hormones

1. Presented by :
Dr. Venisha Pandita
PG Ist Year
Department of Public
Health Dentistry

2. CONTENTS:




Introduction
Anatomy and physiology.
Hormones of pituitar y gland and
associated diseases
Hormones of thyroid gland and
associated diseases
Hormones of parathyroid gland and
associated diseases

3. 





Hormones of adrenal gland and associated
diseases
Hormones of gonads and associated
diseases
Pregnancy
Menopause
Conclusion
References

4. The
word hormone is derived from the Greek
“hormao” meaning “I excite or arouse”, was given by
Starling in 1905.
Hormones
are secretory products of
ductless(endocrine) glands released directly into the
circulation in small amounts in response to a specific
stimulus and on delivery in circulation produces
response on the target cells or organs.

5. CHEMISTRY OF HORMONES



Steroids
Proteins and polypeptides
Amino-acid derivatives.
MECHANISM OF ACTION: Hormone receptors found on target cell
membrane are termed as external receptors
and those within cytoplasm and nucleus are
termed internal receptors.

6. 


The endocrine system is specifically designed to
integrate and control the human body’s
innumerable metabolic activities.
Its functioning components are endocrine
glands.
In most instances, the agent stimulating or
inhibiting their activity is the hormone produced
by the corresponding target gland

7. 
1.
2.
3.
4.
5.
6.


1.
2.
Hormones secreted by anterior lobeGrowth hormone,
Adrenocorticotropic hormone,
Thyroid stimulating hormone,
Follicle stimulating hormone,
Leutinizing hormone
Prolactin
Hormone secreted by intermediate –
melanocytes stimulating hormone
Hormone secreted by posterior lobeVasopressin
oxytocin.

8. DISEASES OF PITUITARY
GLAND
HYPERPITUITARISM


a)
b)
It results from hyper function of anterior lobe of
pituitary gland, most significantly with increased
production of growth hormone.
TYPES:Gigantism
Acromegaly

9. Clinical features of gigantism:



Stature of individual- generalized overgrowth
of most tissue in childhood
Symptoms
Skull

11. ORAL MANIFESTATIONS
Symptoms

Teeth

Jaw bone

Palate

Macroglossia

Lips
Radiological features

Skull changes

Air sinuses

Teeth

Jaw bone

12. 


Surgery- trans sphenoidal surgery may result
in cure of growth hormone excess especially in
patients with macroadenoma.
Medical therapy- octreotide, a long acting
analogue of somatostatin, lowers growth
hormone.
Radiotherapy

13. HYPOPITUITARISM


It results due to reduced secretion of pituitary
hormone which may occur due to pituitary
adenoma that compresses the pituitary gland. It
results in pituitary dwarfism.
Total absence of all pituitary secretions is known
as panhypopituitarism.
Etiology:



Disease of pituitary gland
Space occupying lesion
Sheehan’s syndrome

14. Clinical features: Short stature of individual
 Hypocalcemia
 Diabetic insipidus
 Symptoms
 Sexual characteristics
 Skull
ORAL MANIFESTATIONS


Jaw bone
Teeth

15. 

Radiographic features:Teeth-Complete absence of third molar bud.
Roots of teeth are short and apices are wide
open.
Alveolar bone- there is loss of alveolar bone.
Management:

Removal of cause
Growth hormone replacement therapy

17. 
1.
2.
3.
Thyroid hormones are:
Thyroxine (T4)
Tri-iodo-thyronine (T3)
calcitonin

18. Hyper thyroidism




It is a syndrome in which there is excessive
production of thyroxin in thyroid gland.
Etiology
Exophthalmic goiter
Toxic adenoma
Pituitar y disease

19. Clinical features





Age and sex- higher predilection for females
between 20 and 40 years.
Thyroid features- thyroid is diffusely enlarged,
smooth, possible asymmetrical and nodular, a
thrill may be present, may be tender.
Neuromuscular
Gastrointestinal
Cardiorespiratory

20. 



Ocular
Reproductive
Dermatological
Others- heat intolerance, sweaty and warm
extremities, thin shiny skin, increased pulse rate and
fatigue, thirst and osteoporosis.

