Diabetes Mellitus and its Public Health Significance

1. 2018
PRESENTEDBY:
DR. RADHIKA MITRA
PRESENTED ON:
2/16/2018
DIABETES MELLITUS
DEPARTMENT OF PUBLIC HEALTH DENTISTRY

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CONTENTS
1. INTRODUCTION 03
2. HISTORY 03
3. INSULIN
 SYNTHESIS 4-5
 SECRETION 5-6
 EFFECTS OF INSULIN 06
4. CLASSIFICATIONOF DIABETES MELLITUS 07
5. TYPE I DIABETES MELLITUS
 PATHOPHYSIOLOGY 8-9
 CLINICAL FEATURES 09
6. TYPE II DIABETES MELLITUS
 RISK FACTORS 10
 PATHOPHYSIOLOGY 11
 SIGNS AND SYMPTOMS 11-12
7. GESTATIONAL DIABETES 12
8. DIAGNOSIS 12-15
9. COMPLICATIONS 15-22
10.MANAGEMENT 22-27
11.ADVANCES OF DIABETES MELLITUS 27-31
12.DENTAL ASPECTS OF DIABETES 31-33
13.PUBLIC HEALTH SIGNIFICANCE 36
14.CONCLUSION 36
15.REFERENCES 37

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INTRODUCTION
The word “Diabetes” means passing through and “Mellitus” means sweet/honey.
Definition: Diabetes is a clinically and genetically heterogenous metabolic disease
characterized by abnormally elevated blood glucose levels (hyperglycemia) and
dysregulation of carbohydrate, protein and lipid metabolism.
[Source: Davidson’s Principles and Practice of Medicine- 19th edition]
Globally an estimated 422 million adults are living with diabetes mellitus, according to the
latest 2016 data from the World Health Organization. Diabetes prevalence is increasing
rapidly; previous 2013 estimates from the International Diabetes Federation have put the
number at 381 million people having diabetes.
Diabetes and higher-than-optimal blood glucose together are responsible for 3.7 million
deaths. WHO projects that diabetes will be the 7th leading cause of death in 2030. It leads to
compromised oral health, blindness, kidney failure, lower limb amputation and other long-
term consequences that impact significantly on quality of life.
HISTORY
The term "diabetes" was first coined by Araetus of Cappodocia (81-133AD).
Later, the word mellitus (honey sweet) was added by Thomas Willis of Britain in 1675 after
rediscovering the sweetness of urine and blood of patients (first noticed by the ancient
Indians). It was only in 1776 that Dobson of Britain firstly confirmed the presence of excess
sugar in urine and blood as a cause of their sweetness.
An important milestone in the history of diabetes is the establishment of the role of the liver
in glycogenesis, and the concept that diabetes is due to excess glucose production put forward
by Claude Bernard of France in 1857. The role of the pancreas in pathogenesis of diabetes
was discovered by Mering and Minkowski (Austria) 1889. Later, this discovery constituted
the basis of insulin isolation and clinical use by Banting and Best of Canada in 1921.
Trials to prepare an orally administrated hypoglycemic agent ended successfully by first
marketing of tolbutamide and carbutamide in 1955.

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WORLD DIABETES DAY
November 14th has been celebrated as “WORLD DIABETES DAY”
in memorate birthday of Frederic Banting. He was the person who
discovered insulin.
INSULIN
Insulin is a peptide hormone produced by beta cells of the pancreatic islets which regulates
the metabolism of carbohydrates, fats and protein by promoting the absorption of glucose
from the blood into fat, liver and skeletal muscle cells.
It is a small protein consisting of an A chain of 21 amino acids linked by two disulfide (S—S)
bridges to a B chain of 30 amino acids.
SYNTHESIS
Insulin is secreted by Beta cells in the islets of Langerhans of pancreas.
Beta cells have channels in their plasma membrane that serve as glucose detectors. They
secrete insulin in response to a rising level of circulating glucose. It is stored as β granules
A Chain B Chain

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Insulin is initially produced as preproinsulin which, on proteolysis, yields proinsulin. Clevage
of proinsulin releases C-peptide and insulin A and B chains which are stored together in
secretory granules of beta cells and released into portal circulation together. C-peptide is less
susceptible than insulin to hepatic degradation- hence is a useful marker of insulin secretion
and its measurement helps in differentiation of endogenous source of insulin (insulinoma
where c-peptide levels are high) exogenous source of insulin as the cause of insulin induced
hypoglycaemia.
SECRETION
[SOURCE: Sembulingam K. Sembulingam P. Essentials Of Medical Physiology.5th
ed.2004,]

