2. INTRODUCTION
⢠Corticosteroids, since their introduction in the 1940s, have
become one of the most widely prescribed class of drugs.
⢠They belong to a class of chemicals that includes steroid
hormones that are produced naturally in the adrenal cortex of
vertebrates and analogous to those that are synthesized in
laboratories.
3. HISTORY
⢠Hench (1949) -improvement in rheumatoid arthritis by using
cortisone.
⢠In 1950 Nobel Prize -Kendall and Reichstein and Hench, for
developing corticosteroids
⢠Currently, drugs with one of the broadest spectrum of clinical utility.
4. ⢠Adrenal gland is the source of diverse groups of hormones essential to
metabolic control hormones essential to metabolic control ,regulation of
bodyâs response to stress, regulation of bodyâs response to stress.
⢠The medullary portion secretes epinephrine and epinephrine.
⢠Cortex produce a number of Cortex produce a number of substances,
collectively called CORTICOSTEROIDS.
5. ⢠General physiology-
⢠Corticosteroids are not stored to adrenal glands but are
continuously but are continuously synthesized and secreted .
⢠There is a negative feedback mechanism.
16. Function sof Glucoroticoids-
1)Permissive action
⢠Action of some hormones are executed only in presence of
glucocorticoids.
⢠Examples are :
⢠Calorigenic effect of glucagon.
⢠Lypolytic effect of catecholamines.
⢠Pressor effect of catecholamines.
⢠Bronchodilation by catecholamines.
18. Anti-allergic effect
⢠Exerted by suppression the nuclear factor functions on T cells
and monocytes / macrophages.
⢠Suppresion of recruitment of leucocytes at the site of contact
with antigen and inflammatory response to immunological
injury.
19. Immunosuppressive action-
⢠Glucocorticoids (corticosteroids) have inhibitory effects on a
broad range of immune responses.
⢠Suppresses immune system of body by decreasing number of
circulating T lymphocytes.
⢠Prevent release of IL-2 IL-6 by T-cells
20. Replacement therapy
1.Acute adrenal insufficiency
2.Chronic adrenal insufficiency: (addisonâs disease)
Hydrocortisone given orally,Supplemented with âa mineralocorticoid
(fludrocortisone)
3.Congenital adrenal hyperplasia â
Familial disorder due to def.of of 21-hydroxylase &11 - hydroxylase
enzyme. Treatment: hydrocortisone 0.6 mg /kg/day in divided doses
22. ⢠Aldosterone is the naturally produced mineralocorticoid.
⢠Source- Zona Glomerulosa
⢠Other two synthetic entities â
-DOCA(Desoxycorticosterone acetate)
-Fludrocortisone
23. ACTION ON EFFECT
Sodium metabolism Increases sodium reabsorption
from renal tubules
On ECF Stimulates water reabsorption thus
in term increases ECF volume
Blood pressure Increases
Potassium ions Increases ,excretion of potassium
ions from renal tubules
Hydrogen ion Tubular secretion of hydrogen ion ,
essential to maintain acid base
balance.
24.
25. Fate of corticosteroids
Degraded chiefly in Liver
Conjugated to form glucouronides &
to a lesser extent sulphates
25% is excreted in Bile & faeces
75% excreted in urine
26. ROUTES OF ADMINISTRATION OF
CORTICOSTEROIDS
Topical steroid Beclamethasone,Betamethasone,
Clobetasol,Hydrocortisone,Mometasone
Inhalational steroids Beclomethasone dipropionate,
Budesonide, Fluticasone
Oral forms bethamethasone,prednisone ,prednisolo
ne triamcinolone
methylprednisolone
Systemic form
27. ⢠General principles for cortico-steroid use:
âThe lowest effective dose for the least possible timeâ
⢠Have a clear indication / objective and consider all alternatives before
starting.
⢠Consider prior steroid use, effectiveness and side effects.
⢠Clarify the individual risk-benefit ratio
⢠Ensure specified indications/ doses reflect current evidence base/ best
practice.
⢠Discuss risk factors/incidence of adverse effects with the patient to âgain
consentâ.
⢠Dexamethasone is the corticosteroid of choice . Other steroids can be
converted using the dose equivalent table below: Corticosteroid
Equivalent Dose
30. STEROIDS IN ORAL SURGERY
Chiefly used in â
⢠Post operative pain, edema and trismus after 3rd molar
surgery.