22. Management




Anti thyroid drugs
Subtotal thyroidectomy
Radioactive iodine
Beta-blockers.

23. ORAL MANIFESTATIONS




Teeth- advanced rate of dental development
and early eruption with premature loss of
primary teeth.
Alveolar bone- generalized decrease in bone
density or loss of some areas of edentulous
alveolar bone.
Radiographic features
Generalized osteoporosis
Alveolar resorption

24. HYPOTHYROIDISM


It is caused by insufficient secretion of thyroxin
by the thyroid gland.
Failure of thyrotropic function on the part of the
pituitary gland or any atrophy or destruction of
the thyroid gland or an atrophy or destruction of
thyroid gland leads to an inability of the gland to
produce sufficient hormone to meet the
requirement of the body.

26. Types:
 Cretinism
 Juvenile myxedema
 Myxedema
 Primary hypothyroidism
 Secondary hypothyroidism
Clinical Features:
Cretinism and juvenile
myxedema
 Age
 Symptoms
 Bones
 Signs

27. Myxedema
Symptoms


Early symptoms- weakness, fatigue, cold
intolerance, lethargy, dryness of skin,
headache, menorrhagia and anorexia
Late symptoms- slowing of intellectual and
motor activity, absence of sweating, weight
gain, constipation, pallor, decreased sense of
taste and smell, aches and pains.

28. Signs





Face
Eyes
Skin
Tendon reflexes
Other features- bradycardia , disorientation,
thickened nose.

29. Myxedema

30. Oral manifestations
Cretinism and juvenile myxedema
 Teeth
 Jaw bone
 Tongue
 Skull
 Face
 Lips
Myxedema
 Tongue and lip
 Face
 Teeth

31. Management



Levothyroxine, which is available as 25,
50,100ug tablets.
It is customary to start slowly and a dose of
50ug/day is given for 3 weeks to finally
150ug/day.
In elders and patients with ischemic heart
disease, the initial dose should be 25ug/day.

32. 


Lowering the body temperature
Other therapies like supporting respiration, narcotic
antagonist and oxygen if necessary
Hospitalization if severe.

33. 

Precaution- the use of sedative and
analgesic are dangerous as these agents tend
to precipitate coma in patients with
hypothyroidism.
Inpatients with severe hyperthyroidism the
emergencies likely to occur thyroid crisis,
emotional disturbances, cardiac difficulties.

35. 
Parathyroid hormone- PTH is a single chain
polypeptide of 84- amino acid which are
synthesized by the chief cells and released in
response to a fall in serum ionized calcium
concentration.

36. Hyperparathyroidism

It is an endocrine disorder in which there is an
excess of circulating parathyroid hormone.
 Excess PTH stimulates osteoclast to mobilize
calcium from skeleton leading to hypercalcemia
in addition to PTH increased renal tubular
reabsorption of calcium.
Types: Primary
 Secondary
 Tertiary

37. Clinical features








Age and sex- female :male ratio is 3:1. mainly
30-60 years of age.
Classic triad- bones, grones and stones
Renal calculi
Gastrointestinal problems
Hypercalcemia
Bone pane and fractures.
Cartilage
Eyes

39. 

Oral manifestations
Brown tumor
Teeth- drifting and loss of teeth, malocclusion

40. MANAGEMENT




Surgery- hyperplastic tissue should be removed
surgically
Vitamin D supplement
Parathyroidectomy
Precaution-restriction of dietary phosphate,
phosphate binding agent and aluminum salts
should be done.

41. Hypoparathyroidism

It is an uncommon condition in which there is
insufficient secretion of parathyroid hormone.
Etiology
a)
b)
c)
Surgical damage to parathyroid gland
Damage from radiotherapy
Autoimmune
Clinical features



Hypocalcaemia
Symptoms
Trousseaus sign

42. ORAL MANIFESTATIONS



Teeth- hypoplasia of enamel. Delayed eruption, external
root resorption and root dilacerations
Chvostek sign
Candidiasis

43. 

