1. corticoSTEROIDSShivani gaba
Jr-ii,omfs 1

2. Endocrine system maintains
homeostasis
 The concept that hormones acting on
distant target cells to maintain the stability
of the internal milieu was a major advance
in the historical events of physiological
understanding of human body.
Ernest Henry Starling
(1866-1927)was the first to use the term
hormone(from Greek ὁρμή, "impetus")
2

3. 3

4. This is especially important in
oral surgery because many of
the patients attending the our
clinics face stressful
situations.
Awareness is therefore
necessary of -the risks and
difficulties that may arise
during the surgical
management of patients with
endocrine disorders; and the
most common oral
manifestations.
4

5. objectives
History
Steroids physiology
Actions
Pharmokinetics
Preparations
Therapeutic principals and uses
Steriods withdrawal
Surgical management & Adrenal
crisis
Cushing syndrome
Misuse
From literature
5

6. Steroids 6

7. History of steroid therapy
It has been almost 60 years since corticosteroids were first
recognized for their anti-inflammatory and immunosuppressive
properties, initially in rheumatologic diseases( in 1949) by
Philip S. Hench and colleagues, a discovery for which he received
(together with Edward C. Kendall and Tadeus Reichstein) the
Nobel Prize in medicine in 1950. Currently,corticosteroids are
the drugs with one of the broadest specturm of clinical
utility.
7

8. E D W A RD C. KE N D A L L
The development of cortisone as a therapeutic agent
Nobel Lecture, December 11, 1950
From the time, ages ago, when cortisone was
first made in the adrenal cortex it has continued
to serve as a powerful agent in health and
disease.. What physiologic processes are modified
by cortisone and how this influence is exerted are
matters still locked within this hormone of the
adrenal cortex. Said Shakespeare’s soothsayer, "In
Nature’s infinite book of secrecy a little I can
read."
8

9. corticosteroids
 The term “corticosteriods”(also called simply steroids) refers both
-to the hormones produced in outer layer(cortex) of adrenal glands
and
-to the modified forms of these hormones that are used as drugs.
 Despite the name , corticosteroids should not be confused with
anabolic steroids , substances that mimic the virilizing effects of
testosterone and are some times used illegally by athletes to build up
muscle mass.
9

10. Adrenal glands
 When you think about the adrenal
glands, you should think about
stress. Stress can take many forms:
taking an examination, recovering
from a broken bone, running away
from an invading army, starvation.
For human males, there is even
considerable stress associated
even with shopping .
10

11.  The two adrenal glands are located immediately anterior to the kidneys, encased in a
connective tissue capsule and usually partially buried in an island of fat. Their
combined weight is about .01-.02% of total body weight in both males and females.
 Inspection of a mammalian adrenal gland that has been sectioned reveals two distinct
regions.
 An inner medulla, which is a source of the catecholamines epinephrine and
norepinephrine. The chromaffin cell is the principle cell type. The medulla is richly
innervated by preganglionic sympathetic fibers and is, in essence, an extension of the
sympathetic nervous system.
 An outer cortex, which secretes several classes of steroid hormones (glucocorticoids
and mineralocorticoids, plus a few others). Histologic examination of the cortex reveals
three concentric zones of cells that differ in the major steroid hormones they secrete.
11

12. 12

13. 13

14. Steroids-biosynthesis
Adrenal cortex makes and secretes over 30 different steroid hormones
(collectively called corticosteroids).Corticoids are 21 carbon
compounds having a cyclopentanoperhydro-phenanthene(steroid)
nucleus. Since adrenal cortical cells store only minute quantity of
hormone ,rate of release is governed by the rate of biosynthesis.
14

15. 15

16. Hypothalamic-pituitary-
adrenal axis
 The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop that
includes the hypothalamus, the pituitary and the adrenal glands. The main
hormones that activate the HPA axis are corticotropin-releasing factor (CRF),
arginine vasopressin (AVP) and adrenocorticotropin hormone (ACTH). The
loop is completed by the negative feedback of cortisol on the hypothalamus
and pituitary.
16

17. CORTISOL
ACTH
CRH
STRESS:
Physical stress
Emotional stress
Hypoglycemia
Cold exposure
Pain
Adrenal Cortex
Anterior Lobe of
Pituitary Gland
Hypothalamus
17

