diabetes mellitus / dental implant courses by indian dental academy

INDIAN DENTAL ACADEMY

Leader in Continuing Dental Education

Seminar on

www.indiandentalacademy.com

Learning objective

At the end of the session the learners should be able

to-

Describe regulation of blood sugar level

Describe classification of diabetes mellitus

Enlist diagnostic criteria's for diabetes mellitus

Discuss various treatment modalities of diabetes mellitus

Describe oral manifestations and dental consideration of

diabetes mellitus


Contents: Hormones of Pancreas

Introduction

Insulin

Glucagon

Somatostatin

Pancreatic polypeptide

Regulation of blood sugar level

Hyperinsulinism

Diabetes mellitus

Types of diabetes mellitus

Signs & Symptoms

Investigations

Oral manifestation & Dental consideration www.indiandentalacademy.com

Introduction

Endocrine function of pancreas is performed by islets of

langerhans. There are about 1 to 2 million islets in human

pancreas.

Four types of cells in islets of langerhans are-

1) A or alpha cells secrete glucagon

2) B or beta cells secrete insulin

3) D or delta cells secrete somatostatin

4) F or PP cells secrete pancreatic polypeptide


Insulin

Secreted by B cells in islets of langerhans of pancreas

Actions:-

1) Effect on carbohydrate metabolism-

Only Antidiabetic hormone secreted in the body decreases

the blood sugar level by-

a) Transport & uptake of glucose

b) Peripheral utilization of glucose

c) Storage of glucose

d) Inhibition of glucogenolysis

e) Inhibition of gluconeogenesiswww.indiandentalacademy.com

2) Effect of protein metabolism-

Insulin causes synthesis and storage of protein & decreases

peripheral utilization of proteins by-

a) Increasing permeability of cell membrane for amino acids

b) Increasing synthesis of proteins by influencing

transcription of DNA and increasing translation of mRNA.

c) Decreases catabolism of protein

d) Increases gluconeogenesis

3) Effect on fat metabolism

Insulin causes synthesis, storage and transport of fat in

adipose tissue.

Synthesis of fatty acids & triglycerides-

Insulin causes transport of into liver cells, excess of glucose

is utilized for synthesis of fatty acid and triglyceride.www.indiandentalacademy.com

Promotes synthesis of lipids-

a) Conversion of glucose into fatty acid

b) Conversion of fatty acids into triglycerides

Transport of fatty acids-

Facilitates transport of fatty acid into adipose tissue

Storage of fat-

Promote storage by inhibiting the enzyme which degrade

triglycerides.

4) Effect on growth

Promotes growth by anabolism of proteins


Regulation of insulin secretion

1) Effect of blood glucose level on insulin secretion

Biphasic effect

Initially when meal is taken glucose level is increased after

taking a meal, the release of insulin in blood is rapidly

increased.

Within few minutes concentration of insulin in plasma is

increased up to 90uU/ml from the basal level to 10uU/ml.

Afterwads within 10 to 15 mins the insulin concentration in

blood is reduced to half the value(40-50uU/ml).

After 15 to 20 mins, the insulin secretion rises once again.

This time it rises slowly but steadily. It reaches maximum

between 2 and 21/2 hours.

The prolonged increase in insulin release is due to the

newly formed insulin from pancreas.www.indiandentalacademy.com

2) Effects of proteins on insulin secretion

Excess of amino acid causes increase in insulin secretion.

Amino acids potentiate the action of glucose on insulin

secretion, so that in presence of amino acids, the increase

in blood glucose level causes increase in level of insulin.

3) Effect of lipid derivatives on insulin secretion-

Beta ketoacids such as acetoacetate also increases insulin

secretion.

4) Effect of GIT hormones:-

Increase in insulin secretion causes secretion of GI

hormones like secretin, gastrin & cholocystokinin.


5) Effect of other endocrine hormones

Glucagon, growth hormone and cortisol cause increase in

insulin secretion by potentating the action of increase blood

glucose level on beta cell.

6) Effect on autonomic nerves

Stimulation of parasympathetic nerve to pancreas causes

increase secretion of insulin chemical transmitter involved in

acetylcholine stimulation to sympathetic causes decrease in

insulin secretion & neurotransmitter is noradrenalin.


Glucagon

Actions- Antagonist of insulin

1) Effect on carbohydrate metabolism

Increase blood sugar level by-

a) Increases glycogenolysis (breakdown of glycogen into

glucose)

b) Increases gluconeogenesis (formation of glucose from

proteins)

2) Effect on lipid metabolism

Glucagon has lipolytic &ketogenic actions, it increase

release of free fatty acids from adipose tissue and makes

free fatty acid available for peripheral utilization.www.indiandentalacademy.com

3) Effect on protein metabolism

Increases gluconeogenesis (formation of glucose from

proteins) in liver.