Calcium and Vit D supplement.
Intravenous calcium gluconate

44. Pseudohypoparathyroidism


It is also called Albright hereditary
osteodystrophy.
In this normal parathyroid hormone is present
in the body but biochemical pathway
responsible for activating target cells are
defective in function.
Types
Type I: Type I a- molecular defect of intracellular
binding protein prevents formation of cyclic
adenosine monophosphate. This will hamper
cell metabolism.

45. 

Type I b- defective receptor for the PTH on the
surface of target cells. It Is an autosomal dominant
trait.
Type I c- there is defective adenylate cyclase
Type II- There is induction of camp by PTH in target
cells, but function response by cell is not invoked

46. Clinical features



Stature
Shortened finger
Osteoma cutis
ORAL MANIFESTATIONS


Facial features-mid facial hypoplasia, the face is
rounded in appearance
Teeth- generalized enamel hypoplasia, oligodontia,
delayed eruption of teeth.
Management
vitamin D and calcium

48. 


1.
2.
Parts of glands each gland is divided into
adrenal medulla and a cortex.
ADRENAL MEDULLA- it arises from ectodermal
tissues and function as a part of the
sympathetic nervous system.
It manufactures and secretes two
catecholamine:
epinephrine
nor-epinephrine

49. 
a)
b)
c)
ADRENAL CORTEX – it secretes three major
classes of hormone:Glucocor ticoids or cor tisols
Mineralocor ticoids/ aldosterone
Sex hormones( testosterone, estrogen,
progestrone)

50. Addison’s disease

It is also called as chronic adrenal
insufficiency of the adrenal cortex.
Etiology:


Autoimmune
Infection
Drugs

51. Clinical features

Age and sex- more common in males and
frequently seen in 3rd and 4th decade.

Symptoms- feeble heart action, general debility,
vomiting, diarrhea, postural hypotension,
reduced resistance to infection, trauma and
stress.

Sign- bronzing of skin and pigmentation of oral
mucosa.

52. 
Metabolic function- decreased cortisol level interferes
with the manufacture of carbohydrates from proteins,
causing hypoglycemia and diminished glycogen
storage in liver.

Neuromuscular function- it is inhibited producing
muscle weakness.

53. ORAL MANIFESTATION

bronze pigmentation
Management


Glucocorticoids replacement
Supplement mineralocorticoids

54. Cushing Syndrome
It arises from excess secretion of glucocorticoids
by the adrenal glands.
Etiology



Adrenal tumor
Administration of corticosteroids
Ectopic
Clinical features




Age and sex
Symptoms
Moon face
Buffalo hump

55. ORAL MANIFESTATION

Dental age- in children growth and development
including skeletal and dental age may be
retarded.
Management




Surgery
Radiotherapy
Drugs- Metyrapone 2-6 gm/day in divided doses
by mouth,
Aminoglutethimide, ketoconazole are also given
which act by blocking steroid synthesis.

56. Adrenal insuf ficiency

It is relatively rare and usually occurs in
connection with an acute septicemia and is
called as waterhouse-friderichsen syndrome.
Types: Primar y- It occurs due to disorders of pituitary
or adrenal glands.
 Secondar y- it occurs due to chronic
administration of corticosteroid resulting in the
suppression of endogenous steroid.

57. Etiopathogenesis





Sudden withdrawal of steroid
Following stress
Bilateral adrenalectomy
Destruction of pituitary gland
Trauma
Clinical features



Age- occurs primarily in children
Onset- rapidly fulminating septic course
Symptoms- patient is not able to tolerate stress. There
is anxiety, vomiting, cold clammy skin, lethargy and
partial or complete loss of consciousness.

58. 
Sign- oral, conjunctival, and vaginal mucosa often
show patches of pigmentation.
ORAL MANIFESTATION

Early eruption- teeth may erupt early, compared
with the normal, but the eruption is in harmony
with the skeletal age.

59. Management

Replacement therapy-it is given in combination of
glucocorticoids, mineralocorticoids and anabolic
steroids.
Dental considerations:
 Defer the treatment
 Position the patient
 Airway maintenance
 Saline-i.v 5% dextrose saline
 Hydrocortisone-100-200mg of hydrocortisone

60. 

