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ADRENAL GLAND – ASSOCIATED HORMONES IMPLICATIONS IN DENTISTRY , ORAL& MAXILLOFACIAL SURGERY

ADRENAL GLAND

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ADRENAL GLAND – ASSOCIATED HORMONES, IMPLICATIONS IN DENTISTRY AND ORAL& MAXILLOFACIAL SURGERY

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Page 1: ADRENAL GLAND

ADRENAL GLAND – ASSOCIATED HORMONES

IMPLICATIONS IN DENTISTRY ,ORAL& MAXILLOFACIAL SURGERY

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CONTENTS Adrenal gland anatomy, embryology, histology. Biosynthesis, physiological and pharmacological

actions of hormones of adrenal cortex. Pathological conditions of adrenal cortex. Overview of biosynthesis,functions& pathology. Hormones of adrenal medulla and their actions and

pathology of adrenal medulla. Corticosteroids and their synthetic analogues

classification . Uses , contraindications, adverse effects of

corticosteroids. Corticosteroids and their implications in dentistry. Corticosteroids and their implications in oral &

maaxillofacial surgery

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ANATOMY OF ADRENAL GLAND The adrenal glands are located

in the retroperitoneum superior to the kidneys

Quadrilaterial in shape and are situated bilaterally

The combined weight of the adrenal glands in an adult human ranges from 7 to 10 grams, surrounded by an adipose capsule and renal fascia.

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BLOOD SUPPLY & VENOUS DRAINAGE

The superior suprarenal artery is provided by the inferior phrenic artery

The middle suprarenal artery is provided by the abdominal aorta

The inferior suprarenal artery is provided by the renal artery

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Since the right supra-renal vein is short and drains directly into the inferior vena cava it is likely to injure the latter during removal of right adrenal for various reasons.

The adrenal glands and the thyroid gland are the organs that have the greatest blood supply per gram of tissue. Up to 60 arterioles may enter each adrenal gland. This may be one of the reasons lung cancer commonly metastasizes to the adrenals

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NERVE SUPPLY

The adrenal glands have a rich nerve supply. These nerves are derived from the coeliac plexus

and the thoracic splanchnic nerves.

The nerves supply the chromaffin cells of the medulla,

careful microscopy has shown that nerve trunks

and plexuses may also appear in the cortical layers

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EMBRYOLOGY OF ADRENAL GLAND

Adrenal cortex is of mesodermal origin,developed from cells attached to coelomic cavity lining adjacent to urogenital ridge.

Adrenal medulla develops from cells of neural crest that migrate and penetrate the primitive adrenal cortex to take central position in the gland.

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HISTOLOGICAL CLASSIFICATION

Zona glomerulosa densely packed 5 to6 layer zone secreting aldosterone & not appreciably controlled by ACTH.

Zona fasciculata with rows of chords of cholesterol rich cells secreting cortisol .this zone makes up bulk of adrenal cortex.

Zona reticularis with net like structure secreting weak androgens

Fasciculata&reticularis zones appreciably controlled by ACTH.

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ADRENAL MEDULLA HISTOLOGY Chromaffin cells are

columnar in shape and rather basophilic. At higher magnification, they are seen to have a granular cytoplasm due to hormone-containing granules.

The adrenal medulla is richly innervated by preganglionic sympathetic fibers. Additionally, small numbers of sympathetic ganglion cells are commonly observed in the medulla

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ADRENAL CORTEX & ASSOCIATED HORMONES

BIOSYNTHESIS,FUNCTIONS AND PATHOLOGY

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Cholesterol

Pregnenolone

Progesterone

Corticosterone

11-Desoxy-corticosterone

18-Hydroxy- corticosterone

ALDOSTERONE

17-α- Hydroxy pregnenolone

11- Desoxy- cortisol

17- Hydroxy progesterone21,β hydroxylase

CORTISOL

11,β hydroxylase

Dehydro-epi androsterone

Andro-stenedion

e

Oestrone

Oestriol

TESTOSTERONE OESTRADIOL

ACTH

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COMPARISION OF GLUCOCORTICOID ACTIVITY

PHYSIOLOGICAL Glucose metabolism: Increased gluconeogenesis Decreased peripheral

glucose utilization by skeletal muscles

Inhibition of protein synthesis

Increased lipogenesis{moon face,buffalo hump}

Catabolic action on proteins of muscles&lymphoid tissue

PHARMACOLOGICAL Antinflammatory Due to inhibition of

proliferation of lymphocytes,monocytes,

Inhibition of production of PG’S ,IL’S,interferons,TNF.

Inhibition cox pathway. ANTIALLERGIC IMMUNOSUPPRESSIVE Used in

asthma,ibd ,eczema,sle,RA,prevention of graft rejection

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ACTION OF GLUCOCORTICOIDS ON INDIVIDUAL SYSTEMS

CNS: mood changes

{euphoria ,depression} ,insomnia,lowered thresold for epilepsy.

BLOOD & IMMUNESYSTEM: lymhyocyte,monocyte,eosinophil{decrease} Anti-inflammatory, anti allergic, immunosuppressive

on pharmacological dose.

CVS: ADR or NA induced vasospasm needs physiologic

levels of cortisol, maintains normal tone of blood vessels, prevents microcirculation sluggishness.

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Bone :osteoporosis in chronic therapy.

Healing:inhibition of collagen synthesis,inhibition of wound healing.

Skeletal muscles: glucose utilization sensitivity of muscle cells to insulin. Git: pharmacotherapy by glucocorticoids aggravates

peptic ulcer.

Liver: hepatic glycogenesis.

Lungs: production of surfactant in alveoli.

Endocrine: permissive action on ADR,suppresses ACTH action by –ve feedback mechanism.

