Diabetes

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DIABETES ,
ROLE OF INSULIN &
OTHER ANTIDIABETICS

CONTENTS
 Introduction
 Classification of diabetes mellitus
 Etiology
 Pathophysiology
 Role of Insulin
 Clinical Features and Oral Manifestations
 Diagnosis
 Management/ Dental Management of Diabetic
 Acute Complications
 Long term complications
 Pregnancy and Diabetes
 Conclusion www.indiandentalacademy.com

introduction

Diabetes Mellitus is a clinical syndrome characterized by
hyperglycemia due to absolute or relative deficiency of insulin.
Classification:
1. Primary
 Type 1 or Insulin Dependent DM (IDDM)
 Type 2 or non-insulin Dependent DM (NIDDM)
2. Other specific types of Diabetes
 Pancreatic Disease
 Excess Endogenous production of hormonal antagonists to insulin
 Medication (Corticosteroids, thiazide diuretics, phenytoin)
 Associated with genetic syndromes.
3. Gestational Diabeteswww.indiandentalacademy.com

Etiology
 Precise etiology of both main types of primary
diabetes is uncertain.
Type 1 Diabetes (IDDM)
Genetics
 Inheritance is polygenic
 HLA DR3 and / or DR4 of 6P predispose to IDDM-1.
 Region of insulin gene on 11P predispose to IDDM-2
Environmental Factors
Viruses
 Infection with mumps, coxsackie B4, rubella,
cytomegalovirus and EB virus have been implicated.
 Virus particles may cause cytopathic or autoimmune
damage to Beta cells

Diet :
 Bovine Serum Albumin (BSA), a major constituent of cow’s milk,
has been implicated in triggering type 1 diabetes.
 BSA has close homology with the Beta – chain of HLA classes II
antigen and heat shock protein expressed by Beta cells.
Stress :
 May progress the development of type 1 diabetes by stimulating
secretion of counter regulatory hormones.
Immunological Factors:
 Type 1 diabetes is a slow T-cell mediated autoimmune diseases.
Pancreatic Pathology:
 Insulitis- infiltration of islets with mononuclear cells
 Striking Beta cells specificity of the destructive process.

Type –2 Diabetes (NIDDM)
 Occurs in subjects who are obese and insulin
resistant but these 2 factors are alone in sufficient
to cause diabetes unless accompanied by impaired
beta cells function .
Genetics
 Is associated with many single gene disorders
affecting hepatocyte nuclear factor 4 alfa (HNF4
Alfa) ,Glucokinase, HNF 1 Alfa , Insulin Genes.
Environmental Factors
Life Style
 Overeating, especially when combined with the
obesity and under activity, is associated with the
development of type 2 diabetes.

Malnutrition in utero:
 May damage beta cell development.
Age :
 Type 2 diabetes is principally a disease of the
middle aged and elderly affecting 10% of the
population over the age of 65.
Pregnancy :
 Gestational diabetes refers to hyperglycemia
occurring for the first time during pregnancy
 Repeated pregnancy may increase likelihood of
developing permanent diabetes, particularly in obese
women.

pathophysiology

Clinical Features
 The Classical symptoms of thirst, polyuria,
nocturia and rapid weight loss are prominent in
type 1 diabetes, but are often absent in patients
with type 2 diabetes.
 Increased susceptibility to infection and patients
may present with skin sepsis (boils) and genital
candidiasis .
 In fulminating case with ketoacidosis, the striking
features are those of salt and water depletion,
furred tongue and cracked lips.
 Hypertension is present in 50% of patients with
type 2 diabeteswww.indiandentalacademy.com

Oral Diseases / manifestations
 Oral conditions include burning mouth, altered
wound healing, and an increased incidence of
infection.
 Enlargement of the parotid glands and
xerostomia
 Neuropathy
 Diabetes is a risk factor for the prevalence
and severity of gingivitis and periodontitis.
 Risk of attachment loss and alveolar bone loss
approximately 3 fold when compared to non
diabetic control subjects.