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Glucose enters the beta cells through glucose transporter Glutamine2. In the beta cells,
glucose undergoes glycolysis and high energy ATP molecules are produced by oxidation.
This increased ATP ratio causes blockage of potassium channels and opening of calcium
channels. This causes release of calcium from endoplasmic reticulum into cells. Due to high
concentration of calcium in cells there is release of previously synthesized insulin which is
stored in the secretory vesicles.
EFFECT OF INSULIN
1. On Carbohydrate Metabolism
a) Increases transport and uptake of glucose from blood by increasing the permeability
of cell membrane to insulin.
There are multiple tissues particularly, the liver, muscle, adipose tissue which require
insulin for uptake of glucose but there are also tissues like the brain (except the
hypothalamus), mucous membrane of intestine, RBCs which do not require insulin.
b) Insulin promotes peripheral utilisation of glucose.
c) It promotes storage of glucose- glycogenesis. Insulin causes rapid conversion of
glucose to glycogen which is then stored in the liver and muscle.
d) Inhibits glycogenolysis- Insulin prevents breakdown of glycogen to glucose in liver
and muscle cells.
e) Inhibits gluconeogenesis- Insulin prevents formation of glucose from proteins.
2. On Protein Metabolism
a) Insulin promotes synthesis and storage of proteins.
b) It inhibits the cellular utilization of proteins.
3. On Fat Metabolism
a) Insulin promotes synthesis of fatty acids and triglycerides
b) It helps in transport of fatty acids to adipose tissue
c) Insulin helps in storage of fat- by inhibiting the enzymes which degrades
triglycerides.

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CLASSIFICATION OF DIABETES MELLITUS
1. Primary diabetes
i. Type 1 (Insulin dependent diabetes mellitus-IDDM)
A. Immuned mediated (islet cell anti-bodies)
B. Nonimmune (no antibody)
ii. Type 2 (Non-insulin dependent diabetes mellitus-NIDDM)
A. Obese (insulin resistance with relative insulin deficiency)
B. Non-obese (insulin secretory defect with insulin resistance)
2. Seondary diabetes
a) Pancreatic diabetes due to pancreatitis
b) Hormonal or endocrinal abnormalities- Cushing’s syndrome, acromegaly,
pheochromocytoma.
c) Drug induced (Iatrogenic)- due to thiazides and steroids. Steroids are more likely to
cause type II diabetes. Corticosteroids increases insulin resistance thus allowing blood
glucose level to rise and remain high.
d) Insulin receptor antibodies
e) Genetic Syndromes, i.e., lipodystrophies, muscular dystrophies, Klinefelter’s
syndrome, Turner’s syndrome, Down’s syndrome, DIDMOAD (Diabetes insipidus,
diabetes mellitus, optic atrophy and deafness) syndrome.
3. Gestational diabetes
[SOURCE: Classification and Diagnosis of Diabetes- Diabetes Care, Volume 38, Supplement
1, January 2015]

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TYPE I DIABETES MELLITUS
Once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in
which the pancreas produces little or no insulin, a hormone needed to allow sugar (glucose)
to enter cells to produce energy.
It is considered as an autoimmune disorder. Usually begins below the age of 30 years.
The various CRITERIA for its autoimmunity are:
o Human Leukoid Antigen linkage
o Its association with other autoimmune disorders
o Lymphocytic infiltration of beta cells of pancreas
o Circulating anti-insulin antibodies
o Recurrence of beta cells destruction in grafted pancreas.
PATHOPHYSIOLOGY OF TYPE I DIABETES MELLITUS
Genetic susceptibility HLA (DR3, DR4)
chromosome no.6
Environmental factor- A virus acts as
trigger
Insulitis: inflammation of pancreas with
lymphocytic infiltration
Activation of autoimmunity, distinction
between self and non-self fast
Autoimmune destruction of beta cells of
pancreas.
Alpha cells spared
Type I Diabetes Mellitus

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Genetic susceptibility is a major determinant while environmental factors act as a trigger. The
genetic predisposition is HLA linked class II genes at D locus (DR3 and DR4) on short arm of
chromosome number 6. The appearance of class II molecules on beta cells of pancreas which
normally do not exist has been thought to play a major role in autoimmune process of
destruction. The process of autoimmune destruction is triggered by environmental factors
such as a virus, which has been demonstrated in experimental studies in mice. With onset of
autoimmune process, T-lymphocytes infiltrate the beta cells of pancreas and activate the
immune system with production of both humoral and cell-mediated antibodies.
Two types of antibodies (cytoplasmic and surface) appear and take part in the destructive
process. Surface antibodies have the ability to fix complement (C3 and C4) and lyse the beta
cells. In the process, T-lymphocytes and antibodies dependent killer T cells complete the
process of destruction after its initiation and lead to development of type I diabetes.
CLINICAL FEATURES
It usually begins below the age of 30 years. May develop abruptly; with 3 principal
sequences:
a) Increased blood glucose causing polyuria, polydipsia and polyphagia.
b) Increased utilization of fats for energy and for formation of cholesterol by the liver –
metabolic acidosis (ketoacidosis), rapid and deep breathing, atherosclerosis
c) Depletion of the body’s proteins – rapid weight loss, asthenia, despite of polyphagia

