormone are due to growth hormone itself and which require mediation of
somatomedin. Although growth hormone itself stimulates protein synthesis in liver
and muscle in vitro, these effects are weak and require unphysiologically high doses.
All known growth hormone actions on cartilage are attributable to somatomedin
rather than a direct effect of growth hormone. For most of the extra-skeletal effects
of growth hormone, it remains to be determined which are due to a direct action of
growth hormone and which require induction of somatomedins.
Abnormalities of Growth Hormone Secretion:

1. Dwarfism: Most cases of dwarfism result from generalized deficiency of

anterior pituitary secretion during childhood. In general, the features of the
body develop in proportion to one another, but the rate of development is
greatly decreased. The panhypopituitary dwarf does not pass through puberty
and never secretes a sufficient quantity of gonadotropic hormones to develop
adult sexual functions. In some dwarfs, the deficiency is of growth hormone
alone; these individuals do mature sexually.
2. Gigantism: Gigantism results from acidophilic tumors of the anterior pituitary
during adolescence. As a result, large quantities of growth hormone are
produced. All body tissues grow rapidly, including the bones. If the condition
occurs before adolescence, the person becomes a giant as tall as 8 feet. The
giant ordinarily has hyperglycemia and full-blown diabetes may also occur.
3. Acromegaly: If an acidophilic tumor occurs after adolescence- that is, after
the epiphyses of the long bones have fused with the shafts- the person cannot
grow taller, but the soft tissues can continue to grow and the bones can grow
in thickness. This condition is known as acromegaly. Enlargement is
especially marked in the bones of the hands and feet and in the membranous
bones including the cranium, nose, bosses on the forehead, supraorbital
ridges, lower jawbone and portions of the vertebrae because their growth
does not cease at adolescence. Consequently, the lower jaw protrudes
forward, the forehead slants forward, the nose increases to as much as twice
its normal size, the fingers become extremely thickened and the hands
develop a size twice the normal.
Antidiuretic Hormone (ADH, Vasopressin):
ADH is secreted by the posterior pituitary gland.
Physiological Functions of ADH:
Extremely minute quantities of ADH when injected into a person can cause
antidiuresis, that is, decreased excretion of water by the kidneys. In the
absence of ADH, the collecting tubules and ducts are almost impermeable to
water, which allows extreme loss of water into the urine. In the presence of
ADH, the permeability of the collecting tubules and ducts greatly increases
and allows most of the water to be reabsorbed, thereby conserving water in
the body.

Regulation of ADH Production:

Osmotic concentration of the extracellular fluid regulates ADH production.
Increased concentration of the extracellular fluid stimulates ADH production
and vice versa.

Vasoconstrictor Effects of ADH:

Higher concentrations of ADH have a potent effect of constricting arterioles
everywhere in the body and therefore increasing the arterial blood pressure.
For this reason, ADH is also called vasopressin. One of the stimuli for
causing intense ADH secretion is decreased blood volume. This occurs
especially strongly when the blood volume decreases 15 to 25 percent.

The Thyroid Hormones:

The thyroid gland is located immediately below the larynx on either side and
anterior to the trachea. It secretes two important hormones: thyroxine and
triidothyronine that have a profound effect of increasing the metabolic rate of
the body. Most of the hormone secreted by the thyroid gland is thyroxine.
However, almost all of the thyroxine is eventually converted into
thriidothyronine, the more potent form.
Functions of Thyroid Hormones:
1) Increased transcription of genes: Thyroid hormones cause nuclear
transcription of large numbers of genes. Therefore, in all cells of the
body the number of enzymes, structural proteins and transport
proteins increases. The net result is increase in the functional activity
of all the cells of the body.
2) Effect on growth: Thyroid hormone has both general and specific
effects on growth. In human beings, the effect of thyroid hormone on
growth is manifest mainly in growing children. In hypothyroid
children, the rate of growth is greatly retarded. In hyperthyroid
children, the rate of skeletal growth is greatly accelerated causing the
child to become considerably taller at an earlier age. However, the
bones also mature more rapidly and the epiphyses close at an early
age so that the eventual height of the child may actually be shortened.
The specific effect of thyroid hormone on growth pertains to its
requirement to promote growth and development of the brain at an
early age.
3) Effects on specific bodily mechanisms:
i. On Carbohydrate Metabolism: Thyroid hormone stimulates
all aspects of carbohydrate metabolism including rapid
uptake of glucose by the cells, enhanced glycolysis,
gluconeogenesis and even increased insulin secretion with
all its secondary effects.
ii. On Fat Metabolism: Increased thyroid hormone depletes the
fat stores of the body, decreases the quantity of cholesterol
and increases the free fatty acids in the plasma by causing
 mobilization of lipids from the fat tissue. It also greatly
accelerates the oxidation of free fatty acids by the cells.
iii. On Basal Metabolic Rate: Because thyroid hormone
increases metabolism in all cells of the body, excess
quantities of this hormone can increase the BMR 60 to 100%
above normal.
iv. On Cardiovascular System: Increased BMR increases blood
flow, which increases the cardiac output and heart rate.

Regulation of Thyroid Secretion:

The secretion of thyroid hormones is under feedback control from the
hypothalamus and the anterior pituitary and is affected by the circulating
levels of T3 and T4 in the plasma. When the level of T3 and T4 falls in the
plasma, it sends a negative feedback signal to the hypothalamus and the
anterior pituitary gland. This causes increased secretion of thyrotropin
releasing hormone from the hypothalamus and thyroid stimulating hormone
from the anterior pituitary both of which eventually result in increased
secretion of T3 and T4 from the thyroid gland. This restores the normal
plasma levels of these hormones following which the feedback signal ceases.

Disorders of Thyroid Secretion:

1. Hyperthyroidism (Grave’s Disease, Thyrotoxicosis): The symptoms of
hyperthyroidism include a high state of excitability, intolerance to heat,
increased sweating, mild to extreme weight loss, muscle weakness,
nervousness and other psychic disorders, extreme fatigue but inability to
sleep.
Exophthalmos: Most people with hyperthyroidism develop some degree of
exophthalmos or protrusion of the eyeballs. The cause of exophthalmos is
edematous swelling of the retro-orbital tissues and degenerative changes in
the extraocular muscles. In some patients, the condition becomes severe
enough that the eyeball protrusion stretches the optic nerve enough to damage
vision. More often the eyes are damaged because the eyelids do not close
completely over the protruding eyeballs. As a result, the eyes become dry and
irritated and often infected, resulting in ulceration of the cornea.

2. Hypothyroidism: Hypothyroidism results in myxedema in adults and

cretinism in children.
Myxedema: Myxedema develops in adults with almost total lack of thyroid
function. These patients show fatigue and extreme somnolence with sleeping
up to 12 to 14 hours a day, muscular sluggishness, decreased cardiac output
and weight gain. There is swelling of the face with bagginess under the eyes.
Cretinism: Cretinism is caused by extreme hypothyroidism in fetal life,
infancy and childhood. Apart from the features of hypothyroidism seen in the
adult, this condition is characterized especially by failure of growth and
mental retardation.

The Adrenocortical Hormones:

The two adrenal glands lie at the superior poles of the two kidneys. Each
gland is composed of two distinct parts- the outer adrenal cortex and the inner
adrenal medulla. The adrenal medulla secretes the hormones epinephrine and
norepinephrine in response to sympathetic stimulation. The adrenal cortex
secretes hormones called corticosteroids. These hormones are of two major
types- mineralocorticoids and glucocorticoids. In addition, small amounts of
sex hormones called androgenic hormones are also secreted by the adrenal
cortex.
The mineralocorticoids are so called because they affect the electrolytes of
the extracellular fluids- sodium and potassium in particular. The
glucocorticoids have gained their name because they have an important effect
in increasing the blood glucose concentration. Aldosterone is the principal
mineralocorticoid and cortisol is the principal glucocorticoid.