Enlarged gingival tissues, multiple
periodontal abscesses.
The formation of AGES.
Changes in the function of host defense
cells.
Changes in the collagen metabolism.
wound healing alternations and
periodontal destruction.
Periodontal infection increased the risk
of poor glycemic control by six fold.

Diabetes and prosthodontics
 Abutment Failure.
 Tissue abrasions are more likely in denture
wearers.
 Erythematous candidosis is associated to the use
of upper total denture or prosthesis (denture
stomatitis).
 Oral carrier rate and density of C. albicans in
denture wearers of diabetic group were higher.
 Increased residual ridge resorption.
 Mucostatic impressions.

Diabetes and implant surgery
 Implant dentistry is not contraindicated in most diabetics
 Diabetics patients with blood glucose levels of around 100
Mg/dl…
 Sedative procedures and antibiotics.
 Need for a stress reduction protocol, diet evaluation
before after surgery and control of the risk of infection
are all addressed.
 Corticosteroids, often used to decrease edema, swelling and
pain may not be used in the diabetics patient.
 Detrimental effects of diabetes on osseointegration can be
modified using aminoguanidine systemically. Doxycycline may
also help to an extent.www.indiandentalacademy.com

Diagnosis
 Patient complains of symptoms suggesting diabetes then
 Test urine for glucose and ketones
 Measure random or fasting blood glucose. Diagnosis
confirmed by
Fasting Plasma glucose > 7 mmol / Lit
Random plasma glucose > 11 mmol / Lit.
 Indications for oral glucose tolerance test (OGTT)
random plasma glucose 7-11 mmol/Lit.

Urine Testing
 Sensitive glucose specific dipstick test methods.
 The greatest disadvantage of using urinary glucose as
diagnostic or screening procedure is the individual
variation in renal threshold.
 Ketone bodies can be identified by the nitroprusside
reaction.
 Renal glycosuria
 Alimentary glycosuria
 Glycosuria during pregnancy

The oral glucose tolerance test (OGTT)
 Unrestricted carbohydrate diet for 3 days
before tests
 Fasted overnight
 Rest before test (30 min); no smoking ;
seated
 Plasma glucose measured before 75 gm
glucose load and at 30 min intervals for 2 hrs.

OGTT : Diagnostic criteria :
Plasma Glucose (Venous)
Diabetes
 Fasting > 7.8
 2 Hrs after glucose load > 11.1
Impaired glucose tolerance
 Fasting 7.8
 2 Hrs after glucose load 7.8 – 11

 The revised criteria for the diagnosis of DM
emphasize the FPG (fasting plasma glucose) as
the most reliable and convenient test for
diagnosing DM in asymptomatic individuals.
 FPG is also strongly recommended as a screening
test for type 2 DM.
 HbA 1c can be used as a diagnostic test for DM
but is not universally standardized.

Insulin
Insulin was discovered in 1921
by Banting and Best.
Insulin is synthesized in the
Beta cells of pancreatic islets
as a single chain peptide
preproinsulin (110AA) from
which 24AAs are first removed
to produce proinsulin.
The connecting or ‘c’ peptide
(35AA) is split off by
proteolysis in Golgi apparatus to
produce insulin. www.indiandentalacademy.com

Regulation of Insulin Secretion
 Secretion of Insulin from Beta Cells is
regulated by chemical, hormonal and neural
mechanisms.
Chemical:
 Activation of glucoceptor.
Hormonal:
 A number of hormones, eg. G.H
Corticosteroids, thyroxine modify insulin
release in response to glucose.
 PG E has been shown to inhibit insulin release.

 Stomatostatin
 Glucagon
 Insulin
Neural:
 Adrenergic alpha2 receptor activation decrease
insulin release.
 Adrenergic beta2 stimulation Increases insulin
release
 Cholinergic muscarinic activation by Ach or Vagal
stimulation increase insulin secretion.

