Diabetes Mellitus & Its Oral Manifestations


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Diabetes Mellitus & Its Oral Manifestations

  1. 1. Oral Manifestations Of Diabetes Mellitus By: Md Khateeb Khan
  2. 2. Introduction <ul><li>Diabetes mellitus is a metabolic disorder characterized by relative or absolute insufficiency of insulin and resultant disturbances of carbohydrate metabolism . </li></ul><ul><li>The major function of insulin is to counter the concerted action of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels . </li></ul>
  3. 3. Epidemiology <ul><li>Almost 20% of adult older than 65 year old have DM. </li></ul><ul><li>A dental practice serving an adult population of 2,000 can expect to encounter 40-80 persons with diabetes, about half of whom will be unaware of their condition. </li></ul>
  4. 4. Etiologic classification of DM <ul><li>There are two types of Diabetes Mellitus: </li></ul><ul><ul><li>Type 1, insulin-dependent or juvenile-onset diabetes (IDDM) </li></ul></ul><ul><ul><li>Type 2, non-insulin-dependent or adult-onset diabetes (NIDDM) </li></ul></ul><ul><ul><li>Other specific types </li></ul></ul>
  5. 5. Type 1 (IDDM) <ul><li>Autoimmune destruction of the insulin-producing beta cells of pancreas. </li></ul><ul><li>5-10% of DM cases. </li></ul><ul><li>Commonly occurs in childhood and adolescence. </li></ul><ul><li>Absolute insulin deficiency. </li></ul><ul><li>High incidence of severe complications. </li></ul><ul><li>Prone to autoimmune diseases (Grave’s, Addison, Hashimoto’s thyroiditis). </li></ul>
  6. 6. Pathogenesis of Type I DM Environment ? Viral infection ? Genetic HLA-DR3/DR4 Severe Insulin deficiency ß cell Destruction Type I DM Autoimmune Insulitis
  7. 7. Type 2 (NIDDM) <ul><li>Result from impaired insulin function (insulin resistance). </li></ul><ul><li>Constitutes 90-95% of DM cases. </li></ul><ul><li>Specific causes of this form are unknown. </li></ul><ul><li>Risk factors : age, obesity, alcohol, diet, family history and lack of physical activity, etc. </li></ul>
  8. 8. Pathogenesis of Type II DM Environment Obesity ? ß cell defect Genetic ß cell exhaustion Type II DM Insulin resistance Relative Insulin Deficiency IDDM Abnormal Secretion
  9. 9. Comparison Type 1 Type 2 Clinical onset <20 years onset >30 years   normal weight obesity   decreased blood insulin normal or increased blood insulin   anti-islet cell antibodies no anti-islet cell antibodies Genetics ketoacidosis common ketoacidosis rare   human leukocyte antigen (HLA)-D linked No HLA association Pathogenesis autoimmunity, immunopathologic mechanisms insulin resistance   severe insulin deficiency relative insulin deficiency Islet Cells insulitis early no insulitis   marked atrophy and fibrosis focal atrophy and amyloid deposits   severe beta-cell depletion mild beta-cell depletion
  10. 10. Other specific types <ul><li>Genetic defects of beta-cell functions </li></ul><ul><li>Decrease of exocrine pancreas </li></ul><ul><li>Endocrinopathies </li></ul><ul><li>Drug or chemical usage </li></ul><ul><li>Infections </li></ul>
  11. 11. Gestational diabetes mellitus (GDM) <ul><li>Defined as any degree of glucose intolerance with onset or first recognition during pregnancy. </li></ul><ul><li>4% of pregnancy . </li></ul>
  12. 12. Pathophysiology <ul><li>Healthy people blood glucose level maintained within 60 to 150 mg/dL. </li></ul><ul><li>Insulin synthesized in beta cells of pancreas and secreted rapidly into blood in response to elevations in blood sugar. </li></ul><ul><li>Promoting uptake of glucose from blood into cells and its storage as glycogen </li></ul><ul><li>Fatty acid and amino acids converted to triglyceride and protein stores. </li></ul><ul><li>Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose. </li></ul>
