1. CORTICOSTEROIDS
Dr Vishal Mehrotra
Professor & HOD
Oral Medicine and Radiology,
Rama Dental College, Kanpur

2. DEFINITION:-
Hormones of adrenal cortex are collectively
known as corticosteroids. Three group of
hormones are secreted from gland:-
 Mineralocorticoids
 Glucocorticoids
 Sex hormones

3. HISTORY:-
1849 [South London Medical Society]
Clinical importance of adrenal gland was 1st
appreciated by ADDISON
“He describes fatal outcomes in patient with adrenal
destruction”.
1856,BROWN SEQUARD
“He describes that adrenal gland was necessary for
life”.

4. 1912,CUSHING
“He described patients with hypercorticism
&established the link between anterior pituitary
and adrenal function”
1949,Phillip Hench and assoc
“Isolated a substance from the adrenal gland that
had helpful effect on Rheumatoid Arthritis”.
1951,Hollander
“Revealed how steroids could be used locally with
reduction of systemic side effect”.

5. BIOSYNTHESIS:-
The corticoids are 21 carbon compounds
having a cyclo-pentanoperhydro-
phenanthrene nucleus. They are synthesized
in the adrenal cortical cells from
cholesterol.

7. MINERALOCORTICOIDS:-
They are of two types;-
 Aldosterone
 11-deoxycorticosterone

8. Functions:-
Effect on sodium reabsorption
It acts on the distal convoluted tubule and the collecting duct
and increase the reabsorption of sodium ions.
Effect on extra cellular fluid volume
It increases the sodium reabsorption from the renal tubules
the concentration of sodium in the body does not increase
to that extent.

9. Effect on blood pressure
It cause persistent increase in exrtacellular fluid
volume and the blood volume,finally leads to
increase in blood pressure.
Effect on potassium ions
It increase the K ions excretion through the renal
tubules.
Effect on sweat glands
Sodium is reabsorbed from the gland to prevent the
loss of sodium from the body.

10. Mode of action:-
 Aldosterone acts through the m-RNA
mechanism:-
1. Aldosterone diffuses readily into the interior of the
tubular epithelial cells.
2. In the cytoplasm.aldosterone combines with the specific
receptor protein.
3. Aldosterone-receptor complex diffuses into the
nucleus,and binds to the DNA and formation of m-RNA.
4. m-RNA diffuses back into the cytoplasm,along with
ribosome causes protein synthesis.

11. GLUCOCORTICOIDS:-
They are cortisol and corticosterone.
Cortisol or hydrocortisone is more potent
and has 95%of glucococorticoids activity.
Source of secretion:-
They are mainly secreted by zona fasiculata of
adrenal cortex.

12. Functions:-
Effects on carbohydrate metabolism
It increase the blood glucose level by two ways:-
 By promoting gluconeogenesis in liver from
amino acids.
 By inhibiting glucose uptake and utilization by
peripheral cells.

13. Effect on protein metabolism
It cause catabolism of proteins,decrease the
proteins in the cells and increase plasma
amino acids and protein content in liver by
the following:-
 By inhibiting the amino acid transport into cells
and by inhibiting the formation of RNA.
 At the same time it accelerate protein catabolism
and release of amino acids from tissues.
 It increase the transport of amino acids into
hepatic cells.

14. Effect on fat metabolism
It causes mobilization and redistribution of fats:-
 The fatty acids are mobilized from adipose tissue.
 The concentration of fatty acids increase in blood.
 Utilization of fat for energy is increased.

15. Effect on mineral metabolism
It enhances the retention of sodium and calcium to
some extent and increase the excretion of
potassium.
Effects on water metabolism
Whenever large quantity of water is taken,it
accelerate the excretion of water.
Effect on blood cells
It decrease the number of circulating eosinophils by
increasing the destruction of eosinophils in
reticuloendothelial cells.

16. Effect on vascular response
It is essential for the constrictor action of adrenaline
and nor-adrenaline.
Effect on CNS
Essential for normal function of CNS.
Anti-allergic actions
They prevent the various reactions in allergic
conditions.

17. Effect on resistance to stress
It is assumed that glucocosteroids enhance the
resistance by the following ways:-
 Immediate release of amino acids by hormone is
responsible for synthesis of new proteins,necessary to
withstand with stress.
 The fatty acids released from cells by hormones are
important for supply of more energy during stress.
 It enhance the vascular reactivity to catecholamines and
fatty acid mobilizing action of catecholamines,are
necessary to withstand with stress.

18. Anti-inflammatory effects
This hormone act during all stages of inflammation:-
 It causes the stabilization of the membrane of
lysosome,inhibits the release of proteolytic enzymes.
 Prevents the release of substance like histamine from the
affected tissue.
 It causes vasoconstriction &prevents rush blood to the
injured area.
 It inhibits migration of leukocytes into the affected area.

19.  Loss of fluid from plasma into the affected tissue
is prevented.
 It suppress T-cell and other leukocytes so
that,there is reduction in the reaction of tissues.