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TYPE II DIABETES MELLITUS
Diabetes mellitus type II (also known as type II diabetes) is a long term metabolic disorder
that is characterized by high blood sugar, insulin resistance, and relative lack of insulin.
Disorder begins in middle age. RISK FACTORS FOR TYPE II DM:
1. Genetics
2. Environmental factors: Obesity and physical inactivity are the two diabetogenic
factors only in those patients who are genetically susceptible to type I and type II
diabetes mellitus.
3. Pancreatic beta cell failure: There is reduction in pancreatic beta cell mass with
reduction in insulin levels. The characteristic pathologic change is amyloid deposition
which, in fact, is not the cause of diabetes but reflects pancreatic amyloidosis in type
II diabetes.
4. Age: The occurrence of type II diabetes after 30 years of age indicates the age as an
important risk factor.
5. Pregnancy: Diabetes may occur for the first time in pregnancy in women genetically
predisposed to type I and type II. This is due to relative lack of insulin. Although
insulin levels are high in pregnancy due to stimulating effect of placental lactogens on
beta cells but these are still insufficient to cater to the metabolic needs during
pregnancy resulting in hyperglycemia and development of gestational diabetes.
Therefore, pregnancy is also a factor for determination of diabetes in genetically
predisposed women.
AGE & GENETIC PREDISPOSITION OBESITY
PHYSICAL INACTIVITY PREGNANCY

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PATHOPHYSIOLOGY OF TYPE II DIABETES MELLITUS
In type II diabetes mellitus, there is reduction in beta cell mass causing insufficient insulin
secretion or insulin secretion or insulin resistance. Insulin resistance is a condition in which
multiple cells and tissues of human body become resistant to the effect of insulin causing
blood glucose level to rise (hyperglycaemia). Hyperglycaemia and insulin resistance forces
the pancreas to produce more insulin causing hyperinsulinemia. This causes inflammation by
increased activity and growth of fat cells which further cause cell damage.
SIGNS & SYMPTOMS OF UNDIAGNOSEDDIABETES
i. Polydipsia (excessive thirst)
ii. Polyuria (excessive urination)
iii. Polyphagia (excessive hunger)
iv. Unexplained weight loss
v. Changes in vision
vi. Weakness, malaise
Pancreatic beta cell failure
Insulin resistance Low to moderate insulin
secretion
Hyperglycaemia
Hyperinsulinaemia
Inflammation
Cell damage

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vii. Irritability
viii. Nausea
ix. Dry mouth
x. Ketoacidosis
GESTATIONALDIABETES MELLITUS
o Usually develops during the third trimester and significantly increases perinatal
morbidity and mortality.
o Pathophysiology of gestational diabetes is associated with increased insulin
resistance.
o Most patients with gestational diabetes return to a normoglycemic state after
parturition.
DIAGNOSIS OF DIABETES
Diagnosis can be made from:
 Blood Sugar Testing
 Urine testing
 Glycated Haemoglobin - HbA1c

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BLOOD SUGAR TESTING
Diagnosis is by any of the following three methods and must be confirmed on a subsequent
day by any one of the same three methods:
1. RANDOMPLASMA TEST:
o This test is the simplest test which can be done. It doesn’t require any fasting before
the test.
o Random glucose can be drawn at any time of the day regardless of the time since last
meal.
o Presence of diabetes symptoms plus casual (non fasting) plasma glucose ≥ 200 mg/dl
would show probable chance of diabetes but it needs to be reconfirmed.
2. FASTING GLUCOSE TEST:
o This test requires atleast 8 hours of fasting.
o If the fasting plasma glucose ≥ 126 mg/dl then the diagnosis is confirmed.
3. GLUCOSE TOLERANCE TEST:
o Patient is advised to take 3 days of unrestricted carbohydrate diet prior to the test and
exercise
o Patient should keep an overnight fast of 8-14 hours before the test.
o Rest for 30 minutes before starting the test.
TEST
o Fasting blood sample is drawn on the morning for glucose estimation
o Patient is given 75g of anhydrous glucose dissolved in 250-300 ml water for drinking
over 5 minutes
o Blood and urine sample is collected at 30 minutes interval for next 2 hours for
diagnosis.
o No smoking during the test
o Two-hour postprandial glucose ≥ 200 mg/dl during an oral glucose tolerance test
confirms the diagnosis.
GLUCOSE URINE TEST
o The glucose urine test measures the amount of sugar (glucose) in a urine sample. The
presence of glucose in the urine is called glycosuria or glucosuria.

