ENDOCRINOLOGY AND DISORDERS seminar vish.ppt

OLOGY AND DISORDERS seminar vish.ppt

1. SET A GOAL THAT MAKES YOU
WANT TO JUMP OUT OF THE
BED IN THE MORNING !!!!

2. ENDOCRINOLOGY & IT’S DISORDERS
G. VISHNU LEKSHMI
PG 1
st
YEAR

3. CONTENTS
•INTRODUCTION
•ENDOCRINE GLANDS- DEFINITION
•HORMONES- DEFINITION
•DISCOVERY OF HORMONES
•PITUITARY GLAND
•DISORDERS OF PITUITARY GLAND
•THYROID GLAND
•DISORDERS OF THYROID GLAND
•PARATHYROID GLAND AND DISORDERS
•CONCLUSION

4. INTRODUCTION:
•The activities of various organs in our body are controlled by two systems
namely,
1. Nervous system
2. Endocrine system
•Most of the functions of nervous system are executed by hormonal substances.
And most of the endocrine functions are controlled by nervous system.
•Endocrine system functions by secreting some chemical substances called
hormones.

5. ENDOCRINE GLANDS
•Endocrine glands are the glands which synthesize and release the classical hormones
into the blood. Endocrine glands are also called ductless glands because the hormones
secreted by them are released directly into blood without any duct.
•Endocrine glands are distinct from exocrine glands which release their secretions
through ducts.
•Endocrine glands play an important role in homeostasis and control of various other
activities in the body through their hormones. Hormones are transported by blood to
target organs or tissues in different parts of the body, where the actions are executed.

6. WHAT IS A HORMONE?
•Hormones are chemical messengers, synthesized by endocrine glands.
•Hormones are released directly into the circulation in small amounts in response to
a specific stimulus. On delivery in circulation it produces response on the target cells
or organs.
•Based on chemical nature, hormones are classified into three types :
1.Steroid hormones
2.Protein hormones
3.Derivatives of the amino acid called tyrosine.

8. DISCOVERY OF HORMONE:
•Bayliss and Starling (1902) were studying
digestion and absorption in an isolated loop
of duodenum.
•They found out some blood-borne
substance, which they called "secretin".
•When more of these blood-borne
messengers were discovered they were
given the generic term "hormones".

9. MAJOR ENDOCRINE GLANDS
•Heart - Secretes atrial natriuretic peptide which regulates sodium
reabsorption by the kidneys.
•Kidneys - Secretes erythropoietin (EPO) which stimulates
production of red blood cells in the bone marrow.
•Digestive organs - Secrete several hormones that regulate
digestion and absorption of food.
•Liver - Secretes insulin-like growth factors (IGF's) which promote
tissue growth.
•Skin and Kidneys - Activate vitamin D3 which regulates blood
calcium levels.

12. VARIOUS HORMONES RELATED TO ORTHODONTICS
■GROWTH & DEVELOPMENT

–SKELETAL GROWTH
■GROWTH HORMONE
■THYROID HORMONE
■INSULIN
■CORTICOSTEROIDS
–PUBERTAL GROWTH SPURT
■ESTROGEN
■TESTOSTERONE
■PROGESTERONE
BONE METABOLISM AND TOOTH MOVEMENT
-PARATHYROID HORMONE
-CALCITONIN

13. HORMONAL ACTION
•Hormone does not act directly on target cells. First it combines with receptor
present on the target cells and forms a hormone-receptor complex. This
hormonereceptor complex induces various changes or reactions in the target cells.
•HORMONE RECEPTORS Hormone receptors are the large proteins present in the
target cells. Each cell has thousands of receptors.
•Important characteristic feature of the receptors is that, each receptor is specific
for one single hormone, i.e. each receptor can combine with only one hormone.
Thus, a hormone can act on a target cell, only if the target cell has the receptor for
that particular hormone.

14. SITUATION OF THE HORMONE RECEPTOR:

15. PITUITARY GLAND

16. •Pituitary gland or hypophysis is a small endocrine gland with a diameter of 1
cm and weight of 0.5 to 1 g.
•It is situated in a depression called ‘sella turcica’, present in the sphenoid
bone at the base of skull.
•It is connected with the hypothalamus by the pituitary stalk or hypophyseal
stalk.