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MECHANISM OF ACTION OF GLUCOCORTICOIDS AT MOLECULAR LEVEL

GR RECEPTORS

LIGAND BINDING DOMAIN

DNA BINDING DOMAIN

Binding to ligand domain can cause either inhibition or stimulation of transcription

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Cortisol causes increased synthesis of protein called lipocortin1

Leading to inhibition of PG synthesis

Lipocortin also inhibits ACTH secretion by corticotropes.

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ACTION OF CORTISOL ON STRESS

Neuroendocrine response to stress {NERS}

Greatly increased secretions of ACTH and cortisol

Stress is associated phenomenon like disturbed homeostasis of blood pressure,blood glucose levels,body temperature

Permissive action of glucocorticoids help other hormones in NERS phenomenon {ADH,adr,thyroid hormones}to maintain cellular homeostasis.

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STRESS AND THE ADRENAL GLANDS

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CONTROL OF CORTISOL SECRETION HPA

-ve feedback mechanism

Stress

Circadian rhythm

Products of inflammation

ADH

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INTRODUCTION TO HPA AXIS

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NEGATIVE FEEDBACK MECHANISM

corticotropes of anterior pituitary

Inhibition of ACTH release HYPOTHALAMUS excess cortisol

Inhibition of CRH release inhibition of crh& acth

stopped production of crh& acth

Correction of hypercortisolemia

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Adrenals

Kidney

Posterior Pituitary Gland

Hypothalamus

AnteriorPituitary Gland

ACTH

Stress Circadian

rhythm

CRH

(-)

Glucocorticoids, Catecholamines, etc..

Glucocorticoids, Catecholamines, etc..

Muscle: Net loss of aminoAcids (glucose)

Liver: Deamination of

proteins into amino acids,

gluconeogenesis (glucose)

Fat Cells: Free fatty

acid mobilization

Heart rate: Increased

Immune system: altered

Hypothalamopituitary adrenal (HPA) axis: Negative Feedback

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Circadian rhythm :highest level of cortisol in early morning &lowest in late evening

Stress :stimulation of HPA leading to excess cortisol production

Inspite of high cortisol levels production of CRH&ACTH remain high.

Inflammatory mediators also stimulate HPA eg:IL-1,IL-2

IL-6

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Cholesterol

Pregnenolone

Progesterone

Corticosterone

11-Desoxy-corticosterone

18-Hydroxy- corticosterone

ALDOSTERONE

ACTH

MINERALOCORTICOIDS

target cells for aldosterone

1}kidney 2}GIT 3}sweat glands 4}brain

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in short aldosterone causes na+ conservation k+ excretion

Site of action in kidney is DCT ,principal cells of collecting tubules.

Facilitation of na+ reabsorption from renal tubular fluid

Facilitation of k+ extrusion by renal tubular cells

Excess aldosterone leads

to na+ accumulation {edema ,hypertension}

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ACTION AT MOLECULAR LEVEL

Aldosterone acts on receptors similar to GR receptors and produce na+ channels of tubular epithelial cells and cause vigorous reabsorption of na+ from tubular fluid.

During acidosis instead of k+ extrusion h+ extrusion is coupled with na+ conservation.

Aldosterone also acts on hypothalamusto increase thirst.

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AN OVERVIEW OF SECRETION, MECHANISM& FUNCTIONS & ADVERSE

EFFECTS OF CORTICOSTEROIDS

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PATHOLOGY OF ADRENAL CORTEX CUSHINGS SYNDROME : i]acth dependent

ii] non acth dependent

Acth dependent causes include i]tumour of anterior pituitary ii] tumour of lung secreting ACTH {ectopic acth

secreting tumour}

nonACTH dependent include i]tumour in adrenal cortex ii] iatrogenic(excessive medication by cortisol

analogues)

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Dexamethasone test :exert –ve feedback on HPA.

if following dexamethasone administration there is fall of ACTH level in plasma it is due to hyperfunctioning of corticotropes of API.

If dexa fails to suppress plasma ACTH levels the cause

Is ECTOPIC ACTH secreting tumour.

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HYPERALDOSTERONISM PRIMARY:CONNS SYNDROME : due to tumour or

hyperplasia of zona glomerulosa of adrenal cortex .

Symptoms include hypertension ,edema ,hypokalemia.

SECONDARY:causes include congestive cardiac failure Portal cirrhosis Kidney diseases Due to fall of perfusion pressure of kidney activation of renin angiotensin axis

aldosterone accumulation

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HYPOFUNCTION OF ADRENALS ADDISONS DISEASE:bilateral destruction of adrenal

cortices . causes are i] tb ii] autoimmune disorders iii] fungal infection iv] aids There is destruction of all 3 layers Loss of adrenocorticosteroids + excess of ACTH. Signs&symptoms :low

bp ,hypoglycemia ,intolerance to stress. Lab findings :no rise plasma cortisol level after

ACTH injection.very low plasma cortisol level.high levels of serum ACTH.

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HYPOADRENALISM DUE TO PITUITARY INSUFFICIENCY:

Secondary hypoadrenalism:low plasma ACTH level

Plasma aldosterone levels normal

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CONGENITAL ADRENAL HYPERPLASIA Congenital deficiency of 21 beta hydroxylase or rarely 11 beta hydroxylase.

21 b hydroxylase deficiency leads to both aldosterone and cortisol secretion stops.

11b is inhibited then only cortisol synthesis stops.

Symptoms weakness ,hypoglycemia,hypotension.

Due to lack of cortisol & aldosterone .

Excess ACTH leads to pigmentation .

Excess DHEA+ androstenedione :hirsutism &menstural irregularity

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Excess ACTH leads to excess production of adrenal androgens leading to hirsutism.

Symptoms develop in early in life

Congenital adrenal hyperplasia also known as ADRENAL VIRILISM.