18. Diurnal rhythm
 ACTH is secreted in irregular pulses throughout the day which cause parallel
increases in plasma cortisol . Both the frequency and the amplitude of the
pulses are the greatest in the early morning.
 This early morning increase in ACTH release is initiated by the release of CRH
(corticotropin releasing hormone) and starts approximately a couple of
hours before waking.
 The lowest levels of ACTH in blood occur just before or after falling asleep. This
results in the characteristic diurnal rhythm in ACTH and cortisol secretion
18

19. ACTIONS
.
Cortisol is one of the few hormones
essential for life. Adrenalectomy in
humans is always fatal unless
glucocorticoids are
administered.Exactly why adrenal
insufficiency results in death is not
well understood, but in view of the
widespread actions of the
glucocorticoids, it is not surprising
that they are needed for life
19

20. Pharmacological Actions
Direct Actions
Permissive Actions
•Lipolytic effects
•Effect on BP
•Effect on bronchial muscles
(e . g . sympathomimetic amine)
20

21. Pharmacological Actions
1. Mineralocorticoid actions
2. Glucocorticoid actions
 Carbohydrate
 Protein
 Lipid
 calcium metabolism
 CVS
 Skeletal muscle
 CNS
 Stomach
 Respiratory system
 lymphoid tissue and blood cells
 Inflammatory responses
 Immunological and allergic responses
 Growth & Cell Division
21

22. 22
Mineralocorticoid Actions: Electrolyte and water
balance

23. As a result, blood glucose increases(hyperglycemia,a diabetes like state).
The metabolic effects of glucocorticoids may be counterbalanced by those of other
hormones, particularly insulin, the secretion of which is stimulated by the rise in blood
glucose
23

24. Lipid metabolism
 Permissive action
 Promote adipokinetic agents activity(lipolysis)
 Redistribution of Fat
 Moon face , fish mouth , buffalo hump
24

25. Calcium metabolism
 ↓ Intestinal absorption
 ↑Renal excretion
 OSTEOPOROSIS-spongy bones are
more sensitive(e.g., vertebrae, ribs etc)
Cardiovascular system
Restrict capillary permeability
Maintain tone of arterioles & Myocardial
contractility
Na+ sensitize blood vessels to the
action of catecholamines &
angiotensin-(permissive role in
development of hypertension ,should be
used cautiously in hypertensives)
Skeletal muscle
Optimum level of corticosteroid is needed for
normal muscular activity.
Hypocorticisim : ↓ work capacity &
weakness(due to hypodyanamic circulation)
Hypercorticism :
•excess mineralocorticoid action -
hypokalemia – weakness
•excess glucocorticoid action - muscle
wasting & myopathy -
weakness
CNS
Direct:
Mood(mild euphoria),Behaviour,Brain
excitability,High doses lower seizure
threshold-cautious use in epileptics
Indirect:
maintain glucose, circulation and
electrolyte balance
25

26. Stomach
↑ section of gastric acid &pepsin&↓ in
PG levels in the stomach--
Cytoprotective effect of PG lost--result-
-peptic ulcer
Misoprostol ( A prostaglandin
E1, analogue) may be used to replenish
the depleted stomach PGS
Lymphoid tissue and Blood cells
•Lymphoid tissue:
• ↑ rate of destruction of lymphoid cells(T
cells are more sensitive than B cells)
•Blood cells:
↑ number of RBCs,platlets,neutrophils in
circulation. ↓ lymphocytes,eosinophils and
basophils blood count come back normal
after 24 hours.
Inflammatory responses
Irrespective of type of injury the attending inflammatory response is ↓ed.The cardinal
signs of inflammation –redness,heat,swelling and pain are suppressed.
In early events:↓acute inflammatory response, reduced exudation, ↓ in numbers and
activity of leucocytes, ↓ in inflammatory mediators
In late events:↓numbers and activity of mononuclear cells and fibroblasts, ↓ proliferation
of blood vessels, less fibrosis-thus ↓ chronic inflammation but also ↓ healing
26

27. Phospholipids
Arachidonic acids
lipoxygenase Cycylooxygenase
Leukotriene
Prostaglandins,
Thromboxane
Prostacyclins
Phospholipase A2
Lipocortin
Corticosteroids
27

28. Causes greater suppression of CMI (graft rejection & delayed hypersensitivity)
↓Transplant rejection: ↓antigen expression from grafted tissues, ↓sensitisation of T
lymphocytes.
Which makes the basis of use in autoimmune diseases and organ transplantation.
28