⢠Post operative edema after orthognathic surgery
⢠Prevention of alveolar osteitis
31. Hydrocortisone-
⢠Primarily glucocorticoid
⢠Acts rapidly
⢠Short duration of action
⢠But has significant mineralcorticoid activity also
purpose route dose
Replacement
therapy
orally 20mg in morning
10mg in afternoon
Shock
Status asthmaticus
Acute adrenal
insufficiency
iv 100mg bolus &
100mg 8 hrly
infusion
32. Cortisone-
⢠Inactive
⢠Hydroxylated in liver â hydrocortisone
⢠Primarily glucocorticoid
⢠Occasionally being used now
Route dose
orally 20- 100 mg
im 20- 100mg
33. Prednisolone-
⢠More selective glucocorticoid
⢠4 times more potent than hydrocortisone
⢠Fluid retention with high doses
⢠Less pituitary adrenal axis suppresion
Purpose Route Dose
Allergic
Inflammatory
Autoimmune
Malignant disease
Orally
Im
Intra articular
topically
5-60mg /day
10-40mg /day
34. Methylprednisolone-
⢠Slightly more selective and more potent than prednisolone
⢠Less pituitary adrenal axis suppression
Purpose Route Dose
Retention enema in
ulcerative colitis
orally 4-32mg/day
Nonsuppressive
active rheumatoid
arthritis,
Renal transplant,
pemphigus
Iv 1 gm infused every
6-8 weeks
35. ⢠TMJ arthritis-
⢠Single intra-articular injection of corticosteroid (methylprednisolone)
diluted with 0.5ml of lidocaine or Triamicinolone acetonide significantly
reduced joint pain and other symptoms for 4-6 weeks.
⢠The pharmacologic effect - 3-4 weeks
36. Orthognathic surgery
⢠Glucocorticoids are given to patients to relieve postoperative pain,
swelling, trismus, and nausea and vomiting after a wide variety of surgical
procedures including orthognathic surgery.
⢠Glucocorticoids reduce PONV by depleting 5-HT3 in neural tissue
⢠Also prevent its release in the gut, and they have a synergistic action with
5-HT3 antagonists.
37. ⢠Temporomandibular joint (TMJ) disorder
⢠They are the main cause of chronic facial pain and a major cause of
disability (Horten 1953).
⢠Intra-articular injection of steroids - often diluted with a local anesthetic
prior to injection into the TMJ (Kopp 1981; Alstergren 1996).
⢠Triamcinolone acetonide : 2 to 40 mg, depending upon the size of the
joint injected (Hollander 1951; Silbermann1978). & 10 mg (Gray 1994).
38. ⢠Guidelines for Management of Dental
patients under Corticosteroid therapy
39.
40.
41. Preoperative considerations
Adrenocortical function may be suppressed if â
⢠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
42. CORTICOSTEROIDS IN ORTHODONTIC
TOOTH MOVEMENT
â˘Orthodontic tooth movement is by sequential reactions of the periodontal
tissue in response to biomechanical forces.
⢠The arachidonic acid metabolites also play an important role in the process
of bone remodeling during tooth movement
⢠The acute activity of neutrophils
macrophages is targeted.
43. STEROIDS IN ENDODONTICS
⢠Steroid-antibiotic combinations are often used for eg:-
Ledermix
⢠Steroids like hydrocortisone are
also mixed with zinc oxide eugenol
as root canal sealers.
45. Recurrent aphthous stomatitis
⢠Topical-
Hydrocortisone hemisuccinate (pellets of 2.5 mg)
Triamcinolone acetonide (adhesive paste containing 0.1% of the steroid).
- Inaccessible areas controlled by-
⢠Topical dexamethasone.(0.5 mg/5 ml held over the area or applied with a
saturated gauge pad to the ulcers, 4 times/day for 15 min )
⢠Betamethasone sodium phosphate rinse
46. Major aphthous ulcers-
⢠Systemic treatment -
-Prednisone therapy 40 mg/day for 1 week
-1.0 mg/kg a day as a single dose in severe RAS patients and
gradually tapered after 7-14 days.
47. BEHCETâS DISEASE
⢠The main stay of treatment for Behcetâs disease is
immunosuppressive therapy.
⢠In the acute phase, prednisone, at doses of 40-60 mg/day.
⢠It may be used alone or in combination therapy with other
immunosuppressive agents.
49. ERYTHEMA MULTIFORME
⢠Minor EM â
20 to 40 mg/day of Triamicinolone
acetonide for 4 to 6 days
⢠Severe or rapidly progressing
lesions â
⢠60 mg/day slowly tapered by
10mg/day over 6 weeks
50. Lichen planus
⢠Prednisolone - 1mg/kg/d for <7 days
⢠Triamicinolone acetonide 10mg/ml
(Burkitâs Oral Medicine, 11th edition
⢠Tapered to 10-20mg per day for 2 weeks.