Functions of Mineralocorticoids- Aldosterone

Total loss of adrenocortical secretion causes death of a person unless the
person receives extensive salt therapy. Aldosterone causes reabsorption of
sodium and loss of potassium in the collecting tubules. Without
mineralocorticocoids, the potassium ion concentration of the extracellular
fluid rises, the sodium and chloride concentrations decrease, the total
extracellular fluid volume and blood volume become greatly reduced. The
person develops diminished cardiac output, which proceeds to a shock-like
state followed by death.

Regulation of Aldosterone Secretion:

Four factors are known to play essential roles in aldosterone secretion. In the
probable order of their importance, they are as follows:
1. Increased potassium ion concentration in the extracellular fluid
greatly increases aldosterone secretion
2. Increased activity of the rennin-angiotensin system also greatly
increases aldosterone secretion
3. Increased sodium ion concentration in the extracellular fluid very
slightly decreases aldosterone secretion
4. ACTH from the anterior pituitary is necessary for aldosterone
secretion but has little effect in controlling the rate of secretion.
Functions of Glucocorticoids: Cortisol

1. On Carbohydrate Metabolism:
i. Stimulation of Gluconeogenesis: By far the best-known
metabolic effect of cortisol is gluconeogenesis, that is,
synthesis of carbohydrates from non-carbohydrate sources
such as proteins, fats etc. by the liver
ii. Decreased Glucose Utilization by the Cells: Cortisol causes a
moderate decrease in glucose utilization by cells everywhere
in the body
Both the increased rate of gluconeogenesis and the reduction in the
rate of glucose utilization causes the blood glucose concentrations to
rise. This condition is called adrenal diabetes.

2. On Protein Metabolism: Cortisol causes reduction of the protein

stores in essentially all body cells except those of the liver. This is
caused by both decreased protein synthesis and increased catabolism
of protein already in the cells. Cortisol also depresses the formation of
RNA and subsequent protein synthesis. At the same time, cortisol also
increases the liver and plasma proteins

3. On Fat Metabolism: Cortisol promotes mobilization of fatty acids

from adipose tissue. This increases the concentraton of free fatty acids
in the plasma, which also increases their utilization for energy.

4. In Stress and Inflammation: Almost any type of stress, physical or

neurogenic, causes increased adrenocortical secretion of cortisol. The
 different types of stress that increase cortisol release are trauma of
almost any type, infection, intense heat or cold, surgery etc.
Vitamin D, Parathyroid Hormone and Calcitonin:

Vitamin D and its role in Calcium and Phosphate Absorption:

Vitamin D has a potent role in increasing calcium absorption from the intestinal
tract. However, Vitamin D itself is not the active substance that actually causes
these effects. Instead the Vitamin D must first be converted through a succession of
reactions in the liver and the kidneys to the final active product, 1,25-
dihydroxycholecalciferol also called calcitriol.

Parathyroid Hormone:
Parathyroid hormone is secreted by the four parathyroid glands, which are located
immediately behind the thyroid gland. Parathyroid hormone causes rapid increase in
blood calcium and drop in phosphate levels. The rise in calcium is caused by:
1. Increased calcium and phosphate absorption from the bone
2. Decreased renal excretion of calcium
Decline in phosphate concentration is caused by excessive renal phosphate excretion.

Effect of Parathyroid Hormone on Intestinal Absorption of Calcium and

Phosphate:
Parathyroid hormone greatly enhances both calcium and phosphate absorption from
the intestines by increasing the formation in the kidneys of calcitriol from Vitamin
D.

