Diabetes Mellitus patients

in dental management

Reporter : 吳和泰 Modulator: Dr. 雷文天

Introduction Diabetes mellitus is a metabolic disorder charact

erized by relative or absolute insufficiency of insulin, and resultant disturbances of carbonhydrate 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.

Epidemiology 6% (16 million persons) of the general population

in the US have diabetes mellitus. Almost 20% of adult older than 65 y/o 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.

National Institutes of Health, Aug 2001

國人之糖尿病盛行率

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, adult-onset diabetes (NIDDM)

Other specific types

JADA, Oct 2001

Type 1 (IDDM)

Autoimmune destruction of the insulin-producing beta cells of pancreas.

5-10% of DM cases. Common occurs in childhood and adolescence, o

r any age. Absolute insulin deficiency. High incidence of severe complications. Prone to autoimmune diseases. (Grave’s, Addiso

n, Hashimoto’s thyroiditis)

Type 2 (NIDDM)

Result from impaired insulin function. (insulin resistance)

Constitutes 90-95% of DM Specific causes of this form are unknown. Risk factors : age, obesity, alcohol, diet, family H

x and lack of physical activity..etc.

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

Other specific types

Genetic defects of beta-cell functions Decrease of exocrine pancreas Endocrinepathothies Drug or chemical usage Infections

………….

Gestational diabetes mellitus (GDM)

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

4% of pregnancy in US.

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.

Pathophysiology

Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose.

Triglycerides broken down to fatty acids blood ketones↑ diabelic ketoacidosis.

Pathophysiology

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 excess thirst (polydipsia).

Since cells are starved of glucose, the patient experiences increased hunger (polyphagia).

Paradoxically, the diabetic patient often loss weight, since the cells are unable to take up glucose.

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 infarct; 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

Diagnosis A casual plasma glucose level of 200 mg/dL or g

reater with symptoms presented. Fasting plasma glucose level of 126 or greater.

(Normal <110 mg/dL,IGT,IFG) Oral glucose tolerance test (OGTT) value in bloo

d of 200 mg or greater.

ADA recommend >45 y/o screened every 3 years.

Diabetes Care, 2000National Institutes of Health, Aug 2001

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.

Medical management

Glycated hemoglobin assay (HbA1c ) reflects mean glycemia levels over the proceding 2~3 months. (normal < 7%)

HbA1c also a predictor for development of chronic complications.

Medical management Exercise and diet control Insulin : rapid, short, intermediate, long acting. Oral antidiabetic agents

Oral manifestations and complications

No specific oral lesions associated with diabetes. However, th

ere are a number of problems by present of hyperglycemia.

Periodontal disease Microangiopathy altering antigenic challenge. Altered cell-mediated immune response and impaired of neutrop

hil chemotaxis. Increased Ca+ and glucose lead to plaque formation. Increased collagen breakdown.

Oral manifestations and complications Salivary glands

Xerostomia is common, but reason is unclear. Tenderness, pain and burning sensation of tongue. May secondary enlargement of parotid glands with sialosis.

Dental caries Increase caries prevalence in adult with diabetes. (xerostomia, in

crease saliva glucose) Hyperglycemia state shown a positive association with dental ca

ries.

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 Ab

Candical infection are more common and adding effects with xerostomia

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 sul

phonylurea. (chlopropamide) Ulcers

New Zealand Journal, Jan 1985

Dental management considerations

To minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental tx.

Medical history : take hx and assess glycemic control at initial appt. Glucose levels Frequency of hypoglycemic episodes Medication, dosage and times. Consultation

Dental management considerations Scheduling of visits

Morning appt. (endogeneous cortisol) Do not coincide with peak activity.

Diet Ensure that the patient has eaten normally and taken medications as us

ual. Blood glucose monitoring

Measured before beginning. (<70 mg/dL) Prophylactic antibiotics

Established infection Pre-operation contamination wound Major surgery

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 sensitivit

y avoid aspirin.

Emergency management

Hypoglycemia Initial signs : mood changes, decreased spont

aneity, hunger and weakness.Followed by sweating, incoherence, tachycard

ia.Consequenced in unconsiousness, hypotenti

on, hypothermia, seidures, coma, even death.

Emergency management

15 grams of fast-acting oral carbonhydrate. Measured blood sugua. Loss of conscious, 25-30ml 50% dextrose soluti

on iv. over 3 min period. Glucagon 1mg. 911, 119

Emergency management

Severe hyperglycemiaA prolonged onsetKetoacidosis may develop with nausea, vomiti

ng, abdominal pain and acetone odor.Difficult to different hypo- or hyper-.

Emergency management

Hyperglycemia need medication intervention and insulin administration.

While emergency, give glucose first ! Small amount is unlikely to cause significant

harm.

JADA, Oct 2001

Conclusion

Thanks for ur attention !!

1.Liver

ketone body ATP+co2 acetyl coA TG FAGlycerol-po4 glucose

glucose

glucose glucose

TG glycerol-po4

glycerol +FA

glycerol FA+ALB

2.Adipose

glucose

glucose

3.Muscle