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Diabetes Mellitus & Its Oral Manifestations
- 1. Oral Manifestations OfDiabetes Mellitus By: Md Khateeb Khan
- 2. Introduction Diabetes mellitusis a metabolic disorder characterized by relative or absolute insufficiency of insulin and resultant disturbances of carbohydrate metabolism . 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 .
- 3. Epidemiology Almost 20% of adult older than 65 year old have DM. 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.
- 4. Etiologic classification ofDM There are two types of Diabetes Mellitus: Type 1, insulin-dependent or juvenile-onset diabetes (IDDM) Type 2, non-insulin-dependent or adult-onset diabetes (NIDDM) Other specific types
- 5. Type 1 (IDDM) Autoimmune destruction of the insulin-producing beta cells of pancreas. 5-10% of DM cases. Commonly occurs in childhood and adolescence. Absolute insulin deficiency. High incidence of severe complications. Prone to autoimmune diseases (Grave’s, Addison, Hashimoto’s thyroiditis).
- 6. Pathogenesis of TypeI DM Environment ? Viral infection ? Genetic HLA-DR3/DR4 Severe Insulin deficiency ß cell Destruction Type I DM Autoimmune Insulitis
- 7. Type 2 (NIDDM) Result from impaired insulin function (insulin resistance). Constitutes 90-95% of DM cases. Specific causes of this form are unknown. Risk factors : age, obesity, alcohol, diet, family history and lack of physical activity, etc.
- 8. Pathogenesis of TypeII DM Environment Obesity ? ß cell defect Genetic ß cell exhaustion Type II DM Insulin resistance Relative Insulin Deficiency IDDM Abnormal Secretion
- 9. Comparison Type 1Type 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. Other specific typesGenetic defects of beta-cell functions Decrease of exocrine pancreas Endocrinopathies Drug or chemical usage Infections
- 11. Gestational diabetes mellitus(GDM) Defined as any degree of glucose intolerance with onset or first recognition during pregnancy. 4% of pregnancy .
- 12. Pathophysiology Healthy peopleblood glucose level maintained within 60 to 150 mg/dL. Insulin synthesized in beta cells of pancreas and secreted rapidly into blood in response to elevations in blood sugar. Promoting uptake of glucose from blood into cells and its storage as glycogen Fatty acid and amino acids converted to triglyceride and protein stores. Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose.
- 13. Pathophysiology Triglycerides brokendown to fatty acids blood ketones↑ diabetic ketoacidosis. As blood sugar levels became elevated (hyperglycemia), glucose is excreted in the urine and excessive of urination occurs due to osmotic diuresis (polyuria). Increased fluid loss leads to dehydration and excessive thirst (polydipsia). Since cells are starved of glucose, the patient experiences increased hunger (polyphagia). Paradoxically, the diabetic patient often loses weight, since the cells are unable to take up glucose.
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- 16. Complications People withDM have an increased incidence of both microvascular and macrovascular complications. 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
- 17. Diagnosis A casualplasma glucose level of 200 mg/dL or greater with symptoms presented. Fasting plasma glucose level of 126 or greater.(Normal <100 mg/dL) Oral glucose tolerance test (OGTT) value in blood of 200 mg or greater. ADA recommend >45 year old screened every 3 years.
- 18. Interpretation of theglucose tolerance test 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. 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
- 19. Medical management Objective: Maintain blood glucose levels as close to normal as possible. Good glycemic control inhibits the onset and delay of type 1 DM, similar in type 2 DM.
- 20. Medical management Exerciseand diet control Insulin : rapid, short, intermediate, long acting. Oral antidiabetic agents
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- 22. Oral manifestationsand complications No specific oral lesions associated with diabetes. However, there are a number of problems by presence of hyperglycemia . Periodontal disease Microangiopathy altering antigenic challenge. Altered cell-mediated immune response and impaired of neutrophil chemotaxis. Increased Ca + and glucose lead to plaque formation. Increased collagen breakdown.
- 23. PDL changes inNIDDM Patient from 8 years
- 24. Oral manifestationsand complications Salivary glands Xerostomia is common, but reason is unclear. Tenderness, pain and burning sensation of tongue. May cause secondary enlargement of parotid glands with sialosis. Dental caries Increase caries prevalence in adult with diabetes. (xerostomia, increase saliva glucose) Hyperglycemia state shows a positive association with dental caries.
- 25. Sialosis Carious lesion on teeth with Xerostomia
- 26. Oral manifestationsand complications Increased risk of infection Reasons unknown, but macrophage metabolism altered with inhibition of phagocytosis. Peripheral neuropathy and poor peripheral circulation Immunological deficiency High sugar medium Decrease production of Antibodies Candidal infection are more common and adding effects with xerostomia
- 27. Oral manifestationsand complications Delayed healing of wounds Due to microangiopathy and ultilisation of protein for energy, may retard the repair of tissues. Increase prevalence of dry socket . Miscellaneous conditions Pulpitis : degeneration of vascular. Neuropathies : may affect cranial nerves. (facial) Drug side-effects : lichenoid reaction may be associated with sulphonylureas (chlopropamide) Ulcers
- 28. Subacute Lichenoid Reaction Diabetic Ulcer
- 29. Dental management considerationsTo minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental treatment. Medical history: Take history and assess glycemic control at initial appointment. Glucose levels Frequency of hypoglycemic episodes Medication, dosage and times. Consultation
- 30. Dental management considerationsScheduling of visits Morning appointment Do not coincide with peak activity. Diet Ensure that the patient has eaten normally and taken medications as usual. Blood glucose monitoring Measured before beginning. (<70 mg/dL) Prophylactic antibiotics Established infection Pre-operation contamination wound Major surgery
- 31. Dental management considerationsDuring treatment The most complication of DM occur is hypoglycemia episode. Hyperglycemia After treatment Infection control Dietary intake Medications : salicylates increase insulin secretion and sensitivity avoid aspirin.
- 32. Emergency management HypoglycemiaInitial signs : mood changes, decreased spontaneity, hunger and weakness. Followed by sweating, incoherence, tachycardia. Results in unconsciousness, hypotension, hypothermia, seizures, coma, even death.
- 33. Emergency management 15grams of fast-acting oral carbohydrate. Measured blood sugar. Loss of consciousness: 25-30ml 50% dextrose solution iv. over 3 min period. Glucagon 1mg.
- 34. Emergency management Severehyperglycemia A prolonged onset Ketoacidosis may develop with nausea, vomiting, abdominal pain and acetone odor. Difficult to different hypoglycemia or hyperglycemia.
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- 36. Emergency management Hyperglycemianeeds medical intervention and insulin administration. While emergency, give glucose first ! Small amount is unlikely to cause significant harm.
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