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ASSESSMENT OF ADRENOCORTICAL STATUS Estimation of plasma cortisol level (8 am & 4 pm)

samples

Estimation of 24 hour urinary metabolites of cortisol

Estimation of plasma ACTH levels.

Dexamethasone test, metapyrone test.

For aldosterone :estimation plasma aldosterone level

Estimation serum k+ concentration Plasma rennin activity

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ACUTE ADRENAL INSUFFICIENCY &TREATMENT Occurs irt acute septicemia and is called waterhouse

friderichsen syndrome.

Rapid fulminating septic course ,pronounced purpura ,death within 48 to 72 hours.

Meningococci,streptococci,pneumococci are often responsible.

Cause is bilateral adrenal hemorrhage ,infarction or sepsis.

It can develop in patients taking large doses of steroids for more than two weeks and abruptly stop.

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Treatment includes immediate treatment with normal saline (2-3 litres) rapid infusion and i.v hydrocortisone 100mg every 6hrs.

Blood samples are taken for urea and electrolytes ,blood glucose and for basal cortisol and ACTH levels.

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CHRONIC ADRENAL INSUFFICIENCY & TREATMENT Signs& symptoms: Anorexia ,weight loss,weakness ,

mucosal hyperpigmentation(ACTH mediated),hypotension.

Hyponatremia,hyperkalemia.

Low plasma cortisol

Treatment:oral hydrocortisone maintanenece dose ,

Fludrocorisone in divided doses. Pt.education about lifelong gluco and minerlocorticoid

therapy.

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ADRENAL ANDROGENS ZONA RETICULARIS:

dehydroepiandrosterone ,androstenedione-WEAK androgens

Testosterone- STRONG androgen

Physiologic functions: acne vulgaris,libido.

Escaped into adipose tissue and convert into estrogen

Cushings syndrome: exceesive secretion of weak androgens lead into hirsutism in females.

Estrogen dependent breast cancer weak androgens remain as a source of estrogen and causes recurrence.

Aminoglutethimide is given as treatment.

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ADRENAL MEDULLA ASSOCIATED SECRETIONS,FUNCTIONS AND

PATHOLOGY

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Epinephrine (adr),norepinephrine(NA)

Dopamine intermediate during synthesis of epinephrine.

NA and dopamine are important neurotransmitters in brain & ANS

Catecholamines are produced in response to flight,fright,fight. Emergencies like shock,cold,fatigue,

Emotional conditions like anger etc.

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BIOCHEMICAL&PHYSIOLOGICAL FUNCTIONS OF CATECHOLAMINES

CARBOHYDRATE METABOLISM: glycogenolysis,gluconeogenesis,glycogenesis.

Elevates blood glucose levels and avilability for brain & other tissues.

LIPID METABOLISM: breakdown of triacylglycerols,

Lipolysis, increased free fatty acids in circulation utilized by heart & muscle as fuel source.

Increase adenylate cyclase activity & elevation of cyclic AMP.

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Increased cardiac output,BP ,oxygen consumption.

Smooth muscle relaxation in bronchi,git,blood vessels supplying skeletal muscle.

Stimulate smoothmuscle contraction of blood vessels supplying skin & kidney.

Platelet aggregation is inhibited by catecholamines.

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COMT AND MAO act on catecholamines

Metabolic products metanephrine and vanillyl Mandellic acid (VMA) excreted in urine.

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PATHOLOGY OF ADRENAL MEDULLA PHAEOCHROMOCYTOMA: derived from chromaffin cells of adrenal medulla

(catecholamine producing tumour)

Occurs in association with MEN-2A &MEN -2B

MEN-2A:medullary ca thyroid ,hyperparathyroidism,cutaneous lichen amyloidosis,

MEN-2B:all these features along with multiple mucosal Ganglioneuroma.

Also occurs in association with von –hippel lindau disease.

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Classic manifestations of phaeochromocytoma are

Intermittent episodes of hypertension,headache ,palpitation,sweating(paroxysmal) lasting for minutes to hours.

Acute cardiovascular collapse, stroke, arrythmia during surgicalprocedure under GA or uncontrollable hpertension can occur occassionally.

Drugs like opiates,glucagon,metoclopramide,pancuronium,tricyclic antidepressants may cause crisis in these patients.

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Measurement of urinary catecholamines,or VMA in acidified 24 hour urine collection allows confirmation of diagnosis.

Alpha receptor antagonists like phenoxybenzamine and doxazocine may be given until adrenergic symptoms are releived.

beta blockade should be given only if tachycardia develops and should be instituted after complete alpha blockade completed because of risk of hypertensive crisis.

Laparoscopic adrenalectomy by transperitoneal or retroperitoneal approach is used for surgery

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CORTICOSTEROID ANALOUGES AND THEIR CLASSIFICATION

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USES:

TWO TYPES: 1.REPLACEMENT THERAPY 2.NON ENDOCRINE DISEASES

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REPLACEMENT THERAPY: ACUTE ADRENAL INSUFFICIENCY: hydro or

dexamethasone first given as i.v bolus

then as infusion along with isotonic saline and glucose solution,

monitoring by CVP .short term i.v infusion of dopamine may be needed.

ADDISONS DISEASE (CHRONIC ADRENAL INSUFFICIENCY)

oral hydrocortisone plus salt and water and some times combination of fludrocortisone

should be given.

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Congenital adrenal hyperplasia or adreno genital syndrome,mostly due to deficiency of 21-hydroxylase

Treatment: hydrocortisone 0.6 mg/kg,round the clock to

maintain feedback suppression of pituitary.

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INDICATIONS 1.rheumatoid arthritis

2.osteo arthritis

3.rheumatic fever

4.gout

5.collagen diseases like SLE,polyarteritis nodosa,nephrotic syndrome,glomerular nephritis.

