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STERIODS ITS USES IN DENTISTR
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
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INTRODUCTION
STRUCTURE OF STEROIDS
CHEMISTRY AND SYNTHESIS OF STEROIDS
REGULATION OF SECRETION OF ADRENAL
CORTICOL HORMONES.
ABSORPTION,TRANSPORT,METABOLISM AND
SECRETION OF STEROIDS.
PHYSIOLOGICAL FUNCTION AND PHARMOLOGIC-
-OLOGICAL EFFECTS OF STEROIDS.
THERAPEUTIC USES OF STEROIDS
*GENERAL.
*USES IN DENTISTRY.
ADVERSE EFFECTS OF STERIODS.
CONCLUSION.
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INTRODUCTION
The adrenal cortex secretes three distinct groups of
Steroid hormones .
. Zona glomerulosa-secretes aldosterone and
Desoxycorticosterone( mineralocorticoids).
.Zona fasciculata -secretes cortisone and cortisol
(glucocorticoids).
.Zona reticularis forms dehydroepiandrosterone and
androstenedione (androgens) and traces of estrogens .
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Adrenal cortex is more important than medulla.
Steroids principles were elucidated by kendall.
1949 Hench used steroids in the treatment of rheuma-
toid arthritis.
Corticosteroids are widely used in various conditions.
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Chemistry and synthesis
All the basic structure of steroid is a complex
cyclopentanophenanthrene ring with various functional
groups attached to different carbon atoms.
The steroids can be synthesized basically from 2 carbon
acetate chains via cholesterol.
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.The adrenal glands produce and secrete gluco corticoid-
(cortisol)in response to hormonal and nervous
system stimuli.
.During periods of stress, the centre in the
hypothalamus responds to stimuli and releases
corticotrophin –releasing factor.
.CRF stimulates ACTH secretion from the anterior
pituitary gland.
.This hypothalamic –pituitary axis operates on
the principle of negative feedback system and
regulates the level of circulating cortisol.
.
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.When the level of circulating cortisol has raised
adequately to meet increased demand , further
release of CRF and ACTH is inhibited because
of physiologic needs no longer require
corticosteroid output.
.Normally the average rate of cortisol secretion is 15 to20
mg?/dl.
.Peak cortisol concentration occurs between 6 to 8 am
then slowly decreased in the afternoon and evening.
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Mechanism of action
Adrenocortical steroids enter cells where they combine
with steroid receptors in the cytoplasm.
The combination then enters the nucleus where it
controls the synthesis of proteins, including enzymes that
regulate vital cell activities over a wide range of
metabolic functions including all aspects of inflammation.
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CARBOHYDRATE AND PROTEIN METABOLISM
Important effects are inhibition of incorporation of amino
acids into protein in the peripheral tissues (anti anabolic
action)and stimulation of their conversion into glucose
(neoglucogenesis)in the liver .
During the process of neo-glucogenesis the amino acids are
de--aminated and the nitrogen residue is excreted as urine,
this accounts for.
Inability of the adrenalectomised animal to maintain
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normal blood sugar level while fasting and the ability of
glucocorticoids to correct this ability.
Hyperglycemia and glycosuria induced by chronic admi-
-nistration of glucocorticoid in large doses and encounte-
-red in Cushing’s syndrome.
-Also inhibits peripheral glucose utilisation.
FAT METABOLISM
*Play a permissive role in the metabolisation of fat from
the peripheral fat depots by adrenaline by growth
hormone.such mobilization is markedly inhibited in the
total absence of glucocorticoids.
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-Prolonged administration of excessive glucocorticoid
cause a re-distribution of fat in the body ,with a loss from
the extremities and a deposition is the neck (buffalohump)
supraclavicular area and face (moonFace).
ELECTROLYTE AND WATER METABOLISM
Hydrcortisone has a feeble salt retaining and potassium
Wasting effect.when larger doses 300mg/24hrs are used,
sufficient salt retention occurs to make the concurrent use
of minerals corticoid unnecessary.
