Diabetes Mellitus

patients
in dental management
shabeel pn
http://hi-dentfinishingschool.blogspot.com/
http://apexiondental.com/
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.
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 res

istance)
 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.
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, immunopat insulin resistance
hologic 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
 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 w
ithin 60 to 150 mg/dL.
 Insulin synthesized in beta cells of pancreas and
secreted rapidly into blood in response to elevati
ons in blood sugar.
 Promoting uptake of glucose from blood into cell
s and its storage as glycogen
 Fatty acid and amino acids converted to triglycer
ide and protein stores.
Pathophysiology
 Lack of insulin or insulin resistance, result i
n inability of insulin-dependent cells to use
glucose.
 Triglycerides broken down to fatty acids b
lood ketones↑  diabelic ketoacidosis.
Pathophysiology
 As blood sugar levels became elevated (hyperglycemia),
glucose is excreted in the urine and excessive of urinatio
n occurs due to osmotic diuresis (polyuria).

 Increased fluid loss leads to dehydration and excess thirs

t (polydipsia).

 Since cells are starved of glucose, the patient experience

s increased hunger (polyphagia).

 Paradoxically, the diabetic patient often loss weight, sinc

e the cells are unable to take up glucose.
Complications
 People with DM have an increased incidence of both micr
ovascular and macrovascular complications.
Major organs/systems showing changes Long term complications

Cardiovascular system: heart, myocardial infarct; atherosclerosis; hyperte

nsion; microangiopathy; cerebral vascu
brain, blood vessels lar infarcts; cerebral hemorrhage

Pancreas islet cell loss; insulitis (Type 1); amyloid (Ty

pe 2)

Kidneys nephrosclerosis; glomerulosclerosis; arterio

sclerosis; 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, 2000

National Institutes of Health, Aug 2001
Medical management
 Objective : maintain blood glucose levels a
s close to normal as possible.

 Good glycemic control inhibits the onset a

nd delay of type 1 DM, similar in type 2 D
M.
Medical management
 Glycated hemoglobin assay (HbA1c ) reflec
ts mean glycemia levels over the procedin
g 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 inhib
ition 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 xero
stomia
Oral manifestations and
complications
 Delayed healing of wounds
 Due to microangiopathy and ultilisation of protein for energy, ma
y 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, clinic
ians need to consider some issues before initiating dental tx
.
 Medical history : take hx and assess glycemic control at i
nitial 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 suguar.
 Loss of conscious, 25-30ml 50% dextrose soluti
on iv. over 3 min period.
 Glucagon 1mg.
 911, 119
Emergency management
 Severe hyperglycemia
A prolonged onset
 Ketoacidosis 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
2.Adipose glucose

ketone body glucose

ATP+co2
acetyl coA
TG glycerol-po4
TG
FA
Glycerol-po4 glycerol +FA

glucose glycerol
FA+ALB
 glucose
3.Muscle
glucose

glucose