29. Growth & Cell division
 Delays the process of healing
and scar formation.
 Retards the growth of
children
Respiratory system
•Most potent and most effective
anti-inflammatory
•Effects not seen immediately
(delay 6 or more hrs)
•Inhaled corticosteroids are used
for long term control in bronchial
asthma.
Effects on stress
ACTH and cortisol secretion are increased by stressful stimuli including surgery
, trauma, pain, apprehension, infection, hypoglycemia and hemorrhage. The increase in
cortisol production is necessary for survival, and stresses that are normally tolerated can
become fatal in adrenal insufficiencyRapid deterioration resulting in organ damage and
shock/coma/death can occur, especially in children.
Cortisol response to a minor (dashed line) and major (solid line) surgery
29

30. This process takes 30-60 min.So effects of corticosteroids are not immediate ,and once the
appropriate proteins are synthesized-effects persist much longer than steroid itself
Mechanism of action
30

31. Metabolism:
 Basal Cortisol Production = 8-25 mg/24hrs
 Cortisol Production can be  6-fold in
stress
 Metabolism by liver enzymes
 excretion by urine
 plasma t1/2 of cortisol 60-90 min in
circulation.
 biological t1/2 is longer-effects persist
long after steroid is removed from
plasma.
Bioavailability:
Hydrocortisone undergoes high
first pass metabolism,has low oral:
parentral activity ratio.Oral
bioavailability of synthetic
corticoids is high.
Transport: Transcortin 75%
Albumin 5%
Free form 20%
31

32. Preparations
Glucocorticoids
Short acting
Intermediate acting
Long acting
Mineralocorticoids
Inhalant steroids
Topical steroids
 SYNTHETIC STEROIDS have largely replaced the natural compound
s in therapeutic use ,because they are potent,longer acting,more
selective,for glucu/mineralo action and have high oral activity.
32

33. Short Acting Preparations (t1/2 < 12 h)
Drug Anti-
inflam.
Salt
retaining
Preaparations & dose
Cortisol 1 1.0 • 5 mg tablet , 100 mg/vial (i.m., i.v)
• Topical, enema(in ulcerative colitis)
Uses:for replacement therapy -20 mg morning+10
mg afternoon(oral)
•shock,status ashmaticus,acute adr.insufficiency-
100mg i.v. bolus+100mg 8 hrly infusion.
Cortisone 0.8 0.8 • 5 mg tablet
• 25 mg/vial (i.m)
Intermediate Acting Preparations (t1/2 = 12 -36 h)
Prednisolone 5 0.3 • 5, 10,20 mg tablet , 20 mg/vial (i.m, intrarti)
•Topical,used for allergic,inflammatory,autuimmune
disease,malignancy:5-60 mg/day oral,10-40 mg i.m.
intra-articular
Methyl
prednisolone
5 0 • 0.5, 1.0 gm inj. for i.m. or slow i.v.(4-32mg/day
oral)
Enema,pulse therapy in nonresponsive rh
artritis,renal transplant,pemphigus
Triamcinolone 5 0 • 4 mg Tab.,10, 40 mg/ml for i.m., intrarticular inj.
(4-32mg/day oral,5-40 mg i.m.,intraricular) Topical33

34. Drug Anti-inflam. Salt retaining Preapartions & dose
Dexamethasone 25 0 0.5 mg tab.
4mg/ml inj (i.m., i.v.),Topical
used for: inflammatory and allergic
conditions 0.5-5 mg/day
oral,shock,cerebral edema 4-20mg/day
i.v. infusion/i.m. inj.
Betamethasone 25 0 0.5, 1 mg tab.
4mg/ml inj (i.m., i.v.),topical
Uses:same as dexamethasone
Paramethasone 10 0 2- 20 mg/day (oral)
Long Acting Preparations (t1/2 > 36 h)
34

35. Mineralocorticoids - Preparations
Drug Anti-inflam. Salt
retaining
Preapartions & dose
Fludrocortisone 10 150 100 mcg tab.
DOCA 0 100 10 mg /ml inj.,used
occasionally for replacemen
t therapy in addison’s
disease2-5 mg sublingual ,
10-20 mg i.m. once or twice
weekly
Aldosterone 0.3 3000 Not used clinically
35

36. Prednisolone 10 mg is equivalent to
 Betamethasone 1.5 mg
 Cortisone acetate 50 mg
 Dexamethasone 1.5 mg
 Hydrocortisone 40 mg
 Methylprednisolone 8 mg
36