6.anaphylaxis , angioneurotic edema,urticaria,serum sickness,allergic conjunctivitis,rhinitis

7.AIHA,ITP,active chronic hepatitis

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8.bronchial asthama

9.aspiration pneumonia.pulmonary edema

10.TB,severe lepra reaction,some forms of bacterial meningitis and pneumocystis carini pneumonia with hypoxia in AIDS patients

11.keratitis ,retinitis,optic neuritis,uveitis

12.pemphigus vulgaris,exfoliative dermatitis,steven jhonson syndrome

13. ulcerative colitis. Coeliac disease,

14.cerebral edema

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15.neuro cysticercosis

16.ALL,hodgkins ,harmone responsive breast carcinoma

17.organ trasplantation and skin allogrfts to prevent rejection reaction followed by low maintainance doses

18.septic shock

19.thyroid storm

20.adrenal pitutary acess function

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CONTRAINDICATIONS:

PEPTIC ULCER

DM

HYPERTENSION

VIRAL AND FUNGAL INFECTIONS

TB AND OTHER INFECTIONS

OSTEOPOROSIS

HSV-KERATITIS

EPILEPSY

CHF

RENAL FAILURE

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ADVERSE EFFECTS:- extension of pharmacological actions,

occurring with prolonged therapy

limitation to use corticosteriods in chronic disease

Mineralocorticoids:-

Sodium and water retention,

edema,

hypokalemic alkalosis and progressive rise in B.P.

Glucocorticoids:- Cushing habitués:- characteristic

appearance with rounded face, narrow

mouth,supraclavicular hump, obesity of trunk with

relatively thin limbs.

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Fragile skin purple straiae:- easy brusing,talengectiasis,hirsutism,cutanious atrophy occurs with topical use also.

Hyperglycemia and precipitation of diabetes.

Muscular weakness and myopathy.

Susceptibility to infections: - opportunistic infections like Candida.

Delayed healing of wounds.

Peptic ulceration

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Osteoporosis:- Involving vertebrae and flat spongy

bones.

Growth retardation:- Occurs in children even with

small doses.

Fetal abnormalities:- Cleft palate and other defects

in animals not been encountered in pregnant women.

Psychological disturbances

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GENERAL PRINCIPLES OF CORTICOSTEROID THERAPY

Starting doses can be high in severe illness

Long term duration treatment is hazardous

Duration of treatment and dosage should be kept to minimum

No abrupt withdrawl after a corticoid is given for 2-3 weeks,may precipitate adrenal insufficiency

Infection severe trauma or any stress condition –increase the dose

Use local therapy where-ever possible

ex: cutaneous ,inhaled, intra nasal,intra lesional.

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TAPERING OF STEROID DOSE Pt who has received greater than 20-25mg/day

hydrocortisone or equivalent drugs for a duration of more than 2-3 weeks should be put on gradual scheme of withdrawl

20mg/day reduction every week and then still smaller fractions once this level is achieved

These pts need protection with steroids for stressfull situation upto 1year after withdrawl

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> 2mg Reduce by 2-4mg every 5-7 days (and check for symptoms before next dose reduction), until reaching 2mg.(From higher doses (e.g.16mg dexamethasone) it is reasonable to halve the doses every few days until nearing physiological doses

2mg or less Reduce by 0.5-1mg every 5-7 days, or on alternate days for a more conservative approach

Dexamethasone daily dose

Empirical dose reductions

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REGIMENS FOR STEROID DOSE ON THE DAY OF SURGERY

RECOMMENDATIONS — Several authors have recommended that patients on chronic glucocorticoids undergoing surgery receive only their usual daily dose of glucocorticoid perioperatively.

studies have shown that no surgical patient who was treated with his usual steroid dose developed intraoperative or postoperative hypotension or any other perioperative signs of adrenal insufficiency.

the clinician may decide that even a small risk of

adrenal insufficiency outweighs the risk of 24 to 48 hours of stress doses of glucocorticoid.

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STEROIDS AND SURGERY

Anaesthetists must be informed when patients have taken corticosteroids within 3 months of surgery (10 mg or more) so that

minor surgery under GA either the usual corticosteroid dose

orally, or 25-50 mg of hydrocortisone can be given intravenously (IV) at induction.

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moderate/major surgery

the usual oral dose is taken on the day of surgery with hydrocortisone as above at induction and the same IV dose three times daily for between 24 and 72 hours after surgery, depending on the extent of surgery. This is then followed by the usual oral dose.

Patients on prolonged treatment with potent inhaled or nasal corticosteroids should have the same precautions taken as above before surgery

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STEROIDS AND VACCINES

Corticosteroids and live vaccines

Live vaccines should not be given within 3 months of:

An adult receiving 40 mg/day of prednisolone or equivalent for more than a week.

A child receiving either 2 mg/kg/day for 1 week or 1 mg/kg/day for 1 month.

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STEROIDS IN PREGNANCY Corticosteroids in pregnancy and breast-feeding

The 1997 review of the CSM looked at safety in pregnancy and lactation. :

Corticosteroids vary in their ability to cross the placenta.

Prednisolone is mostly (88%) inactivated as it crosses the placenta,

betamethasone and dexamethasone cross readily.

corticosteroids can cause abnormalities in fetal development in animals, this has also been shown in humans (for example, cleft lip and palate).

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Prolonged or repeated corticosteroid administration in pregnancy increases the risk of intrauterine growth restriction (IUGR).

Short-term treatment carries no such risk.

Prednisolone is excreted in small amounts in breast milk and is unlikely to cause systemic effects in the infant unless doses exceed 40 mg daily.

Above this dose infants should be monitored for

adrenal suppression.

