Corticosteroids in maxillofacial surgery

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cortico steroids in maxillo facial surgery

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  • The normal concentration of aldosterone in bloodis about 6 nanograms (6 billionths of a gram) per100 ml, and the average secretory rate is approximately150 μg/day (0.15 mg/day).The concentration of cortisol in the blood averages12 μg/100 ml, and the secretory rate averages 15 to20 mg/day.
  • Mol Cell Endocrinol. 1993 Jul;94(1):111-9.
  • pro-opiomelanocortin (POMC
  • Bronchial asthma:Status asthmaticus – give i. v, withdraw after emergency is overSevere chronic asthma – as a supplement to bronchodialators or low dose oral therapy is given for longer periodsOther lung diseases:Aspiration pneumoniaPulmonary edemaAccelerate lung maturation in foetus. Therapy may be undertaken if premature delivery is contemplated.
  • Cerebral edema:Due to tumours, tuberculous meningitis etc responds to corticoidsDexa or betamethasone are preferred.Malignancies:Essential component of combined chemotherapy of - Acute lymphatic leukemia - Hodgkin’s lymphoma and other lymphomasOrgan transplantation and skin allograft:High dose of corticosteroids with other immunosupressants are given to prevent rejection reaction followed by low maintenance doses.Shock:I.V glucocorticoids given in septicaemic shock To test the adrenal pituitary axis
  • The applications in the field of oral surgery would include,Prevention of postoperative pain, edema, trismus after 3rd molar surgeryPrevention of postoperative edema after orthognathic surgeryPrevention of alveolar osteitis
  • the key factors that determine the selection of a topical or systemic treatment
  • It also depends upon the concentration
  • Logically, the success of a topical medicine depends mainly on the contact time of the drug with the lesion.
  • TCs have been applied in various vehicles. 2.1 Lotion 2.2 Shake lotion 2.3 Cream 2.4 Ointment 2.5 Gel 2.6 Foam 2.7 Transdermal patch 2.8 Powder 2.9 Solid 2.10 Sponge 2.11 Tape 2.12 Vapor 2.13 Paste 2.14 Tincture
  • Doses of each pulse are notstandardized but are usually 500 to 1000 mg methylprednisoloneor 100 to 200 mg dexamethasone.
  • Doses of each pulse are notstandardized but are usually 500 to 1000 mg methylprednisoloneor 100 to 200 mg dexamethasone.
  • Doses of each pulse are notstandardized but are usually 500 to 1000 mg methylprednisoloneor 100 to 200 mg dexamethasone.
  • 1 mg /kg/day for 7 daysFollowed by reduction of 10mg each subsequent dayBurkits 11th edition
  • Normal HPA suppression recovery may take time to 30 days to 12 month But according to the guideline given by John L. Atlee it is considered normal to return in 6 months

Transcript

  • 1. Corticosteroid s
  • 2. 2 Contents 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
  • 3. 3 Classification of steroids Uses in medicine Steroids in dentistry Adverse effects Drug interactions Precautions Pathologies of adrenal gland
  • 4. 4 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 body’s response to stress. Using cholesterol as a substrate, the adrenal cortex produces a large number of substances collectively known as corticosteroids.
  • 5. 5 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.
  • 6. 6 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.