37. Replacement therapy(for endocrine diseases)
Pharmacotherapy( for non-endocrine diseases)
Diagnostic uses
Uses of steroids therapy
37

38.  Long term use is potentially hazardous.keep dose to
minimum which is found by trial & error; Needs
frequent evaluation.
 Single dose: No harm ,can be used to tide over
mortal crisis.
 Few days therapy (even high doses)unlikely to be
harmful
 Incidence of side effects related to duration of
therapy
 Use is only palliative (except replacement therapy)
 infection,severe trauma or any stress during
therapy:↑ dose
 Abrupt cessation of prolonged high dose(>2-3
weeks) leads to adrenal insufficiency
(contraindicated)
38

39. •Replacement therapy
1.Acute adrenal insufficiency:
 an emergency
 Hydrocortisone
 Amount of fluid infused-governed by-b.p.
 2.Chronic adrenal insufficiency: (addison’s disease):
 Hydrocortisone given orally,Supplemented with –a mineralocorticoid (fludrocortisone)
 3.Congenital adrenal hyperplasia
 Familial disorder due to def.of of 21-  hydroxylase &11 -  hydroxylase enzyme.
 Treatment:hydrocortisone 0.6 mg /kg/day in divided doses .
39

40. •Non-endocrine diseases
1.arthritis: rheumatoid ,osteoarthritis , rheumatic fever , gout
2.Collegen diseses:SLE,polyarteritis nodosa,dermatomyostitis,nephrotic
syndrome,glomerulonephritis
 May be life saving
 Started with high dose-tapered to maintainance dose when remission occurs.
3.Severe allergic reactions: anaphylaxis,angioneurotic edema,urticaria,serum
sickness.
 Even i.v. inj takes 1-2 hours to act,So not a substitute to adr.in anaphylaxis and
angioedema of larynx.
40

41. Non-endocrine diseases
4.Autoimmune diseases :
Hemolytic anaemia , trombocytopenia , MS, active chronic hepatitis , myasthenia
gravis.
5.Bronchial asthma:
 Status asthmaticus ,Severe chronic asthma:as a supplement to bronchodilators.
6.Other lung diseases:
Aspiration pneumonia,pulmonary edema ,for lung maturation in foetus ,to
prevent RDS in cases of premature delivery.
7.Infective diseases :
Under effective chemotherapeutic cover , corticosteroids are indicated only in
serious infective diseases to tide over crisis or to prevent complication.
8.Eye diseases:
Inflammatory ocular diseases-may prevent blindness.
41

42. Non-endocrine diseases
9.Skin diseases:
Life saving in-pemphigus vulgaris,exfoliative dermatitis,stevens johnson sysndrome.
10.Intestinal diseases:
Ulcerative colitis,crohn’disease,coeliac diseses
11.Cerebral edema:
Due to tumors,tubercular meningitis,Dexa or beta-methasone preferred .
12.Malignancies:
ALL,hodgkin’s,other lymphoma,secondary role in breast carcinoma,symptomatic relief
in advance malignancy.
13. Liver diseases
• Subacute hepatic necrosis & chronic active hepatitis: Improves survival rates
• Alcoholic hepatitis: reserved for pts. with severe illness
42

43. Non-endocrine diseases
14. Shock
Septicaemic shock.
15.Organ tranplant and skin allograft:
High dose corticosteroids +other immunosuppressants to prevent rejection followed by
low maintenance dose.
16. Miscellaneous
With chemotherapy(antiemetic),Bell’s palsy,Thrombocytopenia,Spinal cord
injury,Sarcoidosis ,Hypercalcemia,IBD
Diagnostic Uses:
Cushing’s syndrome
To locate the source of androgen production in hirusitism
43

44.  Mineralocoricoids:sodium and water retention,edema,↑ b.p.
 Glucocorticoids:
 1.cushing habitus cutaneous atrophy occurs with topical use
also.
 Precipitation of diabetes.
 Susceptibility to infection.(opportunistic)
 Delayed healing
 Peptic ulceration(silent perforation of ulcers)
 Osteoporosis(spongy bones)(r/g evidence of osteoporosis –
indication of withdrawal of therapy)
 Posterior subcapsular cataract(in children)
 Growth retardation(↓GH)
 FOETAL abnormality
 Psychaitric disturbances
 Suppression of HPA axis
44