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o Normal Results
i. Glucose is not usually found in urine. If it is, further testing is needed.
ii. Normal glucose range in urine: 0 to 0.8 mmol/l (0 to 15 mg/dL)
o Test for diagnosis of glucose in urine is the dipstick method (clinistix test) which
gives a coloured reaction (green colour) if test is positive, which can be compared
with the colour in the bottle.
o The greatest disadvantage of urinary glucose measurement is the individual variation
in renal threshold for glucose. For example, diabetics with raised renal threshold will
give negative urine test for glucose, while on the other hand; normal individual with
low renal threshold may pass glucose in urine.
o Urine for Ketone bodies: Acetotest tablets or ketostix test papers utilising
nitroprusside reactions are employed to detect ketone bodies in urine.
HBA1C CRITERIA
o Allows the determination of blood glucose status over the 30 to 90 days prior to
collection of the blood sample.
o The higher the plasma glucose levels are over time, the greater is the percentage of
hemoglobin that becomes glycated.
o There are two different glycated hemoglobin assays: the hemoglobin A1 (HbA1) test
and the hemoglobin A1c (HbA1c) test.
o The normal HbA1 value is less than approximately 8% whereas the normal HbA1c
value is less than 6.0 to 6.5%.
Symptomatic Asymptomatic
Repeat within 2 weeks
HbA1c ≥ 6.5%
HbA1c ≥ 6.5%
Type II Diabetes Diagnosed

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DIAGNOSIS OF PREDIABETIC CONDITIONS
Impaired fasting glucose (IFG)
It is diagnosed when fasting glucose level is abnormal (between 110 to 126 mg%).
Impaired glucose tolerance
The intermediate values of postprandial blood sugar (140-200 mg%) between normal and
diabetics are classified as impaired glucose tolerance.
DIAGNOSIS OF GESTATIONALDIABETES
FRUCTOSAMINE TEST:
o It is often helpful in managing women with gestational diabetes.
o Assesses glycemic control over the 2 to 4 weeks preceding the test.
o The normal range for fructosamine is 2.0 to 2.8 mmol/L
COMPLICATIONS OF DIABETES
1) Acute Complications of DM
• Hypoglycemia
• Diabetic ketoacidosis (DKA)
• Hyperglycemic hyperosmolar state (HHS)
2) Chronic Complications of DM
MICROVASCULAR
a. Eye disease
 Retinopathy (nonproliferative/proliferative)
 Macular edema
b. Neuropathy
c. Nephropathy

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MACROVASCULAR
a. Coronary artery disease
b. Peripheral arterial disease
c. Cerebrovascular disease
OTHER
a. Gastrointestinal
b. Genitourinary
c. Dermatologic
d. Infections
e. Cataracts
f. Glaucoma
g. Periodontal disease
HYPOGLYCAEMIA
It is defined as ‘fall in blood glucose concentration below 3.1 mmol/l (<55 mg%)’. Severe
hypoglycaemia refers to fall in blood glucose concentration below 40 mg% requiring help
from outside for recovery.
Hypoglycemia is classified traditionally into:
i. Postprandial or reactive which occurs only in response to meals
ii. Fasting which occurs after few hours of fasting
FACTORS RESPONSIBLE FOR HYPOGLYCAEMIA IN DIABETES:
1. Intake of too little food or no food but insulin is taken as regular
2. Unaccustomed exercise is attempted but preceding dose of insulin is not reduced
3. Alcohol intake
4. Poorly designed insulin regimen. There is a mismatch between insulin administration
and food habits.
5. Defective counter-regulatory mechanisms such as release of glucagon and
catecholamines in diabetes.
6. Impaired gastric emptying
7. Malabsorption of food