17. DIVISIONS OF PITUITARY GLAND
Pituitary gland is divided into two divisions:
1.Anterior pituitary or adenohypophysis
2.Posterior pituitary or neurohypophysis.
•Both the divisions are situated close to each other. Still both are entirely different
in their development, structure and function.
•Between the two divisions, there is a small and relatively avascular structure
called pars intermedia. Actually, it forms a part of anterior pituitary

19. DEVELOPMENT OF PITUITARY GLAND
•Both the divisions of pituitary glands develop from different sources.
•Anterior pituitary is ectodermal in origin and arises from the pharyngeal epithelium as an
upward growth known as Rathke pouch.
•Posterior pituitary is neuro-ectodermal in origin and arises from hypothalamus as a
downward diverticulum.
•Rathke pouch and the downward diverticulum from hypothalamus grow towards each
other and meet in the midway between the roof of the buccal cavity and base of brain.
There, the two structures lie close together.

20. HYPOTHALAMO-HYPOPHYSEAL RELATIONSHIP
•The relationship between hypothalamus and pituitary gland is called hypothalamo-
hypophyseal relationship.
•Hormones secreted by hypothalamus are transported to anterior pituitary and posterior
pituitary.
•But the mode of transport of these hormones is different. Hormones from hypothalamus
are transported to anterior pituitary through hypothalamo-hypophysial portal blood
vessels.
•But, the hormones from hypothalamus to posterior pituitary are transported by nerve
fibers of hypothalamo-hypophyseal tract

21. HORMONES SECRETED BY ANT. PITUITARY

22. HORMONES SECRETED BY POST. PITUITARY

23. HYPOTHALAMIC RELEASING AND INHIBITORY 
HORMONES
•Special neurons in the hypothalamus synthesize and secrete the hypothalamic
releasing and inhibitory hormones that control secretion of the anterior
pituitary hormones.
•For most of the anterior pituitary hormones, it is the releasing hormones that
are important, but for prolactin, a hypothalamic inhibitory hormone probably
exerts more control.

24. Hypothalamic Releasing 
and Inhibitory Hormones

25. 1. GROWTH HORMONE / SOMATOTROPIC HORMONE OR
SOMATOTROPIN,
•Source of Secretion Growth hormone is secreted by somatotropes which are the
acidophilic cells of anterior pituitary.
•Chemistry, Blood Level and Daily Output GH is protein in nature, having a single-chain
polypeptide with 191 amino acids. Its molecular weight is 21,500. Basal level of GH
concentration in blood of normal adult is up to 300 g/dL and in children, it is up to
500 ng/ dL. Its daily output in adults is 0.5 to1.0 mg.
•Transport Growth hormone is transported in blood by GH-binding proteins (GHBPs).
•Half-life and Metabolism Half-life of circulating growth hormone is about 20 minutes. It is
degraded in liver and kidney

26. ACTIONS OF GROWTH HORMONE
1.GROWTH HORMONE STIMULATES CARTILAGE AND BONE GROWTH
•In embryonic stage, GH is responsible for the differentiation and development of bone
cells.
•In later stages, GH increases the growth of the skeleton. It increases both the length as
well as the thickness of the bones.

27. •In bones, GH increases:
i.Synthesis and deposition of proteins by chondrocytes and osteogenic cells
ii.Multiplication of chondrocytes and osteogenic cells by enhancing the intestinal calcium
absorption
iii.Formation of new bones by converting chondrocytes into osteogenic cells
iv.Availability of calcium for mineralization of bone matrix.
•GH acts on bones, growth and protein metabolism through somatomedin secreted by
liver. GH stimulates the liver to secrete somatomedin.

28. SOMATOMEDIN
•Somatomedin is defined as a substance through which growth hormone acts. It is a
polypeptide with the molecular weight of about 7,500.
•Types of somatomedin :

1.Insulin-like growth factor-I (IGF-I), which is also called somatomedin C
2.Insulin-like growth factor-II.
•Somatomedin C (IGF-I) acts on the bones and protein metabolism.
•Insulin-like growth factor-II plays an important role in the growth of fetus.
•Duration of action of GH is 20 min;
•Duration of action of somatomedian C is 20 hrs.

29. 2. EFFECT ON METABOLISM
1.On protein metabolism :
•GH accelerates the synthesis of proteins by:
1. Increasing amino acid transport through cell membrane
2. Increasing ribonucleic acid (RNA) translation
3. Increasing transcription of DNA to RNA
4. Decreasing catabolism of protein
5. Promoting anabolism of proteins indirectly

30. 2.On fat metabolism
•GH mobilizes fats from adipose tissue.
•So, the concentration of fatty acids increases in the body fluids. These fatty acids are
used for the production of energy by the cells. Thus, the proteins are spared.
•During the utilization of fatty acids for energy production, lot of acetoacetic acid is
produced by liver and is released into the body fluids, leading to ketosis. Sometimes,
excess mobilization of fat from the adipose tissue causes accumulation of fat in liver,
resulting in fatty liver.
•Hence under the influence of GH fat is used for energy in preference to carbohydrates
and proteins.