Actions of Insulin
 Insulin facilitates glucose transport across cell
membrane; skeletal muscle and fat are highly sensitive.
 Insulin enhances the production of glucokinase. Insulin
facilitates glycogen synthesis.
 Insulin inhibits gluconeogenesis, lipolysis, glycogenolysis.
 Insulin Increase clearance of VLDL and Chylomicrons.
 Insulin facilitates protein synthesis.

Mechanism of Action.
Insulin receptors are
heterotetrameric glycoproteins
consisting of 2 extracellulor alfa
and 2 transmembrane beta
subunits linked together by
disulphide bonds.
 Insulin stimulates glucose
transport across cell membrane by
ATP dependent translocation of
glucose transporters GLUT4 and
GLUT 1 to the plasma membrane.www.indiandentalacademy.com

Conventional preparations of Insulin
The conventional commercial preparation of insulin are
derived from beef and pork pancreas.
Type
Peak (Hr) Duration (Hr)
1) Short acting
regular Insulin 2-4 6-8
Semilente 3-6 12-6
2) Intermediate acting
Lente 8-10 20-24
Isophone Insulin 8-10 20-24
3) Long Acting
Ultralente 14-18 24-36
Protamine Zn Insulin 14-20 24-36www.indiandentalacademy.com

Highly purified Insulin preparations
 According to the purification method used
the preparation can be categorized into :
1) Single Peak Insulin : Purified by gel filtration
and repeated crystallization; they contain 50-
200 ppm proinsulin
2) Monocomponent Insulin : After gel filtration,
it is further purified by ion exchange
chromatography; the content of proinsulin is
reduced to < 20 ppm.www.indiandentalacademy.com

Human Insulins :
 In 1980’s the human insulins were produced by recombinant
DNA Technology in E. Coli , yeast or by enzymatic
modification of porcine insulin
 Human insulin is more water soluble as well as hydrophobic
than porcine or bovine insulin.
 It has more rapid S.C. absorption, earlier and more defined
peak and slightly shorter duration of action.
Reactions of Insulin:
 Hypoglycemia
 Local reactions: lipodystrophy
 Allergy
 Edema

Insulin Delivery
Insulin is injected into subcutaneous sites namely the
anterior abdominal wall, upper arms, outer thighs and
buttocks.
Pen injectors
Open loop systems are battery powered portable pumps
providing continuous subcutaneous or intravenous infusion
of insulin.

Insulin Regimens
 Twice daily administration of short acting and
intermediate acting insulin given in combination before
breakfast and the evening meal, is the simplest and most
commonly used regimen.
Short acting insulin is injected atleast 30 min before a
meal.
Rapidly absorbed insulin analogues can be administered
5-10 min before food.
Once absorbed into blood, insulin has half life of 7
minutes.

Oral Hypoglycaemic Drugs
Classification
1) Sulfonylureas
First
Generation
Second Generation
Tolbutamide Gilbenclamide
Chlorpropamide Glipizide
Glicazide
Glimepiride

2) Biguanides
 Phenformin Metformin
3) Meglitinide analogues
 Repaglinide Nateglinide
4) Thiazolidinediones
 Rosiglitazone Pioglitazone
5) Alfa Glucosidase Inhibitors
 Acarbose Miglitol

Sulfonylureas
Mechanism of action
 They act on the so called sulfonylurea
receptors on the pancreatic Beta cell membrane.
Adverse effects
 Chloropropamide
 Tolbutamide reduces iodide uptake by thyroid.

Biguanides
Mechanism of action
 Supress hepatic gluconeogenesis and glucose output
from liver : Major action
Adverse effects
 Lactic acidosis
 Vit B12 deficiency
Meglitinide analogues
 Induces rapid onset short lasting insulin release

Thiazolidinediones
Mechanism of action : They are selective agonists for
the nuclear peroxisome proliferator activated receptor –
gamma ( PPAR gamma) which enhances the transcription
of several insulin responsive genes.
Alfa Glucosidase Inhibitors
Mechanism of action
Inhibit alfa glucosidases, the final enzymes in the
digestion of carbohydrates in the brush border of small
intestine mucosa.