45. Longer the duration of therapy, slower the withdrawal
Less than 1 week: withdrawal in few steps
 Rapid withdrawal: 50% reduction of dose every day
 Slow withdrawal: 2.5 – 5 mg prednisolone reduced at an interval
of 2-3 days
 Longer period & high dose:
 Half the dose weekly until 25 mg prednisolone or equivalent is
reached
 Later reduce by about 1mg every 3-7 days.
HPA axis recovery may take months or up to 2 years
45

46.  In The patients with steroids therapy for long time,the adrenal cortex atrophies and
stoppage of exogenous steroids precipitates a withdrawal syndrome-
Malaise,fever,weakness,pain in muscles and joints and reactivation of disease.
 Subjected to stress these patients may go into acute adrenal insufficiency.
 So any patient who has received >20-25 mg/day hydrocortisone or equivalent for
longer than2-3 weeks should be put on a scheme of gradual withdrawal .
 Such patients may need protection with steroids if a stressful situation developes
upto one year after withdrawal.
 If a patient on steoids develops an infection –the steroids should not be discontinued
despite its propensity weaken host defence.Rather,the dose may have to be increased
to meet the stress of infection.
46

47.  Use shorter acting
steroids(hydrocortisone,prednisolone) at the
lowest possible dose.
 Use steroids for the shortest peroids of time
possible.
 Give entire daily dose at one time in
morning.
 Switch to alternate day therapy if possible.
 If appropiate ,use
(dermal,inhaled,ocular,nasal,rectal,intrasyno
vial)prep.of steroid with poor systemic
availability(beclomethasone,triamcinolone,fl
uticasone)
47

48. Contraindications
(relative)
 Infections
 Hypertension with CCF
 Psychosis
 Peptic ulcer
 Diabetes mellitus
 Osteoporosis
 Glaucoma
 Pregnancy : (methylprednisolone preferred)
 Epilepsy
 Renal failure
48

49. 1.Moonface’ – excess adipose tissue in face
2 ‘Buffalo Hump’ – excess cervical adipose
tissue
3 Striae
4 Excess adipose tissue in trunk
5 Thin limbs
6 Thinning of skin on limbs
7 Bruising on extremities
8 Amenorrhea, decreased libido
9 Osteoporosis, fractures easily
10 Hirsutism 11 Acne 12 Mood swings
There are no specific oral
manifestations,but,though it may be hard
to believe ,patients have been referred to
dentists,for suspected cause of the swollen
face!!
Cushing syndrome-clinical features
Dental management in these patients consists in ---LA is preffered for pain control.
preventionof infections
pathological fractures during surgical treatments
complications such as hypertension,CVS problems, hyperglycemia, depression and
delayed healing.
Consider supplementation.
49
If the steroid dose is reduced too quickly
after replacement therapy in post
surgical patients with cushing
syndrome,,features:lethargy,abdominal
pain,hypotentionscaly desquamation of
facial skin,paticularly of forehead,is a
characteristic sign.

50. Adrenocortical hypofunction
 1⁰-due to adrenal disesae(addision’s disease)
 2⁰-following use of systemic steroids
 addision;’s disease- (autoimmune)
 c/f-hypotention,hypogyycemia,hyperpigmentation,vulnerable to any
stress such as
infection, trauma, surgery, aneasthesia, fatigue, weakness, lethargy,weigh
t loss,anorexia,dizziness
 Rᵪ-most patients are treated with oral hyrocortisone and fludrocortisone
 Dental aspects:risk of ppt hypotensive collapse,prefer LA for pain control
(over concious sedation and GA),oral hyperpigmentation
50

51. Adrenal Crisis
 Life-threatening emergency characterised by collapse ,
 bradycardia,hypotension,profound weakness,hypoglycemia,vomiting,and dehydration
 The early indicators of an adrenal-crisis onset can be vague and non-specific.
 Management:
 Lay patient flat and leg raised
 Give 200 mg hydrocortisone i.v. and summon medical assistance
 Take blood for glucose and electrolyte estimation
 Give glucose if there is hypoglycemia(25 mg orally or i.v.)
 Put up an infusion of NS or glucose –saline.
 Give I litre. For two hours together with 200mg hydrocortisone sodium
succinate,repeating this at 4-6 hourly intervals as req. and monitor b.p.
 Determine and deal with underlying cause,control of pain &infection
 Steroids supplementation must be continued for 3 days after the b.p.has retuned to
normal.
51