20. Immunosuppressive effects
It suppress the immune system of the body by
decreasing the number of circulating T-
lymphocytes,also prevents the release of
interleukin-2 by T-cells.

21. The immunosuppressive and anti-
inflammatory actions of glucocorticoids are
inextricably linked perhaps because they
both largely result from inhibition of
specific functions of leukocytes.[Chrousos
1995]

22. CELL TYPE FACTOR COMMENTS
Macrophages and
monocytes
A]Arachidonic
acid(prostaglandin
,leukotrienes)
B]cytokines,interl
eukin
Inhibited by the
hormone
Production&relea
se are blocked
Endothelial cells Acute phase
reactants,cytokina
se
Same as above for
mocrephages and
monocytes
Basophils Histamine
&leukotriene C4
IgE-dependent
release inhibited

23. Fibroblasts Arachidonic
acid
metabolites
Hormone
suppress the
factors
Lymphocytes Cytokines,TNF
-alpha
Hormone
suppress the
factors

24. PHARMACOKINETICS:-
 Corticosteroids are effective by oral as well by I.v
and I.m routes.
 These are metabolized in liver and some are
excreted unchanged by kidney.
 Plasma t ½ of hydrocortisone is 1.5hrs.
 Synthetic metabolites are more resistant and long
acting.

25. CLASSIFICATION:-
MINERALOCORTICOIDS
Compound Gluco Miner
alo
Equiv.dose
Desoxycorticosterone
acetate
0 100 2.5mg
Aldosterone 0.3 3000 0.2mg not
used clinically

26. GLUCOCOTRICOIDS
Compound Gluco Mineralo Equiv.dose
Short acting
(t ½ <12hrs)
1. Cortisol
2. Cortisone
1
0.8
1 20mg
25mg
Intermediate acting(t
½12-36 hrs)
1. Prednisolone 4 0.8 5mg

27. 2.Methlyprednisolone
3.Triamcinolone
5
5
0.5
0
4mg
4mg
Long acting(t ½ >36hrs)
1. Paramethasone
2. Dexametasone
3. Betametasone
10
25
25
0
0
0
2mg
0.75mg
0.75mg

28. PREPARATIONS & DOSE:-
CORTISOL
Used in:-
 Replacement therapy-20mg mor+10 mg afternoon
orally
 In shock,acute adrenal insufficiency-100mg
I.v.+10 mg/8hr infusion

29.  PREDNISOLONE
Used in
allergy,inflammatory
condition,autoimmune
disease and in
malignancies.
 5-60mg/day oral
 10-40mg I.m.
 TRIAMICINOLONE
More potent than
prednisolone.
 4-32mg/day oral
 5-40mg I.m.
 Can be used topically

30.  DEXAMETHASONE
Used as anti-
inflammatory and in
allergy conditions.
 0.5-5mg/day oral
 4-20mg/day I.v.
 Can be used topically
 BETAMETHASONE
 0.5-5mg/day oral
 4-20mg/day I.v./I.m.
 Also topical

31. ROUTES OF ADMINSTRATION:-

34. USES:-
[A] Replacement therapy
 Acute adrenal insufficiency
 Addison’s disease
 Congenital adrenal hyperplasia
DOSE:-0.6mg/kg/day in divided dose

35.  Pharmacotherapy
 Arthritides
 Collagen disease
 Severe allergic reactions
 Autoimmune disease
 Bronchial asthma
 Eye disease
 Skin disease
 Cerebral edema
 Malignancies
 Organ transplantation
 Shock

36. ADVERSE EFFECTS:-
MINERALOCORTICOIDS
 Sodium and water retention
 Edema
 Hypokalemic alkalosis
 Rise in BP

37. GLUCOCORTICOIDS
 Cushing’s habitus
 Fragile skin[purple striae]
 Hyperglycaemia
 Muscular weakness
 Susceptibility to infections
 Delayed healing
 Peptic ulcerations
 Osteoporosis

38.  Posterior subcapsular cataract
 Glaucoma
 Growth retardation
 Psychiatric disturbances
 Suppression of hypothalamo-pituitary-adrenal axis

40. CONTRAINDICATIONS:-
 Peptic ulcer
 Diabetes mellitus
 Hypertension
 Pregnancy
 Tuberculosis and other infections
 Epilepsy
 CHF
 Renal failure

41. THERAPUTIC USES IN DENTISTRY:-

42. [A] Oral ulcerations:-
 Denture induced ulcer
 Traumatic ulcer
 Recurrent ulcerative(aphthous)stomatitis
 Erosive lichen planus
 Erythema multiforme
 Pemphigus
 Desquamative gingivitis & stomatitis
 Geographic tongue
 Allergic stomatitis
 Herpes simplex

43.  Major aphthous ulcer
 Behcet’s syndrome
 Bullous pemphigoid
 Mucous membrane pemphigoid
 O.S.M.F

44. [B] OTHERS:-
 T.M.J disorders
 Postoperative pain
 Post herpetic neuralgia