Corticosteroids in Dentistry Seminar by Dr Pratik

• 1. Corticosteroi ds SEMINAR I I PRESENTER : DR PRATIK PIPALIA

2. G O O D 2M O R N I N G 3. Corticosteroi ds SEMINAR II PRESENTER: DR PRATIK PIPALIA PPT available at https://www.dropbox.com/s/unzzzyaotqhs1vz/Steroids%20seminar%20Dr%20Prat ik.pptx 4. Introduction History Functional anatomy and histology of adrenal glands Biosynthesis of steroids Fate of steroids Mineralocorticoids (source, action, regulation) Glucocorticoids (source, action, regulation) Mechanism of action at cellular level Contents 4 5. 5Classification of steroids Uses in medicine Steroids in dentistry Adverse effects Drug interactions Precautions Pathologies of adrenal gland 6. Introduction The adrenal gland is the source of a diverse group of hormones essential for metabolic control, regulation of water and electrolyte balance, and regulation of bodys response to stress. Using cholesterol as a substrate, the adrenal cortex produces a large number of substances collectively known as corticosteroids. 6 7. History By the middle of 19th century it was demonstrated that adrenal glands were essential for life Later, it was appreciated that the cortex was more important than the medulla A number of steroidal active principles were isolated and their structures were elucidated by kendall and his coworkers in the 1930s. 7 8. However, the gate to their great therapeutic potential was opened by Hench (1949) who obtained striking improvement in rheumatoid arthritis by using cortisone. The nobel prize was awarded the very next year to kendall and Hench. Currently, corticosteroids are drugs with one of the broadest spectrum of clinical utility. 8 9. Functional anatomy and histology of adrenal glands 9 10. 10 11. 11 12. Zones of adrenal cortex Hormones Zona glomerulosa Aldosterone Desoxycorticosterone Zona fasciculata Cortisone Cortisol Zona reticularis Dehydroepiandrosterone Androstenidione Traces of estrogens 12 Essentials Of Medical Physiology 3rd Edition, K Sembulingam 13. Cholesterol Pregnenolone Progesterone 11- Deoxy corticosterone Corticosterone Aldosterone 17 Hydroxy pregnenolone 17 Hydroxy progesterone 11 Desoxyhydro cortisone Hydrocortisone Dehydroepiandrosterone Androstenidione Testosterone Biosynthesis of steroids 13 14. Mineralocorticoids Aldosterone 11- Deoxy corticosterone Glucocorticoids Cortisol Corticosterone Cortisone 14 Essentials Of Medical Physiology 3rd Edition, K Sembulingam 15. Rate of secretion of the principal steroids Glucorticoids 10-20 mg daily Mineralocorticoids 0.125 mg daily Textbook of Medical Physiology 11th Edition, Arthur C. Guyton, John E. Hall - 2006 15 16. Regulation by Hypothalamus (CRH) & Pituitary (ACTH) Negative feedback effect from plasma cortisol levels Pulsatile secretion of ACTH based on Circadian rhythm Neural effects on HPA axis due to emotional / physical stress 16 REGULATION OF SECRETION 17. Fate of corticosteroids 17 Degraded mainly in liver Conjugated to form glucuronides and to a lesser extent form sulphates 25% - excreted in bile and feces 75% - excreted in urine 18. 18 MECHANISM OF ACTION plasma memb Corticosteroids CYTOPLASMIC RECEPTOR PROTEIN GLUCOCORTICOID RESPONSE ELEMENT Nucleus Transcription of m - RNA New protein synthesis TOTAL TIME 30 60 mins 19. Mineralocortico ids 19 20. Mineralocorticoids Source : Zona glomerulosa Functions: 90% of mineralocorticoid activity is provided by aldosterone Aldosterone life saving hormone 20 Essentials Of Medical Physiology 3rd Edition, K Sembulingam 21. On Na+ metabolism Increase in the reabsorption of sodium from renal tubules Actions 21 Essentials Of Medical Physiology 3rd Edition, K Sembulingam 22. 22 On ECF volume Na reabsorption from renal tubules Simultaneous water reabsorption Increase in ECF volume Essentials Of Medical Physiology 3rd Edition, K Sembulingam 23. 23 On BP Increases ECF volume Increases BP Essentials Of Medical Physiology 3rd Edition, K Sembulingam 24. 24 On K+ ions Increase in the excretion of potassium from renal tubules Essentials Of Medical Physiology 3rd Edition, K Sembulingam 25. 