  • 7. 7 Functional anatomy and histology of adrenal glands
  • 8. 8
  • 9. 9
  • 10. 10 Zones of adrenal cortex Zona glomerulosa Hormones Aldosterone Desoxycorticosterone Zona fasciculata Cortisone Cortisol Zona reticularis Dehydroepiandrosterone Androstenidione Traces of estrogens Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 11. 11 Biosynthesis of steroids Cholesterol Pregnenolone Progesterone 17α Hydroxy pregnenolone Dehydroepiandrosterone 11- Deoxy corticosterone 17α Hydroxy progesterone Androstenidione Corticosterone 11 Desoxyhydro cortisone Aldosterone Hydrocortisone Testosterone
  • 12. 12 Mineralocorticoids Glucocorticoids Cortisol Aldosterone Corticosterone 11- Deoxy corticosterone Cortisone Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 13. 13 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
  • 14. 14 REGULATION OF SECRETION  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
  • 15. 15 Fate of corticosteroids 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
  • 16. 16 MECHANISM OF ACTION plasma memb CYTOPLASMIC Corticosteroids RECEPTOR PROTEIN GLUCOCORTICOID RESPONSE ELEMENT Transcription of m - RNA New protein synthesis Nucleus TOTAL TIME 30 – 60 mins
  • 17. 17 Mineralocorticoid s
  • 18. 18 Mineralocorticoids Source : Zona glomerulosa Functions: 90% of mineralocorticoid activity is provided by aldosterone Aldosterone – life saving hormone Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 19. 19 Actions On Na+ metabolism • Increase in the reabsorption of sodium from renal tubules Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 20. 20 On ECF volume • Na reabsorption from renal tubules • Simultaneous water reabsorption • Increase in ECF volume Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 21. 21 On BP • Increases ECF volume • Increases BP Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 22. 22 On K+ ions •Increase in the excretion of potassium from renal tubules Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 23. 23 On H+ ion concentration • Causes tubular secretion of hydrogen ions • Essential to maintain acid - base balance Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 24. 24 On intestine •Greatly enhances sodium absorption from the intestine Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 25. 25 Regulation of aldosterone secretion Increase in K+ concentration Decrease in Na+ Concentration Decrease in ECF volume Decrease in K+ concentration Increase in Na+ Concentration Increase in ECF volume Feedback inhibition Stimulation angiotensinogen Angiotensin - 1 Angiotensin - 2 Renin Converting enzyme Juxtaglomerular apparatus Excretion of K+ Retention of Na+ Retention of water Lungs kidneys Adrenal cortex Aldosterone Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 26. 26 Glucocorticoids
  • 27. 27 Glucocorticoids Source : zona fasciculata Functions: Hormone Glucocorticoid activity Cortisol 95% Corticosterone 4% Cortisone 1% Cortisol – Life protecting hormone Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 28. 28 Actions: 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
  • 29. 29 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
  • 30. 30 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
  • 31. 31 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
  • 32. 32 On water metabolism • Accelerate the excretion of water Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 33. 33 On muscles • Increase the release of aminoacids from muscles by catabolism of proteins Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 34. 34 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
  • 35. 35 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
  • 36. 36 On CNS • Essential for normal functioning • Insufficiency causes personality changes like irritablity and lack of concentration Essentials Of Medical Physiology 3rd Edition, K Sembulingam
  • 37. 37 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
  • 38. Anti-inflammatory actions Lipocortin Recruitment of WBC & monocytemacrophage into affected area & elaboration of chemotactic substances ELAM & ICAM in endothelial cells TNF from phagocytic cells IL1 from monocyte-macrophage Expression of cyclooxygenase II GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006) 38
  • 39. Corticosteroids Lipocortin Phospholipids Phospholipase A2 Arachidonic acids lipoxygenase Leukotriene Cycylooxygenase Prostaglandins, Thromboxane Prostacyclins 39
  • 40. On resistance to stress 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) 40
  • 41. 41 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)
  • 42. 42 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)
  • 43. 43 Regulation of cortisol secretion Emotion, stress, trauma Feedback inhibition Hypothalamus Corticotropin releasing factor Anterior pituitary ACTH Adrenal cortex Cortisol
  • 44. 44 Mechanism of action at cellular level
  • 45. 45 Mechanism of action at cellular level Translocation of glucose transporters from plasma membrane to deeper sites Decreased glucose uptake and utilization in peripheral tissues GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
  • 46. 46 Induction of hepatic gluconeogenetic enzymes Increased production of glucose from aminoacids GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
  • 47. 47 Induction of hepatic glycogen synthetase Deposition of glycogen in hepatocytes GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
  • 48. 48 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)
  • 49. 49 Decreased expression of POMC gene in pituitary corticotropes Decreased production of ACTH GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
  • 50. 50 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)
  • 51. 51 Negative regulation of genes for cytokines in macrophages, endothelial cells and lymphocytes Decreased production of IL1,2,3,6,TNFα,GM-CSF, Interferon – γFibroblast proliferation and T lymphocyte function are suppressed. chemotaxis interfered. GOODMAN & GILMAN'S THE PHARMACOLOGICAL BASIS OF THERAPEUTICS - 11th Ed. (2006)
  • 52. 52 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)
  • 53. 53 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)
  • 54. 54 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)
  • 55. 55 Classificatio n
  • 56. 56 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
  • 57. 57 Mineralocorticoids • Desoxycorticosterone acetate(DOCA) • Fludrocortisone • Aldosterone
  • 58. 58 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
  • 59. 59 According to Potency Agent Antiinflammator y 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 Basic and Clinical Pharmacology LANGE-11th Edition
  • 60. 60 Some Commonly Prescribed Steroids
  • 61. 61 Triamcinolone Kenacort, Tricort, kenalog, 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
  • 62. 62 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.
