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DENTAL MANAGEMENT

CONSIDERATION FOR
DIABETES MELLITUS
PATIENTS

Dr. Dewi Priandini. Drg.SpPM


Introduction
 Diabetes mellitus is a metabolic disorder
characterized 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.
 Indonesian Population 2,4 – 3,75 million have DM

National Institutes of Health, Aug 2001; JADA,vol 132, Oct 2001


Epidemiology

 There for, it is important for dentist to be


aware of medical and Dental management
consideration for this expandinh patient
population …
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

In type-1 diabetes the patient can not produce the hormone


insulin, while in type-2 diabetes the patient produces insulin,
but it is not used properly. An estimated 90% of diabetic
patients suffer from type-2 disease.
American Academy of Oral Medicine,2007; 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. (Grave’s, Addison,
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


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

Genetics ketoacidosis common ketoacidosis rare


human leukocyte antigen No HLA association
(HLA)-D linked
Pathogenesis autoimmunity, insulin resistance
immunopathologic
mechanisms
severe insulin deficiency relative insulin deficiency
Islet Cells insulitis early no insulitis
marked atrophy and focal atrophy and amyloid
fibrosis deposits
severe beta-cell depletion mild beta-cell depletion
Other specific types

 Genetic defects of beta-cell functions


 Decrease of exocrine pancreas

 Endocrinopathies

 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.
 In the majority cases, glucose regulation will return
to normal after delivery.
 However, woman who have had GDM  increased
risk of developing type 2 DM later .
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, myocardial infarct; atherosclerosis;


hypertension; microangiopathy; cerebral
brain, blood vessels 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


Oral Changes Associated with Diabetes Mellitus

Periodontal Disease. Periodontal disease is a commonly


observed dental problem for patients with diabetes. It is similar
to the periodontal disease encountered among nondiabetic
patients. However, as a consequence of the impaired immunity
and healing associated with diabetes, it may be more severe
and progress more rapidly . The potential for these changes
points to the need for periodic professional evaluation and
treatment
Oral Changes Associated with Diabetes Mellitus

 Salivary Gland Dysfunction. Several changes to


the salivary glands may occur in association with
diabetes. The most commonly observed concern is
dry mouth ,but other findings may include gland
enlargement, and an increased risk for developing
salivary duct stones and gland infection.
Oral Changes Associated with Diabetes
Mellitus

Infections.
Poorly controlled diabetes can lead to a variety of
tissue infections. The most commonly encountered is
a yeast infection (Candida) and the presence of dry
mouth further increases one’s risk
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 usual.
 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


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 sugua.
 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 !!

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