52.  Systemic steroids are often effective in the
treatment of oral lesions due to
noninfectious inflammatory disease.
 Topical use: non-infections, ulcerative
diseases in oral cavity. Inhibit the
inflammatory reaction, redness and edema,
 Systemic use: third molar extraction, minor
and major surgery to reduce
edema,pain,trismus .Temporomandibular
joint disorders,oral submucous fibrosis
52

53. Surgical management of a
patient on steroid therapy
53

54. Implication
 Barely three years later after the
discovery of steroids , Fraser and
coworkers reported the death of a
34-year-old man after routine
orthopedic surgery due to
shock, adrenal insufficiency, and
circulatory collapse. The patient
had been on corticosteroids for
rheumatoid arthritis, but the
treatment had been stopped prior
to surgery.
54

55. Surgery-activation of HPA axis
 Surgery is one of the most potent stressors that can cause activation of the HPA axis. The
degree of activation depends on the type and duration of surgery and anesthesia, with
many other variables adding to the picture, including analgesics, antihypertensive
medications, infections, and age.
 The maximum stimulation of the HPA axis is occur during reversal of anesthesia and in
the immediate postoperative period.
55

56. Significant hypotension??
 Significant hypotension which cannot be explained
by acute blood loss, myocardial
infarction, anesthesia, drugs, or electrolyte
imbalance should suggest the possibility of an acute
adrenal insufficiency. This is especially true if the
blood pressure does not respond promptly to blood
transfusions or vasopressors.
 It is suggested that an increase in capillary
resistance and potentiation of the effect of
vasoconstrictors on blood vessels may be factors in
the blood pressure response to adrenal
corticosteroids.
Adams, R., and Siderius, N.: Postoperative Acute Adrenal Cortical Insufficiency, J. A. M. A.
165:41-44 (Sept. 7) 1957 56

57. SUPPLEMENTATION
 Lack of increase in cortisol production during stress would cause the host to
succumb to it. On the other hand, too much cortisol would be detrimental,
causing increased tissue breakdown, poor wound healing, and
immunosuppression.
 Given this background, it is clear that any patient who has inadequate
cortisol production in response to surgical stress will fare poorly in such a
situation. This patient will need to be recognized, and his acute steroid
requirement will have to be estimated and supplemented.
57

58. Preoperative considerations
Adrenocortical function may be suppressed if:
 The patient is currently on daily systemic corticosteroids at doses above 7.5 mg
prednisolone(or equivalent)
 Cortisteroids has been taken regularly during the past 30 days.
 Corticosteroids have been taken for more than one month during past one year.
 Although the evidence for the need of steroid cover may be questionable,medicolegal
and other considerations suggest that one should act on the side of caution and fully
inform and discuss with patient,take medical advice in case of doubt,give a steroid cover
unless confident that collapse is unlikely.
58

59. Intraoperative consideration
 B.p. must be carefully watched during surgery and especially during
recovery.,and steroid supplementation must be given if b.p. starts to fall.
 Drugs especially sedative and GA ,are a hazard and it is extremely
important to avoid hypoxia,hypotention and haemorrhage
 Patient may also require special management as a result of
diabetes,hypertention ,poor wound healing and infections.
59

60. Procedure No steroids for
previous 12 months
Steroids taken
during previous 12
months
Steroids currently
taken
Conservative
dentistry or
dentoalveolar
surgery ↓LA
No cover required Give usual oral
steroids dose in
morning or
hydrocortisone 25-
50mg i.v. preop
Double oral steroids
dose in morning or
hydrocortisone 25-
50 mg i.v.
preop,continue
normal steroid
medication postop
Intermediate
surgery(multiple
extractions,or
surgery ↓GA)
Consider cover if
large doses of
steroids were given
Give usual steroids
dose in morning
+hydrocortisone 25-
50 mg i,.v. preop +
i.m. 6 hourly for 24 h
Double oral steriod
dose in morning
+hydrocortisone 25-
50mg i.v.preop +
i.m.6 hourly for 24
h,then continue
normal med.
Maxillofacial surgery
or trauma
Consider cover if
large doses were
given
Same+i,.m 6 houly
for 72 h
Same +i.m. 6 hourly
for 72 h+normal
thereafter
60