  • 63. 63 Betamethasone Oral: oral drops – 0.5 mg/ ml, tablets – 0.5 to 1 mg. Betnesol, Betnovate, Topical – 0.1% eye drops, Betnesol forte, ointment,0.05% nasal drops, Betawin forte, 0.12% skin creams Walacort, Parenteral:4 mg/ml for IM, Stemin IV, intralesional, intraarticular
  • 64. 64 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
  • 65. 65 Cortisone Oral: 5, 10, 25 mg tablets Corlin, Cortone Parentral:22,25 mg/ml of solution
  • 66. 66 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
  • 67. 67 Uses In medicine In dentistry
  • 68. 68 Medicine Replacement therapy Pharmacotherapy
  • 69. 69 Replacement therapy: Acute adrenal insufficiency Chronic 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. • 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
  • 70. 70 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
  • 71. 71 • 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
  • 72. 72 Arthritis Rheumatoid arthritis Osteoarthritis Rheumatic fever Gout
  • 73. 73 Collagen diseases SLE Polyarteritis nodosa Dermatomyositis Nephrotic syndrome Glomerulonephritis
  • 74. 74 Severe allergic reactions Used for short periods in anaphylaxis Angioneurotic edema Utricaria Serum sickness
  • 75. 75 Autoimmune disorders Autoimmune hemolytic anemia Thrombocytopenia Active chronic hepatitis Myasthenia gravis
  • 76. 76 Bronchial asthma Status asthmaticus Severe chronic asthma
  • 77. 77 Infective diseases Severe forms of tuberculosis Severe lepra reaction Certain form of bacterial meningitis Pneumocystitis carini pneumonia with hypoxia in AIDS patients.
  • 78. 78 Eye diseases Effective in diseases of anterior chamber Allergic conjuctivitis Iritis keratitis
  • 79. 79 Skin diseases Eczematous skin diseases Pemphigus vulgaris Exfoliative dermatitis Steven johnsons syndrome
  • 80. 80 Intestinal diseases Ulcerative colitis Chron’s disease
  • 81. 81 Others Cerebral edema Malignancies Organ transplantation and skin allograft Shock To test the adrenal pituitary axis
  • 82. Steroids in Dentistry Used primarily to decrease postoperative edema and manage oral inflammatory diseases 82
  • 83. 83 Steroids in oral surgery Prevention of postoperative pain, edema, trismus after 3rd molar surgery Prevention of postoperative edema after orthognathic surgery Prevention of alveolar osteitis
  • 84. 84 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 International Endodontic Journal,Volume 36 Issue12, Pages 868 - 75
  • 85. 85 Corticosteroids in Oral Medicine
  • 86. 86 • Eg: Erosive LP Ulcerative, Vesiculoerosive diseases • RAS Benign lesions Salivary gland disorders TMJ Disorders Neuralgia Treatment Miscellanous • Eg: CGCG • Eg: Mucocele • Eg: Osteoarthritis • Rheumatiid arthritis • Eg. Post herpatic neuralgia • OSMF
  • 87. 87 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 reddening, debilitating. clinical with features pain that are can ulceration and be and severe
  • 88. 88 • 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)
  • 89. 89 Criteria for use short course of TCs Accelerate remission without adverse effects TCs must be used for longer, less predictable periods Recurrent aphthous stomatitis (RAS), some cases of erythema multiforme (EM), and Drug-induced ulceration. Severe RAS, Erosive oral lichen planus (OLP), specific forms of EM, and mucous membrane pemphigoid (MMP) Scully et al., 1999; Chan et al., 2002
  • 90. 90 CODS Davangere 24/01/2014 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
  • 91. 91 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. JDR April 2005 vol. 84 no. 4 294-301
  • 92. 92 The key factors The specific diagnosis The severity of the oral disease The presence or absence of extra-oral lesions The medical history of the patient JDR April 2005 vol. 84 no. 4 294-301
