Steroids in oral & maxillofacial surgery

4,654 views

Published on

Published in: Health & Medicine, Technology
2 Comments
35 Likes
Statistics
Notes
  • hi!!! can u please mail me this presentation at garimaverma19@gmail.com
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • very nice presentation, kindly can u give me this presentation, i urgently want..
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
No Downloads
Views
Total views
4,654
On SlideShare
0
From Embeds
0
Number of Embeds
11
Actions
Shares
0
Downloads
0
Comments
2
Likes
35
Embeds 0
No embeds

No notes for slide
  • All the physiological activity in human Is …..To regulate the body function…..
  • Location : Immediately superior and slightly anterior to the upper pole of either kidney ( Golden yellow in colour, each gland possesses two functionally and structurally distinct areas, an outer cortex and an inner medulla. The glands are surrounded by connective tissue containing perinephric fat, enclosed within the renal fascia, and separated from the kidneys by a small amount of fibrous tissue.The dimensions of the suprarenal glands in adults in vivo have been defined by Vincent and colleagues (1994) using computed tomography (CT). The mean transverse dimensions of the body of the suprarenal gland are 61 mm (right) and 79 mm (left) and the mean transverse dimensions of suprarenal limbs are 28 mm (right) and 33 mm (left). No individual suprarenal limb should measure more than 6.5 mm in transverse section. The suprarenal glands each weigh approximately 5 g (the medulla contributes about one-tenth of the total weight).
  • Aldosterone secretion is regulated by renin-angiotensin system, ACTH, sodium, and potassium levels . When renal blood pressure decreases, renin is released, which stimulates release of angiotensin and activates the secretion of aldosteronevia a negative feedback loop.
  • Steroids in oral & maxillofacial surgery

    1. 1. PRESENTED BY – DR. SHEETAL KAPSE 2nd YEAR, P.G. STUDENT MODERATORS - DR. SUNIL DUTT C. DR. M. SATISH DR. DEEPAK THAKUR DR. MANISH PANDIT
    2. 2. 1. Introduction 2. History 3. Physiological action 4. Biosynthesis 5. Classification 6. Pharmacokinetics 7. Preparations & Dosages 8. Indications/uses 9. Important uses in oral & maxillofacial surgery 10. Adverse effects 11. Contraindications 12. Conclusion 13. References
    3. 3.  Hormone (hormaein = to stir up).  Hormone is a substance of intense biological activity that is produced by specific cells in the body and is transported through the circulation to act on is target cells.  Hormones regulate body function to bring about a programmed pattern of life events and maintain homeostasis in the face of markedly variable external or internal environment.
    4. 4. 1. Protein hormone 2. Steroids hormone 3. Derivatives of amino acids (tyrosine)
    5. 5.  These hormones are secreted by endocrine (ductless) glands. Sr. no. Body function Major regulator hormone(s) 1 Availability of fuel Insulin, glucagon, growth hormone 2 Metabolic rate Triiodothyronine, thyroxin 3 Somatic growth growth hormone, insulin like growth factors, 4 Sex & reproduction Gonadotropins, androgens, estrogens, progestins 5 Circulating volume Aldosterone, antidiuretic hormone 6 Adaptation to stress Gucocorticoids, adrenaline 7 Calcium balance Parathormone, calcitonine, vitamin D
    6. 6.  Location  Colour  Dimensions  weight
    7. 7.  The adrenal cortex secretes steroidal hormones .  Conventionally the term – ―corticosteroids‖ or ―corticoids‖ includes – natural glucocorticoids, mineralocorticoid & their synthetic analogues.
    8. 8.  In human important corticosteroids are – 1. Mineralocorticoids - Aldosterone 2. Glucocorticoids – Hydrocortisone (cortisol)
    9. 9.  Clinical importance of adrenal gland was 1st described by – Addison (1849) as fetal outcome of patients with adrenal damage.  Cortex is more important than medulla.  Isolation & characterization of various corticosteroids based on their importance in body metabolism.
    10. 10.  Their great therapeutic potential was opened by ―Hench” (1949) - Rheumatoid Arthritis, Got the Nobel Prize in 1950.  Currently corticosteroids are the drugs with one of the broadest spectrum of clinical activity.
    11. 11.  Diverse effects include – 1. Carbohydrate, lipid & protein metabolism. 2. Preservation of normal function of Cardiovascular system, immune system, nervous system, kidney, skeletal muscle. 3. Prepare the body to withstand with all kinds of noxious stimuli & stress.
    12. 12.  Some permissive actions are also present – - They don’t themselves produce their effect but Their presence facilitates other hormones to exert that action. Example – corticosteroids don’t have direct effect on BP but pressure action of Adr is blunted in their absence.
    13. 13. Decreased maximum tubular rebsorptive capacity for Na+ (even in Na+ deficient state) Kidney absorb water without attended Na+ (to maintain ECF) Dilutional hyponatemia Excessive water enters in the cell Decrease blood volume & increased hematocrit Fluid electrolyte imbalance Circulatory collapse IN DCT ↑ Na+ reabsorption ↑ K+ & H+ excretion ↑ Na+ excretion ↑ K+ & H+ retention hyponatremia hyperkalemia acidosis
    14. 14. Gene mediate increased transcription of AIP (Aldosterone induced protein) which is responsible for maintaining the gradients of ions across the membrane.
    15. 15.  Hypertension  Fluid retention  Oedema  Hypokalemia  Alkalosis  Promote CHF associated myocardial fibrosis & progression of the disease IN DCT ↑ Na+ reabsorption ↑ K+ & H+ excretion
    16. 16. 1. Carbohydrate & protein metabolism 2. Fat metabolism 3. Calcium metabolism 4. Water excretion 5. Cardiovascular system 6. Skeletal muscles 7. Central nervous system 8. Stomach 9. Lymphoid tissue & blood cells 10. Inflammatory responses 11. Immunological & allergic responses
    17. 17.  Promotes glycogen deposition in liver by- 1. Hepatic glycogen synthetase induction 2. Gluconeogenesis 3. Inhibition of glucose utilization by peripheral tissues 4. Increase glucose release from liver
    18. 18.  Protein breakdown.  Mobilization of amino acid from peripheral tissue (used in gluconeogenesis, formation of plasma proteins, excessive urea production & nitrogen imbalance).  Muscle wasting, thinning of skin, lympholysis, loss of osteoid from bone.