25 On H+ ion concentration Causes tubular secretion of hydrogen ions Essential to maintain acid - base balance Essentials Of Medical Physiology 3rd Edition, K Sembulingam 26. 26 On intestine Greatly enhances sodium absorption from the intestine Essentials Of Medical Physiology 3rd Edition, K Sembulingam 27. Increase in K+ concentration Decrease in Na+ Concentration Decrease in ECF volume Decrease in K+ concentration Increase in Na+ Concentration Increase in ECF volume Juxtaglomerular apparatus Excretion of K+ Retention of Na+ Retention of water kidneysLungs AldosteroneAdrenal cortex angiotensinogen Angiotensin - 1 Angiotensin - 2 Renin Converting enzyme Stimulation Feedback inhibition Regulation of aldosterone secretion 27 Essentials Of Medical Physiology 3rd Edition, K Sembulingam 28. 28 Glucocorticoids 29. Glucocorticoids Source : zona fasciculata Functions: Cortisol Life protecting hormone Hormone Glucocorticoid activity Cortisol 95% Corticosterone 4% Cortisone 1% 29 Essentials Of Medical Physiology 3rd Edition, K Sembulingam 30. Actions: 30 On carbohydrate metabolism Increases blood glucose level in two ways, Promotes gluconeogenesis Inhibits glucose uptake and utilization by peripheral cells Essentials Of Medical Physiology 3rd Edition, K Sembulingam 31. 31 On protein metabolism Promote catabolism of protein in cell Increase plasma amino acid and protein content in the cell. Essentials Of Medical Physiology 3rd Edition, K Sembulingam 32. 32 On fat metabolism Causes mobilization and redistribution of fat Actions are - Mobilization of fatty acids from adipose tissue - Increase the concentration of fatty acids in blood - Increases the utilization of fat for energy Essentials Of Medical Physiology 3rd Edition, K Sembulingam 33. 33 On mineral metabolism Enhances sodium retention Slightly increase potassium excretion Decreases blood calcium by inhibiting absorption from intestine Essentials Of Medical Physiology 3rd Edition, K Sembulingam 34. 34 On water metabolism Accelerate the excretion of water Essentials Of Medical Physiology 3rd Edition, K Sembulingam 35. 35 On muscles Increase the release of aminoacids from muscles by catabolism of proteins Essentials Of Medical Physiology 3rd Edition, K Sembulingam 36. 36 On blood vessels Decreases the number of circulating eosinophills in retculoendothelial cells Decrease the number of basophils and lymphocytes Increase the number of neutrophills, RBCs and platelets. Essentials Of Medical Physiology 3rd Edition, K Sembulingam 37. 37 On vascular response Glucocorticoids is essential for the constrictor action of adrenaline and noradrenaline In adrenal deficiency, the blood vessels fail to respond to Adr and NA leading to vascular collapse. Essentials Of Medical Physiology 3rd Edition, K Sembulingam 38. 38 On CNS Essential for normal functioning Insufficiency causes personality changes like irritablity and lack of concentration Essentials Of Medical Physiology 3rd Edition, K Sembulingam 39. 39 Permissive action of glucocorticoids The action of some hormones are executed only in the presence of glucocorticoids. Eg: Calorigenic effect of glucagon Lipolytic effect of catecholamines Pressor effects of catecholamines Bronchodialation by catecholamines Essentials Of Medical Physiology 3rd Edition, K Sembulingam 40. Lipocortin Recruitment of WBC & monocyte- macrophage into affected area & elaboration of chemotactic substances ELAM & ICAM in endothelial cells TNF from phagocytic cells IL1 from monocyte-macrophage Expression of cyclooxygenase II 40 Anti-inflammatory actions GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 41. 41 Phospholipids Arachidonic acids lipoxygenase Cycylooxygenase Leukotriene Prostaglandins, Thromboxane Prostacyclins Phospholipase A2 Lipocortin Corticosteroids 42. On resistance to stress 42 Physical or mental stress Increases ACTH Increase in glucocorticoid secretion High resistance to body against stress GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 43. 43 Anti allergic action Suppress all types of hypersensitivity and allergic phenomena. Suppression of recruitment of leucocytes at the site of contact with antigen and of inflammatory response to immunological injury. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 44. 44 Immunosuppresive effects Suppress the immune system of the body by decreasing the number of circulating T lymphocytes Prevent release of interleukin-2 by T cells GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 45. Emotion, stress, trauma Hypothalamus Corticotropin releasing factor Anterior pituitary ACTH Adrenal cortex Cortisol Feedbackinhibition Regulation of cortisol secretion 45 46. Mechanism of action at cellular level 46 47. Translocation of glucose transporters from plasma membrane to deeper sites Decreased glucose uptake and utilization in peripheral tissues 47 GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) Mechanism of action at cellular level 48. 48 Induction of hepatic gluconeogenetic enzymes Increased production of glucose from aminoacids GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 49. 49 Induction of hepatic glycogen synthetase Deposition of glycogen in hepatocytes GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 50. 50 Site specific changes in sensitivity of adipocytes to GH, Adr, insulin Altered distribution of body fat GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 51. 51 Decreased expression of POMC gene in pituitary corticotropes Decreased production of ACTH GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 52. 52 Induction of lipocortins in macrophages, endothelium and fibroblasts Lipocortins inhibit phospolipase A2 decreased production of PGs,LTs&PAF GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 53. 53 Negative regulation of genes for cytokines in macrophages, endothelial cells and lymphocytes Decreased production of IL- 1,2,3,6,TNF,GM-CSF, Interferon Fibroblast proliferation and T lymphocyte function are suppressed. chemotaxis interfered. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 54. 54 Decreased production of acute phase reactants from macrophages and endothelial cells Complement function is interfered. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 55. 55 Decreased production of ELAM-1 and ICAM-1 in endothelial cells Adhesion and localization of leukocytes is interfered. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 56. 56 Inhibit IgE mediated histamine and LT-C4 release from basophils Effects of antigen antibody reaction not mediated GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 57. Classificatio n 57 58. Classification of steroids based on their relative activity Glucocorticoids: Short acting (t1/2 < 12 hr) Hydrocortisone Cortisone Intermediate acting: (t1/2 12 36) Prednisole Methyl prednisole Triamcinolone Long acting: (t1/2 > 36 hrs) Paramethasone Dexamethasone Betamethasone 58 59. Mineralocorticoids Desoxycorticosterone acetate(DOCA) Fludrocortisone Aldosterone 59 60. 60 Potency Examples Highest 0.05% Clobetasol propionate 0.05%Betamethasone dipropionate High 0.1% Halcinonide 0.25% Desoximethasone 0.05% Fluocinonide 0.5% Triamcinolone acetinode 0.05% Betamethasone dipropionate 0.05% Diflorasone diacetate cream Intermediate 0.2% Fluo-cinolone acetonide 0.05% Desoxymethasone 0.025% Betamethasone benzoate 0.2% Hydrocortisone valerate Low 0.025% Fluo-metholone 0.025% Triamcinolone acetonide 0.03% Fluocinolone pivalate 0.01% Betamethasone valerate Lowest 0.25-2.5% Hydrocortisone 0.5% Prednisolone 0.2% Betamethasone Handbook of Applied therapeutics 8th Edition, 2007 61. Agent Anti- inflammatory Topical Equivalent oral dose (mg) Forms Available Hydrocortisone 1 1 20 O, I, T Cortisone 0.8 0 25 O Prednisolone 5 4 5 O, I Triamcinolone 5 5 4 O, I, T Flu-prednisolone 15 7 1.5 O Betamethasone 25-40 10 0.6 O, I, T Dexamethasone 30 10 0.75 O, I, T 61 According to Potency Basic and Clinical Pharmacology LANGE-11th Edition 62. Some Commonly Prescribed Steroids 62 63. 63 Triamcinolone Kenacort, Tricort, k enalog, Tess buccal paste Oral:1,4,8mg syrup Topical:0.1% eye drops, ointment Parentral: 3,10,40 mg/ml for I.M, intraarticular, intralesional injections 64. 64 Dexamethasone Decadron, Dexasone, Wymesone Oral:0.25,0.5,0.75,1,2,4,6mg tablets Topical:0.1% eye drops, ear drops, skin ointment Parenteral: 4,8,10,20 mg/ml for IV, IM, intralesional and intraarticular. 