  • 93. 93 Factors that influence the effectiveness of TCs: 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). JDR April 2005 vol. 84 no. 4 294-301
  • 94. 94 Factors that influence the effectiveness of TCs: The contact time between the drug and lesion and the vehicle used to apply it; JDR April 2005 vol. 84 no. 4 294-301
  • 95. 95 Factors that influence the effectiveness of TCs: Concentration which can increase its clinical effectiveness, although no additional advantage is obtained beyond certain limits. (Regezi and Sciubba, 1999). JDR April 2005 vol. 84 no. 4 294-301
  • 96. 96 Success of a topical medicine Two main factors Number of applications per day High-potency (2-3 times) The vehicle used Low potency (5-10 times) JDR April 2005 vol. 84 no. 4 294-301 Various vehicles
  • 97. 97 Various vehicles. 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). JDR April 2005 vol. 84 no. 4 294-301
  • 98. 98 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. JDR April 2005 vol. 84 no. 4 294-301
  • 99. 100 • 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. JDR April 2005 vol. 84 no. 4 294-301
  • 100. 101 Systemic steroids for ulcerative vesiculobullous diseases
  • 101. 102 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. Natah SS, Konttinen YT. IJOMS 2004;33:221-34.
  • 102. 103 Erythema multiforme Minor EM Severe or rapidly progressing lesions 20 – 40 mg/day for 4 – 6 days 60 mg/day slowly tapered by 10 mg/day over 6 weeks Indian J Ophthalmol Jan-Feb 2010;58(1):64-66
  • 103. 104 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. Burkit’s Oral Medicine, 11th edition
  • 104. 105 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
  • 105. 106 Benefits • Avoids complications & side effects of long term steroid therapy • To achieve immunosuppressive effects similar to those with higher doses of steroids
  • 106. 108 Cicatricial 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
  • 107. 109 Bullous pemphigoid Clobetasol propionate 20 -40 mg/day is more effective for the treatment. JIAOMR, April-June 2011;23(2):128-131
  • 108. 110 Lichen planus Prednisolone 1mg/kg/d for <7 days Tapered to 10-20mg per day for 2 weeks Burkit’s Oral Medicine, 11th edition JIAOMR, April-June 2011;23(2):128-131
  • 109. 111 Lupus erythematosus Predisolone – 20 - 30 mg/day for 2- 6 weeks Tapered gradually
  • 110. 112 Steroids in the treatment of benign lesions CGCG HEMANGIOMA
  • 111. 113 CGCG 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. J Med Assoc Thai 2008; 91 (Suppl 3): S90-6
  • 112. 116 Hemangioma Prednisone at a dose of 20-30 mg/d can be given for 2 weeks to 4 months ( Fost and Esterly) Intralesional triamcinolone acetonide (4 mg/mL) (Hawkins et al)
  • 113. 117 Steroids in salivary gland disorders MUCOCELE
  • 114. 118 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. (JOMS 2008;66:1737-9)
  • 115. 121 Steroids in neuralgia POST HERPETIC NEURALGIA
  • 116. 122 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 (Treatment of oral diseases, George Lascaris)
  • 117. 125 Steroids for TMJ disorders OSTEOARTHRITIS RHEUMATOID ARTHRITIS
  • 118. 126 24/01/2014 Arthritis Rheumatoid arthritis osteoarthritis Intraarticular injection – 10 to 40 mg/ml Intraarticular injection – 20 mg/ml(2 injections 14 days apart) Oral Surgery Volume 1 Issue 2, Pages 88 - 95
  • 119. 127 Miscellaneous OSMF BELL’S PALSY
  • 120. 128 Bell’s palsy  Significant improvement can be achived when Prednisolone is started within 72 hours of symptom onset  1 mg/kg body weight (maximum 70 mg) in divided doses with meals for six days, and the dose can be reduced gradually over the next four days.