No data are available on other corticosteroids

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patients who have taken any dose of glucocorticoids for less than three weeks or who have taken chronic alternate day therapy are unlikely to have a suppressed HPA axis and should continue on their usual dose of glucocorticoids perioperatively.

HPA axis suppression should be assumed to be present in patients taking prednisone at a dose greaterthan 20 mg/day for three weeks or more, and in patients with a Cushingoid appearance.

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a replacement dosage of glucocorticoid appears to be sufficient for most patients during major surgery.

If higher dosages are used, patients should revert to the usual replacement dose within 48 hours of surgery,unless other circumstances intervene.

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MINIMIZE HPA-AXIS SUPPRESSION

Minimal HPA-AXIS suppression achieved by

short acting steroids with lowest possible dose example:hydrocortisone

prednisolone

Using steroids for shortest period as possible

Entire daily dose at one time in the morning

Switch to alternate day therapy if possible

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STEROIDS AND CHICKEN POX Patients on corticosteroids (systemic) or who have used

them within 3 months and are non-immune to varicella infection, are at risk of severe chickenpox.

Infection can be severe (fulminant pneumonia, hepatitis and

disseminated intravascular coagulation, often without prominent rash).

Exposed non-immune patients on or within 3 months of taking corticosteroids should be given passive immunisation with varicella-zoster immunoglobulin

(within 3 days, and no later than 10 days, after exposure).

Confirmed chickenpox in such patients warrants urgent referral and treatment

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CORTICOSTEROIDS AND THEIR IMPLICATIONS IN DENTISTRY

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SYSTEMIC CORTICOSTEROIDS USED FOR TREATMENT OF ORAL LESIONS

INDICATIONS:

Severe recurrent aphthous stomatitis, Behcet's syndrome, pemphigus vulgaris, pemphigoid, erythema multiforme

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RECURRENT APTHOUS ULCERS& BEHCETS SYNDROME

Recurrent aphthous stomatitis:

These superficial painful ulcers occur commonly in the oral cavity.

Minor form of the disease has 1 to 5 ulcers at one episode.

The ulcers which are under 1 cm in diameter persist 8 to 14 days, and heal spontaneously without sequelae.

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major aphthous ulcers are larger than 1 cm, and persist for weeks to months.

Corticosteroids either alone or in combination with other drugs have been used for treatment of these lesions.

Topical steroids, such as triamcinolone acetonide and prednisolone (2 times/day), are formulated as oral pastes.

Therapeutic benefit can be derived from a mouthwash containing betamethasone. It shouldbe noted that the long-term use of topical steroids may predispose patient to developing oral candidiasis.

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Topical and injectable (intralesional) corticosteroids are useful for large and painful lesions.

Systemic administration of corticosteroids is reserved

for severe cases to prevent lesion formation or to reduce the number of lesions.

Systemic corticosteroids should be prescribed in short

courses, and only for severe outbreaks or cases that don't respond to topical or injectable corticosteroids.

Behcet's syndrome:The treatment of oral lesions of

Behcet's syndrome is similar to the treatment of severe or major RAS.

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Common ingredients include:

Diphenhydramine - an antihistamine to reduce inflammation

Glucocorticoids - to reduce inflammation

Lidocaine - a local anesthetic to relieve pain

Maalox & sucralfate - an antacid acts as a coating agent

Nystatin- an antifungal for candidiasis

Tetracycline & erythromycin : antibiotics

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DESQUAMATIVE GINGIVITIS Various differential diagnosis for desquamative

gingivitis are: lichen planus

bullous pemphigoid

mucous membrane pemphigoid

pemphigus vulgaris

EM

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LICHEN PLANUS

0.05% FLUOCINONIDE OINTMENT for erosive ,bullous or ulcerative type of LP .

Gingival tray with 0.05% clobetasol propionate along with 1lakh I.U/ML of nystatin in orabase.

Intra lesional injections of triamcinolone acetonide (10-20mg) or short term regime of 40 mg prednisolone for 5 days followed by 10-20mg for additional 2 weeks in case of severe cases

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BULLOUS& MUCOUS MEMBRANE PEMPHIGOID

The choice of drugs used for the treatment of pemphigoid is based

sites of involvement,

clinical severity,

disease progression.

more severe disease, or with rapid progression, systemic corticosteroids are the agents of choice for initial treatment,

combined with steroid-sparing agents for longterm maintenance.

Topical and injectable corticosteroids are useful for treatment of mild or localized oral lesions.

Clobetasol propionate 20-40mg/day or

prednisone+other immunomodulator drugs

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Note tense blisters on a background of red hive-like rash in classic case of Bullous Pemphigoid

Bullous pemphigoid blisters in floor of mouth

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symblapheron charecteristic of ocular mucous membrane pemphigoid

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ERYTHEMA MULTIFORMAE & STEVEN-JOHNSONS SYNDROME

Erythema multiforme (EM) &Stevens-Johnson

syndrome (SJS):corticosteroids have a favorable influence on the outcome of EM and SJS,

if administered in high doses, over a short period of time, early in the course of the disease, and with proper tapering of medication.

the dosing and route of administration that provides

the mostbenefit for EMM and SJS patients is in question.

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TREATMENT PROTOCOLS: 1. early therapy systemic prednisone (0.5 to

1.0mg/kg/day) or

2. pulse methylprednisolone (1mg/kg/day for 3 days)

3. intravenous pulsed dose methylprednisolone (3 consecutive daily infusions of 20–30mg/kg to a

maximum of 500mg given over 2 to 3 hours)

4.dexamethasone pulse therapy (1.5mg/kg IV over 30 to 60 minutes on 3 consecutive days) all have been shown to be effective.

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INFECTIOUS MONONUCLEOSIS Characterised by palatal petechiae

1:4096 raised titer of agglutinins and hemolysins of human rbc agianst sheep rbc.