65. 65 Betamethasone Betnesol, Betn ovate, Betnes ol forte, Betawin forte, Walacort , Stemin Oral: oral drops 0.5 mg/ ml, tablets 0.5 to 1 mg. Topical 0.1% eye drops, ointment,0.05% nasal drops, 0.12% skin creams Parenteral:4 mg/ml for IM, IV, intralesional, intraarticular 66. 66 Hydrocortisone Wycort, Hycort, Unicort, Cipcorlin, Efcorlin Oral:5mg,10mg,20mgtab Topical: 1%eye drops 0.025%nasal drops 0.25-2.5%skin cream Parenteral:25, 50 mg/ml for IV,IM,SC Injections 67. 67 Cortisone Corlin, Cortone Oral: 5, 10, 25 mg tablets Parentral:22,25 mg/ml of solution 68. 68 Prednisolone Wysolone, Prelone, Nucort, Cecort, Oral:5,10, 20 mg tablets, 15mg/5 ml syrup, 5mg/ml suspension as pediatric drops Parenteral:25,50 mg/ml IM,IV,Intralesional 69. In medicine In dentistry 69 Uses 70. Medicine 70 Replacement therapy Pharmacotherapy 71. Acute adrenal insufficiency Hydrocortisone or dexamethasone are given i.v, first as a bolus injection and then as infusion along with istonic saline and glucose solutions. Chronic adrenal insufficiency : Hydrocortisone given orally is the most commonly used drug with adequate salt and water allowance Congenital adrenal hypoplasia : 0.6 mg/kg daily in divided doses round the clock Replacement therapy: 71 72. Pharmacotherapy: Single dose (even excessive) is not harmful can be used to tide over mortal crisis even when benefit is not certain. Short courses (even high doses) are not likely to be harmful in the absence of contraindications. Starting doses can be high in severe illness 72 73. Long term use is potentially hazardous: keep the dose to minimum which is found by trial and error, even partial relief may have to be tolerated. No abrupt withdrawal after a corticoid has been given for > 2 to 3 weeks: may precipitate adrenal insufficiency 73 74. Arthritis Rheumatoid arthritis Osteoarthritis Rheumatic fever Gout 74 75. Collagen diseases SLE Polyarteritis nodosa Dermatomyositis Nephrotic syndrome Glomerulonephritis 75 76. Severe allergic reactions Used for short periods in anaphylaxis Angioneurotic edema Utricaria Serum sickness 76 77. Autoimmune disorders Autoimmune hemolytic anemia Thrombocytopenia Active chronic hepatitis Myasthenia gravis 77 78. Bronchial asthma Status asthmaticus Severe chronic asthma 78 79. Infective diseases Severe forms of tuberculosis Severe lepra reaction Certain form of bacterial meningitis Pneumocystitis carini pneumonia with hypoxia in AIDS patients. 79 80. Eye diseases Effective in diseases of anterior chamber Allergic conjuctivitis Iritis keratitis 80 81. Skin diseases Eczematous skin diseases Pemphigus vulgaris Exfoliative dermatitis Steven johnsons syndrome 81 82. Intestinal diseases Ulcerative colitis Chrons disease 82 83. Others 83 Cerebral edema Malignancies Organ transplantation and skin allograft Shock To test the adrenal pituitary axis 84. Steroids in Dentistry Used primarily to decrease postoperative edema and manage oral inflammatory diseases 84 85. Steroids in oral surgery 85 Prevention of postoperative pain, edema, trismus after 3rd molar surgery Prevention of postoperative edema after orthognathic surgery Prevention of alveolar osteitis 86. steroids in Endodontics Steroids are used as intracanal medicaments in endodontics Ledermix is corticosteroid- antibiotic intracanal paste Painful teeth with acute apical periodontitis that had been dressed with ledermix paste gave rise to less pain and it has proved to be an effective intracanal medicament for the control of postoperative pain associated with acute apical periodontitis with a rapid onset of pain reduction 86 International Endodontic Journal,Volume 36 Issue12, Pages 868 - 75 87. Corticosteroi ds in Oral Medicine 87 88. Thank You... 88 89. GOO D 89 MORNING 90. Corticosteroi ds SEMINAR II SESSION-2 PRESENTER: DR PRATIK PIPALIA CHAIR PERSON: DR ALI I M 91. Previous Session Questions 91 92. Mineralosorticoid Lifesaving .. Why ?? Without mineralocorticoids, potassium ion concentration of the extracellular fluid rises markedly, sodium and chloride are rapidly lost from the body, and the total extracellular fluid volume and blood volume become greatly reduced. The person soon develops diminished cardiac output, which progresses to a shock like state, followed by death. This entire sequence can be prevented by the administration of aldosterone or some other mineralocorticoid 92 93. 