Dental Management of diabetic patient
Key dental treatment considerations for
diabetic patients include :
Establishing the levels of glycemic control
early in the treatment process:
 Patients recent glycated Hb values

Stress Reduction :
 Endogenous production of epinephrine and
cortisol increase during stressful situations .
 Profound anesthesia reduces pain and minimizes
endogenous epinephrine release.
 Conscious sedation should be considered for
extremely anxious patient.
Treatment Settings.
The use of antibiotics.
Diet Modification.

Appointment Timings
 Diabetic patients can receive dental
treatment in the morning.
 But, it is generally best to plan dental
treatment to occur either before or after
periods of peak insulin activity.
 Greatest risk of hypoglycemia will occur about
 30-90 min after injecting Lispro Insulin.
 2 – 3 Hours after injecting regular insulin
 4-10 hours after injecting Lente Insulin

Diabetic Emergencies Management
 The most common diabetic emergency in the
dental office is hypoglycemia.
 Signs and symptoms of hypoglycemia include ;-
Confusion , sweating, tremors, agitation, anxiety,
dizziness, tingling or numbness, and tachycardia.
Severe hypoglycemia may result in seizures or
loss of consciousness.
 Blood glucose with a glucometer should be
checked.

 If glucometer is not available, condition is
treated as hypoglycemic episode and the patient
should be given approx. 15g of oral carbohydrate.
 If patient is unable to take food by mouth, IV
line is in place, 25-50 ml of 50% dextose solution
(D50) or 1mg of glucagon can be given
intraveneously.
 Signs and symptoms of hypoglycemia should
reduce in 10-15 min.
Marked Hyperglycemia : If glucometer is not
available, these symptoms must be treated as
hypoglycemia.

Acute Complications of Diabetes
1) Hypoglycemia
 Occurs often in diabetic patients treated with insulin
but relatively infrequent in those taking sulfonyl urea
drug.
Symptoms
Autonomic (activation of ANS)
 Sweating, trembling, pounding heart, hunger, anxiety.
Neuroglycopenic (Secondary to glucose deprivation of
brain)
 Confusion, drowsiness, speech difficulty, inability to
concentrate, in coordination,
Non specific
 Nausea, tiredness, headache.

2) Diabetic Ketoacidosis
 Ketoacidosis is caused by insulin deficiency and an
increase in catabolic hormones leading to hepatic
overproduction of glucose and ketone bodies.
 Any form of stress , particularly that produced by
infection, may precipitate severe ketoacidosis ,
even in patients with type 2 diabetes.
 The cardinal biochemical features of diabetic
ketoacidosis are ;
 Hyperglycemia
 Hyper ketonaemia
 Metabolic acidosis
 The Severity of ketoacidosis can be assessed
rapidly by measuring the plasma bicarbonate.www.indiandentalacademy.com

Clinical features of diabetic ketoacidosis
Symptoms Signs
Polyuria, Thirst Dehydration
Weight loss Hypotension
Weakness Tachycardia
Nausea vomiting Kussmaul breathing
Leg cramps Smell of acetone
Blurred vision Hypothermia
Abdominal pain Confusion, drowsiness, coma.

Management
Principal components of treatment are ;
 The administration of short acting(soluble) insulin.
 Fluid replacement(0.9% NaCl)
 K+
Replacement (IV KCl)
 Na bicarbonate (300ml, 1.25% over 30 min into large
vein)
 Administration of antibiotics, if infection present
Insulin : Loading dose of 10-20 units of soluble insulin
can be given by IM injection, immediately followed by 4-6
units hourly thereafter.

Non Ketotic hyperosmolar diabetic coma
 This condition is characterized by severe
hyperglycemia ( > 50 mmol/l) without significant
hyperketonaemia or acidosis
 Half the dose of insulin recommended for
treatment of ketoacidosis is employed.
 0.45% saline administered.
Lactic Acidosis
 Patient is likely to be taking a biguanide for
type 2 diabetes.
 IV Na bicarbonate given.