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8. Factitious hypoglycaemia
9. An unrecognised low renal threshold for glucose
10. Renal failure
11. Other endocrinal causes, e.g., pitutary insufficiency, Addison’s disease and
premenstrual insulin sensitivity.
SYMPTOMS & SIGNS
CVS: Palpitation, tachycardia, anxiety, cardiac arrhythmias
CNS: Tremors, confusion, headache, tiredness, difficulty in concentration,
incoordination, slurred speech, drowsiness, convulsions, coma
GI tract: Nausea, vomiting
Skin: Sweating, hypothermia
TREATMENT
I. IF PATIENT IS UNCONSCIOUS
 Stop anti-diabetic medication
 Give 50 ml of 50% intravenous glucose through a large vein to avoid
thrombophlebitis
 As soon as patient recovers consciousness, start oral carbohydrate intake, otherwise 5-
10% glucose infusion- till patients recovers consciousness.
 Intramuscular injection of 1.0 ml of glucagon given if hypoglycaemia is insulin
induced.
 If patient does not regain consciousness inspite of normal blood glucose levels, then
cerebral oedema is likely possibility which should be treated with intravenous
dexamethasone or mannitol.
II. IF PATIENT IS CONSCIOUS
 Oral glucose intake must be encouraged to reverse hypoglycaemia. Full recovery
occurs in mild cases.
 In case of hypoglycaemia induced by OHA or by depot preparation of insulin,
recovery takes longer time and even relapse may occur within a day or two after
stoppage of glucose.

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DIABETIC KETOACIDOSIS
The basic defect of diabetes ketoacidosis is poor metabolic control due to lack of insulin.
SYMPTOMS
a. Nausea/vomiting
b. Thirst/polyuria
c. Abdominal pain
d. Shortness of breath
PHYSICAL FINDINGS
a. Tachycardia
b. Dehydration / hypotension
c. Tachypnea / Kussmaul respirations/respiratory distress
d. Abdominal tenderness (may resemble acute pancreatitis or surgical abdomen
e. Lethargy / cerebral edema / possibly coma
MANAGEMENT
1. Correction of dehydration by intravenous fluids.
 In diabetes ketoacidosis there is loss of both extracellular and intracellular
fluid.
 The extracellular fluid deficit is replaced by infusion of normal saline (0.9%) -
first 1 litre in first half hour, second 1 litre in next 1 hour and last 1 litre in
next 2 hours.
 The intracellular fluid deficit is corrected by infusion of 5-10% dextrose.
2. Correction of acidosis
 Severe acidosis (pH<7), sodium bicarbonate 300-500ml may be given over a
period of half an hour.
3. Use of unmodified (soluble/rapid acting) insulin
 This can be done in two ways-
- 6 units i.v stat followed by 6 units/hour
- Alternatively, it can be given as a bolus dose of 20 units i.m followed by
6 units/hour by the same route, till ketoacidosis is reversed.

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4. Replacement of potassium
 If potassium level remains between 3.5- 5.5 mmol/l; 20 mmol/l of potassium
may be infused. But, if level falls below 3.5 mmol, then 40 mmol should be
infused to correct hypokalemia.
5. Treatment of precipitating factor such as an infection by appropriate antibiotics.
HYPEROSMOLAR NON-KETOTIC DIABETIC COMA
o This is common in type 2 diabetes patients.
o It is precipitated by some factors, e.g., procedures, drugs, infection
o The clinical hallmark of the syndrome is-
i) hyperglycemia
ii) hyperosmolarity
iii) dehydration
o Treatment is infusion of half normal saline (0.45% NaCl) with small doses of insulin.
DIABETIC RETINOPATHY
o It is important cause of blindness among diabetics. Early detection and early
management are mandatory.
o Characteristic Features:
a. Microaneurysms: These are small, discrete red spots near to the retinal blood
vessels.
b. Hard and soft exudates which appear as white specks or patches on the retina.
c. Retinal haemorrhage or blot haemorrhage are round and are deeply situated.
d. Neovascularisation: Formations of new blood vessels are seen on the retina near the
optic disc.
e. Vitreous haemorrhages are followed by proliferation of connective tissue which
appear as dense white sheets and fibres, known as ‘retinitis proliferans.’

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f. Fibrosis
o Treatment: Photocoagulation
DIABETIC NEPHROPATHY
o Two types of pathological lesions seen:
- diffuse glomerulosclerosis
- nodular glomerulosclerosis
o 3 clinical phases can be seen:
- Early phase: patient is asymptomatic but has high GFR
- Renal hypertrophy giving rise to microalbuminuria
- Advanced: macroproteinuria and passes on to nephrotic syndrome