93Sources of cholesterolEgg Yolk Dairy Products, ice cream cheese, butter Oil, ghee, soyaben oil, sun flower oil Red Meat, pork, beef, mutton 94. Lipids Total Lipid Range mg% Mean Total Lipid 350-800mg% 570 Cholesterole 150-250 200 HDL 30-6 45 LDL 70-200 135 VLDL 1/5th of TG Phospholipid 125-400 210 Triglycerol 75-175 140 Free Fatty acids 5-15 10 94 95. How exactly stress induces increases Corticosteroid production? At the hypothalamus, fear-signaling impulses activate both the sympathetic nervous system and the modulating systems of the HPA axis. E/NE will positively feedback to the pituitary and increase the breakdown of POMCs(Pro-opiomelanocortin ) into ACTH 95 96. 96 Steroids in Oram Medicine Adverse effects Drug interactions Precautions Pathologies of adrenal gland Content 97. Corticosteroi ds in Oral Medicine 97 98. 98 Eg: Erosive LP RASUlcerative, Vesiculoerosive diseases Eg: CGCG Benign lesions Eg: Mucocele Salivary gland disorders Eg: Osteoarthritis Rheumatiid arthritisTMJ Disorders Eg. Post herpatic neuralgia Neuralgia Treatment OSMF Miscellanous 99. Ulcerative Vesiculoerosive diseases Immunologically mediated diseases that affect the oral mucosa present with inflammation and loss of epithelial integrity, through cellular and/or humoral immunity- mediated attack on epithelial connective tissue targets. The main clinical features are ulceration and reddening, with pain that can be severe and debilitating. 99 100. Corticosteroids play a central role in the treatment of vesiculoerosive lesions. However, the frequency and severity of the adverse effects associated with the use of systemic corticosteroids have led to the increased use of topical corticosteroids (TCs) 10 0 101. 10 1 short course of TCs Accelerate remission without adverse effects Recurrent aphthous stomatitis (RAS), some cases of erythema multiforme (EM), and Drug-induced ulceration. TCs must be used for longer, less predictable periods Severe RAS, Erosive oral lichen planus (OLP), specific forms of EM, and mucous membrane pemphigoid (MMP) Scully et al., 1999; Chan et al., 2002 Criteria for use 102. 10 2 very severe cases of ulceration Short course of systemic corticosteroids followed by maintenance regimen of TCs and or can also be started simultaneously with the systemic therapy Pemphigus vulgaris ,10-30% of Pemphigoid patients, Erosive lichen planus Inevitably be treated with systemic corticosteroids and/or other immunosuppressant therapies Laskaris and Angelopoulos, 1981; Nisengard and Neiders, 1981; Fine et al., 1984; Domloge-Hultsch et al., 1994; Dayan et al., 1999 103. Protocols for use When a TC is prescribed, and especially when a prolonged course is predicted, the basic rule is that a TC of a potency appropriate to the severity of the clinical symptoms should be used, at the lowest possible concentration and frequency, with maintaining the effectiveness of the treatment. It should always be taken into account that these drugs do not cure the disease but rather control or relieve the symptoms. 10 3 JDR April 2005 vol. 84 no. 4 294-301 104. The key factors 10 4 JDR April 2005 vol. 84 no. 4 294-301 The specific diagnosis The severity of the oral disease The presence or absence of extra-oral lesions The medical history of the patient 105. Factors that influence the effectiveness of TCs: 10 5 JDR April 2005 vol. 84 no. 4 294-301 The intrinsic potency of the drug which can be significantly increased by the halogenation of the steroid; esterification, which makes the drug more lipophilic and gives it greater penetrability (Regezi and Sciubba, 1999). 106. Factors that influence the effectiveness of TCs: 10 6 JDR April 2005 vol. 84 no. 4 294-301 The contact time between the drug and lesion and the vehicle used to apply it; 107. Factors that influence the effectiveness of TCs: 10 7 JDR April 2005 vol. 84 no. 4 294-301 Concentration which can increase its clinical effectiveness, although no additional advantage is obtained beyond certain limits. (Regezi and Sciubba, 1999). 