Diabetes Mellitus & Its Oral Manifestations

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Oral Manifestations Of Diabetes Mellitus By: Md Khateeb Khan

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Transcript of Diabetes Mellitus & Its Oral Manifestations

Page 1: Diabetes Mellitus & Its Oral Manifestations

Oral Manifestations Of Diabetes Mellitus

By: Md Khateeb Khan

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Introduction

Diabetes mellitus is 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.

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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.

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Etiologic classification of DM

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

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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).

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Pathogenesis of Type I DM

Environment ?Environment ?

Viral infection ?Viral infection ?Genetic Genetic

HLA-DR3/DR4HLA-DR3/DR4

Severe Insulin deficiencySevere Insulin deficiency

ß cell Destructionß cell Destruction

Type I DMType I DM

Autoimmune Insulitis Autoimmune Insulitis

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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.

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Pathogenesis of Type II DM

EnvironmentEnvironment

Obesity ?Obesity ?ß cell defectß cell defect

GeneticGenetic

ß cell ß cell

exhaustionexhaustion Type II DMType II DM

Insulin resistanceInsulin resistance

Relative Insulin DeficiencyRelative Insulin Deficiency

IDDMIDDM

Abnormal SecretionAbnormal Secretion

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ComparisonComparison 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

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Other specific types

Genetic defects of beta-cell functions

Decrease of exocrine pancreas

Endocrinopathies

Drug or chemical usage

Infections

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Gestational diabetes mellitus (GDM)

Defined as any degree of glucose intolerance with onset or first recognition during pregnancy.

4% of pregnancy.

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Pathophysiology Healthy people blood 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.

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Pathophysiology Triglycerides broken down 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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Factors Causing

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Complications People with DM 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

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Diagnosis

A casual plasma 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.

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Interpretation of the glucose tolerance testA 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.

Fastingmmol/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

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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.

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Medical management Exercise and diet control

Insulin : rapid, short, intermediate, long acting.

Oral antidiabetic agents

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Oral manifestations and 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.

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PDL changes in NIDDM Patient from 8 years

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Oral manifestations and 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.

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Sialosis Carious lesion on teeth with Xerostomia

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Oral manifestations and 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

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Oral manifestations and 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

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Subacute Lichenoid Reaction Diabetic Ulcer

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Dental management considerations

To 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

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Dental management considerations Scheduling 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

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Dental management considerations

During 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.

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Emergency management

Hypoglycemia

Initial signs : mood changes, decreased spontaneity, hunger and weakness.

Followed by sweating, incoherence, tachycardia.

Results in unconsciousness, hypotension, hypothermia, seizures, coma, even death.

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Emergency management

15 grams of fast-acting oral carbohydrate.

Measured blood sugar.

Loss of consciousness: 25-30ml 50% dextrose solution iv. over 3 min period.

Glucagon 1mg.

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Emergency management

Severe hyperglycemia A prolonged onset

Ketoacidosis may develop with nausea, vomiting, abdominal pain and acetone odor.

Difficult to different hypoglycemia or hyperglycemia.

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Emergency management

Hyperglycemia needs medical intervention and insulin administration.

While emergency, give glucose first !

Small amount is unlikely to cause significant harm.

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Conclusion

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