    19. 19.  Permissive action.  Promote : lipolysis  Ketogenic effect  Fat deposition occurs differently in different areas of the body.  Redistribution of body fat.  Extremities - loose fat  Deposited over – face, neck & shoulder, abdomen, causing – moon face, fish mouth, buffalo hump.
    20. 20.  Inhibit intestinal absorption & decreases renal excretion of Ca++  Loss of osteoid negative calcium balance  Hypercalcemia.  Spongy bone.
    21. 21.  Independent of Na+ transport  Water retention – in adrenal insufficiency.  Enhances secretory activity of renal tubules.
    22. 22.  Restrict capillary permeability  Maintain tone of arteriole & myocardial contractility.  Permissive action on pressor effect of adrenaline & angiotensin.  In adrenal insuffiency – hypovolumia & circulatory collapse.
    23. 23.  Optimal level of glucocorticoid is required.  Hypocorticism – weakness due to hypodynamic circulation.  Hypecorticism – weakness due to muscle wasting & hypokalemia.
    24. 24.  Mild euphoria  Increased motor activity, insomnia, anxiety or depression.  Maintains the level of sensory perception & neuronal excitability.  High doses lower the seizure threshold.
    25. 25.  Blockade of prostaglandin (protective for gastric mucosa).  Secretion of gastric acid & pepsin is increased.  May aggravate the peptic ulcer.
    26. 26.  Increases the rate of destruction. ( T cells are more sensitive than B cells)  Treatment in malignancy of lymphatic tissues – lymphomas  ↓ in lymphocytes, eosinophils & basophils (due to their sequestration in tissues)  ↑ in neutrophils, RBCs & platelets in circulation.  Blood count come back to normal level after 24 hours.
    27. 27.  Basis of most of their clinical use.  Inhibit the release of arachidonic acid from membrane lipids by production of proteins – annexins & lipocortins which inhibits the phospholipase A2
    28. 28.  ↓ production of IL& TNF-α – chemotaxis is interfered.  Complement function is interfered.  Adhesion & localization of leukocytes are interfered.  Inhibit Ig E mediated histamine release – no antigen- antibody reaction.  ↓ production of collagenase – prevention of tissue destruction.
    29. 29.  Corticosteroids are 21 carbon compounds.  Synthesized in adrenal cortical cells from cholesterol.  Steroidogenesis takes place under the influence of ACTH, which makes the cholesterol available for conversion into Pregnenolone.
    30. 30.  Since the adrenal cortical cells store only minute quantities of hormones, the rate of release is governed by the rate of biosynthesis. Normal Production rates & circulating levels of two principle corticosteroids Rate of secretion under normal circumstances 10.0 mg/day 0.125mg/day Concentration in peripheral plasma 8 :00 AM 16 µg/100ml 0.01µg/100ml 4: 00 PM 4 µg/100ml 0.01µg/100ml HYDROCORTISONE ALDOSTERONE
    31. 31.  Effective by oral route  Water soluble esters can be given I.V. or I.M. e.g. hydrocortisone hemisuccinate Dexamethasone sodium phosphate  Water insoluble esters can’t be given I.V. , but I.M. can be given. E.g. – hydrocortisone acetate & triamcinolone acetonide.
    32. 32.  Hydrocortisone undergoes high 1st pass metabolism.  Oral bioavailability of synthetic corticoids are high.  Hydrocortisone is 90% bound to specific corticosteroid binding globulin (protein) - Transcortin as well as to the albumin.  Transcortin concentration increases in pregnancy & by oral contraceptives – but hypercorticism doesn’t occur.
    33. 33.  Metabolizes primarily in liver.  Excreted in urine(75 %) and in bile & feces (25%) .  t1/2 = 1.5 hour, but biological t1/2 is longer because of action through intracellular receptors & regulation of protein synthesis.  Synthetic derivatives are more resistance to metabolism, so are longer acting.  Phenobarbitone & phenytoin induce metabolism of hydrocortisone, prednisolone & Dexamethasone.
    34. 34.  Animals – Insects - ecdysterone that controls moulting Vertebrate - Steroid hormones & Cholesterol  Plants – Phytosterols, Brassinosteroids & Steroidal alkaloids  Fungus - Ergosterols
    35. 35.  - Class Examples Number of carbon atoms Cholestanes cholesterol 27 Cholanes cholic acid 24 Pregnanes progesterone 21 Androstanes testosterone 19 Estranes estradiol 18
    36. 36. interact with androgen receptors to increase muscle and bone synthesis. 1. Glucocorticoids 2. Mineralocorticoid 3. Sex steroids Most medical 'steroid' drugs are corticosteroids. Hydrocortisone, cortisone Prednisolone, methylprednisolone, triamcinolone Dexamethasone, betamethasone, paramethasone Aldosterone, fludrocortisones, deoxycorticosterone acetate (DOCA) androgens, estrogens, and progestagens.
    37. 37. Short-Acting (biological t1/2 is <12 hr) Intermediate-Acting (biological t1/2 is 12-36 hr) Long-Acting (biological t1/2 is >36 hr) 1. Cortisol (hydrocortisone) 2. Cortisone 1. Triamcinolone 2. Prednisolone 3. Methylprednisolone 1. Betamethasone 2. Dexamethasone 3. Paramethasone
    38. 38.  Group A — Hydrocortisone type Hydrocortisone, hydrocortisone acetate, cortisone acetate, tixocortol pivalate, prednisolone, methylprednisolone, and prednisone (Short- to medium-acting glucocorticoids).  Group B — Acetonides (and related substances) Triamcinolone acetonide, triamcinolone alcohol, mometasone, amcinonide, budesonide, desonide, fluocinonide, fluocinolone acetonide, and halcinonide.  Group C — Betamethasone type Betamethasone, betamethasone sodium phosphate, dexamethasone, dexamethasone sodium phosphate, and fluocortolone.  Group D — Esters  Group D1 — Halogenated (less labile) Hydrocortisone-17- valerate, halometasone, alclometasone dipropionate, betamethasone valerate, betamethasone dipropionate, prednicarbate, clobetasone-17-butyrate, clobetasol-17-propionate, fluocortolone caproate, fluocortolone pivalate, and fluprednidene acetate.  Group D2 — Labile prodrug esters Hydrocortisone-17-butyrate, hydrocortisone-17- aceponate, hydrocortisone-17-buteprate, and prednicarbate.