Control of Parathyroid Secretion:

Even the slightest decrease in calcium ion concentration in the extracellular fluid
causes the parathyroid glands to increase their rate of secretion within minutes. If the
decreased calcium ion concentration persists, as in rickets, the glands will
hypertrophy. On the other hand, any condition that increases the calcium ion
concentration above normal causes decreased activity and reduced size of the
parathyroid glands. Such conditions include: (1) excess quantities of calcium in the
diet (2) increased Vitamin D in the diet (3) bone absorption caused by other factors

Hypoparathyroidism and Hyperparathyroidism:

Hypoparathyroidism: Hypoparathyroidism causes hypocalcemia, which results in

tetany. Whem the extracellular fluid calcium ion concentration falls below normal,
the nervous system becomes progressively more excitablebecause this causes this
causes increased neuronal membrane permeability of to sodium, allowing easy
initiation of action potentials and causing them to discharge spontaneously to elicit
tetanic muscle contractions. Tetany in the hands, which usually develops before
tetany develops in other parts of the body, is called “carpopedal spasm”. Tetany
ordinarily occurs when the calcium ion concentration falls from its normal level of 9-
11 mg/dl to about 6 mg/dl.

Hyperparathyroidism: Hyperfunctioning of the parathyroid glands results in

hypercalcemia. When the level of calcium in the body fluids rises above, the nervous
system is depressed and the reflex activities of the central nervous system can
become sluggish. Other features include constipation and lack of appetite. Symptoms
of hypercalcemia begin to appear when the blood level of calcium rises above 12
mg/dl and become marked above 15 mg/dl.

Calcitonin:
Calcitonin is secreted by the thyroid gland. This hormone also plays an important
role in calcium metabolism. It is antagonistic in its action to parathormone and
decreases the blood calcium levels by the following two mechanisms:
1. It decreases the absorptive activity of the osteoclasts
2. It also decreases the formation of new osteoclasts
Insulin and Glucagon:
Insulin is secreted by the β cells of the Islets of Langerhans. The hormone is
associated with energy abundance, that is, when there is great abundance of
energy giving foods in the diet, especially excess amounts of carbohydrates
and proteins, insulin is secreted in great quantity.

Effects of Insulin:
1. On Carbohydrate Metabolism:
i. Muscle: The resting muscle membrane is only slightly
permeable to glucose. However, when the muscle is
stimulated by insulin, the membrane permeability greatly
increases. Insulin also stimulates the synthesis of muscle
glycogen.
ii. Liver: One of the most important effects of insulin is to
cause most of the glucose absorbed after a meal to be
immediately stored as glycogen. Then, between meals, when
the blood glucose level begins to fall, insulin secretion
decreases rapidly and the liver glycogen is split back to
glucose. When the quantity of glucose entering the liver
cells is more than can be stored as glycogen, insulin
promotes the conversion of all this excess glucose into fatty
acids. Insulin also inhibits gluconeogenesis.
 iii. Brain: Secretion of insulin has little or no effect on uptake of
glucose by the brain as even in the absence of insulin brain
tissue can take up glucose, unlike other cells of the body.

2. On Fat Metabolism: Insulin is a “fat sparer.” First insulin increases

the utilization of glucose by most of the body’s tissues, which
automatically decreases the utilization of fat. Insulin also promotes
fatty acid synthesis, all of which lead to fat storage in adipose tissue.
3. On Protein Metabolism: Insulin promotes protein formation and
prevents the degradation of proteins.
4. On Growth: Insulin has a synergistic effect on growth along with
growth hormone since it is required for the synthesis of proteins. It
has been seen that in depancreatized and hypophysectomized rats, the
administration of either growth hormone or insulin one at a time
causes almost no growth. Yet a combination of these two hormones
causes dramatic growth.

Control of Insulin Secretion:

Formerly, it was believed that insulin secretion is controlled almost entirely by blood
glucose concentration. However, it is now known that there are other factors that
play an important role as well.
Amino acids administered in the absence of a rise in blood glucose concentration
cause only a small increase in insulin secretion. However, when administered at the
time of raised blood glucose levels, the glucose-induced secretion of insulin may be
twice as much in the presence of excess amino acids. Thus, amino acids strongly
potentiate the glucose stimulus for insulin secretion.
Gastrointestinal hormones like gastrin, secretin which are secreted after a meal cause
an anticipatory increase in insulin secretion in preparation for the glucose and amino
acids to be absorbed from the meal.

