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STEROIDS IN DENTISTRY
Presented by-Shibani Sarangi
Postgraduate IInd year
(Dept of Oral & Maxillofacial surgery)
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.
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.
• Adrenal gland is the source of diverse groups of hormones essential to
metabolic control hormones essential to metabolic control ,regulation of
body’s response to stress, regulation of body’s response to stress.
• The medullary portion secretes epinephrine and epinephrine.
• Cortex produce a number of Cortex produce a number of substances,
collectively called CORTICOSTEROIDS.
• General physiology-
• Corticosteroids are not stored to adrenal glands but are
continuously but are continuously synthesized and secreted .
• There is a negative feedback mechanism.
Mineralocorticoid-
Aldosterone
Desoxycorticosterone
Glucocoticoid-
Cortisone
Hydrocortisone
Androgens-
DHEA,Androstenedione
Catecholamines-
Adrenaline
SOURCE
• NORMAL ADULT DAILY PRODUCTION
•Cortisol 20 mg/ day
•Corticosterone 02 mg / day
•Aldosterone 0.125 mg/day
• Dehydroepiandro sterone 30 mg/day.
BIOSYNTHESIS
CLASSIFICATION
GLUCOCORTICOIDS
SHORT ACTING INTERMEDIATE ACTING LONG ACTING
•Hydrocortisone
(Cortisol)
•Prednislone
•Methylprednislone
•Triamicinolone
•Deflazacort
Dexamethasone
Betamethasone
MINERALOCORTICOIDS
•DOCA(Desoxy-corticosterone actete)
•Aldosterone
•Fludrocortisone
Coopman’s classification-Based on chemical structure
• Group A –( Hydrocortisone type)
• Hydrocortisone,
Hydrocortisone acetate,
Cortisone acetate,
Prednisolone, Methylprednisolone.
•Group B- Acetonides (and related substances)
Triamcinolone acetonide
Mometasone,
Amcinonide,
Budesonide,
Flucocortlone
Group C- ( Betamethasone type)
Betamethasone sodium phosphate,
Dexamethasone
Dexamethasone sodium phosphate
Group D – Esters
Group D1 – Halogenated (less labile)
Aclometasone dipropionate
Betamethasone valerate
Betamethasone dipropionate
Group D2 – Labile prodrug esters
Ciclesonide,
Hydrocortisone acetate,
Hydrocortisone butyrate
GLUCOCORTICOIDS
FUNTIONS OF GLUCORTICOIDS
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.
Anti- inflammatory Action
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.
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
Replacement therapy
1.Acute adrenal insufficiency
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
MINERALOCORTICOIDS
• Aldosterone is the naturally produced mineralocorticoid.
• Source- Zona Glomerulosa
• Other two synthetic entities –
-DOCA(Desoxycorticosterone acetate)
-Fludrocortisone
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.
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
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
• General principles for cortico-steroid use:
“The lowest effective dose for the least possible time”
• 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 ‘gain
consent’.
• Dexamethasone is the corticosteroid of choice . Other steroids can be
converted using the dose equivalent table below: Corticosteroid
Equivalent Dose
CLINICAL IMPLICATIONS
STEROIDS IN ORAL SURGERY
Chiefly used in –
• Post operative pain, edema and trismus after 3rd molar
surgery.
• Post operative edema after orthognathic surgery
• Prevention of alveolar osteitis
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
Cortisone-
• Inactive
• Hydroxylated in liver – hydrocortisone
• Primarily glucocorticoid
• Occasionally being used now
Route dose
orally 20- 100 mg
im 20- 100mg
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
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
• 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
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.
• 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).
• Guidelines for Management of Dental
patients under Corticosteroid therapy
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
CORTICOSTEROIDS IN ORTHODONTIC
TOOTH MOVEMENT
•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.
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.
STEROIDIN ORALMEDICINE
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
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.
BEHCET’S DISEASE
• The main stay of treatment for Behcet’s 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.
ULCERATIVE VESICULOEROSIVE
DISEASES
• Immunologically mediated diseases affecting oral mucosa
• Inflammation and loss of epithelial integrity
• Corticosteroids central role in the treatment
ERYTHEMA MULTIFORME
• Minor EM –
20 to 40 mg/day of Triamicinolone
acetonide for 4 to 6 days
• Severe or rapidly progressing
lesions –
• 60 mg/day slowly tapered by
10mg/day over 6 weeks
Lichen planus
• Prednisolone - 1mg/kg/d for <7 days
• Triamicinolone acetonide 10mg/ml
(Burkit’s Oral Medicine, 11th edition
• Tapered to 10-20mg per day for 2 weeks.
• Combination of [Prednisolone + Levamisole)-
orally 50mg for first three days
Indications for use
• Short course of TC –
• Accelerates remission without producing adverse effects
• Ulcerative disease that have tendency to remit spontaneously
•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
STEROIDS IN THE TREATMENT OF
BENIGN LESIONS
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.
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)
• 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 –
To reduce incidence of post herpetic neuralgia: • Prednisolone 20 to 30
mg/day for 7 – 10 days tapered to 10 mg/day for 1 week
ORAL SUBMUCOUS FIBROSIS
•The initial symptomatic relief the anti- inflammatory action of the steroid
• Biweekly submucosal injections combination of –
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
• Medical emergencies in Dental
Practice
Adrenal crisis prophylaxis
• Hydrocortisone i.v. initially.
• If improvement within 24 hours – 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).
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
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 –
• Never steroid discontinuation
increase the dose
Adverse effects
• Seen in long term use
• Depends on drug potency, duration of therapy, frequency
of application
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.
Systemic adverse effects
• Mineralocorticoid :
-Sodium & water retention,
-oedema,
-hypokalemic
- alkalosis & a progressive raise in BP.
Glucocorticoid :
1. Cushing’s habitus: round face,
narrow mouth,
supraclavicular hump,
obesity of trunk with relatively thin limbs.
• Fragile skin & purple striae :
-typically on thighs & lower abdomen
-easy bruising
-telengiactasis
-hirstuism,
-cutaneous atrophy due to topical use
telengiactasis
Psychiatric disturbances : mild euphoria
nervousness
decreased sleep
mood changes
depressive illness
Suppression of hypothalamo-pitutary axis (HPA) :
adrenal atrophy + stoppage of exogenous steroid = withdrawal syndrome
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
Steroids in dentistry