    39. 39.  Primarily glucocorticoid  Acts rapidly  Short duration of action  But has significant mineralocorticoid activity also. Purpose Route Dose Replacement therapy orally 20mg in morning 10mg in afternoon Shock, Status asthmaticus, Acute adrenal insufficiency i.v. 100mg bolus & 100mg 8 hourly infusion
    40. 40.  Inactive  Hydroxylated in liver - hydrocortisone  Primarily glucocorticoid  Occasionally being used now Route Dose orally 20 - 100mg i.m. 20 - 100mg
    41. 41.  More selective glucocorticoid  4 times more potent than hydrocortisone  Fluid retention with high doses  Less pituitary adrenal axis suppression Purpose Route Dose Allergic, inflammatory, autoimmune & malignant diseases Orally i.m. Intra-articular topically 5-60 mg/day 10-40 mg/day
    42. 42.  Slightly more selective & more potent than prednisolone  Less pituitary adrenal axis suppression Purpose Route Dose Retention enema in ulcerative colitis Orally 4-32 mg/day Nonsuppressive active Rheumatoid arthritis, renal transplant, pemphigus i.v. 1gm infused every 6-8 weeks
    43. 43.  More potent than prednisolone  Highly selective glucocorticoid Route Dose Orally 4-32 mg/day i.m. Intra-articular topically 5-40 mg
    44. 44.  Very potent & highly selective glucocorticoid  Long acting  Marked pituitary adrenal axis suppression  No fluid retention or hypertension problem Purpose Route Dose Allergic, inflammatory Orally 0.5-5 mg/day Shock, cerebral edema i.v. i.m. 4-20 mg/day
    45. 45.  Similar to Dexamethasone .  Can be used topically. Purpose Route Dose Allergic, inflammatory Orally 0.5-5 mg/day Shock, cerebral edema i.v. i.m. 4-20 mg/day
    46. 46.  Dexamethasone & Betamethasone are preferred in cerebral edema & other states in which fluid retention must be avoided.
    47. 47.  Having intermediate action between Dexamethasone & Betamethasone Route Dose Orally 2-20 mg/day
    48. 48.  Only mineralocorticoid activity. Purpose Route Dose Occasionally for replacement therapy in Addison’s disease Sublingual i.m. 2-5 mg 10-20 mg once or twice weekly
    49. 49.  Potent mineralocorticoid activity.  Some glucocorticoid activity.  Orally active Purpose Route Dose Replacement therapy in Addison’s disease Congenital adrenal hyperplasia with salt wasting oral 50-200 µg/day Idiopathic postural hypotension Oral 100-200 µg/day
    50. 50.  Selective mineralocorticoid  Not used clinically because of low oral bioavailability & difficulties in regulating doses.
    51. 51. Compound Anti- inflammatory potency Na retaining potency Duration of action Equivalent dose Cortisol 1 1 S 20 Cortisone 0.8 0.8 S 25 Dexamethasone 25 0 L 0.75 Betamethasone 25 0 L 0.75 Prednisone 4 0.8 I 5 Prednisolone 4 0.8 I 5 6-methyl Prednisolone 5 0.5 I 4 Triamcinolone 5 0 I 4
    52. 52. 1. Acute & chronic adrenal insufficiency 2. Arthritis– rheumatoid arthritis, osteoarthritis, rheumatic fever & gout 3. Severe allergic reactions – 4. Autoimmune diseases 5. Bronchial asthma 6. Other lung diseases – anaphylaxis, angioneurotic edema, utricaria, serum sickness. can’t take the place of adrenaline aspiration pneumonia, pulmonary edema, to mother for foetus
    53. 53. 7. Infective diseases – 8. Eye diseases – 9. Skin diseases – 10. Intestinal diseases - Severe form of tuberculosis, severe lepra reactions, certain form of bacterial meningitis, pneumonia with hypoxia in AIDS patients. Allergic conjunctivitis, iritis, iridocyclitis, keratitis. Contraindicated in herpes simplex keratitis & ocular injuries. Eczematous diseases, pemphigus vulgaris, exfoliative dermatitis, Steven’s Johnson's syndrome & other severe afflictions. Ulcerative colitis, Chron’s disease, chronic inflammatory bowel disease .
    54. 54. 11. Cerebral edema 12. Malignancies 13. Organ transplantation & skin allograft 14. Shock 15. To test adrenal-pituitary axis function
    55. 55.  The use of topical and systemic steroids in an attempt to manage apthus stomatitis is based on the resumption that the aphthae are the result of a infectious inflammatory process.  Corticosteroids may act directly on T lymphocytes or alter the response of effect or cells to precipitants of immunopathogenesis (Vincent 1992).
    56. 56.  Hydrocortisone hemisuccinate (as pellets of 2. 5 mg) and triamcinolone acetonide (in an adhesive paste containing 0. 1% of the steroid).  There is little risk of adrenal suppression provided that the recommended dose (four times daily) is adhered to (Field 2003).  High potency topical steroid preparation such as fluocinonide, betamethasone or clobetasol placed directly on the lesions shortens healing time and reduces the size of lesion.  The gel can be carefully applied directly to the lesion after meals and at bedtime 2-3 times a day or mixed with an adhesive such as orabase prior to application.