  • 121. 129 OSMF Predisolone – 20 - 30 mg/day for 2 – 4 weeks Gradually taper Discontinue in 12 months
  • 122. 130 Injections of triamcinolone 10mg/ml diluted in 1 ml of 2% lidocaine with hyaluronidase 1500 IU, biweekly for 4 weeks. (Borle et al)
  • 123. 131  Biweekly submucosal injections of a combination of dexamethasone (4mg/ml) and two parts of hyaluronidase, diluted in 1.0 ml of 2% xylocaine by means of a 27 gauge needle, not more than 0.2ml solution per site, for a period of 20 weeks.  Significant relief of burning sensation (88%) and improvement of trismus (83%) can be seen in most patients.
  • 124. 132 Adverse effects Due to extention of pharmacological action occuring with prolonged therapy Mineralocorticoids:  Sodium and water retention  Edema  Hypokalemic alkalosis  Progressive rise in B.P  Weight gain  Fluid and electrolyte disturbance
  • 125. 133 Glucocorticoid: GIT:  Acute erosive gastritis with hemorrhage  Peptic ulcer  Intestitial perfortion  Pancreatitis Metabolic effects:  Hyperglycemia  Ketoacidosis  Hyperosmolar coma  Hypophosphatemia
  • 126. 134 Cushingoidism: Prolonged therapy causes  Central obesity with moon face  Buffalo hump  Pink florid striae are liable to appear on the abdomen, hips and pectoral region and skin may become friable
  • 127. 135 CVS and renal system:  Hypertension  Salt and water retention  Hypokalemic alkalosis CNS:  Influence mood, sleep pattern  Insomnia  Acute psychotic reactions  Benign intracranial hypertension  Epilepsy
  • 128. 136 Musculoskeletal effects:  Proximal myopathy and osteoporosis with compression fractures of vertebrae  Acute aseptic necrosis of bone Eyes:  Glaucoma
  • 129. 137 Suppression of inflammation and immune response:  Latent infection may flare  Oppurtunistic infection with low grade pathogens Retardation of linear growth:  Occurs in children who receive more than 50 mg of cortisone per m2 of body surface per day.
  • 130. 138 Relative Contraindications:       Peptic ulcer Diabetes mellitus Hypertension Pregnancy Herpes simplex keratitis Tuberculosis Osteoporosis  Psycosis  Epilepsy  Renal failure 
  • 131. 139 Drug interactions Glucocorticoid dosage decreased:  Antibiotics (Erythromycin)  Cyclosporine  Isoniazid  Ketakonazole  Estrogen Reduce metabolic clearance
  • 132. 140 Glucocorticoid dosage increased:  Cholestyramine  Antiepileptic Drugs (Barbiturates, Phenytoin, Carbamazepine)  Rifampicin Glucocorticoid dosage needs adjustment:  Antianxiety and antipsychotic drugs  Antihypertensives  Hypoglycemics  sympathomimetics
  • 133. 141 Precautions during therapy Before starting therapy:  Enquire and check for hypertension, diabetes mellitus, peptic ulcer, any infection
  • 134. 142 During therapy:  Prescribe drug with food  Diet low in calories and sodium and rich in potassium  Check periodically for weight gain, hypertension, hyperglycemia
  • 135. 143  Increase dose in case of stress  Instruct patient not to stop abruptly While stopping therapy:  Taper therapy
  • 136. 144 Rule of 2 Adrenocortical suppression should be suspected if a patient has received Glucocoticoid therapy through two of the following methods In a dose of 20 mg or more of cortisone or its equivalent Via oral or parenteral route or a continuous period of 2 weeks or longer Within 6 months -2 years of therapy Medical emergencies in dental office, Stanley F.Malamed Complications in Anesthesia - John L. Atlee; Page-132
  • 137. 145 Protocol for Supplementation of Patients on Glucocorticoid Therapy Who Are Undergoing Dental Care (Burket’s 10th ed)