31. Growth hormone
1. Increased glucose production by liver
2. Decreased uptake of
glucose by skeletal muscles
and fat
Type II Diabetes
3. compensatory increase in

insulin secretion
3. On carbohydrate metabolism

32. Diabetogenic effect of GH:
•Hypersecretion of GH increases blood glucose level enormously. It causes
continuous stimulation of the β-cells in the islets of Langerhans in pancreas and
increase in secretion of insulin.
•In addition to this, the GH also stimulates β-cells directly and causes secretion of
insulin. Because of the excess stimulation, β-cells are burnt out at one stage.
•This causes deficiency of insulin, leading to true diabetes mellitus or full-blown
diabetes mellitus. This effect of GH is called the diabetogenic effect.

33. short-loop feedback
FEEDBACK CONTROL

35. 2.THYROID STIMULATING HORMONE (TSH)
•Glycoprotein in nature
•It stimulates the synthesis and secretion of 2 thyroid hormones
triiodothyronine (T3) and thyroxine (T4)

36. 3. ADRENOCORTICOTROPIC HORMONE (ACTH)
•It’s polypeptide in nature.
•Controls the production and secretion of cortisol and other glucocorticoids by
the adrenal glands.
•Stress related stimuli such as low blood glucose, physical trauma stimulate
release of ACTH.

37. 4. FOLLICLE-STIMULATING HORMONE (FSH)
•Follicle-stimulating hormone is a glycoprotein made up of one α-subunit and a β-subunit.
The α-subunit has 92 amino acids and β-subunit has 118 amino acids. The half-life of FSH
is about 3 to 4 hours.
•Actions of FSH In males, FSH acts along with testosterone and accelerates the process of
spermeogenesis.
•In females FSH:
1.Causes the development of graafian follicle from primordial follicle
2.Stimulates the theca cells of graafian follicle and causes secretion of estrogen
3.Promotes the aromatase activity in granulosa cells, resulting in conversion of androgens
into estrogen.

39. 5.LUTEINIZING HORMONE (LH)
•LH is a glycoprotein made up of one α-subunit and one β-subunit. The α-subunit has 92
amino acids and β-subunit has 141 amino acids.
•The half-life of LH is about 60 minutes.
•Actions of LH In males, LH is known as interstitial cell-stimulating hormone (ICSH)
because it stimulates the interstitial cells of Leydig in testes.
•This hormone is essential for the secretion of testosterone from Leydig cells.

40. In females, LH:
1. Causes maturation of vesicular follicle into graafian follicle along with follicle-
stimulating hormone
2. Induces synthesis of androgens from theca cells of growing follicle
3. Is responsible for ovulation
4. Is necessary for the formation of corpus luteum
5. Activates the secretory functions of corpus luteum

41. 6. PROLACTIN
•Prolactin is a single chain polypeptide with 199 amino acids.
•Its half-life is about 20 minutes.
•Prolactin is necessary for the final preparation of mammary glands for the
production and secretion of milk. Prolactin acts directly on the epithelial cells of
mammary glands and causes localized alveolar hyperplasia

42. HORMONES OF POSTERIOR PITUITARY
„ ANTIDIURETIC HORMONE
•Source of Secretion Antidiuretic hormone (ADH) is secreted mainly by supraoptic
nucleus of hypothalamus. It is also secreted by paraventricular nucleus in small
quantity.
•From here, this hormone is transported to posterior pituitary through the nerve
fibers of hypothalamo-hypophyseal tract, by means of axonic flow.

43. •Actions: Antidiuretic hormone has two actions:
1.Retention of water :
2. Vasopressor action.

44. In the absence of ADH, the distal
convoluted tubule and collecting duct
are totally impermeable to water. So,
reabsorption of water does not occur in
the renal tubules and dilute urine is
excreted. This leads to loss of large
amount of water through urine. This
condition is called diabetes insipidus

45. „OXYTOCIN:
•Oxytocin is secreted mainly by paraventricular nucleus of hypothalamus. It is also secreted
by supraoptic nucleus in small quantity and it is transported from hypothalamus to
posterior pituitary through the nerve fibers of hypothalamo-hypophyseal tract.
•Action of oxytocin on mammary glands Oxytocin causes ejection of milk from the
mammary glands.
•Action on uterus Oxytocin acts on pregnant uterus and also non-pregnant uterus.
•On pregnant uterus Oxytocin causes contraction of uterus and helps in the expulsion of
fetus
•On non-pregnant uterus The action of oxytocin on non-pregnant uterus is to facilitate the
transport of sperms through female genital tract up to the fallopian tube, by producing the
uterine contraction.