    57. 57.  Larger lesions can be treated by placing a gauge sponge containing the topical steroid on the ulcer and leaving it in place for 15-30 min to allow for longer contact of the medication.  Ulcerations located in the areas that make them difficult to see or reach can be controlled by 1. topical dexamethasone elixir, 0. 5 mg / 5 ml held over the area or applied with a saturated gauge pad to the ulcers, four times per day for 15 min (Lo Muzio 2001) 2. Betamethasone sodium phosphate rinse (dissolve 0. 5 mg in 5 ml of water and rinse for 2–3 min), 3. Steroid aerosol (e. g. beclometasone diproprionate, 100 lg/puff) , 4. high-potency topical corticosteroid, such as clobetasol 0. 05% in orabase or fluocinonide 0. 05% in orabase (Natah 2004).
    58. 58.  Major apthus ulcers often require systemic treatment as an initial approach. Therapy with prednisone 40 mg/day for one week is usually adequate to control the presenting outbreak.  Systemic prednisone therapy should be started at 1. 0 mg/kg a day as a single dose in patients with severe RAS and should be tapered after 1-2 weeks.
    59. 59.  Injectable steroids, e.g. methylprednisolone, may be useful in treating painful ulcerations and their combined use with topical steroids has been recommended .  Although advocated by some authors , systemic steroid therapy is indicated only rarely.
    60. 60.  In the acute phase, prednisone, at doses of 40-60 mg/day, may be helpful, used alone or in combination with other immunosuppressive agents (Reich 1998).  Successful treatment consists of anti-inflammatory agents that modify neutrophil activity.
    61. 61.  Lichen planus is a mucocutaneous disease of unknown etiology, which represents a cell-mediated immunological response to induced antigenic changes in the skin and mucosa.  They are widely used in the treatment of OLP to reduce pain and inflammation.  Options (decreasing potency) include0.05% clobetasol proprionate> gel, >0. 1-0. 05% betamethasone valerate gel, >0. 05% fluocinonide gel, >0. 05% clobetasol ointment or cream > 0. 1% triamcinolone acetonide ointment (Levin 2002).Cawson R. Treatment of oral lichen planus with betamethasone. Br Med J 1968: 1: 864. Tyldesley WR, Harding SM. Betamethasone valerate aerosol in the treatment of oral lichen planus. Br J Dermatol 1977: 96: 659-62.
    62. 62.  To assess the effectiveness of intralesional injection of methylprednisolone and habit control in the management of oral submucous fibrosis.  Bilateral submucosal injection of methylprednisolone 20 mg/0.5 mL was given to predetermined areas of the buccal mucosa once a month for 5 consecutive months. Maximum unaided mouth opening was measured using the same measuring device after each injection. Anura Ariyawardana, Tharanga Nawagamuwa, Ajith W Ranasinghe, Mohamed Sitheeque, Nishanthi Vithanaarachchi. Conservative Management of Oral Submucous Fibrosis Asian Journal of Oral and Maxillofacial Surgery. March 2005;17(1) : p26-30
    63. 63.  Intralesional injections of corticosteroids have been used successfully to treat the Mucocele. British Journal of Oral and Maxillofacial Surgery (1999) 37, 312–315
    64. 64.  Characterized by intraepithelial bulla formation, due to autoantibodies directed against proteins of the desmosome-tonofilament complex between keratinocytes (Sirois 2000).  Topical corticosteroids - 0. 05% fluocinolone acetonide or 0. 05% clobetasol propionate (Hashimoto; Prajapati 2008).
    65. 65.  Systemic corticosteroid therapy -  The starting dose is high; a total oral dose of 100–200 mg Prednisone is administered daily until subsidence of clinical signs. This dose can gradually be decreased to a maintenance level of 40 to 50 mg daily.  Intralesional corticosteroid therapy  accelerates the scarring process of a lesion or is used to treat persistent lesions.  gives inconsistent results,  involves sublesional injection given every 7 to 15 days  treatment is stopped after 3 injections if there is no improvement.  A daily 0. 5–2 mg/kg is recommended (Fellner; Toth 2001).
    66. 66.  Oral ulcerations of systemic lupus erythematosus are transient, occurring with acute lupus flares.  Treated with 1. High potency topical corticoids 2. Intralesional steroid injections (triamcinolone acetonide 3mg/mL) 3. Systemically low dose prednisone 10-20 mg /day or an alternate day dose of 20-40 mg may be needed (Pedersen 1984; Reich 1998).
    67. 67.  Studies have shown the benefit of high-dose corticosteroids for acute Bell palsy (Sullivan 2007; Engström 2008). 1. N Julian Holland, Graeme M Weiner. Recent developments in Bell’s palsy. BMJ 2004;329:553–7. 2. Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell’s palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:830-6.  Taverner in 1954 was the first to design a controlled treatment trial of steroids.  Attempts to treat Bell’s palsy with steroids changed in the 1970s. After the initial publication of Adour et al. several series of treatments with prednisone for Bell’s palsy were designed, but almost all of them were of unsatisfactory quality (Adour 1972).
    68. 68.  Immunocompetent patients without specific contraindications are prescribed prednisone at 1 mg/kg/day (maximum 80 mg) for the first week, which is tapered over the second week.  Around a fifth of patients will progress from partial palsy, so these patients should also be treated (Ramsey 2000). 1. Ramsey MJ, DerSimonian R, Holtel MR, Burgess LP. Corticosteroid treatment for idiopathic facial nerve paralysis: a meta-analysis. Laryngoscope 2000;110:335-41. 2. Williamson IG, Whelan TR. The clinical problem of Bell’s palsy: is treatment with steroids effective? Br J Gen Pract 1996;46:743-7. 3. Shafshak TS, Essa AY, Bakey FA. The possible contributing factors for the success of steroid therapy in Bell’s palsy: a clinical and electrophysiological study. J Laryngol Otol 1994;108:940-3.