  • 138. 146 Dental Procedure Previous Systemic Steroid Use Routine procedures If prior usage No lasted for > 2 supplementatio weeks and ceased n needed < 14–30 days ago, give previous maintenance dose If prior usage ceased > 14–30 days ago, no supplementation needed Current Systemic Steroid Use Daily alternating Systemic Steroid Use Current topical Systemic Steroid Use Treat on No steroid dosage supplementatio day; no further n needed supplementatio n needed
  • 139. 147 Dental Procedure Previous Systemic Steroid Use Current Systemic Steroid Use Extractions, surgery, or extensive procedures If prior usage Double daily lasted > 2 weeks dose on day of and ceased < procedure 14–30 days ago, give previous maintenance dose Treat on steroid dosage day, and give double daily dose on day of procedure If prior usage ceased > 14–30 days ago, no supplementatio n needed Give normal daily dose on first postoperative day when pain is anticipated Double daily dose on first postoperative day when pain is anticipated Daily alternating Systemic Steroid Use Current topical Systemic Steroid Use No supplementatio n needed
  • 140. 148 Scenario One 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 Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001
  • 141. 149 Scenario Two Patient requiring extractions is taking 10 mg of prednisone for the past year to treat rheumatoid arthritis This patient’s 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 Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001
  • 142. Scenario Three 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 Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001 150
  • 143. Scenario Four Patient requiring extractions was previously taking 50 mg of prednisone for Crohn’s 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 151
  • 144. 152 Scenario Five 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 Clinical update by Naval Postgraduate Dental School, Maryland Vol. 23, No. 7 July 2001
  • 145. 153 Pathology of Adrenal Gland
  • 146. 154 Pathologies of the adrenal gland Adrenal cortex Hyperactivity Hypoactivity
  • 147. 155 Hyperactivity Cushing’s syndrome Hyperaldosteronism Adrenogenital syndrome
  • 148. 156 Cushing’s syndrome  Hypersecretion of glucocorticoids particularly cortisol Due to pituitary origin Due to adrenal origin Cushing’s disease Cushing’s syndrome
  • 149. 157 Disproportionate body fat distribution Moon face Buffalo hump Pot belly Purple striae Thinning of skin Pigmentation Facial redness Hirsutism Muscle weakness
  • 150. 158 Bone resorption Hyperglycemia Hypertension Susceptiblity to infections Poor wound healing
  • 151. 159 Hyperaldosteronism  Hypersecretion of aldosterone Primary Secondary Adrenal cause Extra adrenal causes
  • 152. 160 Hyperaldosteronism • • • • • Increase in ECF volume and blood volume Hypertension Severe depletion of potassium Muscle weakness Metabolic alkalosis
  • 153. 163 Hypoactivity Addison’s disease Adrenal crisis Chronic adrenal hyperplasia
  • 154. 164 Addison’s disease  Failure of adrenal cortex to secrete all the corticosteroids Primary Adrenal cause Secondary Failure of anterior pituitary to secrete ACTH Tertiary Failure of hypothalamus to secrete CRF
  • 155. 165 Pigmentation of skin and mucous membrane Muscle weakness Dehydration Hypotension Decreased cardiac output Hypoglycemia Nausea, vomiting, diarrhoea Inability to withstand stress
  • 156. 166 Adrenal crisis  Common symptom of addison’s disease characterized by sudden collapse associated with an increase in need for large quantities of glucocorticoids.  Fatal if not treated in time
  • 157. 167 Adrenal crisis Causes • Exposure to even mild stress Hypoglycemia due to fasting Surgical operation Sudden withdrawal of glucocorticoid treatment
  • 158. 168 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.
  • 159. 169 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.
  • 160. 170 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.