Glucagon:
Glucagon, a hormone secreted by the α-cells of the Islets of Langerhans when the
blood glucose concentration falls, has several functions that are diametrically
opposite to those of insulin.

Effects on Glucose Metabolism:

The major effects of glucagon on glucose metabolism are: (1) breakdown of liver
glycogen (glycogenolysis) (2) increased gluconeogenesis in the liver. Both these
effects greatly enhance the availability of glucose to other parts of the body.
Other Effects:
Glucagon activates adipose cell lipase making increased quantities of fatty acids
available to the energy systems of the body. It also inhibits the storage of
triglycerides in the liver, which prevents the liver from removing fatty acids from the
blood; this also makes fatty acids available to other tissues of the body.

Regulation of Glucagon Secretion:

Increased blood glucose concentration inhibits glucagon secretion. The blood
glucose concentration is the most potent factor that controls glucagon secretion. The
effect of blood glucose concentration on glucagon secretion is exactly opposite to
that of insulin secretion.

Excitatory Effect of Amino Acids: High concentrations of amino acids, as occur in

the blood after a protein meal, stimulate the secretion of glucagon. This is the same
effect that amino acids have on insulin secretion. Thus, in this instance, the glucagon
and insulin responses are not opposite.

Excitatory Effect of Exercise: In exhaustive exercise, the blood concentration of

glucagon increases fourfold to fivefold. What causes this is not understood because
the blood glucose concentration does not necessarily fall. A beneficial effect of
glucagon is that it prevents a fall in blood glucose.

Testosterone:
Apart from its effects in causing growth of the secondary sexual characters,
testosterone has some other functions as well:

Effect on Bone Formation and Muscle Development: One of the most important
male characteristics is the development of increasing musculature after puberty,
about 50 percent more than the females, which is a function of testosterone. Because
of the great effect that testosterone has on the body musculature, it is widely used by
athletes to improve their muscular performance. Testosterone is also used in old age
as a “youth hormone” to improve muscle strength and vigor.

Effect on Bone Growth and Calcium Retention: Testosterone increases the total
quantity of bone matrix and causes calcium retention. The increase in bone matrix is
believed to result from the general protein anabolic functions of testosterone.
Because of the ability of testosterone to increase the size and strength of bones, it is
often used in old aged men to treat osteoporosis.

Estrogen:
Apart from its effect in causing growth of the female secondary sexual characters,
estrogens serve other functions such as:
Effect of Estrogens on the Skeleton: Estrogens cause increased osteoblastic
activity. Therefore, at puberty, the female growth rate becomes rapid for several
years. However, estrogens also cause early uniting of the epiphysis with the shafts of
the long bones. This effect is much stronger in the female than in the male. As a
result, growth of the female usually ceases several years earlier than growth of the
male.

Osteoporosis of the Bones Caused by Estrogen Deficiency in Old Age: After

menopause, the ovaries secrete almost no estrogens. This estrogen deficiency leads
to (1) diminished osteoblastic activity (2) decreased bone matrix (3) decreased
deposition of bone calcium and phosphate. In severe cases, this can lead to
osteoporosis. Because this can greatly weaken the bones and lead to bone fracture, a
large share of post-menopausal women are treated prophylactically with estrogen
substitutes.
 Bibliography

 Contemporary orthodontics-Proffit

 Current Principles and Techniques –Graber Vanarsdall

 Nutrition and oral health-Pollack

 Introductory nutrition-Helen Andrews

 Principles of nutrition-Wilson,Fisher

 Clinical dietetics and nutrition-F.P.Antia

 Basic pathology-Robbins

 Pathology for dental students-Harsh Mohan

 Textbook of Medical Physiology- Guyton and Hall

 Control mechanisms in craniofacial growth- James A. McNamara