    69. 69.  Caused by the reactivation of a previous Varicella zoster virus (VZV) infection.  Acyclovir at 800 mg orally 5 times/day for 7-10 days and Prednisone at 1 mg/kg/day orally for 5 days followed by a taper (Murakami 1997). C Sweeney, D Gilden. Ramsay Hunt syndrome. J Neurol Neurosurg Psychiatry. 2001 August; 71(2): 149–154.
    70. 70.  Prednisone 40 mg daily for 10 days,  Gradually tailed off over the following 3 weeks  Reduces the occurrence of post herpetic neuralgia.  Steroids should not be given alone (without antiviral therapy) , owing to concern about the promotion of viral replication (Van Wijck 2006).  Intrathecal administration of methylprednisolone – decrease the duration of neuralgia and the pain (Kotani 2000).
    71. 71.  Temporomandibular joint (TMJ) disorders 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).
    72. 72.  TMJ arthritis, a single intra-articular injection of corticosteroid (methylprednisolone) diluted with lidocaine significantly reduced joint pain and other symptoms for 4-6 weeks.  The pharmacologic effect - 3-4 weeks. No adverse events were reported (Alstergren 1996).
    73. 73.  The use of steroid injections for the treatment of temperomandibular joint capsulitis following arthroscopy. A prospective outcome assessment A. Khan, A. Sidebottom. Queens Medical Centre, Nottingham University Hospitals, UK  Patients with TMJ related pain and restriction associated with post arthroscopy TMJ capsulitis and who have failed to respond to routine conservative measures may be submitted to intracapsular steroid injections, which has been associated with significant therapeutic improvement in 74% or more patients.
    74. 74.  The patient had been treated with increasing doses of prednisolone up to 60 mg/day. The anterior open bite had begun after prednisolone medication.  Magnetic resonance imaging scans disclosed internal and erosive damage to the condyles without disk displacement, but showed no sign of adaptive changes or functional remodeling. T. Hata, M. Hosoda, Y. Hamada, K. Kobayashi: Steroid-induced damage to the condyles in treatment of idiopathic thrombocytopenia. Int. J. Oral Maxillofac. Surg. 2009; 38: 193–195.
    75. 75.  Oral prednisone the vast majority of patients respond to a dose of 1 mg/kg/d, or between 40 and 60 mg/day (Salvarani 2002; Weyand 2003).  The dose of prednisone is lowered after 2–4 weeks, and slowly tapered over 9–12 months (Chan 2001).  Higher doses of 80 to 100 mg/day - patients with visual or neurological symptoms of GCA.  IV pulse methylprednisolone has been proposed as an induction therapy, particularly in cases where vision is at risk (Rahman; Rahman 2005).
    76. 76.  Effects of corticosteroids for prevention of pain and edema associated with oral surgery.  The most commonly - Dexamethasone (oral), dexamethasone sodium phosphate, dexamethasone acetate, and methylprednisolone acetate and methyl prednisolone sodium succinate.  Dexamethasone has a longer duration of action than methylprednisolone and is considered more potent (Alexander 2000).
    77. 77.  Dexamethasone 4mg given submucosally is an effective way of minimising swelling, trismus, and pain after removal of impacted lower third molars, and is comparable with the intramuscular route.  Methylprednisolone is usually administered via the intramuscular or intravenous ,though the possibility of topical (intra-alveolar) application has been described, with a reduction in morbidity and possible side effects. Omer Waleed Majid ∗, Waseem Khalid Mahmood. Effect of submucosal and intramuscular dexamethasone on postoperative sequelae after third molar surgery: comparative study. British Journal of Oral and Maxillofacial Surgery 49 (2011) 647–652
    78. 78.  The study group received 40 mg of methylprednisolone injected into the masseter muscle via the intrabuccal approach, immediately after suturing of the surgical wound.  The control group received no intramuscular corticoid.  Evaluations were made of postoperative pain, trismus and swelling.  The results obtained show that 40 mg of methylprednisolone injected into the masseter muscle in the immediate postoperative period reduces swelling, trismus and pain. E. Vegas-Bustamante, J. Mico´-Llorens, J. Gargallo-Albiol, M. Satorres-Nieto, L. Berini-Ayte´s, C. Gay-Escoda: Efficacy of methylprednisolone injected into the masseter muscle following the surgical extraction of impacted lower third molars. Int. J. Oral Maxillofac. Surg. 2008; 37: 260–263.
    79. 79.  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 and prevent its release in the gut, and they have a synergistic action with 5-HT3 antagonists. Soudeh Chegini , Daljit K. Dhariwal. Review of evidence for the use of steroids in orthognathic Surgery. British Journal of Oral and Maxillofacial Surgery 50 (2012) 97–101
    80. 80.  Disadvantages - Allergic reaction, Skin changes, Increased serum glucose, Adrenal suppression, Disturbance of wound healing, Impaired immunity, Increased cardiovascular risk, Increased morbidity in pre-existing peptic ulcer disease, Glaucoma, Psychiatric disturbance.  Regimens used currently may be reduced if combined with cold-press and drains, and they benefit from a cumulative effect with NSAIDs and synergistic antiemetics. Soudeh Chegini , Daljit K. Dhariwal. Review of evidence for the use of steroids in orthognathic Surgery. British Journal of Oral and Maxillofacial Surgery 50 (2012) 97–101
    81. 81.  Upper airway obstruction (UAO) is a well known complication of cleft palate repair.  Local steroid injection of the tongue base during cleft palate surgery reduced the incidence and severity of post-palatoplasty UAO. M. Abdel-Aziz, A. Ahmed, N. Naguib, M. I. Abdel-Khalik: The effect of steroid injection of the tongue base on reducing postoperative airway obstruction in cleft palate repair. Int. J. Oral Maxillofac. Surg. 2012; 41: 612–615.
    82. 82.  Case series with a minimum of 5 patients with enlarging, problematic cutaneous hemangiomas treated with systemic corticosteroids.  Patients were given a mean prednisone equivalent daily dose of 2.9 mg/kg 2.7-3.1 mg/kg) for a mean of 1.8 months.  Systemic corticosteroid treatment seems to be effective for problematic cutaneous hemangiomas of infancy. Bennett ML, Fleischer AB Jr, Chamlin SL, Frieden IJ. Oral corticosteroid use is effective for cutaneous hemangiomas: an evidence-based evaluation. Arch ermatol. 2001 Sep;137(9):1208-13.