  13. 13. Pathophysiology <ul><li>Triglycerides broken down to fatty acids  blood ketones↑  diabetic ketoacidosis. </li></ul><ul><li>As blood sugar levels became elevated (hyperglycemia), glucose is excreted in the urine and excessive of urination occurs due to osmotic diuresis (polyuria). </li></ul><ul><li>Increased fluid loss leads to dehydration and excessive thirst (polydipsia). </li></ul><ul><li>Since cells are starved of glucose, the patient experiences increased hunger (polyphagia). </li></ul><ul><li>Paradoxically, the diabetic patient often loses weight, since the cells are unable to take up glucose. </li></ul>
  14. 14. Factors Causing
  15. 16. Complications <ul><li>People with DM have an increased incidence of both microvascular and macrovascular complications. </li></ul>Major organs/systems showing changes Long term complications Cardiovascular system: heart, brain, blood vessels Myocardial infarction; atherosclerosis; hypertension; microangiopathy; cerebral vascular infarcts; cerebral hemorrhage Pancreas Islet cell loss; insulitis (Type 1); amyloid (Type 2) Kidneys Nephrosclerosis; glomerulosclerosis; arteriosclerosis; pyelonephritis Eyes Retinopathy; cataracts; glaucoma Nervous system Autonomic neuropathy; peripheral neuropathy Peripherals Peripheral vascular atherosclerosis; infections; gangrene
  16. 17. Diagnosis <ul><li>A casual plasma glucose level of 200 mg/dL or greater with symptoms presented. </li></ul><ul><li>Fasting plasma glucose level of 126 or greater.(Normal <100 mg/dL) </li></ul><ul><li>Oral glucose tolerance test (OGTT) value in blood of 200 mg or greater. </li></ul><ul><li>ADA recommend >45 year old screened every 3 years. </li></ul>
  17. 18. Interpretation of the glucose tolerance test <ul><li>A 75 gram oral glucose tolerance test (OGTT) is used to follow up people with equivocal results who may have Diabetes, Impaired Fasting Glucose or Impaired Glucose Tolerance. </li></ul>Fasting mmol/L 2 hours post load mmol/L Normal < 5.5 and < 7.8 IFG 6.1 – 6.9 and < 7.8 IGT < 7.0 and 7.8 – 11.0 Diabetes mellitus ≥ 7.0 and/or ≥ 11.1 GDM ≥ 5.5 and/or ≥ 9.0
  18. 19. Medical management <ul><li>Objective : Maintain blood glucose levels as close to normal as possible. </li></ul><ul><li>Good glycemic control inhibits the onset and delay of type 1 DM, similar in type 2 DM. </li></ul>
  19. 20. Medical management <ul><li>Exercise and diet control </li></ul><ul><li>Insulin : rapid, short, intermediate, long acting. </li></ul><ul><li>Oral antidiabetic agents </li></ul>
  20. 22. Oral manifestations and complications <ul><li>No specific oral lesions associated with diabetes. However, there are a number of problems by presence of hyperglycemia . </li></ul><ul><li>Periodontal disease </li></ul><ul><ul><li>Microangiopathy altering antigenic challenge. </li></ul></ul><ul><ul><li>Altered cell-mediated immune response and impaired of neutrophil chemotaxis. </li></ul></ul><ul><ul><li>Increased Ca + and glucose lead to plaque formation. </li></ul></ul><ul><ul><li>Increased collagen breakdown. </li></ul></ul>
  21. 23. PDL changes in NIDDM Patient from 8 years
  22. 24. Oral manifestations and complications <ul><li>Salivary glands </li></ul><ul><ul><li>Xerostomia is common, but reason is unclear. </li></ul></ul><ul><ul><li>Tenderness, pain and burning sensation of tongue. </li></ul></ul><ul><ul><li>May cause secondary enlargement of parotid glands with sialosis. </li></ul></ul><ul><li>Dental caries </li></ul><ul><ul><li>Increase caries prevalence in adult with diabetes. (xerostomia, increase saliva glucose) </li></ul></ul><ul><ul><li>Hyperglycemia state shows a positive association with dental caries. </li></ul></ul>
  23. 25. Sialosis Carious lesion on teeth with Xerostomia