46. GROWTH HORMONE IN ORTHODONTICS
•Growth hormone has a strong effect on bone growth, including the bones of the face, ie maxilla
and mandible.
  It has the potential to regulate odontogenesis, bone modeling and remodelling,
exerting its anabolic effects on both trabecular and cortical bone.
•In growth hormone deficiency it is common to see a growth disorder of the jaws.
•Growth hormone deficiency also significantly delays eruption of permanent teeth in particular
•GH deficiency reduces bone mass
•On assessing the role of GH in the field of orthodontics, it induces orthodontic tooth
movement by acting on specific signalling pathways thus activating certain cytokines to control
the activity of osteoclasts and osteoblasts for selective formation and remodelling of the bone

47. •Minayao et al ; Children who received long-term GH therapy (more than 2 years) showed
increased growth of the craniofacial skeleton, especially the maxilla and mandibular
ramus.
•These findings suggest that GH accelerates craniofacial development, which improves
occlusion and the facial profile.
Effects of Growth Hormone on Craniofacial Growth: Angle Orthod (2006) 76 (6): 970–977.

48. DISORDERS OF PITUITARY GLAND

49. HYPERACTIVITY OF ANTERIOR PITUITARY
1. GIGANTISM
•Gigantism is the pituitary disorder characterized by
excess growth of the body. The subjects look like the
giants with average height of about 7 to 8 feet.
•Gigantism is due to hyper-secretion of GH in childhood
or in pre-adult life before the fusion of epiphysis of bone
with shaft.
•Hyper-secretion of GH can be also because of tumor of
acidophil cells in the anterior pituitary.

50. Signs and symptoms
•General overgrowth of the person leads to the development of a huge stature, with a
height of more than 7 or 8 feet.
• Giants are hyperglycemic and they develop glycosuria and pituitary diabetes
•Tumor of the pituitary gland itself causes constant headache
•Pituitary tumor also causes visual disturbances. It compresses the lateral fibers of optic
chiasma, leading to bitemporal hemianopia

51. ORAL & FACIAL FEATURES
•Overgrowth of alveolar process in height and breadth with
increased spacing between teeth.
•Vertical height of face increased and paranasal sinuses
overdeveloped.
•Enlargement of tongue.
•Acceleration of tooth eruption and increase in occlusal height.
•Thickening of cortical plate of mandible.
•Radiographically, bones are poorly calcified and have large
trabeculae, hypercementosis of the roots.
•Prognathic mandible, frontal bossing.

52. 2. ACROMEGALY
•Acromegaly is the disorder characterized by
the enlargement, thickening and broadening of
bones, particularly in the extremities of the
body.
•Acromegaly is due to hypersecretion of GH in
adults after the fusion of epiphysis with shaft of
the bone.
•Hypersecretion of GH is because of tumor of
acidophil cells in the anterior pituitary.

53. SIGNS AND SYMPTOMS
1.Enlargement of hands and feet
2.Kyphosis (extreme curvature of upper back – thoracic spine)
3.Thickening of scalp. Scalp is also thrown into folds or wrinkles like
bulldog scalp
4.Overgrowth of body hair .
5.Enlargement of visceral organs such as lungs, thymus, heart, liver
and spleen
6.Hyperactivity of thyroid, parathyroid and adrenal glands
7.Hyperglycemia and glucosuria, resulting in diabetes mellitus
8.Hypertension
9.Headache
10.Visual disturbance

54. FACIAL AND ORAL FEATURES:
•Acromegalic or gorilla face: Face with rough features
such as protrusion of supraorbital ridges, broadening of
nose, thickening of lips, thickening and wrinkles formation
on forehead and prognathism
•spacing in the teeth, malocclusion, aperthognathia,
macroglossia, hypertrophy of palatal tissues which may
cause or accentuate sleep apnea.
•Dental radiograph may demonstrate large pulp
chambers(taurodontism) and excessive deposition of
cementum on the roots.

55. HYPOACTIVITY OF ANTERIOR PITUITARY
1.Dwarfism
•Dwarfism is a pituitary disorder in children,
characterized by the stunted growth.
•In general, all the physical parts of the body develop
in appropriate proportion to one another, but the rate
of development is greatly decreased.
•A child who has reached the age of 10 years may have
the bodily development of a child aged 4 to 5 years,
and the same person at age 20 years may have the
bodily development of a child aged 7 to 10 years.