⢠Combination of [Prednisolone + Levamisole)-
orally 50mg for first three days
51. Indications for use
⢠Short course of TC â
⢠Accelerates remission without producing adverse effects
⢠Ulcerative disease that have tendency to remit spontaneously
â˘Eg RAS, some cases of EM, drug induced ulceration
⢠In severe cases of ulceration-
⢠After a short course of systemic corticosteroids, maintenance
regimen of TC
⢠Prevent recurrence, and avoids adverse effects associated
with long course of systemic corticosteroids
53. CENTRAL GIANT CELL GRANULOMA
⢠Intralesional injection of triamcinolone
can be given in a dose of 1 to 2 mg/kg/d
(maximum of 60 mg).
⢠The treatment interval at 4 to 6 weeks.
54. Hemangioma
⢠Prednisone at a dose of 20-30 mg/d
can be given for 2 weeks to 4
months
⢠Intralesional triamcinolone
acetonide (4 mg/mL)
55. ⢠STEROIDS IN SALIVARY GLAND
DISORDERS
⢠Mucocele
⢠0.05% clobetasol propionate 3 times a
day for 4 weeks in a mucosal adhesive base.
⢠Intralesional injections have also been
tried with success
STERIODS IN NEURALGIA
Post herpetic neuralgia â
To reduce incidence of post herpetic neuralgia: ⢠Prednisolone 20 to 30
mg/day for 7 â 10 days tapered to 10 mg/day for 1 week
56. ORAL SUBMUCOUS FIBROSIS
â˘The initial symptomatic relief the anti- inflammatory action of the steroid
⢠Biweekly submucosal injections combination of â
Dexamethasone (4mg/ml) + hyaluronidase + diluted in 1.0 ml of 2%
Lignocaine
Systemic-
⢠Therapy with Hydrocortisone 25 mg orally QID
⢠Triamicinolone or 90mg of Dexamethasone supplemented with biweekly
intraleisonal injections.
For a period of 20 weeks
58. Adrenal crisis prophylaxis
⢠Hydrocortisone i.v. initially.
⢠If improvement within 24 hours â changed to an oral formulation.
⢠The dose can be decreased by one third to one half the dose daily until a
maintenance dose of 20 mg in the morning and 10 mg in the afternoon or
at night is attained.
⢠Some patients may need only a dose of 20 mg/day total (i.e., 20 mg every
morning, or 15 mg in the morning and 5 mg in the afternoon or at night).
59. Anaphylatic shock
⢠They have a delayed onset of 4 to 6 hours.
⢠Are unlikely to be helpful in the treatment of acute anaphylaxis. Play a
role in preventing rebound anaphylaxis.
⢠Prednisone 1 mg/kg up to 50 mg orally,.
⢠Hydrocortisone 1. 5- 3 mg/kg IV particularly in patients with airway
involvement and bronchospasm, based empirically on their important role
in asthma
60. Scheme for Steroid withdrawal
⢠Any patient taking > 20 -25 mg /day hydrocortisone or equivalent dose for
longer than 2-3 week.
⢠20mg hydrocortisone/day reduction every week
⢠Such patients need protection with steroids if a stressful condition
develop up to 1 year after withdrawal.
⢠If a patient on steroid therapy develops infection â
⢠Never steroid discontinuation
increase the dose
61. Adverse effects
⢠Seen in long term use
⢠Depends on drug potency, duration of therapy, frequency
of application
62. Local adverse effects
⢠Tachyphylaxis
⢠Burning Mouth
⢠Hypogeusia
⢠Oral Hairy Leukoplakia
⢠Hypersensitive Reactions to the Drug
⢠Topical Steroid Allergy
⢠Skin Atrophy
⢠Striae - Stretch Marks
⢠Acne form/Rosacea like eruptions
⢠Candidiasis
⢠Delayed Healing of application and anatomical area.
63. Systemic adverse effects
⢠Mineralocorticoid :
-Sodium & water retention,
-oedema,
-hypokalemic
- alkalosis & a progressive raise in BP.
Glucocorticoid :
1. Cushingâs habitus: round face,
narrow mouth,
supraclavicular hump,
obesity of trunk with relatively thin limbs.
64. ⢠Fragile skin & purple striae :
-typically on thighs & lower abdomen
-easy bruising
-telengiactasis
-hirstuism,
-cutaneous atrophy due to topical use
telengiactasis
66. References
⢠Essential of Pharmaclogy:K D Tripathi
⢠Textboot of Oral Medicine: Burkitt
⢠The Journal of Anesthesia :Britain society of anesthesiologist
⢠Textbbook of oral medicine: Anil Govindrao Ghom
⢠Internet