  24. 26. Oral manifestations and complications <ul><li>Increased risk of infection </li></ul><ul><ul><li>Reasons unknown, but macrophage metabolism altered with inhibition of phagocytosis. </li></ul></ul><ul><ul><li>Peripheral neuropathy and poor peripheral circulation </li></ul></ul><ul><ul><li>Immunological deficiency </li></ul></ul><ul><ul><li>High sugar medium </li></ul></ul><ul><ul><li>Decrease production of Antibodies </li></ul></ul><ul><ul><li>Candidal infection are more common and adding effects with xerostomia </li></ul></ul>
  25. 27. Oral manifestations and complications <ul><li>Delayed healing of wounds </li></ul><ul><ul><li>Due to microangiopathy and ultilisation of protein for energy, may retard the repair of tissues. </li></ul></ul><ul><ul><li>Increase prevalence of dry socket . </li></ul></ul><ul><li>Miscellaneous conditions </li></ul><ul><ul><li>Pulpitis : degeneration of vascular. </li></ul></ul><ul><ul><li>Neuropathies : may affect cranial nerves. (facial) </li></ul></ul><ul><ul><li>Drug side-effects : lichenoid reaction may be associated with sulphonylureas (chlopropamide) </li></ul></ul><ul><ul><li>Ulcers </li></ul></ul>
  26. 28. Subacute Lichenoid Reaction Diabetic Ulcer
  27. 29. Dental management considerations <ul><ul><li>To minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental treatment. </li></ul></ul><ul><li>Medical history: Take history and assess glycemic control at initial appointment. </li></ul><ul><ul><li>Glucose levels </li></ul></ul><ul><ul><li>Frequency of hypoglycemic episodes </li></ul></ul><ul><ul><li>Medication, dosage and times. </li></ul></ul><ul><ul><li>Consultation </li></ul></ul>
  28. 30. Dental management considerations <ul><li>Scheduling of visits </li></ul><ul><ul><li>Morning appointment </li></ul></ul><ul><ul><li>Do not coincide with peak activity. </li></ul></ul><ul><li>Diet </li></ul><ul><ul><li>Ensure that the patient has eaten normally and taken medications as usual. </li></ul></ul><ul><li>Blood glucose monitoring </li></ul><ul><ul><li>Measured before beginning. (<70 mg/dL) </li></ul></ul><ul><li>Prophylactic antibiotics </li></ul><ul><ul><li>Established infection </li></ul></ul><ul><ul><li>Pre-operation contamination wound </li></ul></ul><ul><ul><li>Major surgery </li></ul></ul>
  29. 31. Dental management considerations <ul><li>During treatment </li></ul><ul><ul><li>The most complication of DM occur is hypoglycemia episode. </li></ul></ul><ul><ul><li>Hyperglycemia </li></ul></ul><ul><li>After treatment </li></ul><ul><ul><li>Infection control </li></ul></ul><ul><ul><li>Dietary intake </li></ul></ul><ul><ul><li>Medications : salicylates increase insulin secretion and sensitivity  avoid aspirin. </li></ul></ul>
  30. 32. Emergency management <ul><li>Hypoglycemia </li></ul><ul><ul><li>Initial signs : mood changes, decreased spontaneity, hunger and weakness. </li></ul></ul><ul><ul><li>Followed by sweating, incoherence, tachycardia. </li></ul></ul><ul><ul><li>Results in unconsciousness, hypotension, hypothermia, seizures, coma, even death. </li></ul></ul>
  31. 33. Emergency management <ul><li>15 grams of fast-acting oral carbohydrate. </li></ul><ul><li>Measured blood sugar. </li></ul><ul><li>Loss of consciousness: 25-30ml 50% dextrose solution iv. over 3 min period. </li></ul><ul><li>Glucagon 1mg. </li></ul>
  32. 34. Emergency management <ul><li>Severe hyperglycemia </li></ul><ul><ul><li>A prolonged onset </li></ul></ul><ul><ul><li>Ketoacidosis may develop with nausea, vomiting, abdominal pain and acetone odor. </li></ul></ul><ul><ul><li>Difficult to different hypoglycemia or hyperglycemia. </li></ul></ul>
  33. 36. Emergency management <ul><li>Hyperglycemia needs medical intervention and insulin administration. </li></ul><ul><li>While emergency, give glucose first ! </li></ul><ul><li>Small amount is unlikely to cause significant harm. </li></ul>
  34. 37. Conclusion