61. ROUTINE DENTAL PROCEDURES
REMEMBER:
 Conducting treatment in the morning.
 Control of anxiety and emotional stress.
 Use long-acting anesthetics.
 Treatment of postoperative pain.
 Minimum use of NSAIDs
 Aseptis surgery ,Antibiotic prophylaxis
 Prevention of iatrogenic fracture during surgery .
 topical steroids for use in mouth predispose to oral candidiosis.
61

62. From litreture
Gersema L, Baker K. Use of corticosteroids in oral surgery.J Oral Maxillofac Surg. 1992
Mar;50(3):270-
Perioperative use of corticosteroids has been advocated for reduction of pain, edema, and
trismus following oral surgical procedures. It was demonstrated that corticosteroids
reduced the amount of inflammation , especially edema. No significant adverse reactions
were noted. Based on these studies, the use of perioperative corticosteroids appears to be a
safe and rational method of reducing postoperative complications following the removal of
impacted third molars
62
 Oral submucous fibrosis: etiology, pathogenesis, and future researchR. Rajendran1. Bulletin of
the World Health Organization, 1994, 72 (6): 985-996
 Immunomodulatory drugs and systemic application of glucocorticoids and placental extract are
commonly used. By opposing the action of soluble factors released by sensitized lymphocytes
following activation by specific antigens, glucocorticoids act as immunosuppressive agents .
These also prevent or suppress inflammatory reactions, thereby preventing fibrosis by
decreasing fibroblastic proliferation and deposition of collagen.

63. From litreture
63
Emerging intra-articular drug delivery systems for the temporomandibular joint.
Mountziaris PM, Kramer PR, Mikos AG.Methods. 2009 Feb;47(2):134-40.
Intra-articular injections of corticosteroids and hyaluronic acid are currently used to treat
chronic painof TMJ.The most common treatment strategy is either a single injection or a
series of two injections spaced 14 days apart .A single corticosteroid injection is beneficial
for patients with severe TMJ pain, while further injections do not provide added pain relief,
and may increase the risk of joint degeneration and other complications
Kondoh T et al ..Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 Dec;98(6):651-6
Aim was to compare the the clinical outcome of intra-articular irrigation and corticosteroid
injection into the superior joint compartment (SJC) of patients and conventional closed
reduction with IMF with fresh mandibular condyle fractures. Clinical outcome was
determined by clinical examination of jaw motion, joint pain, and occlusal changes.
It was concluded that the modified treatment protocol involving intra-articular
corticosteroid injection is a more effective and quick-acting modality than conventional
closed reduction with IMF for functional recovery and control of clinical symptoms of
patients with unilateral fresh condylar fractures

64. Say “NO” to the mis-use!!
A patient consults a general dental practitioner for burning sensation in the mouth
The dentist looks into the mouth, finds red patches on the buccal mucosa and tongue
prescribes a topical steroid.
Within few days the burning sensation increases manifold times making life miserable for
the patient
Such events are not uncommon in today’s practice. This patient probably had oral
candidiasis predisposed by some underlying factor (e.g. diabetes). The use of a steroid
further increased the immune suppression locally, resulting in the flare up of the fungal
infection
This is a clear case of misuse of steroid
64

65. USE TOPICAL STEROIDS WISELY!!
Althoughthe practitioners have learnt (as students) that steroids are “double edged
weapons” many of them consider steroids as panacea
Steroids are used by every practitioner irrespective of their speciality. Steroids can be
administered in various forms, but its use or misuse is generally restricted to topical
preparations in dentistry(KENACORT)
Some general practitioners use them for any ulcer or even an area of erythema in the oral
cavity.
Unfortunately these preparations can also be bought over the counter
.... It doesn’t end there. The patient uses the preparation till he feels better and stops or
keeps using it for an unlimited period without consulting the dentist again
To make the situation worse, the patient recommends its use to anyone who has an ulcer in
the mouth. Although nothing catastrophic is going to happen, such misuse for prolonged
periods can result in unexpected and unwanted effects and delay in the correct diagnosis
and proper management.
Somasundaram Elangovan,A RETHINK ON THE USE OF TOPICAL STEROIDSe-Journal of
Dentistry July - Sep 2011 Vol 1 Issue 3 65

66. conclusion
In Addison’s disease: We must conduct treatment
in the morning and control of anxiety. In
patients with corticotherapy, we must evaluate
the necessity to administer additional
corticosteroids.
In Addisonian crises: we should interrupt dental
procedure. Unexplained hyponatremia and
hyperkalemia in the setting of hypotension
unresponsive to catecholamine and fluid
administration… should receive 100mg
hydrocortisone intravenously
In hyperadrenocorcism: we must prevent infection
and pathological fractures.
66