1.
2.
Exocrine secretion of pancreas:
Pancreatic juices( promote digestion of
carbohydrates,fats and proteins)
Endocrine secretion:
Insulin
glucagon

61. Diabetes mellitus



It may be caused by autoimmune response.
Principal laboratory sign are hyperglycemia.
It is caused by disorders of carbohydrate
mechanism resulting from insulin deficiency or
ineffectiveness, producing hyperglycemia and
glycosuria.

62. T YPES

Type I or insulin dependent- it occurs due to
deficiency. There is lack of insulin production
resulting in severe hyperglycemia and ketoacidosis.

Type II or non-insulin dependent- it occurs due
to insulin resistance.

65. Pathogenesis

a)
b)
c)
d)
Type I diabetes mellitus
Autoimmune disorder.
Increase blood glucose level- as there is deficiency
of insulin glucose will remain in blood as absorption
of it hampered. So blood glucose level is increased.
Glucose as main energy source
Polyuria and polydipsia
Type II diabetes mellitus
a) Decrease in number of insulin receptor- This
results in non absorption of glucose in the body.


66. Etiology
Type I diabetes mellitus
 Viruses
 Diet
 Stress
 Immunological factors
Type II diabetes mellitus
 Genetic
 Environmental factors- lifestyle, malnutrition, eg,
pregnancy.

67. Clinical features










Polydipsia
Polyuria
Polyphagia
Breath
Visual activity
Atherosclerosis
Diabetic neuropathy
Infection
Other symptoms- nocturia, weight loss,
fatigue, obesity, temperature and hypertension
Symptoms of type II diabetes mellitus- mild in
nature with this disease discovered on routine
hematological examination.

68. ORAL MANIFESTATIONS










Effect on periodontium
Periodontitis
Median rhomboid glossitis
Oral candidiasis
Localized osteitis
Burning mouth
Trigeminal nerve involvement
Xerostomia and increase caries activity
Delayed healing
Radiographic features
loss of lamina Dura with blurring of alveolar crest,

69. ADA criteria 1997 endorsed by WHO 1998 for diagnosis of
diabetes mellitus 2hours after giving 75gm glucose load:
Fasting
Normal
DM
Impaired fasting
glycemia
IGT
< 110
> 126
> 110 & <126
< 126
Post- Prandial
< 140
> 200
< 140
>140 & <200

70. Complications




Microangiopathy
Coronary artery disease
Blindness
Ketoacidosis, diabetic coma, premature
mortality.

72. Management



Diet control
Oral hypoglycemic drugs- sulfonylureas, biguanides,
alfa-glucosidase inhibitors
Insulin therapy

73. Diabetes Insipidus



Causes- It occurs due to insufficiency of the
posterior pituitary hormone. In these patients
there is damage to the neurohypophyseal
mechanism for the production of vasopressin.
Symptoms- There is increased thirst and
passage of large quantities of urine. There is
also dehydration, headache, irritability, and
fatigue due to restriction of fluid.
Management- Administration of vasoprssin is
the treatment of choice. Desmopressin can be
given intranasal in a dose of 5-10mg once or
twice daily.

74. 

a)
b)
c)
d)
e)
f)
g)
DENTAL CONSIDERATIONS
Emergency
Dental managementAppointment should be of short duration and
in the morning
Glucose drink should be available.
Local anesthesia without epinephrine
Suturing
Physician referral
Antibiotic prophylaxis
Avoid complicated oral procedure.

75. Hypergonadism


It occurs in children, results in precocious
puberty.
The long bone develops quickly and child may
initially turn toward tallness, but this is offset by
the early fusion of epiphyses so that adult’s person
may be short.

76. Hypogonadism



It occurs in equal frequency in males and females.
The bones are long and slender and epiphyses are
late in fusion.
The supracilliary ridges, malar bone, and mandible
show greater development.

77. 


The chin is pointed, the palate is high and
markedly arched and irregularities of the teeth
occur.
The mandible tends to become enlarged.
The skull is small and there is marked or even
excessive enlargement of the frontal and
sphenoid sinuses and especially mastoid air
sinus.