108. Success of a topical medicine 10 8 Two main factors Number of applications per day High-potency (2-3 times) Low potency (5-10 times) The vehicle used Various vehicles JDR April 2005 vol. 84 no. 4 294-301 109. Various vehicles. 10 9 JDR April 2005 vol. 84 no. 4 294-301 Orabase (Stoy, 1966), Cyanoacrylate (Jasmin et al., 1993), Bioadhesive patches made of cellulose derivatives (Mahdi et al., 1996), Gels (Regezi and Sciubba, 1999), and Denture adhesive paste (Lo Muzio et al., 2001). 110. Patients prescribed TC in an adherent vehicle should be instructed to Apply a small amount to the target area after meals, and Not to eat or drink for at least 30 min. It is best not to rub the TC in, because this can produce irritation. 11 0 JDR April 2005 vol. 84 no. 4 294-301 111. For small and accessible erosive lesions, or those located on the gingiva and palate, the lesions can be treated by the Use of an adherent paste in a tray, Which allows for accurate control over the contact time and Ensures that the entire lesional surface is exposed to the drug. 11 2 JDR April 2005 vol. 84 no. 4 294-301 112. Systemic steroids for ulcerative vesiculobullous diseases 11 3 113. major aphthae or severe multiple minor aphthae Prednisone therapy should be started at 1.0 mg/kg/day in patients with severe RAU and should be tapered after 1 to 2 weeks. 11 4 Natah SS, Konttinen YT. IJOMS 2004;33:221-34. 114. 11 5 Minor EM 20 40 mg/day for 4 6 days Severe or rapidly progressing lesions 60 mg/day slowly tapered by 10 mg/day over 6 weeks Erythema multiforme Indian J Ophthalmol Jan-Feb 2010;58(1):64-66 115. Pemphigus Vulgaris Mainstay 1-2mg/kg/d. Initial dose of treatment 0.5 mg/kg/day to 3 mg/kg/d Dose that achieves clinical control is maintained for 2- 3 weeks and then gradually tapered. 11 6 Burkits Oral Medicine, 11th edition 116. Pulse therapy Also called short term therapy High dose therapy involves a 48-72 hrs course of intensive steroid administration Single i.v injection of a supra-physiological dose of steroid Dose of 0.5-2g of prednisolone or equivalent 11 7 117. Benefits Avoids complications & side effects of long term steroid therapy To achieve immunosuppressive effects similar to those with higher doses of steroids 11 8 118. 12 0Cicatricial pemphigoid Predisolone 30 to 60 mg/day 2-3 weeks to stop new bullae formation Tapered by 20% every 2-3 weeks until the dose of 10 mg is reached Dose maintained on alternate days and reduced by 5 mg every 2 weeks, then stopped 119. 12 1Bullous pemphigoid Clobetasol propionate 20 -40 mg/day is more effective for the treatment. JIAOMR, April-June 2011;23(2):128-131 120. 12 2Lichen planus Prednisolone 1mg/kg/d for 2 weeks and ceased < 1430 days ago, give previous maintenance dose If prior usage ceased > 1430 days ago, no supplementation needed No supplementation needed Treat on steroid dosage day; no further supplementatio n needed No supplementatio n needed 152. 16 1Dental Procedure Previous Systemic Steroid Use Current Systemic Steroid Use Daily alternating Systemic Steroid Use Current topical Systemic Steroid Use Extractions, surgery, or extensive procedures If prior usage lasted > 2 weeks and ceased < 1430 days ago, give previous maintenance dose If prior usage ceased > 1430 days ago, no supplementation needed Double daily dose on day of procedure Double daily dose on first postoperative day when pain is anticipated Treat on steroid dosage day, and give double daily dose on day of procedure Give normal daily dose on first postoperative day when pain is anticipated No supplementatio n needed 153. 16 2 Patient requiring extractions took a 7 day course of 20 mg. of prednisone for exacerbation of asthma one week ago No supplementation required. Even though the dose was supraphysiologic, the course of time it was taken was less than 2 weeks Scenario One Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 154. 