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DIABETIC NEUROPATHY
The most common form of diabetic neuropathy is distal symmetric polyneuropathy. It most
frequently presents with distal sensory loss, but up to 50% of patients do not have symptoms
of neuropathy.
Hyperesthesia, paresthesia, and dysesthesia also may occur. Any combination of these
symptoms may develop as neuropathy progresses.
Symptoms may include a sensation of numbness, tingling, sharpness, or burning that begins
in the feet and spreads proximally.
Pain typically involves the lower extremities, is usually present at rest, and worsens at night
DIABETIC FOOT
The pathogenic components of diabetic foot are:
1. Neuropathy
2. Peripheral vascular disease producing ischaemia (vasculopathy)
3. Secondary infection following ulceration
Clinical Features:
- Pain
- Numbness
- Claudication
Signs:
- Ulcer
- Sepsis, abscess
- Osteomyelitis
- Gangrene
- Charcot’s joint
- Loss of toes

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Management of diabetic foot ulcers:
a) Removal of callous skin
b) Treatment of infection by appropriate antibiotics
c) Avoid weight bearing
MANAGEMENT OF DIABETES MELLITUS
A. DIET FORMULATIONS
o Diet is a basic part of management in every case. Treatment cannot be effective unless
adequate attention is given to ensuring appropriate nutrition.
 Dietary treatment should aim at:
◦ ensuring weight control
◦ providing nutritional requirements
◦ allowing good glycaemic control with blood glucose levels
as close to normal as possible
◦ correcting any associated blood lipid abnormalities
 Nutritional Recommendations for Adults with Diabetes:
◦ Carbohydrates- 50-55% of total caloric intake is recommended. All the
carbohydrates prescribed should be taken in the form of starch and complex
sugars. Fibre content of the diet should be high.
◦ Proteins- 10-15% of total caloric intake is recommended. Amino acids
stimulate insulin secretion, hence, proteins combined with carbohydrates in
die,t lower the blood sugar effectively. Daily intake of proteins should be 60-
100g divided between meals.
◦ Fats- 30-35% of total caloric intake is recommended. Fats should be used in
the form of polyunsaturated fatty acid (PUFA) for cooking.
◦ Alcohol- Alcohol is prohibited if a person is obese, hypertensive and
hyperlipidaemic.

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◦ Salts & Sweetening Agents- Normal salt intake of 6.0g daily is allowed to
diabetics. It is reduced to half if the diabetic is hypertensive also. Saccharin
and sucramate, non-nutririve sweeteners are allowed.
B. EXERCISE
o Physical activity promotes weight reduction and improves insulin sensitivity, thus
lowering blood glucose levels.
o Together with dietary treatment, a programme of regular physical activity and
exercise should be considered for each person. Such a programme must be tailored to
the individual’s health status and fitness.

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C. ORAL HYPOGLYCEMIC AGENTS
o Oral hypoglycemics are the drugs which, when administered orally bring down the
blood glucose.
o Usually, these drugs are used in patients of type II diabetes (NIDDM) who do not
respond to dietary management and who would otherwise require treatment with
insulin; in later situation, they are used adjuvant to insulin in obese patients.
o These drugs require presence of insulin secreting beta cells for their action and that is
the reason why they are not effective in type I diabetes.
[SOURCE: Sembulingam K. Sembulingam P. Essentials Of Medical Physiology.5th
ed.2004,]
SIDE EFFECTS OF ORAL HYPOGLYCEMIC AGENTS:
 Sulfonylureas: low blood sugar, upset stomach, skin rash or itching, weight gain
 Biguanides/Metformin: sickness with alcohol, kidney complications, upset stomach,
tiredness or dizziness, metal taste
 Alpha-glucosidase inhibitors: gas, bloating and diarrhoea

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 Thiazolidinediones: weight gain, risk of liver disease, anaemia risk, swelling of legs
or ankles,
 Meglitinides: weight gain, low blood sugar
D. INSULIN THERAPY
o Type 1 diabetes is dependent on insulin for survival.
o Insulin is classified by source or duration of action.
o Human insulin has less allergy or lipoatrophy.
o More than one injection is needed and different types.
INSULIN DELIVERY DEVICES:
i. Syringe
ii. Pump
iii. Pen device
Though the pen device has advantages like it is easy and convineant to use and also has a
psycologic benefit to patients with needle phobias but it also has disadvantages. Zinc insulins
cannot be used coz they aggregate on the pen catridges and also pens produced by one
manufacturer cannot be used with the insulin produced by another.