56. Causes
•Reduction in GH secretion in infancy or early childhood causes dwarfism. It occurs because
of the following reasons:
1.Tumor of chromophobes
2.Deficiency of GH-releasing hormone secreted by hypothalamus
3.Deficiency of somatomedin C
4.Atrophy or degeneration of acidophilic cells in the anterior pituitary.
5.Panhypopituitarism: In this condition, there is reduction in the secretion of all the
hormones of anterior pituitary gland. This type of dwarfism is associated with other
symptoms due to the deficiency of other anterior pituitary hormones.

57. Signs and symptoms
i.Primary symptom of hypopituitarism in children is the stunted skeletal growth. The
maximum height of anterior pituitary dwarf at the adult age is only about 3 feet
ii.But the proportions of different parts of the body are almost normal. Only the head
becomes slightly larger in relation to the body
iii.Pituitary dwarfs do not show any deformity and their mental activity is normal with no
mental retardation
iv.Reproductive function is not affected, if there is only GH deficiency. However, during
panhypopituitarism, the dwarfs do not obtain puberty due to the deficiency of gonadotropic
hormones.

58. ORAL MANIFESTATIONS
•The maxilla and mandible of affected patients are smaller than the normal and the face
appears smaller, with the permanent teeth showing a delayed pattern of eruption.
•Often the shedding pattern of deciduous teeth is delayed by several years, and also the
development of roots of permanent teeth appears to be delayed.
•The dental arches are smaller than the normal and therefore cannot accommodate all
the teeth resulting in dental malocclusion.
•Complete absence of buds of wisdom tooth even in patient in fourth decade of life is
also reported.
•Other rare findings such as agenesis of the upper central incisor and solitary maxillary
central incisor have been observed.

59. Laron dwarfism
•Laron dwarfism is a genetic disorder. It is also called
GH insensitivity.
•It occurs due to the presence of abnormal growth
hormone secretagogue (GHS) receptors in liver.
•GHS receptors become abnormal because of the
mutation of genes for the receptors.
•GH secretion is normal or high. But the hormone
cannot stimulate growth because of the abnormal GHS
receptors. So, dwarfism occurs.

60. 2. SIMMOND DISEASE
•Simmond disease is a rare pituitary disease. It is also called
pituitary cachexia.
•It occurs mostly in panhypopituitarism, i.e. hyposecretion of
all the anterior pituitary hormones due to the atrophy or
degeneration of anterior pituitary.
•A major feature of Simmond disease is the rapidly developing
senile decay. Thus, a 30years-old person looks like a 60-
years-old person.
•Skin on face becomes dry and wrinkled. So, there is a
shrunken appearance of facial features.

62. THYROID GLAND

63. •Thyroid is the largest endocrine gland situated at
the root of the neck on either side of the trachea.
It has two lobes, which are connected in the
middle by an isthmus .
•It weighs about 20 to 40 g in adults. Thyroid is
larger in females than in males. The structure and
the function of the thyroid gland change in
different stages of the sexual cycle in females.
•Its function increases slightly during pregnancy
and lactation and decreases during menopause

64. HORMONES SECRETED BY THYROID GLAND
Thyroid gland secretes three hormones:
1.Tetraiodothyronine or T4 (thyroxine) (90% )
2.Tri-iodothyronine or T3 (9-10%)
3.Calcitonin
•Synthesis of thyroid hormones takes place in thyroglobulin,
present in follicular cavity.
•For the synthesis of normal quantities of thyroid hormones,
approximately 1 mg of iodine is required per week or about 50
mg per year.
•The potency of T3 is four times more than that of T4.
•T4 acts for longer period than T3. Duration of T4 action is four
times more than T3 action

66. FUNCTIONS OF THYROID HORMONES
Thyroid hormones have two major effects on the body:
I.To increase basal metabolic rate
II.To stimulate growth in children.

67. METABOLIC EFFECTS OF THYROID HORMONES
Carbohydrate metabolism:
•Stimulates carbohydrate metabolism.
•Increases the rate of glucose uptake by cells
•Increases insulin secretion as a secondary effect.
Fat metabolism:
•Stimulates fat metabolism.
•Increases the free fatty acid concentration in plasma.
Basal metabolic rate:
•Thyroxine increases the metabolic activities in most of the body tissues, except
brain, retina, spleen, testes and lungs.

68. CVS:
•Increases blood flow, heart rate, cardiac out put and
pulse pressure .
Respiratory:
•Increases rate and depth of respiration.
CNS:
•Promotes the growth and development of brain and CNS
during fetal life.
•Thyroid deficiency in infants results in abnormal
development of synapses, defective myelination and
mental retardation.

