Se ha denunciado esta presentación.
Utilizamos tu perfil de LinkedIn y tus datos de actividad para personalizar los anuncios y mostrarte publicidad más relevante. Puedes cambiar tus preferencias de publicidad en cualquier momento.

Corticosteriods uses in dentistry/ oral surgery courses  

2.306 visualizaciones

Publicado el

The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit

Publicado en: Educación
  • Inicia sesión para ver los comentarios

Corticosteriods uses in dentistry/ oral surgery courses  

  1. 1. STERIODS ITS USES IN DENTISTR INDIAN DENTAL ACADEMY Leader in continuing Dental Education
  3. 3. INTRODUCTION The adrenal cortex secretes three distinct groups of Steroid hormones . . Zona glomerulosa-secretes aldosterone and Desoxycorticosterone( mineralocorticoids). .Zona fasciculata -secretes cortisone and cortisol (glucocorticoids). .Zona reticularis forms dehydroepiandrosterone and androstenedione (androgens) and traces of estrogens .
  4. 4. Adrenal cortex is more important than medulla. Steroids principles were elucidated by kendall. 1949 Hench used steroids in the treatment of rheuma- toid arthritis. Corticosteroids are widely used in various conditions.
  5. 5. Chemistry and synthesis All the basic structure of steroid is a complex cyclopentanophenanthrene ring with various functional groups attached to different carbon atoms. The steroids can be synthesized basically from 2 carbon acetate chains via cholesterol.
  6. 6. .The adrenal glands produce and secrete gluco corticoid- (cortisol)in response to hormonal and nervous system stimuli. .During periods of stress, the centre in the hypothalamus responds to stimuli and releases corticotrophin –releasing factor. .CRF stimulates ACTH secretion from the anterior pituitary gland. .This hypothalamic –pituitary axis operates on the principle of negative feedback system and regulates the level of circulating cortisol. .
  7. 7. .When the level of circulating cortisol has raised adequately to meet increased demand , further release of CRF and ACTH is inhibited because of physiologic needs no longer require corticosteroid output. .Normally the average rate of cortisol secretion is 15 to20 mg?/dl. .Peak cortisol concentration occurs between 6 to 8 am then slowly decreased in the afternoon and evening.
  8. 8. Mechanism of action Adrenocortical steroids enter cells where they combine with steroid receptors in the cytoplasm. The combination then enters the nucleus where it controls the synthesis of proteins, including enzymes that regulate vital cell activities over a wide range of metabolic functions including all aspects of inflammation.
  9. 9. CARBOHYDRATE AND PROTEIN METABOLISM Important effects are inhibition of incorporation of amino acids into protein in the peripheral tissues (anti anabolic action)and stimulation of their conversion into glucose (neoglucogenesis)in the liver . During the process of neo-glucogenesis the amino acids are de--aminated and the nitrogen residue is excreted as urine, this accounts for. Inability of the adrenalectomised animal to maintain
  10. 10. normal blood sugar level while fasting and the ability of glucocorticoids to correct this ability. Hyperglycemia and glycosuria induced by chronic admi- -nistration of glucocorticoid in large doses and encounte- -red in Cushing’s syndrome. -Also inhibits peripheral glucose utilisation. FAT METABOLISM *Play a permissive role in the metabolisation of fat from the peripheral fat depots by adrenaline by growth hormone.such mobilization is markedly inhibited in the total absence of glucocorticoids.
  11. 11. -Prolonged administration of excessive glucocorticoid cause a re-distribution of fat in the body ,with a loss from the extremities and a deposition is the neck (buffalohump) supraclavicular area and face (moonFace). ELECTROLYTE AND WATER METABOLISM Hydrcortisone has a feeble salt retaining and potassium Wasting effect.when larger doses 300mg/24hrs are used, sufficient salt retention occurs to make the concurrent use of minerals corticoid unnecessary. Cortisol is essential for excreting a water load.Adrenale- -ctomised animals cannot excrete a water load and tend to develop water intoxications.