16 3 Patient requiring extractions is taking 10 mg of prednisone for the past year to treat rheumatoid arthritis This patients HPA axis is probably suppressed due to supraphysiologic dose of corticosteroids for longer than 2 weeks. Supplement with at least 100 mg of cortisol equivalent (25 mg prednisone) in the morning on the day of the surgery Scenario Two Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 155. 16 4 Patient requiring extractions is taking 2.5 mg of prednisone daily for the past 3 months to treat his psoriasis No supplementation required. Even though the patient has been on prednisone for over 2 weeks, the dose is subphysiologic and will not adversely impact his stress response Scenario Three Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 156. 16 5 Patient requiring extractions was previously taking 50 mg of prednisone for Crohns disease. He was on a 6-month course of prednisone but took his last dose 5 weeks ago No supplementation needed. A functional stress response returns in 14-30 days after the last dose of steroids Scenario Four 157. 16 6 Patient requiring extractions is taking 75 mg of prednisone daily for the past 8 weeks to treat pemphigus No supplementation needed as 75 mg of prednisone is the maximum dose equivalent to 300 mg of endogenous cortisol Scenario Five Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 158. Pathology of Adrenal Gland 16 7 159. 16 8Pathologies of the adrenal gland Adrenal cortex HypoactivityHyperactivity 160. 16 9 Hyperactivity Cushings syndrome Hyper- aldosteronism Adreno- genital syndrome 161. 17 0 Due to pituitary origin Cushings disease Due to adrenal origin Cushings syndrome Cushings syndrome Hypersecretion of glucocorticoids particularly cortisol 162. 17 1Disproportionate body fat distribution Moon face Buffalo hump Pot belly Purple striae Thinning of skin Pigmentation Facial redness Hirsutism Muscle weakness 163. 17 2 Bone resorption Hyperglycemia Hypertension Susceptiblity to infections Poor wound healing 164. 17 3 Primary Adrenal cause Secondary Extra adrenal causes Hyperaldosteronism Hypersecretion of aldosterone 165. 17 4 Hyperaldosteronism Increase in ECF volume and blood volume Hypertension Severe depletion of potassium Muscle weakness Metabolic alkalosis 166. 17 7 Hypoactivity Addisons disease Adrenal crisis Chronic adrenal hyperplasia 167. 17 8 Primary Adrenal cause Secondary Failure of anterior pituitary to secrete ACTH Addisons disease Failure of adrenal cortex to secrete all the corticosteroids Tertiary Failure of hypothalamus to secrete CRF 168. 17 9 Pigmentation of skin and mucous membrane Muscle weakness Dehydration Hypotension Decreased cardiac output Hypoglycemia Nausea, vomiting, diarrhoea Inability to withstand stress 169. 18 0Adrenal crisis Common symptom of addisons disease characterized by sudden collapse associated with an increase in need for large quantities of glucocorticoids. Fatal if not treated in time 170. 18 1Adrenal crisis Causes Exposure to even mild stress Hypoglycemia due to fasting Surgical operation Sudden withdrawal of glucocorticoid treatment 171. Congenital adrenal hyperplasia Congenital disorder characterized by increase in size of adrenal cortex. Eventhough the size of the gland increases the cortisol secretion decreases. Congenital enzymes necessary for synthesis of cortisol, particularly 21- hydroxylase. 18 2 172. In boys: Precocious body growth, causing stocky appearance called infant Hercules Precocious sexual development with enlarged penis even at age of 4 years. In girls: Produces Masculinization Female child born with external genitalia of male type. 18 3 173. Conclusion 18 4 174. Conclusion Corticosteroids play an important role in control of pain & inflammation associated with numerous disease states of oral cavity. Currently corticosteroids are drugs with one of the broadest spectrum of clinical utility. But it should never be used as a substitute to other treatments Lets keep it mind that these drugs do not cure the disease but rather control or relieve the symptoms. It should be used cautiously as it is two edged sword. 18 5 175. Thank You 18 6 PPT available at https://www.dropbox.com/s/unzzzyaotqhs1vz/Steroids%20seminar%20Dr%20Prat ik.pptx