Diabetes Mellitus

patients
in dental management
shabeel pn

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 hyperglycemiagenerating 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

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,
or any age.
Absolute insulin deficiency.
High incidence of severe complications.
Prone to autoimmune diseases. (Graves,
Addison, Hashimotos 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
Hx and lack of physical activity..etc.

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

ketoacidosis common

ketoacidosis rare

human leukocyte antigen

(HLA)-D linked

No HLA association

autoimmunity,
immunopathologic
mechanisms

insulin resistance

severe insulin deficiency

relative insulin deficiency

insulitis early

no insulitis

marked atrophy and

fibrosis

focal atrophy and amyloid

deposits

severe beta-cell depletion

mild beta-cell depletion

Genetics

Pathogenesis

Islet Cells

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

greater with symptoms presented.
Fasting plasma glucose level of 126 or greater.
(Normal <110 mg/dL,IGT,IFG)
Oral glucose tolerance test (OGTT) value in
blood of 200 mg or greater.

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

Diabetes Care, 2000
National 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,
there are a number of problems by present 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.

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,

increase saliva glucose)
Hyperglycemia state shown a positive association with dental
caries.

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
sulphonylurea. (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

Blood glucose monitoring

Ensure that the patient has eaten normally and taken medications as
usual.
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
sensitivity avoid aspirin.

Emergency management

Hypoglycemia
Initial

signs : mood changes, decreased

spontaneity, hunger and weakness.
Followed by sweating, incoherence,
tachycardia.
Consequenced in unconsiousness,
hypotention, hypothermia, seidures, coma,
even death.

Emergency management

15 grams of fast-acting oral carbonhydrate.

Measured blood suguar.
Loss of conscious, 25-30ml 50% dextrose
solution iv. over 3 min period.
Glucagon 1mg.
911, 119

Emergency management

Severe hyperglycemia
A prolonged

onset
Ketoacidosis may develop with nausea,
vomiting, 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

glucose

2.Adipose
glucose

ketone body
ATP+co2
acetyl coA
TG
FA
Glycerol-po4
glucose

TG

glycerol-po4

glycerol +FA
glycerol
FA+ALB

glucose

3.Muscle
glucose
glucose