  12. 12. This defect is corrected by administration of glucocorticoid CALCIUM METABOLISM AND BONE. In pharmacological doses,glucocorticoids antagonize the action of vitamin D on the gut and reduce absorption of calcium Given in large doses for prolonged periods they interferes with the development of cartilage and inhibit the linear growth in children. As a result of protein catabolic action ,gluco corticoids inhibit the formation of new bony tissue and contin- -uous resorption lead to severe osteoporosis in chronic cases of hypercorticism.
  13. 13. C.V.S Important changes which occur in adrenal insuffic-- iency are partly due to mineralo-corticoid and partly due to glucocorticoid deficiency. Usually the blood volume and blood pressure are reduced and blood viscosity is increased.These defects are partly corrected by administration of sodium chloride or mineralocorticoid.Addition of a glucocorticoid completely restores the circulation to normal. Absence of gluco corticoids leads increase in the capillary permeability ,Inadequate vasomotor response of smaller blood vessels and decrease in cardiac output.
  14. 14. Glucocorticoid potentiates pressor response of blood vessels to adrenaline and noradrenaline , Hypertension is sometimes seen during chronic administration of glucocorticoids. SKELETAL MUSCLE Maintenance of normal muscle function requires adequate concentration of corticosteroids,but excessive amounts lead to abnormalities. Muscle weakness in adrenal insufficiency is largely due to inability of the circulatory system to respond to the stress of increased muscle activity .
  15. 15. CNS Patients receiving large doses of glucocorticiods sometimes show mood elevation ,euphoria, nervousness, restlessness and Psychosis. HEMATOLOGICAL ACTIONS. Hyperplasia of lymphoid tissues and peripheral lymphoc- -ytosis is in Addison disease. Lymphocyotpenia and dissolution of lymphatic masses in the body is seen in cushing syndrome. Glucocorticoids causes increasing in number of circulating neutrophils and decrease in number of lymphocytes and esonophils in blood.
  16. 16. GIT Causes increases in basal and nocturnal gastric acid secretion. ANTI INFLAMMATORY ACTION Supress the features of inflammation such as heat , swelling and tenderness. At tissues level ,they suppress the phenomena such as edema .
  17. 17. ABSORPTION, TRANSPORT, METABOLISM AND EXCRETION: ABSORPTION: .Hydrocortisone and numerous congeners including the synthesis analogs are effective when given by mouth. .Glucocorticoids also are absorbed systemically from sites of local administration,such as synovial spaces ,the conjun- -tival sac,skin and respiratory tract. .90% or more of cortisol in plasma is reversably bound to protein under normal circumstance.
  18. 18. Two plasma protein account for almost all of the steroid binding capacity. Corticosteroid binding globulin and albumin.
  19. 19. THERAPEUTIC USES *Acute adrenal insufficiency. *Chronic primary adrenal insufficiency. *Secondary adrenal insufficiency. *Congenital adrenal hyperplasia. *Rheumatic disorders. *Renal diseases. *Allergic disease. *Bronchial asthma. *Infectious disease. *ocular disease. *skin disease.
  20. 20. *Gastro intestinal disease. *Hepatic disease. *Malignancies. *cerebral edema. *organ transplantation
  21. 21. THERPEUTIC USES IN DENTISTRY Oral ulcerations: .Denture induced and other traumatic ulcers, *Recurrent ulcerative stomatitis. *Erosive lichen planus. *Erythema multiforme. *Pemphigus. *Desequamative gingivitis. *Stomatitis. *Geographic tongue. *Angular chelitis.