Cortisol is essential for excreting a water load.Adrenale-
-ctomised animals cannot excrete a water load and tend
to develop water intoxications.
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This defect is corrected by administration of glucocorticoid
CALCIUM METABOLISM AND BONE.
In pharmacological doses,glucocorticoids antagonize the
action of vitamin D on the gut and reduce absorption of
calcium Given in large doses for prolonged periods they
interferes with the development of cartilage and inhibit the
linear growth in children.
As a result of protein catabolic action ,gluco corticoids
inhibit the formation of new bony tissue and contin-
-uous resorption lead to severe osteoporosis in chronic cases
of hypercorticism.
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C.V.S
Important changes which occur in adrenal insuffic--
iency are partly due to mineralo-corticoid and partly due
to glucocorticoid deficiency.
Usually the blood volume and blood pressure are reduced
and blood viscosity is increased.These defects are partly
corrected by administration of sodium chloride or
mineralocorticoid.Addition of a glucocorticoid completely
restores the circulation to normal.
Absence of gluco corticoids leads increase in the capillary
permeability ,Inadequate vasomotor response of smaller
blood vessels and decrease in cardiac output.
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Glucocorticoid potentiates pressor response of blood
vessels to adrenaline and noradrenaline , Hypertension is
sometimes seen during chronic administration of
glucocorticoids.
SKELETAL MUSCLE
Maintenance of normal muscle function requires adequate
concentration of corticosteroids,but excessive amounts
lead to abnormalities.
Muscle weakness in adrenal insufficiency is largely due to
inability of the circulatory system to respond to the stress
of increased muscle activity .
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CNS
Patients receiving large doses of glucocorticiods
sometimes show mood elevation ,euphoria, nervousness,
restlessness and Psychosis.
HEMATOLOGICAL ACTIONS.
Hyperplasia of lymphoid tissues and peripheral lymphoc-
-ytosis is in Addison disease.
Lymphocyotpenia and dissolution of lymphatic masses in
the body is seen in cushing syndrome.
Glucocorticoids causes increasing in number of circulating
neutrophils and decrease in number of lymphocytes
and esonophils in blood.
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GIT
Causes increases in basal and nocturnal gastric acid
secretion.
ANTI INFLAMMATORY ACTION
Supress the features of inflammation such as heat ,
swelling and tenderness.
At tissues level ,they suppress the phenomena such as
edema .
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ABSORPTION, TRANSPORT, METABOLISM AND
EXCRETION:
ABSORPTION:
.Hydrocortisone and numerous congeners including the
synthesis analogs are effective when given by mouth.
.Glucocorticoids also are absorbed systemically from sites
of local administration,such as synovial spaces ,the conjun-
-tival sac,skin and respiratory tract.
.90% or more of cortisol in plasma is reversably bound to
protein under normal circumstance.
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Two plasma protein account for almost all of the steroid
binding capacity.
Corticosteroid binding globulin and albumin.
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THERAPEUTIC USES
*Acute adrenal insufficiency.
*Chronic primary adrenal insufficiency.
*Secondary adrenal insufficiency.
*Congenital adrenal hyperplasia.
*Rheumatic disorders.
*Renal diseases.
*Allergic disease.
*Bronchial asthma.
*Infectious disease.
*ocular disease.
*skin disease.
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*Gastro intestinal disease.
*Hepatic disease.
*Malignancies.
*cerebral edema.
*organ transplantation
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THERPEUTIC USES IN DENTISTRY
Oral ulcerations:
.Denture induced and other traumatic ulcers,
*Recurrent ulcerative stomatitis.
*Erosive lichen planus.
*Erythema multiforme.
*Pemphigus.
*Desequamative gingivitis.
*Stomatitis.
*Geographic tongue.
*Angular chelitis.
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Temporomandibular joint disorders:
Intra articular injection of glucocorticoid such as
dexamethasone is benefical.
Post operative:
Glucocorticoid can be used to lessen postoperative compl
-ications,mainly edema and trismus
Other uses are after third molar extraction,orthognathic
Surgery, bells palsy ,sub mucous fibrosis.