    83. 83.  Systemic corticosteroids are efficacious in stopping the proliferation of hemangiomas. The oral corticosteroids offered more clinical and biological benefit than the pulse steroids with higher risk of adverse effects. Pope E, Krafchik BR, Macarthur C, Stempak D, Stephens D, Weinstein M, Ho N, Baruchel S. Oral versus high-dose pulse corticosteroids for problematic infantile hemangiomas: a randomized, controlled trial. Pediatrics. 2007 Jun; 119(6):e1239- 47. Epub 2007 May 7
    84. 84.  Glucocorticoid receptor expression in the multinucleated giant cells was higher in patients with a good response. It can be postulated that immunohistochemical staining for glucocorticoid receptors may provide a tool for selecting the therapeutic strategy.  An H-score greater than 48 for glucocorticoid receptors in multinucleated giant cells predicted a good response in this study. R. L. M. Nogueira, M. H. G. Faria, R. L. V. Osterne, R. B. Cavalcante, R. A. Ribeiro, S. H. B. Rabenhorst: Glucocorticoid and calcitonin receptor expression in central giant cell lesions: implications for therapy. Int. J. Oral Maxillofac. Surg. 2012; 41: 994–1000. C. Kermer, W. Millesi, L M. Watzke: Local injection of corticosteroids for central giant cell granulorna, A case report. Int. J. Oral Maxillofac. Surg. 1994; 23." 366 368.
    85. 85.  Intralesional injection of 20 mg/ml triamcinolone hexacetonide diluted in an anesthetic solution of 2% lidocaine/ epinephrine 1:200,000 in the proportion 1:1; 1.0 ml of the solution was infiltrated for every 1 cm3 of area of the lesion.  The advantages of this therapy are its less-invasive nature, the probable lower cost to the patient, lower risk and the ability to treat the lesion surgically in the future, if necessary. R. L. M. Nogueira, R. C. Teixeira, R. B. Cavalcante, R. A. Ribeiro, S. H. B. Rabenhosrt: Intralesional injection of triamcinolone hexacetonide as an alternative treatment for central giant-cell granuloma in 21 cases. Int. J.OralMaxillofac. Surg. 2010; 39: 1204– 1210.
    86. 86.  Three patients (female, 28 months; male, 9 years; male, 15 years) with LLCH of the mandible were treated in an one stage procedure with intralesional injection of 40 and 80 mg methylprednisolone succinate, respectively, as the primary form of treatment.  Patients were seen for clinical and radiological evolution 1, 3, 6, 9 and 12 months after treatment, and yearly thereafter.  The lesions showed clinically and radiologically complete remission approximately 6 months after treatment.  There were no complications nor morbidity of the treatment. Th. F. Putters, J. G. A. M. de Visscher, A. van Veen, F. K. L. Spijkervet:Intralesional infiltration of corticosteroids in the treatment of localised langerhans’ cell histiocytosis of the mandible Report of known cases and three new cases. Int. J. Oral Maxillofac. Surg. 2005; 34: 571–575.
    87. 87.  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).
    88. 88.  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; (Review anaphylaxis in the emergency department 2008) (Ring 2002; Greenberger 2007).  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 (Soar 2008).
    89. 89.  Adrenal suppression may occur if a patient is taking 20 mg of cortisone or its equivalent daily, for 2 weeks within 2 years of dental treatment.  General anesthesia, infection, and pain can increase the risk of adrenal crisis in susceptible patients. Dental Procedures and Recommended Corticosteroid Supplementation in Patients with Adrenal Insufficiency Negligible Risk Category Nonsurgical dental procedures Regimen: No supplementation required Mild Risk Category Minor oral surgery: A few simple extractions, biopsy Minor periodontal surgery Regimen: The glucocorticoid target is about 25 mg of hydrocortisone equivalent on the day of surgery Moderate to Major Risk Category Major oral surgery: Multiple extractions, quadrant periodontal surgery, extraction of bony impactions, osseous surgery, osteotomy, bone resections, cancer surgery, surgical procedures involving general anesthesia, procedures lasting more than 1 hour, procedures associated with significant blood loss Regimen: The glucocorticoid target is about 50 to 100 mg per day of hydrocortisone equivalent on the day of surgery and for at least 1 post-operative day
    90. 90. Doses of drugs equivalent to 20 mg of cortisone Drug Equivalent Dose (mg) Hydrocortisone 20 mg Prednisone 5 mg Triamcinolone 4 mg Dexamethasone 0.75 mg
    91. 91.  Long-term steroid therapy must never be stopped suddenly.  Doses should be reduced very gradually, with most being given in the morning at the time of withdrawal — this minimizes adrenal suppression.  Other physicians, anesthetists and dentists must be told about steroid therapy.  Patients should also be informed of potential side-effects and all this information should be documented in the clinical record.
    92. 92.  Any patient taking > 20 -25 mg /day hydrocortisone or equivalent dose for longer than 2-3 weeks……  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 - steroid discontinuation - increase the dose
    93. 93. 1. Use shorter acting steroids at lowest possible dose. 2. Use for shorter period 3. Entire daily dose for once 4. Switch to alternate day therapy – less immunological suppression but incapacitation in steroid dependent patients on OFF day 5. Use local preparation with poor systemic availability
    94. 94.  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  Fine Hair Growth • Seen with long-term use, • Some may be noticed within days of starting therapy. • Is related to drug potency, duration of therapy, frequency of application and anatomical area. (Key2003; Baid 2006):
    95. 95.  Extensions of pharmacological actions on long term use (in case of chronic disease).  Mineralocorticoid :  Sodium & water retention, oedema, hypokalemic, alkalosis & a progressive raise in BP. Gradual raise in BP occurs due to excess glucocorticoid action as well.