78. PREGNANCY
•condition of having a developing embryo or fetus in
the body
•In Human duration of pregnancy is about 266
days after conception.
•Roughly divided in three trimesters of about three
calendar months each-into the embryonic period
lasting from fertilization through the first eight
weeks of pregnancy and the fetal period during the
remainder of pregnancy

79. ORAL MANIFESTATION
•The Popular notion that pregnancy cause tooth
loss “a tooth for every pregnancy” and that
calcium is withdrawn in significant
amounts from the maternal dentition to
supply fetal requirements has no histological,
chemical, evident to support it.
•In other hand, calcium is readily mobilized from
bone to supply these demands and
demineralization of alveolar processes can result.

80. •Caries activity is attributed to an increase in
local cariogenic factors
•Condition that may influence the pregnant
patient’s teeth is acid erosion, which may
caused by repeated regurgitation of gastric
contents associated with morning sickness or
esophageal reflux.
•Periodontal disease occurs in 50% to
100%of all pregnant women
•Gingival changes occur most frequently in
association with poor oral hygiene and local
irritants, esp bacterial plaque.

81. •Clinically, the appearance of inflamed
gingiva during pregnancy is
characterized by a fiery red color of
marginal gingiva and interdental
papillae
•Tissue is edematous, with a smooth,
shiny surface texture, loss of resiliency,
and tendency to bleed easily.
•Interdental papillae may hypertrophy
and form pseudopocket.

82. 
Tumor like growths, usually on the interdental papillae
or other areas of the frequent irritation..it is referred
to as a “pregnancy tumor”, epulis gravidarum,
or pregnancy granuloma .

Poor oral hygiene invariably is present, and often
there are deposits of plaque or calculus on the teeth
adjacent to the lesion.

83. •Full development granuloma is a sessile or
pedunculated lesion that is usually painless.
•Color varies from purplish red to deep blue.
•Bone destruction is rarely observed around
pregnancy granulomas.
•Oral findings that may be seen in pregnant women
is generalized tooth mobility.
•probably related to the degree of the gingival
disease and the disturbance of the attachment
apparatus, as well as to mineralisation; changes in
the lamina dura.
•Condition usually reversed after delivery.

84. Dental Management
•Pregnant patients begins with thorough medical
history.
•History should note any complications the patient
has encountered in the pregnancy to date and record
any previous miscarriages, recent cramping,
•No elective dental care should be undertaken during
the tri-semester.
•Prolong chair time is avoided
•Emergency dental care may be rendered at any time
during pregnancy, after consultation to physician

85. MENOPAUSE




Menopause is not a disease, it is a natural
transition period in ever woman's life.
Menopause is a time of declining ovarian
function
However, during menopause, many women may
experience uncomfortable symptoms such as
hot flashes, vaginal dryness, depression,
sleeplessness, etc.
Traditionally women have sought hormone
replacement

86. 








Some Possible Symptoms
Associated with various Stages
Hot flashes, flushes, night sweats and/or cold
of Menopause
flashes, clammy feeling
Bouts of rapid heart beat
Irritability, Mood swings, sudden tears
Trouble sleeping through the night (with or without
night sweats)
Irregular periods; shorter, lighter periods; heavier
periods, flooding; phantom periods, shorter cycles,
longer cycles
Loss of libido
Crashing fatigue
Anxiety, feeling ill at ease
Feelings of dread, apprehension, doom

87. Dental Management
•Postmenopausal osteoporosis can be prevented
and treated by sound dietary control adequate
levels of dietary calcium.
•The condition may be prevalent because of dietary
adequacies of young women and could become an
important issue in dental care for postmenopausal
women
•Counseling may be indicated for some patients,
and it is most appropriate for the dentist to refer
the menopausal patient for medical evaluation and
treatment to optimize the befits of dental
treatment.

88. 
Hormones form an integrate regulatory system
of human body. They regulate various human
systems like growth,digestion,reproduction ,etc.
Any dearrangement in hormonal function
immense effects on human body. Hence a
deeper understanding of hormones ,their
chemistry, mechanism and side effects are
important.

89. 






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