Glandular fever

O/F: acute gingivitis and stomatitis

TREATMENT: 60-80mg/day of prednisolone used initially,with rapid reduction on clinical improvement

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palatal petechiae charecteristic of infectious mononucleosis

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CENTRAL GIANT CELL GRANULOMA

Central giant cell granuloma of the jaws is a benign tumor which occurs most often in children and young adults.

This tumor is made up of loose fibrous connective tissue stroma with many interspersed proliferating fibroblasts, aggregations of multinucleated giant cells, and foci of hemorrhage.

.

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Various surgical and nonsurgical treatments havebeen advocated for this lesion.

Mainly treatment for CGCG is surgical. One of the nonsurgical treatments proposed is

intralesional corticosteroid injection

Intralesional injection of triamcinolone acetonide has been shown to induce partial and in some cases complete resolution of central giant cell granuloma.

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Equal parts of triamcinolone acetonide (10 mg )& lidocaine (0.5%),3 ml of solution was injected into the lesion by multiple penetrations with a needle of 0.5 mm diameter.

The mechanism of action of corticosteroids in the treatment of central giant cell granuloma is unknown.

rationale for its use has been histologic resemblance of

CGCC to sarcoid. corticosteroids have been effective in the treatment of sarcoid, it may have a similar therapeutic effect on central giant cell granuloma.

In addition, corticosteroids may act by suppressing any angiogenic component of the lesion.

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BELL’S PALSY Bell's palsy is an idiopathic inflammation of the facial

nerve (the seventh cranial nerves) which occurs almost always on one side only.

It is characterized by facial muscle weakness,

hyperacusis,

decreased hearing, and

loss of taste on the anterior two thirds of the tongue.

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Bell's palsy results from inflammation and edema of the facial nerve, corticosteroids constitute the standard medicine in its treatment.

For adults, prednisolone at doses of 1 mg/kg/day for 7 to 10 days, taken in divided doses in the morning and evening, is suggested

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Mucocele: lower lip(60%) bluish

translucent excision intra lesional

injection of steroids used occassionally.

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ORAL SUBMUCOUS FIBROSIS

submucosal injections: COMBINATION dexa methasone 4mg/ml 2 parts of hyaluronidase(200usp unit/ml) diluted in 1ml of 2%xylocaine with 27 guage

dental needle not more than 2 ml /inj site for a period of 20 weeks

Sub mucosal inj of triamcinolone 10 mg/ml diluted in 1ml of 2% lidocaine to avoid immediate tissue irritation and facilitate proper drug distribution at the inj site bi- weekly recommended

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STEROIDS IN ENDODONTIA Endodontic anodyne.

Along with broad spectrum antibiotics as pulp-capping agent.

pulpovital= prednisolone+chloramphenicol+neomycin

Dontisolon=prednisolone+neomycin

Septomixine=dexamethasone+polymycin sulphate+neomycin

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Cavity liners 1%prednisolone +25% chloram phenicol+50%gum camphor to reduce post op. thermal sensitivity

Tramcinolone acetonide: potent drug for reduction of inflammation secondary to post endo treatment.

Steroids applied for exposed dentin after cavity prep.

Ipc,pulpal exposure,pulpal remanents in periapical area during rct to eliminate post op pain and inflammation

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POSTHERPETIC NEURALGIA Reduced pain and disability and had no

adverse effect on incidence and severity of postherpetic neuralgia.

Subcutaneous infiltration of 0.2% triamcinolone acetonide in normal saline injected daily in sites of pain upto 20 days.

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KELOID AND HYPERTROPHIC SCAR

Keloid and hypertrophic scar (HS) represent pathologic over healing conditions caused by excessive production of fibrous tissue following healing of skin injuries.

Keloid produces significantly more collagen than HS.

exact cause is unknown but inflammation, tension, and genetic background are mentioned as contributing factors.

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.

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Various treatment modalities have been used for prevention and treatment of keloid and HSs such as pressure therapy, silicone gel sheeting, topical flavonoids, corticosteroid therapy, radiotherapy, and surgery

Topical and intralesional glucocorticoids are frequently used to treat existing keloid and HS or, prophylactically, to prevent their formation or recurrence after surgical removal.

Intralesional steroid injection, either on its own or in combination with other treatment modalities is the most common treatment used for keloid and HSs.

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Glucocorticoids have a multiplicity of effects on scars includingsuppressive effects on the inflammatory process in the wound,

diminishing collagen

glycosaminoglycan synthesis

inhibition of fibroblast growth

enhancing collagen and fibroblast degeneration.

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Triamcinolone acetonide is the most commonly used steroid for the treatment of HS and keloid.

It is used in a concentration of 10-20 mg/ml, at a dose of 40 mg/ml for a tough bulky lesion;

the concentration depends upon the size and site of the lesion and age of the individual.

Side effects of steroid injection include hypopigmentation, dermal atrophy, telangiectasia and cushingoid effects from systemic absorption.

Cushing's syndrome secondary to injection of triamcinolone acetonide for the treatment of keloids have been reported by several investigators

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CORTICOSTEROIDS AND THEIR IMPLICATIONS IN ORAL & MAXILLOFACIAL

SURGERY

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TEMPOROMANDIBULAR DISORDERS (TMDS)

TMDs : clinical problems involving the temporomandibular joints (TMJs), the masticatory muscles, or both.

TMDs affect a significant number of individuals, and

are the most common musculoskeletal disorders that cause orofacial pain.

Trauma to the joint structures, especially microtrauma,

accounts for the majority of patients who develop TMJ problems.

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a small number of joint diseases are caused by nontraumatic etiologic factors: benign and malignant neoplasms (osteoma,

chondroma, and synovial sarcoma),

congenital or developmental anomalies (condylar agenesis and hyperplasia), arthritides (rheumatoid arthritis), and

systemic diseases.