    96. 96.  Glucocorticoid : 1. Cushing’s habitus: round face, narrow mouth, supraclavicular hump, obesity of trunk with relatively thin limbs.
    97. 97. 2. Fragile skin & purple striae : typically on thighs & lower abdomen, easy bruising, telengiactasis, herstuism, cutaneous atrophy due to topical use. telengiactasis Herstuism purple striae
    98. 98. 3. Muscular weakness 4. hyperglycaemia 5. Susceptibility to opportunistic infections 6. Delayed wound healing 7. Peptic ulcerations : risk is doubled, bleeding & silent perforation 8. Osteoporosis : vertebrae & flat spongy bones 9. Glaucoma : after prolong topical therapy 10. Growth retardation in children 11. Foetal abnormalities : cleft lip & cleft palate (in animals, not in human) foetal growth retardation after prolong use neurological & behavioral disturbances in offspring
    99. 99. 12. Psychiatric disturbances : mild euphoria, nervousness, decreased sleep, mood changes & rarely depressive illness 13. Suppression of hypothalamo-pitutary axis (HPA) : dose & duration dependent.  adrenal atrophy + stoppage of exogenous steroid = withdrawal syndrome (malaise, fever, weakness, pain in muscle & joints, reactivation of disease)  Subjected to stress - acute adrenal insufficiency
    100. 100.  Comorbidities of steroid use along with bisphosphonates may cause osteonecrosis of the jaw to occur sooner, be more severe, and respond more slowly to a drug discontinuation. Chang-Ta Chiu, Wei-Fan Chiang, Ching-Ya Chuang, Sung-Wen Chang. Resolution of Oral Bisphosphonate and Steroid-Related Osteonecrosis of the Jaw—A Serial Case Analysis. Journal of Oral and Maxillofacial Surgery, Volume 68, Issue 5, May 2010, Pages 1055-1063
    101. 101.  Have to be used as life saving drug.  Relative contraindications (may aggravate) –  Combination of any drug with corticosteroids in fixed dose formulation for internal use is banned. 1. Peptic ulcer 2. Diabetes mellitus 3. Hypertension 4. Viral & fungal infection 5. Tuberculosis 6. Osteoporosis 7. Herpes simplex keratitis 8. Psychosis 9. CHF 10. Epilepsy 11. Renal failure
    102. 102. • Steroid are have been proven to be archetypal, double edged sword of medicine. • The risk associated with steroids parallels the benefits of their therapeutic power.
    103. 103. BOOKS 1 . G O O D M A N G I L M A N ’ S T H E P H A R M A C O L O G I C A L B A S I S O F T H E R A P E U T I C S , 11 T H E D I T I O N . 2 . T R I PAT H I K D , E S S E N T I A L S O F M E D I C A L P H A R M A C O L O G Y, 6 T H E D I T I O N . 3 . G Y TO N & H A L L T E XT B O O K O F M E D I C A L P H Y S I O L O G Y, 1 0 T H E D I T I O N . References
    104. 104. Others  M o h a m m a d z a n d i , t h e r o l e o f c o r t i c o s t e r o i d s i n t o d a y ‘ s o r a l a n d m a x i l l o f a c i a l s u r g e r y . H t t p : / / d x . D o i . O r g / 1 0 . 5 7 7 2 / 4 8 6 5 5  B r i t i s h j o u r n a l o f o r a l a n d ma x i l l o f a c i a l s u rg e r y ( 1 9 9 9 ) 3 7 , 3 1 2 – 3 1 5 .  N j u l i a n h o l l a n d , g r a e me M w e i n e r. R e c e n t d e v e l o p me n t s i n b e l l ’s p a l s y. B mj 2 0 0 4 ; 3 2 9 : 5 5 3 – 7 .  G r o g a n p m, g r o n s e t h g s . P r a c t i c e p a r a me t e r : s t e r o i d s , a c y c l o v i r, a n d s u rg e r y f o r b e l l ’s p a l s y ( a n e v i d e n c e - b a s e d r e v i e w ) : r e p o r t o f t h e q u a l i t y s t a n d a r d s s u b c o mmi t t e e o f t h e a me r i c a n a c a d e my o f n e u r o l o g y. N e u r o l o g y 2 0 0 1 ; 5 6 : 8 3 0 - 6 .  C s w e e n e y , d g i l d e n . R a m s a y h u n t s y n d r o m e . J n e u r o l n e u r o s u r g p s y c h i a t r y . 2 0 0 1 a u g u s t ; 7 1 ( 2 ) : 1 4 9 – 1 5 4 . References
    105. 105.  T . H a t a , M . H o s o d a , Y . H a m a d a , K . K o b a y a s h i : s t e r o i d - i n d u c e d d a m a g e t o t h e c o n d y l e s i n t r e a t m e n t o f i d i o p a t h i c t h r o m b o c y t o p e n i a . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 0 9 ; 3 8 : 1 9 3 – 1 9 5 .  O m e r w a l e e d m a j i d ∗ , w a s e e m k h a l i d m a h m o o d . E f f e c t o f s u b m u c o s a l a n d i n t r a m u s c u l a r d e x a m e t h a s o n e o n p o s t o p e r a t i v e s e q u e l a e a f t e r t h i r d m o l a r s u r g e r y : c o m p a r a t i v e s t u d y . B r i t i s h j o u r n a l o f o r a l a n d m a x i l l o f a c i a l s u r g e r y 4 9 ( 2 0 1 1 ) 6 4 7 – 6 5 2  E . V e g a s - b u s t a m a n t e , J . M i c o ´ - l l o r e n s , J . G a r g a l l o - a l b i o l , M . S a t o r r e s - n i e t o , L . B e r i n i - a y t e ´ s , C . G a y - e s c o d a : e f f i c a c y o f m e t h y l p r e d n i s o l o n e i n j e c t e d i n t o t h e m a s s e t e r m u s c l e f o l l o w i n g t h e s u r g i c a l e x t r a c t i o n o f i m p a c t e d l o w e r t h i r d m o l a r s . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 0 8 ; 3 7 : 2 6 0 – 2 6 3 .  E . V e g a s - b u s t a m a n t e , J . M i c o ´ - l l o r e n s , J . G a r g a l l o - a l b i o l , M . S a t o r r e s - n i e t o , L . B e r i n i - a y t e ´ s , C . G a y - e s c o d a : e f f i c a c y o f m e t h y l p r e d n i s o l o n e i n j e c t e d i n t o t h e m a s s e t e r m u s c l e f o l l o w i n g t h e s u r g i c a l e x t r a c t i o n o f i m p a c t e d l o w e r t h i r d m o l a r s . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 0 8 ; 3 7 : 2 6 0 – 2 6 3 .