67. •Jabbour SA. Steroids and the surgical patient. Med Clin North Am. 2001
Sep;85(5):1311-1317.
•Hume DM, Bell CC, Bartter F. Direct measurement of adrenal secretion during operative
trauma and convalescence. Surgery. 1962 Jul;52:174-187.
•Kehlet H. A rational approach to dosage and preparation of parenteral glucocorticoid
substitution therapy during surgical procedures. A short review. Acta Anaesthesiol
Scand. 1975;19(4):260-26
•Kehlet H. Clinical course and hypothalamic-pituitary-adrenocortical function in
glucocorticoid-treated surgical patients. Copenhagen: FADL; 1976.
•Somasundaram Elangovan,A RETHINK ON THE USE OF TOPICAL STEROIDSe-Journal of
Dentistry July - Sep 2011 Vol 1 Issue 3
67
references

68. 68
•Steroid cover for dental patients on long-term steroid medication: proposed clinical
guidelines based upon a critical review of the literatureN. Gibson1 and J. W.
Ferguson2.British Dental Journal 2004; 197: 681–685
 Oral submucous fibrosis: etiology, pathogenesis, and future researchR. Rajendran1.
Bulletin of the World Health Organization, 1994, 72 (6): 985-996
•Crispian Scully and Roderick A. Cowson,5TH edition-medical problems in dentistry
Chapter-7,endocrine disorder II,p-85-92.
•Salem M, Tainsh RE Jr, Bromberg J, et al. Perioperative glucocorticoid coverage. A
reassessment 42 years after emergence of a problem. Ann Surg. 1994
Apr;219(4):416-425.

69. THANKYOU
69

70. Glucocorticoids antagonists
 Mitotane:structure similar to DDT, used in inoperable adrenal
cancer
 Metyrapone: inhibit 11 -hydroxylase
 Aminoglutethamide: inhibit conversion of cholesterol to
pregnolone, medical adrenelectomy
 Trilostane: inhibit conversion of pregnolone to progesterone;
used in Cushing’s syndrome
 Ketoconazole: anti-fungal, inhibit CYP450 enzymes, inhibit
steroid synthesis in ad.cortex and testis; used in Cushing’s
syndrome & Ca.prostate
 Mifepristone: glucocorticoid receptor antagonist; anti-
progesterone, used in Cushing’s syndrome 70

71. 71

72.  The effect of anabolic steroids on muscle mass is caused in at least two ways:first, they increase the
production of proteins; second, they reduce recovery time by blocking the effects of stress hormone
cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized
that this reduction in muscle breakdown may occur through anabolic steroids inhibiting the action
of other steroid hormones called glucocorticoids that promote the breakdown of muscles.[26]
Anabolic steroids also affect the number of cells that develop into fat-storage cells, by favouring
cellular differentiation into muscle cells instead. Anabolic steroids can also decrease fat by
increasing basal metabolic rate(BMR), since an increase in muscle mass increases BMR
72
Major effects of steroid abuse can include liver damage; jaundice; fluid retention; high blood
pressure; increases in "bad" cholesterol. Also, males risk shrinking of the testicles, baldness,
breast development, and infertility. Females risk growth of facial hair, menstrual changes,
male-pattern baldness, and deepened voice. Teens risk permanently stunted height,
accelerated puberty changes, and severe acne. All users, but particularly those who inject
the drug, risk infectious diseases such as HIV/AIDS and hepatitis.
Most anabolic steroids are synthetic substances similar to the male sex hormone testosterone

73. 73
This short review should underscore the primary problems associated with the
development of ‘guidelines’ defining the appropriate use of intra-articular corticosteroid
injection: there is just too little science evaluating short and long term efficacy, assessing
the most efficient technique for drug delivery and the most effective formulation, and
documenting the risks associated with repeated articular injection.
Nonetheless, it is clear that intra-articular injection of the TMJ with local anesthetic and
corticosteroid may be useful with some forms of temporomandibular joint disease including
juvenile rheumatoid arthritis and uncomplicated TM joint arthralgia associated with acute
inflammation and osteoarthritis. However, as is noted by JJ Buescher in the American
Family Physician (http://www.aafp.org/afp/2007/1115/p1477.html), “repeated intra-
articular corticosteroid injections are not recommended”

74. 74