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ANABOLIC STEROIDS
They artificially raises the amount of anabolic
hormone in the blood and permit further growth.
They are analogue of the reproductive hormones
such as testosterone.
They increase muscle tissue.
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CATOBOLIC STEROIDS.
They are analogues of naturally occurring hormone
released from adrenal gland when stressed.
Catabolic steroids decreases the muscle tissue by
breakdown of muscle and release of energy in patients
with stress.
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MANAGEMENT OF PATIENTS RECEVING
SYSTEMIC GLUCOCORTICOSTEROIDS.
Screen the patient for T.B, D.M,BP,Glaucoma,Cataracts,.
Prepare the patient and family for possible adverse effects
On mood and memory changes.
Inform them about the side effects.
Administer calcium,vitamin, bisphonates.
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Avoid prolonged bed rest that will accelerate muscle
weakness and bone mineral loss.
Avoid elective surgery,if possible.
Avoid elective work that would cause fall or trauma.
Treat infections .
Weigh daily.
Measure height.
Avoid smoking
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Taper the dose before you stop .
With dosage reduction ,watch for signs of adrenal
Insufficiency or withdrawal syndrome.
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BASIC PRINCIPLE OF TOPICAL STEROIDS.
Ointment is more potent than cream.
Potency of topical steroid can increase by covering with
a occlusive dressing.
Caution should be taken while they are used on areas of
thin skin.
Avoid soaps and detergents.
Use it 10-20 minutes after the use of emollients.
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Avoid on a infected skin.
Use rule of FTU(Finger tip unit )
Large areas use the rule of nines.
Used usually bid or tid (orally after food )
Donot apply on the unaffected area
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GLUCOCORTICOID AND THE PERIODONTAL
TISSUE.
Topical applications of corticosteroids to the inflamed
marginal gingivae of patients with periodontal disease
resulted in a reduction of inflammation and sulcus bleeding.
With no effect on the progression of periodontitis(stwawins-
-ki) 1960;Haim 1962).However Iusem et al.(1956) injected
cortisol preparations directly into the gingival tissues of five
patients with periodontal disease and showed,histologi-
-cally,reduced capillary permeability, fewer plasma cells in
the granulation tissue ,inhibition of collagen synthesis and
clinical improvement in haemorrhagic and hyperplastic
gingivitis. www.indiandentalacademy.com

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The effects of prednisone therapy upon gingival inflama-
-tion and periodontal bone loss have been studied in a
group of patients suffering from multiple sclerosis who
had been on steroid therapy for up to four years (safkan
and knuuttila 1984 ) .
comparisons were made between this group ,a group of
patients who suffered from neurological disorders but
were not receiving steroids,and healthy controls.
There were no difference in the frequency and severity of
periodontal disease between the groups and it was concl-
-uded that corticosteroid therapy over 1-4 years had no
influence on the measures of periodontal disease in
patients suffering from neurological disorders.
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32.
CONTRA INDICATIONS :
Peptic ulcer
Diabetic mellitus
Hypertension
Tuberculosis.
Osteoporosis.
Herpes simplex.
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Pschychosis.
Glaucoma.
Epilepsy
Renal failure.
CHF.
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Adverse effects
Cushings habitus
Hyperglycemia
Muscular weakness.
Susceptibility of infection.
Delayed healing
Peptic ulceration.
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Osteoporosis.
Glaucoma.
Growth retardation.
HPA axis suppression.
Edema
Rise in BP.
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36.
BIBLOGRAPHY.
GOODMAN AND GILMANS – The Pharmacological
Basis of therapeutics.
Clinical Pharmacology in dentistry: L.A CAWSON
R.G SPECTOR.
Pharmacology and pharmacotherapeutics –
R.S SATOSKAR
CMDT -2004 – TRENEY, MACPHAEE.
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37.
Text book of clinical pharmacology .
H.T.ROGER
Drugs ,diseases and Periodontium-
ROBIN .A .SEYMOUR
PETER .A.HEASMAN
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