    106. 106.  C . E . P . A l c a ˆ n t a r a , S . G . M . F a l c i , F . O l i v e i r a - f e r r e i r a , C . R . R . S a n t o s , M . L . P . P i n h e i r o : p r e - e m p t i v e e f f e c t o f d e x a m e t h a s o n e a n d m e t h y l p r e d n i s o l o n e o n p a i n , s w e l l i n g , a n d t r i s m u s a f t e r t h i r d m o l a r s u r g e r y : a s p l i t - m o u t h r a n d o m i z e d t r i p l e - b l i n d c l i n i c a l t r i a l . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 1 3 ; x x x : x x x – x x x .  S o u d e h c h e g i n i , d a l j i t k . D h a r i w a l . R e v i e w o f e v i d e n c e f o r t h e u s e o f s t e r o i d s i n o r t h o g n a t h i c s u r g e r y . B r i t i s h j o u r n a l o f o r a l a n d m a x i l l o f a c i a l s u r g e r y 5 0 ( 2 0 1 2 ) 9 7 – 1 0 1  M . A b d e l - a z i z , A . A h m e d , N . N a g u i b , M . I . A b d e l - k h a l i k : t h e e f f e c t o f s t e r o i d i n j e c t i o n o f t h e t o n g u e b a s e o n r e d u c i n g p o s t o p e r a t i v e a i r w a y o b s t r u c t i o n i n c l e f t p a l a t e r e p a i r . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 1 2 ; 4 1 : 6 1 2 – 6 1 5 .  T . R . F l o o d , J . M c m a n n e r s , A . E l a t t a r , K . F . M o o s . R a n d o m i z e d p r o s p e c t i v e s t u d y o f t h e i n f l u e n c e o f s t e r o i d s o n p o s t o p e r a t i v e e y e - o p e n i n g a f t e r e x p l o r a t i o n o f t h e o r b i t a l f l o o r . B r i t i s h j o u r n a l o f o r a l a n d m a x i l l o f a c i a l s u r g e r y ( 1 9 9 9 ) 3 7 , 3 1 2 – 3 1 5
    107. 107.  B e n n e t t M L , f l e i s c h e r A B j r , c h a m l i n S L , f r i e d e n I J . O r a l c o r t i c o s t e r o i d u s e i s e f f e c t i v e f o r c u t a n e o u s h e m a n g i o m a s : a n e v i d e n c e - b a s e d e v a l u a t i o n . A r c h e r m a t o l . 2 0 0 1 s e p ; 1 3 7 ( 9 ) : 1 2 0 8 - 1 3 .  P o p e e , k r a f c h i k b r , m a c a r t h u r c , s t e m p a k d , s t e p h e n s d , w e i n s t e i n m , h o n , b a r u c h e l s . O r a l v e r s u s h i g h - d o s e p u l s e c o r t i c o s t e r o i d s f o r p r o b l e m a t i c i n f a n t i l e h e m a n g i o m a s : a r a n d o m i z e d , c o n t r o l l e d t r i a l . P e d i a t r i c s . 2 0 0 7 j u n ; 1 1 9 ( 6 ) : e 1 2 3 9 - 4 7 . E p u b 2 0 0 7 m a y 7  R . L . M . N o g u e i r a , M . H . G . F a r i a , R . L . V . O s t e r n e , R . B . C a v a l c a n t e , R . A . R i b e i r o , S . H . B . R a b e n h o r s t : g l u c o c o r t i c o i d a n d c a l c i t o n i n r e c e p t o r e x p r e s s i o n i n c e n t r a l g i a n t c e l l l e s i o n s : i m p l i c a t i o n s f o r t h e r a p y . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 1 2 ; 4 1 : 9 9 4 – 1 0 0 0 .  C . K e r m e r , W . M i l l e s i , L M . W a t z k e : L o c a l i n j e c t i o n o f c o r t i c o s t e r o i d s f o r c e n t r a l g i a n t c e l l g r a n u l o r n a , A c a s e r e p o r t . I n t . J . O r a l M a x i l l o f a c . S u r g . 1 9 9 4 ; 2 3 . " 3 6 6 - 3 6 8 .
    108. 108.  R . L . M . N o g u e i r a , R . C . T e i x e i r a , R . B . C a v a l c a n t e , R . A . R i b e i r o , S . H . B . R a b e n h o s r t : i n t r a l e s i o n a l i n j e c t i o n o f t r i a m c i n o l o n e h e x a c e t o n i d e a s a n a l t e r n a t i v e t r e a t m e n t f o r c e n t r a l g i a n t - c e l l g r a n u l o m a i n 2 1 c a s e s . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 1 0 ; 3 9 : 1 2 0 4 – 1 2 1 0 .  T h . F . P u t t e r s , J . G . A . M . D e v i s s c h e r , A . V a n v e e n , F . K . L . S p i j k e r v e t : i n t r a l e s i o n a l i n f i l t r a t i o n o f c o r t i c o s t e r o i d s i n t h e t r e a t m e n t o f l o c a l i s e d l a n g e r h a n s ’ c e l l h i s t i o c y t o s i s o f t h e m a n d i b l e r e p o r t o f k n o w n c a s e s a n d t h r e e n e w c a s e s . I n t . J . O r a l m a x i l l o f a c . S u r g . 2 0 0 5 ; 3 4 : 5 7 1 – 5 7 5 .

    ×