The most common signs and symptoms of TMDs are pain, altered mandibular movements, and the elicitation of joint noise.

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Treatment of TMDs varies according to their etiologic basis.

Conservative managements (splint therapy, thermal application, pharmacotherapy, and physiotherapy),

surgical treatments, or a combination of them may be required.

A variety of medications have been used to relieve pain, inflammation, muscle spasm and other signs and symptoms associated with TMDs.

They include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, analgesics, and muscle relaxants

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Various glucocorticoids are used in the treatment of TMDs .

These drugs have dramatic effects on pain, hypomobility, and inflammation associated with acute TMJ problems.

Oral corticosteroids are used mainly for treatment of acute TMJ discomforts or for diagnostic purposes.

Theyshould be used in a short term basis (tapering dose lasting 5 to 7 days), and repeated as infrequently as possible.

Long term use of corticosteroids for the treatment of TMDs is contraindicated;

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ORAL CORTICOSTEROIDS USED IN TMDS

drug Alternative name

Usual dose

Hydrocortisone hydrocortone 20-240mg /day

Prednisone Deltasone,orasone 5-60mg/day

Prednisolone Delta-cortef 5-60mg/day

Dexamethasone decadron 0.75-9.0mg/day

betamethasone celestone 0.6-7.2mg/day

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Intracapsular injection of glucocortcoids decreases pain in patients with pain & limited mouth opening secondary to inflammatory disorders of the joint, such as arthritis and capsulitis.

intra- articular corticosteroid injection has been used to improve mouth opening in patients of anterior disk displacement without reduction (ADDWOR), i.e., closed lock.

glucocorticoids: inhibit inflammatory mediator release from many cell types involved in inflammation such as macrophages,T-lymphocytes, mast cells, dendritic cells, and neutrophilic leukocytes.

Glucocorticoids also reduce prostaglandin production by blocking the phospholipase A2enzyme.

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The most striking effect of glucocorticoids

inhibition of expression of multiple inflammatory genes encoding cytokines, chemokines, inflammatory enzymes, receptors & adhesion molecules.

Changes in gene transcription

regulated by proinflammatory transcription factors, such as

nuclear factor-κB (NF-κB) and activator protein-1 (AP-1).

proinflammatory transcription factors switch on inflammatory genes via

recruitment of transcriptional coactivator proteins & changes in chromatin modifications such as histone acetylation.

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Glucocorticoids binding and activating cytoplasmic glucocorticoid

receptor.

anti inflammatory effect on responsive cells

activated glucocorticoid receptor & proinflammatory transcription factors interaction

deacetylation of histones and repression of inflammatory genes

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In chronic inflammatory disorders of TMJ,

macrophages, T-lymphocytes, and other cell types

release of cytokines and chemokines.

induce expression of adhesion molecules,

release of various enzymes from fibroblasts & osteoclasts bone erosion.

IL-8, a chemokine, is known to cause the infiltration of neutrophils into synovial fluid and promote joint inflammation.

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LONG-TERM COMPLICATIONS ASSOCIATED WITH INTRA-ARTICULAR GLUCOCORTICOID INJECTION

Wenneberg et al. evaluated the long-term prognosis of intra-articular glucocorticoid injections for TMJ arthritis observed that this treatment modality was helpful

there were no radiographically demonstrable side

effects of the treatment.

In contrast, Haddad IK showed that intra-articular

injections of corticosteroids ( triamcinolone acetonide ) cause damage to fibrous layer, cartilage, and bone of TMJ

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JUVENILE IDIOPATHIC ARTHRITIS

Juvenile idiopathic arthritis (JIA): chronic rheumatologic disease of children which may involves TMJ region & causes significant craniofacial growth disturbances.

rx of TMJ arthritis is controversial, glucocorticoid

injection of the TMJ reduces pain and inflammation & improves the function of TMJ in children with JIA.

Other studies also confirmed that corticosteroid injection of the TMJ can be safely performed in children with JIA, and is effective.

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TREATMENT PROTOCOLS 1 cc (40 mg) of triamcinolone acetonide

1 cc (20 mg) of triamcinolone hexacetonide in 0.5 to 1 cc of the diluted (with 1% lidocaine HCL) triamcinolone hexacetonide in into each of the involved TMJs.

The peak effect occurs after approximately 6 weeks of treatment, and the expected duration is 6-17 months.

The children may receive a second injection

approximately 6 months after the first.

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SIDE EFFECTS OF INTRA-ARTICULAR STEROID INJECTION IN CHILDREN:

immediate reactions, such as pain and headache

delayed side effects, such as joint infection and loss of subcutaneous fat.

mandibular endochondral growth zone is located at the head of condyle (at the site of corticosteroid injection),

Stoustrup et al.: intra-articular glucocorticoid injection may result in even more pronounced mandibular growth reduction than that caused by the arthritis alone.

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MANAGEMENT OF POST-OPERATIVE MORBIDITIES ASSOCIATED WITH

MAXILLOFACIAL SURGERIES Facial pain, edema, ecchymosis and limitation of

mouth opening are expected sequelae of oral and maxillofacial surgeries.

Many modalities are used to abate sequelae are use of

ice pack, pressure dressing, surgical drain, and drugs.

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Corticosteroids are commonly used to control post-operative morbidities and to provide comfort for patients.

there are no definite protocols relative to molecules, doses, schedules, and routes of administration.

The most commonly administered types of are

betamethasone, dexamethasone, an methylprednisolone, administered intravenously, orally or by injection into the masseter muscle.

The morbidity-management protocol also varies

depending upon the type of surgery being performed.