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WHERE TO GIVE INSULIN: ON TARGET!
SIDE-EFFECTS OF INSULIN THERAPY:
• Hypoglycaemia
- The Somogyi effect: refers to rebound hyperglycaemia following an episode of
hypoglycaemia due to counter-regulatory hormone release.
- The Dawn phenomenon: refers to an early morning hyperglycaemia requiring
increased amount of insulin to achieve normoglycaemia.
INSULIN PEN DEVICE
o Injections are given at
90⁰ into subcutaneous
tissue
o The injection site must be
changed regularly
o Common sites:
abdomen, thigh
buttocks, upper arms

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• Lipodystrophy: Small dent or lump formed on the skin due to repeated injection at
the same site.
• Allergic Reactions: might be caused due to IgE antibodies
to insulin. It includes itching, swelling, redness at the site
of injection.
• Weight gain
ADVANCES IN DIABETES MELLITUS
1) MONITORING
a) Pain Free Glucose Test: Uses a unique disposable test strip to obtain blood samples
from the forearm, thigh or upper arm, areas that have fewer nerve endings so it doesn't
hurt as much as a finger stick.
b) Continuous Monitoring Device: The GlucoWatch Biographer extracts fluid through
the skin by sending out tiny electric currents. The watch may be worn for 12
consecutive hours, producing 3 measurements every hour, even while asleep.

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2) INSULIN DELIVERY
a) Implantable Insulin Pumps: Implantable capsule that continuously produces insulin
and releases it to the bloodstream. It contains insulin-secreting cells that borrow
nutrients from the body to keep producing insulin indefinitely.
b) Insulin Inhalers: These inhalers are about the size of a flashlight and uses rapid-
acting insulin. The sprayed insulin is inhaled into the mouth and coats the mouth,
throat and tongue. The insulin passes quickly into the bloodstream.
c) Insulin Pill: A new polymer has been discovered that may allow development of an
effective insulin pill. When the polymer is used as a pill coating, it allows insulin to
get into the bloodstream without being destroyed by the digestive system.

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d) New Insulin: Three new formulations of insulin have become available derived from
recombinant DNA technology. They are:
 Glargine
 Aspart
 A 75/25 lispro mixture
3) NEW TREATMENT MODALITIES
a) Islet Cell Transplant: The Edmonton technique uses islet cells (cells from the
pancreas) from two or more donor pancreases. The cells are transplanted into a person
with diabetes and then special medications are given to prevent rejection of the new
cells.
b) Gene Therapy: Researchers have developed ways of using the three genes to
encourage insulin production in cells that don't normally make insulin. Beta-cell-
specific insulin gene transcription factor RIPE3b1, SHIP2 and INGAP (Islet
Neogenesis Associated Protein). They believe it is the third and last gene that
regulates insulin production.
c) Artificial Pancreas= insulin pump+ continuous glucose monitoring:
 Closed loop system
 Data from continuous glucose monitoring blood glucose reading every few minutes.

30. 30
 Sensor is connected via wire to the insulin pump
 Blood glucose variation is signalling to the pump how much insulin to deliver.
d) Herbal Medication for Type II Diabetes Mellitus
 The Council for Scientific and Industrial Research (CSIR) launched its ayurvedic
antidiabetic drug BGR34 in 2016.
 Aimed at managing type 2 diabetes, BGR34 has been jointly developed by National
Botanical Research Institute (NBRI) and Central Institute for Medicinal and Aromatic
Plants (CIMAP).
 The modern diabetes drugs are known for side effects and toxicity while BGR34
works by controlling blood sugar and limiting the harmful effects of other drugs.
e) Other Alternative Therapies for Type II Diabetes Mellitus
 Ginseng
 Bitter gourd or karela
 Fenugreek
 Garlic and onions
 Ginger

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 Aloe vera
 Minerals like chromium, magnesium, vanadium
 Physical Interventions: Acupuncture and Hydrotherapy
DENTAL ASPECTS OF DIABETES MELLITUS
1. EFFECTS ON ORAL MUCOSA
a) Burning mouth syndrome
b) Oral Candidiasis
c) More risks of laceration
d) Delayed wound healing
e) Increased incidence of infections
a) Burning Mouth Syndrome: Neuropathy of the autonomic system cause changes in
salivary secretion since salivary flow is controlled by the sympathetic and
parasympathetic pathways. Dry mucosal surfaces are easily irritated and are
associated with “burning mouth” syndrome.
b) Oral Candidiasis: This also provides a favorable environment for the growth of
fungal organisms. Other reasons for an association between DM & Candidiasis :
-increased genetic susceptibility
-altered immune response
- a change in oral environment.