69. Musculoskeletal system:
•Thyroxine is essential for the normal activity of skeletal muscles,
•Excessive quantity causes muscle weakness because of protein catabolism. This
condition is called thyrotoxic myopathy.
Sleep:
•It stimulates the neurons, hence in case of hyperthyroidism even though the
patient is sleepy because of tiredness he/she can’t sleep.
•On the other hand, hyposecretion of thyroxine causes somnolence.

70. ACTION ON GROWTH
•Thyroid hormones have general and specific effects on growth.

•Increase in thyroxine secretion accelerates the growth of the body, especially in growing children.
•Lack of thyroxine arrests the growth.
•At the same time, thyroxine causes early closure of epiphysis. So, the height of the individual may
be slightly less in hypothyroidism.
•Thyroxine is more important to promote growth and development of brain during fetal life and first
few years of postnatal life.
•Deficiency of thyroid hormones during this period leads to mental retardation.

72. Body temperature
Metabolism
Excess iodine intake
Metabolism
Regulation of secretion of thyroid
hormones
Iodide is an important factor regulating the
synthesis of thyroid hormones. When the
dietary level of iodine is moderate, the
blood level of thyroid hormones is normal.
However, when iodine intake is high, the
enzymes necessary for synthesis of thyroid
hormones are inhibited by iodide itself,
resulting in suppression of hormone
synthesis. This effect of iodide is called
WolffChaikoff effect

73. CALCITONIN
•Calcitonin is a peptide containing 32 amino acids.
•It is secreted by Para follicular cells / C cells of thyroid gland.
•Also called as thyrocalcitonin.
•Plasma concentration – 10-20pg/ml
•The action of CT on calcium metabolism is antagonistic to that of PTH

74. •calcitonin promotes calcification by increasing the activity of osteoblasts.
•Decreases ability of osteoclasts to resorb bone .
•calcitonin decreases bone resorption and increases the excretion of Ca into
urine.
•CT, therefore has a decreasing influence on blood calcium.
OSTEOCLASTS CELLS

• Lose their ruffled borders
•Undergo cytoskeletal
rearrangement
•Decreased mobility
•Detach from bone

75. DISORDERS OF THYROID GLAND

76. HYPOTHYROIDISM
•Decreased secretion of thyroid hormones is called hypothyroidism.
Hypothyroidism leads to myxedema in adults and cretinism in children

77. 1.MYXEDEMA
•Myxedema is the hypothyroidism in adults,
characterized by generalized edematous appearance.
•Myxedema occurs due to diseases of thyroid gland,
genetic disorder or iodine deficiency.
•Common cause of myxedema is the autoimmune disease
called Hashimoto’s thyroiditis, which is common in late
middle-aged women

78. SIGNS & SYMPTOMS
1.Swelling of the face
2.Bagginess under the eyes
3.Non-pitting type of edema (It is because of accumulation of proteins with
hyaluronic acid and chondroitin sulfate, which form a hard tissue with
increased accumulation of fluid.
4. Atherosclerosis

79. ORAL MANIFESTATION
•macroglossia and enlarged lips are seen as a result of the deposition of water
and protein.
•Facial swelling of non-pitting type may be seen.
•Mandible will be underdeveloped.
•There is greater tendency to periodontal diseases

80. 2. CRETINISM
•Cretinism is the hypothyroidism in children, characterized by stunted growth.
•Cretinism occurs due to congenital absence of thyroid gland, genetic
disorder or lack of iodine in the diet.

81. •A newborn baby with thyroid deficiency may appear
normal at the time of birth because thyroxine might have
been supplied from mother. But a few weeks after birth,
the baby starts developing the signs like sluggish
movements and croaking sound while crying. Unless
treated immediately, the baby will be mentally retarded
permanently.

•Skeletal growth is more affected than the soft tissues. So,
there is stunted growth with bloated body.
•The tongue becomes so big that it hangs down with
dripping of saliva. The big tongue obstructs swallowing
and breathing. The tongue produces characteristic
guttural breathing that may sometimes choke the baby

83. HYPERTHYROIDISM
•Increased secretion of thyroid hormones is called hyperthyroidism.
Hyperthyroidism is caused by:
1.Graves’ disease
2.Thyroid adenoma.