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Steroids in dentistry

  • 1. STEROIDS IN DENTISTRY Presented by-Shibani Sarangi Postgraduate IInd year (Dept of Oral & Maxillofacial surgery)
  • 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 body’s response to stress, regulation of body’s 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.
  • 7. • NORMAL ADULT DAILY PRODUCTION •Cortisol 20 mg/ day •Corticosterone 02 mg / day •Aldosterone 0.125 mg/day • Dehydroepiandro sterone 30 mg/day.
  • 9. CLASSIFICATION GLUCOCORTICOIDS SHORT ACTING INTERMEDIATE ACTING LONG ACTING •Hydrocortisone (Cortisol) •Prednislone •Methylprednislone •Triamicinolone •Deflazacort Dexamethasone Betamethasone MINERALOCORTICOIDS •DOCA(Desoxy-corticosterone actete) •Aldosterone •Fludrocortisone
  • 10. Coopman’s classification-Based on chemical structure • Group A –( Hydrocortisone type) • Hydrocortisone, Hydrocortisone acetate, Cortisone acetate, Prednisolone, Methylprednisolone. •Group B- Acetonides (and related substances) Triamcinolone acetonide Mometasone, Amcinonide, Budesonide, Flucocortlone
  • 11. Group C- ( Betamethasone type) Betamethasone sodium phosphate, Dexamethasone Dexamethasone sodium phosphate Group D – Esters Group D1 – Halogenated (less labile) Aclometasone dipropionate Betamethasone valerate Betamethasone dipropionate Group D2 – Labile prodrug esters Ciclesonide, Hydrocortisone acetate, Hydrocortisone butyrate
  • 12.
  • 13.
  • 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: (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
  • 22. • Aldosterone is the naturally produced mineralocorticoid. • Source- Zona Glomerulosa • Other two synthetic entities – -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: “The lowest effective dose for the least possible time” • 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 ‘gain consent’. • Dexamethasone is the corticosteroid of choice . Other steroids can be converted using the dose equivalent table below: Corticosteroid Equivalent Dose
  • 28.
  • 30. STEROIDS IN ORAL SURGERY Chiefly used in – • 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 – 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 – • 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 •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. BEHCET’S DISEASE • The main stay of treatment for Behcet’s 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.
  • 48. ULCERATIVE VESICULOEROSIVE DISEASES • Immunologically mediated diseases affecting oral mucosa • Inflammation and loss of epithelial integrity • Corticosteroids central role in the treatment
  • 49. ERYTHEMA MULTIFORME • Minor EM – 20 to 40 mg/day of Triamicinolone acetonide for 4 to 6 days • Severe or rapidly progressing lesions – • 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 (Burkit’s 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 – • Accelerates remission without producing adverse effects • Ulcerative disease that have tendency to remit spontaneously •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
  • 52. STEROIDS IN THE TREATMENT OF BENIGN LESIONS
  • 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 – To reduce incidence of post herpetic neuralgia: • Prednisolone 20 to 30 mg/day for 7 – 10 days tapered to 10 mg/day for 1 week
  • 56. ORAL SUBMUCOUS FIBROSIS •The initial symptomatic relief the anti- inflammatory action of the steroid • Biweekly submucosal injections combination of – 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
  • 57. • Medical emergencies in Dental Practice
  • 58. Adrenal crisis prophylaxis • Hydrocortisone i.v. initially. • If improvement within 24 hours – 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 – • 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. Cushing’s 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
  • 65. Psychiatric disturbances : mild euphoria nervousness decreased sleep mood changes depressive illness Suppression of hypothalamo-pitutary axis (HPA) : adrenal atrophy + stoppage of exogenous steroid = withdrawal syndrome
  • 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

Editor's Notes

  1. Basophilic cells of ant pituatory
  2. RESORPTION FROM DCT