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c) More Risks of Laceration: As tissue tolerance is reduced, collagen metabolism is
altered, thus more risks of lacerations with slight manipulation.
d) Delayed Wound Healing: Increase in glucose content and altered immunity causes
delayed wound healing.
e) Infections: Increased incidence of infection due to an abnormal neutrophil function,
microangiopathy, altered microflora.
2. EFFECTS ON TONGUE
a) Median rhomboid glossitis: due to impairment of blood supply to dorsum of the
tongue due to atherosclerotic changes in blood vessels supplying that area;
b) atrophy of lingual papillae,
c) dry tongue,
d) fissured tongue and
e) altered taste sensation
3. EFFECTS ON PAROTID GLAND
a) Diffuse enlargement
b) decreasing the salivary flow.
4. EFFECTS ON LIPS
a) Dry lips
b) angular cheilitis
5. EFFECTS ON HARD TISSUE
a) Due to excessive fluid loss and decreased salivary flow, the detergent action of saliva
is reduced, thereby increasing caries susceptibility.
b) Increase in glucose in GCF increases root caries.

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6. EFFECTS ON GINGIVAL & PERIODONTAL TISSUES
a) Rapid progressive periodontitis with periodontal abscess formation and tooth mobility
b) Alveolar bone loss
c) Delayed wound healing
d) Bleeding on slight probing
7. RECURRENT ABSCESS FORMATION
 Classically periodontitis in diabetics is associated with recurrent abscess formation
and suppuration
 This pattern is consistent with increased neutrophil influx into and through the pocket
which leads to suppuration and if blocked to microabcess formation
 There is naturally concentration gradient of IL-8 produced by keratinocytes in the
sulcular and junctional epithelium.

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DENTAL MANAGEMENT OF A DIABETIC PATIENT
Medical History
 The hypoglycemic action of sulfonylureas may be potentiated by drugs that are highly
protein-bound, such as salicylates, dicumerol, β-adrenergic blockers, monoamine
oxidase inhibitors, sulfonamides and ACE inhibitors.
 Epinephrine, corticosteroids, thiazides, oral contraceptives, phenytoin, thyroid
products and calcium channel–blocking drugs have hyperglycemic effects.
Scheduling of Visits
 In general, morning appointments are advisable
 For patients receiving insulin therapy, appointments should be scheduled so that they
do not coincide with peaks of insulin activity, since that is the period of maximal risk
of developing hypoglycemia.
Diet
 It is important for clinicians to ensure that the patient has eaten normally and taken
medications as usual.
Blood Glucose Monitoring
 This can be done using commercially available electronic blood glucose monitors,
which are relatively inexpensive and have a high degree of accuracy.
During Treatment
 The most common complication of DM therapy that can occur in the dental office is a
HYPOGLYCEMIC EPISODE.
 Initial signs and symptoms include mood changes, decreased spontaneity, hunger and
weakness. These may be followed by sweating, incoherence and tachycardia. If
untreated, possible consequences include unconsciousness, hypotension, hypothermia,
seizures, coma and death.

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After Treatment
 Salicylates increase insulin secretion and sensitivity and can potentiate the effects of
sulfonylureas, resulting in hypoglycemia.
 Therefore, Aspirin and Aspirin containing compounds generally should be avoided
for patients with DM
Dental managementduring surgicalprocedures
 Physicians’ advice should be taken priorly.
 Antibiotic prophylaxis should be given before the surgery.
 Local anaesthesia should have low content of epinephrine.
 After extraction, suturing of socket is done to aid hemostasis.
 Postoperatively, 5% glucose infusion with 10-12 units of insulin maybe started with
20mmol of potassium.
 Physicians’ advice to be taken before GA.
Managementof diabetic pediatric patient
 Comprehensive medical history along with screening tests are essential.
 Appointment should be short and in the morning.
 Atraumatic procedures are preferred.
 Vital pulp therapy should be preferred to stressed extraction.
 During orthodontic treatment, preference should be given to maintenance of oral
health.
Managementof diabetic prosthetic patient
 In case of complete denture patient:
 Minimal pressure techniques are preferred during impression.
 Frequent check-ups to assess bone loss.
 Frequent relining and rebasing of denture is required.
 In case of implant placement, success is questionable if glucose level is not
maintained properly.

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PUBLIC HEALTH SIGNIFICANCE
Diabetes Mellitus is a disease of increasing public health importance.
The general public know little about diabetes and there is need for more enlightenment as
part of a campaign for the primary and secondary prevention of the disease and its
complications.
Local health authorities have a role to play in this public education, as part of a
comprehensive scheme for the prevention of diabetes and for the care and after-care of
sufferers from that disease.
CONCLUSION
The intimate relationship between oral health and systemic health in individuals with diabetes
suggests a need for increased interaction between the dental and medical professionals who
are charged with the management of these patients.
Dental professionals with a thorough understanding of current medical treatment regimens
and the implications of diabetes on dental care are able to help their diabetic patients achieve
and maintain the best possible oral health.

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