Long term Complications
 Large blood vessel disease or macroangiopathy
(atherosclerosis) accounts for about 70% of all
deaths in diabetics
 Diseases of small blood vessels (diabetic
microangiopathy) contributes to mortality by
causing renal failure to due diabetic nephropathy.
 Both vascular diseases cause diabetic retinopathy
chronic ulceration, diabetic neuropathy, angina,
cardiac failure and gangrene.

Diabetic Retinopathy
Clinical features
Micro aneurysms
Haemoharages (blot haemorrhages)
Hard exudates
Soft exudates (Cotton wool spots)
Neovascularisation
Venous changes (dilation, beading, oxbow
lakes or loops)

Classification
 Non proliferative background retinopathy without
maculopathy.
 Pre-proliferative retinopathy and / or
maculopathy
 Proliferative retinopathy and / or exudative
macrolopathy.
Management
 Retinal photocoagulation
 2 types of photo coagulation – xenon arc (white
light ) Laser Beam (Monochromatic green light)
 Vitrectomy may also be done.

Diabetic Neuropathy
Classification
Somatic Visceral
Polyneuropathy Cardiovascular
Mononeuropathy Gastrointestinal
Genitourinary
Sudomotor
Vasomotor
Pupillary

Clinical Features
 Symmetrical sensory polyneuropathy
 Asymmetrical motor diabetic neuropathy
 Mononeuropathy
 Autonomic neuropathy
Management
 Intensive insulin therapy
 Tricyclic antidepressants
 Anticonvulsants

The diabetic foot
 Foot ulceration occurs as a result of trauma in
presence of neuropathy and or peripheral
vascular disease, with infection occurring as a
secondary phenomenon following ulceration.
Clinical Features
Neuropathy Ischaemia
Paraesthesiae Claudication
Pain Rest Pain
Numbness None
None

The most common cause of Ulceration is a plaque of callous
skin, beneath which tissue necrosis occurs.
Management
 Remove callous skin
 Treat infectionwww.indiandentalacademy.com

Diabetic nephropathy
Most common cause of end stage renal failure
Pathology:
Thickening of glomerular basement membrane and
accumulation of matrix material in the mesangium
Microalbuminura is an important indicator of risk
of developing diabetic nephropathy.

Management
In case of incipient
nephropathy,
Improve control of blood
glucose
Reduction of blood pressure
Institution of ACE inhibitor
therapy

Pregnancy and diabetes
 Pregnancy in diabetic women is associated with an increased
perinatal mortality rate.
 The main causes of this are ;
 Intrauterine death in 3rd trimester of pregnancy.
 Prematurity.
 Low birth weight and congenital malformation.
Management of pregnancy in established diabetic
women
 Maintain good glycemic control i.e., HbA1c within the range
6.5 – 8% by use of 3-4 injections of insulin daily.
 Check blood glucose during the night periodically.
 Check overnight sample of urine for ketones regularly.

Gestational
Diabetes
It is defined as
hyperglycemia diagnosed
for the first time in
pregnancy

 A screening procedure for gestational diabetes
involves measurement of fasting true venous
plasma glucose concentration.
up to 20 weeks - >5.5 mmol/lit
20 – 40 weeks - >6.5 mmol/lit
Management of diabetes at Delivery :
 Diabetic women are delivered between 38 and 39
weeks gestation
 On morning of delivery, IV infusion of 10%
dextrose with 10 units of short acting insulin
added to each 500 ml.

conclusion

references
 Davidson’s Principles and practice of medicine-18th
edition
 Principles of general medicine.- Harrision.
 Burket’s Oral Medicine.Diagnosis and treatment.
- -10th
edition
 Essentials of medical pharmacology.
-KD Tripathi. 5th
edition.
 Contemporary implant dentistry. –Carl E Micsh.
2ND
edition.
 Prosthodontics for the elderly.Diagnosis and treatment.
-Jorgensen
 New microbiology 1998 jan;21(1):41-8
 J Periodontol 1994 jun;18;67-9
 J of oral Rehab 1999;26;345-55www.indiandentalacademy.com

Diabetes

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