84. •Graves’ disease Graves’ disease is an autoimmune disease and it is the most common
cause of hyperthyroidism.
•In Graves’ disease, the B lymphocytes (plasma cells) produce autoimmune antibodies
called thyroid-stimulating autoantibodies (TSAbs).
•the concentration of TSH is low or almost zero in plasma of most of the hyperthyroid
patients.
characteristic features of thyroid eye disease including marked chemosis and eyelid oedema (A); eyelid retraction, swelling and
exophthalmos (B). Also shown are features of thyroid acropachy in a patient with Graves’ disease including soft-tissue oedema and
clubbing (C) with the characteristic eroded bone margins of the phalanges suggestive of new periosteal bone formation and periosteitis (D)

85. Signs and Symptoms of Hyperthyroidism
1.Intolerance to heat
2.Increased sweating
3.Decreased body weight due to fat mobilization
4.Diarrhea due to increased motility of GI tract
5.Muscular weakness
6.Nervousness, extreme fatigue, mild tremor in the hands.
7.Toxic goiter
8.Oligomenorrhea or amenorrhea
9.Exophthalmos
10.Polycythemia
11.achycardia and atrial fibrillation

86. ORAL MANIFESTATION
•The accelerated dental eruption in children is seen in this condition.
•Maxillary or mandibular osteoporosis, high index of caries and periodontal
diseases, burning sensation of tongue, incidence of Sjogren’s syndrome and
systemic lupus erythematosus are also reported

87. THYROID HORMONE IN ORTHODONTICS
•Poumpros (1994): Reported a protective effect of thyroxine on root resorption that had
been induced by orthodontic tooth movement.
•Shirazi and colleagues (1999): Thyroid hormone administration increases rate of tooth
movement in rats and also reduces the extent of root resorption.
•Seunghye Kim et al (2010): Increased rate of tooth movement during the forced
eruption procedure was observed in a young girl in correlation with the high level of
serum thyroid hormone.
•In this case, the rate of orthodontic movement of the impacted canine was increased
during the hyperthyroid period. Then, the rate decreased when antithyroid drugs
(propylthiourasil) were administered to adjust the level of serum thyroid hormone.

88. PARATHYROID GLAND

89. •Human beings have four parathyroid glands, which
are situated on the posterior surface of upper and
lower poles of thyroid gland (Fig. 68.1).
•Parathyroid glands are very small in size, measuring
about 6 mm long, 3 mm wide and 2 mm thick,
with dark brown color.
•Each parathyroid gland is made up of chief cells
and oxyphil cells.
•Chief cells secrete parathormone.

90. PARATHORMONE
•Parathormone secreted by parathyroid gland is essential for the maintenance of blood
calcium level within a very narrow critical level.
•It also controls blood phosphate level.
•Primary action of PTH is to maintain the blood calcium level within the critical range of 9
to 11 mg/dL.
•PTH maintains blood calcium level by acting on:
1.Bones
2.Kidney
3.Gastrointestinal tract
•The prime function of PTH is to elevate serum calcium level

92. ROLE OF PTH IN RATE OF ORTHODONTIC TOOTH MOVEMENT
•Local or systemic application of PTH increases the rate of OTM.
•The same effect is seen when endogenous PTH synthesis is stimulated by, for example, a
low-calcium diet.
•Intermittent short administration of PTH or its active fragment (1-36) (teriparatide), on the
other hand, has an anabolic effect on bone.
Medication effects on the rate of orthodontic tooth movement: A systematic literature review (Am J
Orthod Dentofacial Orthop 2015;135: 16-26)

93. DISORDERS OF PARA-THYROID GLAND

94. HYPERPARATHYROIDISM
•Hypersecretion of PTH is called hyperparathyroidism. It results in
hypercalcemia. Hyperparathyroidism is of three types:
•Primary hyperparathyroidism
•Secondary hyperparathyroidism
•Tertiary hyperparathyroidism.

95. PRIMARY HYPERPARATHYROIDISM
•An abnormality of the parathyroid glands causes inappropriate, excess PTH
secretion (tumour) Eg Parathyroid adenoma or parathyroid hyperplasia.
SECONDARY HYPERPARATHYROIDISM
•High levels of PTH occur as a compensation for hypocalcemia, rather than as
a primary abnormality of the parathyroid glands.
• Occurs in pathological conditions such as:
i. Chronic renal failure.
Ii. Vitamin D deficiency.

96. TERTIARY HYPERPARATHYROIDISM
•Tertiary hyperparathyroidism is due to hyperplasia (abnormal increase in
the number of cells) of all the parathyroid glands that develops due to
chronic secondary hyperparathyroidism.

97. HYPERCALCEMIA
•Hypercalcemia is the increase in plasma calcium level. It occurs in
hyperparathyroidism because of increased resorption of calcium from bones.
•Depressive effects of hypercalcemia are noticed when the blood calcium level
increases to 12 mg/dL.
•The condition becomes severe with 15 mg/dL and it becomes lethal when
blood calcium level reaches 17 mg/dL.