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To decrease POST-RHINOPLASTY EDEMA, the administration of corticosteroids has been advocated.

study by Gurlek et al., i shown that high dose methylprednisolone was effective in preventing & reducing both the periorbital ecchymosis & edema in open rhinoplasty.

Kargi et al.& Kara & Gokalan showed perioperative use

of corticosteroids reduced edema & ecchymosis associated with rhinoplasty surgery.

In contrast, Hoffmann et al. did not observe any increase either in edema or ecchymosis after rhinoplasty surgery.

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Regarding orthognathic surgery, several investigations demonstrated that perioperative corticosteroid administration significantly reduced post-operative inflammation and edema.

In contrast, Munro et al. did not observe any significant decrease in postoperative edema even with the highest doses and the longest durations of corticosteroid treatment

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THE EFFECTS OF CORTICOSTEROIDS ON POST-OPERATIVE EDEMA AFTER ORAL

SURGERY

Many prior studies demonstrated a significant decrease in post-operative edema after administration of corticosteroids.

In a study by Zandi, it was shown that steroids reduced the facial swelling & also the severity of pain after surgery.

Similarly, several studies, indicated strong correlation between post-op edema and pain decreases with steroids.

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OTHER USES OF CORTICOSTEROIDS

management of acute trigeminal nerve injuries,

traumatic facial nerve paralysis,

chronic facial pain

allergic diseases involving maxillofacial area.

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PERIOPERATIVE MANAGEMENT OF PATIENTS WITH ADRENAL INSUFFICIENCY

Adrenal suppression suspected in pt.s receiving 20 mg of prednisone daily for one week or of 7.5 mg prednisone daily for one month within past year or its equivalent doses.

In adrenal suppression body is not able to cope up stresses such as medical illness, surgery & trauma.

precipitation of adrenal crisis

signaled by the onset of fever, restlessness, flank and abdominal pain, vomiting, lethargy, hypotension, or coma.

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pt. suspected having adrenal insufficiency

evaluated with ACTH (cortrosyn) stimulation test

orgiven supplemental corticosteroids empirically perioperatively.

Cortrosyn stimulation test measures how well the

adrenal glands respond to a synthetic ACTH administered to the patient.

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RECOMMENDED CORTICOSTEROID COVERAGE

MINOR SURGICAL STRESS tooth extraction, biopsy, periodontal surgery,

genioplasty, etc: 25 mg of hydrocortisone equivalent, the day of surgery. Submucosal dexamethasone(4 mg) inj. In apicectomy of

max.anteriors MODERATE SURGICAL STRESS panfacial fractures, two jaw surgery, etc: 50-75 mg of hydrocortisone equivalent for 1 to 2 days.

MAJOR SURGICAL STRESS extensive head and neck resection and reconstruction, etc: 100-150 mg of hydrocortisone equivalent for 2 to 3 days.

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MATERNAL CORTICOSTEROID USE AND THE RISK OF OROFACIAL CLEFTS IN

INFANTS Orofacial clefts are the most common congenital deformity affecting maxillofacial area.

both major and minor genetic influences involved, with

variable interactions from environmental factors. environmental factors suchas maternal drug intake, trauma, smoking, exposure to x-rays during the pregnancy period suggested

to increase the chance of cleft development in infants.

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Pregnant women use topical, inhaled, or systemic corticosteroid drugs for a variety of inflammatory and allergic conditions.

use of corticosteroids during early pregnancy is associated with a 3- to 6-fold increased risk of orofacial clefts.

systemic corticosteroids are associated with higher

risk of orofacial clefts than topical corticosteroids, the latter is not without risk.

application of hydrocortisone cream on eczematous

skin is associated with significant increase in the level of plasma cortisol.

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study by Edwards et al., showed significant association

between topical corticosteroids and orofacial cleft.

Epidemiologic data have shown low-to-moderate doses of inhaled corticosteroids taken during the first trimester of pregnancy are safe but raise concerns about high doses

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Glucocorticoids may cause cleft palate deformity by delaying palatal shelf elevation.

Corticosteroids reduce the collagen content of

connective tissue by inhibiting collagen synthesis.

This disrupts cell-cell interaction and tissue-tissue

interactions

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STEROIDS AS LIFE SAVING DRUGS corticoids (i.v soluble corticosteroids)along with

bronchodilator drugs are given as life saving drugs in status asthmaticus (acute severe asthma).

Life threatening Pemphigus vulgaris conditions large doses of oral prednisolone (40-120 mg per day) is given.

Corticoids also used as life saving drugs in septicaemic shock.

In cerebral oedema due to tuberculosis and infections also it is used as a life saving drug (dexamethasone).

It is used as second line drug in anaphylactic reaction after adrenaline.

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CONCLUSION Steroids are frequently used to minimize expected

post-operative morbidities such as pain and edema after oral and maxillofacial surgeries.

anti-inflammatory and anti-allergic actions of glucocorticoids, have widest application in management of acute and chronic conditions with allergic, immunologic, or inflammatory basis.

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corticosteroids carry the risk of potential side effects which are sometimes severe and life threatening.

benefits from corticosteroids should always be weighed

against their potential risks

Prescribing the minimal dose ,

least potent type of corticosteroids necessary to produce a given therapeutic effect,

simultaneous use of NSAIDS to reduce the dose of

corticosteroids,

prescribing corticosteroids for a short period of time should be followed.

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REFERENCES

CONSICE MEDICAL PHYSIOLOGY:CHAUDHURI BIOCHEMISTRY:U.SATYANARAYANA PHARMACOLOGY:K.D TRIPATHI SHORT PRACTICE OF SURGERY BY BAILLEY &

LOVE TODAYS ORAL & MAXILLOFACIAL SURGERY AND

CORTICOSTEROIDS: MOHD.ZANDI ORAL MEDICINE : BURKETTS INTERNET SOURCES.

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THANK YOU