  22. 22. Temporomandibular joint disorders: Intra articular injection of glucocorticoid such as dexamethasone is benefical. Post operative: Glucocorticoid can be used to lessen postoperative compl -ications,mainly edema and trismus Other uses are after third molar extraction,orthognathic Surgery, bells palsy ,sub mucous fibrosis.
  23. 23. ANABOLIC STEROIDS They artificially raises the amount of anabolic hormone in the blood and permit further growth. They are analogue of the reproductive hormones such as testosterone. They increase muscle tissue.
  24. 24. CATOBOLIC STEROIDS. They are analogues of naturally occurring hormone released from adrenal gland when stressed. Catabolic steroids decreases the muscle tissue by breakdown of muscle and release of energy in patients with stress.
  25. 25. MANAGEMENT OF PATIENTS RECEVING SYSTEMIC GLUCOCORTICOSTEROIDS. Screen the patient for T.B, D.M,BP,Glaucoma,Cataracts,. Prepare the patient and family for possible adverse effects On mood and memory changes. Inform them about the side effects. Administer calcium,vitamin, bisphonates.
  26. 26. Avoid prolonged bed rest that will accelerate muscle weakness and bone mineral loss. Avoid elective surgery,if possible. Avoid elective work that would cause fall or trauma. Treat infections . Weigh daily. Measure height. Avoid smoking
  27. 27. Taper the dose before you stop . With dosage reduction ,watch for signs of adrenal Insufficiency or withdrawal syndrome.
  28. 28. BASIC PRINCIPLE OF TOPICAL STEROIDS. Ointment is more potent than cream. Potency of topical steroid can increase by covering with a occlusive dressing. Caution should be taken while they are used on areas of thin skin. Avoid soaps and detergents. Use it 10-20 minutes after the use of emollients.
  29. 29. Avoid on a infected skin. Use rule of FTU(Finger tip unit ) Large areas use the rule of nines. Used usually bid or tid (orally after food ) Donot apply on the unaffected area
  30. 30. GLUCOCORTICOID AND THE PERIODONTAL TISSUE. Topical applications of corticosteroids to the inflamed marginal gingivae of patients with periodontal disease resulted in a reduction of inflammation and sulcus bleeding. With no effect on the progression of periodontitis(stwawins- -ki) 1960;Haim 1962).However Iusem et al.(1956) injected cortisol preparations directly into the gingival tissues of five patients with periodontal disease and showed,histologi- -cally,reduced capillary permeability, fewer plasma cells in the granulation tissue ,inhibition of collagen synthesis and clinical improvement in haemorrhagic and hyperplastic gingivitis.
  31. 31. The effects of prednisone therapy upon gingival inflama- -tion and periodontal bone loss have been studied in a group of patients suffering from multiple sclerosis who had been on steroid therapy for up to four years (safkan and knuuttila 1984 ) . comparisons were made between this group ,a group of patients who suffered from neurological disorders but were not receiving steroids,and healthy controls. There were no difference in the frequency and severity of periodontal disease between the groups and it was concl- -uded that corticosteroid therapy over 1-4 years had no influence on the measures of periodontal disease in patients suffering from neurological disorders.
  32. 32. CONTRA INDICATIONS : Peptic ulcer Diabetic mellitus Hypertension Tuberculosis. Osteoporosis. Herpes simplex.
  33. 33. Pschychosis. Glaucoma. Epilepsy Renal failure. CHF.
  34. 34. Adverse effects Cushings habitus Hyperglycemia Muscular weakness. Susceptibility of infection. Delayed healing Peptic ulceration.
  35. 35. Osteoporosis. Glaucoma. Growth retardation. HPA axis suppression. Edema Rise in BP.
  36. 36. BIBLOGRAPHY. GOODMAN AND GILMANS – The Pharmacological Basis of therapeutics. Clinical Pharmacology in dentistry: L.A CAWSON R.G SPECTOR. Pharmacology and pharmacotherapeutics – R.S SATOSKAR CMDT -2004 – TRENEY, MACPHAEE.
  37. 37. Text book of clinical pharmacology . H.T.ROGER Drugs ,diseases and Periodontium- ROBIN .A .SEYMOUR PETER .A.HEASMAN
  38. 38.
  39. 39.