98. CLINICAL FEATURES

99. ORAL MANIFESTATION
•Common oral manifestations in patients with hyperparathyroidism (HPT) are brown
tumor, loss of bone density, soft tissue calcification, and
•Dental abnormalities, such as development defects, alterations in dental eruption.
•Malocclusion due to drifting of teeth, with definite spacing of the teeth may be one of
the first signs of the disease.
•Loss of lamina dura
•Pseudocystic lesion can also be presents,
•Oral radiographs (intraoral and panoramic) of hyperparathyroid patient reveal
generalized rarification of the jaws.
•The radiograph is typically described as loss of medullary trabecular pattern, jaw
appears finely radiopaque described as clear "ground glass" appearance

100. Hyperparathyroidism. A, B; intraoral radiographs of cases with secondary hyperparathyroidism demonstrate loss of
lamina dura and granular pattern of alveolar bone. C; lateral oblique radiographs of a different case with primary
hyperparathyroidism shows a brown tumor of the mandibular body causing cortical expansion and root resorption.

101. HYPOPARATHYROIDISM
•Hyposecretion of PTH is called hypoparathyroidism. It leads to hypocalcemia (decrease in
blood calcium level).
CAUSES
•Accidental removal of gland during surgery
•occasionally from autoimmune destruction of the gland.
•Congenital absence of the gland.
•Atrophy of the gland- Idiopathic
•Deficiency of receptors for PTH inthe target cells. In this, the PTH secretion is normal
or increased but the hormone cannot act on the target cells. This condition is called
pseudohypoparathyroidism

102. HYPOCALCEMIC TETANY
•Tetany is an abnormal condition characterized by violent and painful muscular
spasm, particularly in feet and hand. It is because of hyperexcitability of nerves
and skeletal muscle due to calcium deficiency.

103. SIGNS AND SYMPTOMS
•Hyper-reflexia and convulsions
•Carpopedal spasm
•Laryngeal stridor
•Cardiovascular changes :
i.Dilatation of the heart
ii.Prolonged duration of ST segment and QT interval in
ECG
iii.Arrhythmias (irregular heartbeat)
iv.Hypotension
v.Heart failure

104. LATENT TETANY
•Latent tetany, also known as subclinical tetany is the neuromuscular hyper excitability due to
hypocalcemia that develops before the onset of tetany.
•It is characterized by general weakness and cramps in feet and hand. Hyper excitability in these
patients is detected by some signs, which do not appear in normal persons.
1.Trousseau sign
2.Chvostek sign
3.Erb sign (Hyperexcitability of the skeletal muscles even to a mild electrical stimulus is called Erb sign.
It is also called Erb-Westphal sign)

105. ORAL MANIFESTATIONS OF HYPOPARATHYROIDISM
•enamel hypoplasia,
•widened pulp chambers, dental pulp calcifications, shortened tooth roots,
hypodontia
•Delay or cessation of dental development, mandibular tori and fungal infections
like chronic candidiasis,
• Paresthesia of the tongue or lips,
•delayed eruption, and there may be multiple unerupted teeth

106. ORTHODONTIC CONSIDERATIONS
•Relative studies have confirmed that parathyroid hormone could stimulate both
osteoclast-mediated bone resorption and osteoblast-mediated bone formation, therefore
accelerating the bone turnover rate.
•Continuous infusion of parathyroid hormone results in a catabolic effect, whereas
intermittent injection leads to an anabolic effect.
•Intermittent low-dose parathyroid hormone analogs have been widely administered in the
clinical treatment of osteoporosis.
•Salazar et al evaluated the tooth movement with intermittent parathyroid hormone
injections mentioned that unlike other osteoporosis treatment drugs such as
bisphosphonates, calcitonin, and calcium with vitamin D, which diminish bone resorption,
parathyroid hormones stimulated osteoblast function with no interference in osteoclast
activity and facilitated bone remodelling.

107. CONCLUSION
•Endocrinal disorders are relatively rare in a day to day practice.
However, adequate knowledge of this complex topic will help the
clinician to anticipate and prevent avoidable complications in the
dental management

108. REFERENCES
•Text book of medical physiology- gyton and hall (11th edition)
•Essentials of medical physiology ( 3rd edition- sembulingam)
•Role of Hormones in Orthodontics: A Review (Review Article) by Dr Sourabh Jindal, Dr
Amit Khera , Pradeep Raghav
•Oral manifestations of endocrine disorders by Sunitha Kesidi and Harsha Bhayya
(International Journal of Applied Dental Sciences 2019; 5(2): 476-478)
•Shafers text book of oral pathology- 10 edition
•The effect of hyperthyroidism on the rate of orthodontic tooth movement(Seunghye
Kim, Seong Oh Kim, Chul Hee Kim*, Jae-Ho Lee, Heung-Kyu Son J Korean Acad Pediatr
Dent 37(2) 2010)