4) Other actions of glucagon

i) Increases secretion of bile

ii)Decreases secretion of gastric juice


Regulation of glucagon secretion

1) Effect of blood glucose level on glucagon secretion

Hypoglycaemia decrease blood sugar level

alpha cells of islets are stimulated

more glucagon is released

2) Effect of amino acid level on glucagon

Increase in amino acids causes increases glucagon which

further converts amino acids into glucose and thus increase

blood sugar level.

3) Effect of other factors on glucagon secretion

Factors that increase glucagon secretion are stress, gastrin,

choleocystokinin & cholestrol.

Somatostatin, insulin, free fatty acids & ketones inhibit secretion

of glucagon.


Somatostatin

It has 3 sources of secretion

i) Hypothalamus

ii) D cells of islets of langerhans

iii) D cells in stomach and upper part of small intestine

Actions:-

1) Acts within islets of langerhans and inhibits alpha and

beta cells and thus inhibit secretion of insulin and

glucagon.

2) It decreases motility of stomach, duodenum & gall

bladder

3) Hypothalamic stomatostatin inhibits secretion of anterior

pituitary and also known as growth hormone inhibitory

hormone(GHIH)www.indiandentalacademy.com

Regulation of secretion

Secretion of pancreatic stomatostatin is increased by

glucose, amino acids & cholecystokinin.

Tumor of D cells of islets of langerhans causes

hypersecretion of somatostatin which causes

hyperglycaemia and other symptoms of Diabetis mellitus


Pancreatic Polypeptide

Secreted by F cells or PP cells in islets of langerhans.

Action:-

It is believed to increase secretion of glucagon from the alpha

cells of langerhans.

Regulation of secretion:-

Secretion is stimulated by the presence of chyme containing

more proteins in small intestine.


Regulation of Blood sugar level

Normal blood sugar

Early morning blood sugar level is 80-90 mg/dl of blood.

Between first and second hour after meals it becomes 120-

140mg/dl

After second hour of meals it is brought to normal.

The blood sugar regulating mechanism is operated through

liver and also through muscles by the influence of

pancreatic hormones insulin and glucagon.

Hormones which increase blood sugar level are known as

antiinsulin or diabetogenic hormone.


Why regulation of Blood glucose level

necessary ???

It is important because glucose is the

only nutrient that can be utilized by

the tissues of brain, retina and

germinal epithelium of gonads


Liver acts as an important glucose buffer system.

Role of liver in regulation of blood sugar level


Role of insulin in maintainance of

blood sugar level

Decrease blood sugar level

Transport &uptake of

glucose

Peripheral utilization of

glucose

Storage of glucose

(glycogenesis)Inhibition of

glycogenolysis

Inhibition of

gluconeogenesis


Role of glucagon in maintenance of

blood sugar level


Role of other hormones in maintenance of

blood sugar level

1) Growth hormone- Increase blood sugar level by

a) Decrease peripheral utilization of glucose for production of

energy.

b) Increase deposition of glycogen in the cells

c) Decrease in uptake of glucose by the cells

d) Diabetogenic effect of GH

2) Cortisol- Increase blood sugar level by-

a) Increase the gluconeogenesis in liver from amino acids.

b) Decrease the glucose uptake by the peripheral cells &

utilization of glucose.


3) Adrenaline

Increases blood sugar level by increasing glycogenolysis in

liver & muscle, so large quantity of glucose enter cell.

4) Thyroxine

Increase blood sugar level by

a) Increase absorption of glucose from the GIT tract.

b) Increase the breakdown of glycogen into glucose.

c) Increase gluconeogenesis


Hyperinsulinism

The excessive secretion of insulin from pancreas is called

hyperinsulinism.

Cause

It occurs due to tumor of beta cells in the islets of langerhans.

Signs & Symptoms

1) Hypoglycaemia : blood sugar level falls below 50 mg/dl

2) Manifestation of CNS: It occurs when the blood sugar

level falls down. All the manifestation are together called

neuroglycopenic symptoms.

Initially, the activity of neurons is increased leading to

nervousness, tremor all over the body and excessive

sweating. If not treated it leads to clonic convulsions and

unconsciousness. Slowly, the convulsions cease and

coma occurs due to damage of neurons.www.indiandentalacademy.com

Diabetes mellitus

Diabetes is a group of metabolic diseases characterized by

hyperglycemia resulting from defects in insulin secretion,

insulin action, or both.

The chronic hyperglycemia of diabetes is associated with

long-term damage, dysfunction, and failure of different

organs, especially the eyes, kidneys, nerves, heart, and

blood vessels.


Diabetes has been classified by National

Diabetes Data Group

Classification of Diabetes and other categories of glucose

intolerance

Idiopathic diabetes mellitus

Insulin dependent type(type 1)

Noninsulin dependent type(type 2)

Nonobese

Obese

Impaired glucose tolerance

Gestational diabetes

Previous abnormality of glucose intolerance

Potential abnormality of glucose tolerance

Glucose intolerance associated with certain conditionswww.indiandentalacademy.com

Etiologic classification of Diabetes mellitus by the

American Diabetes Association (1997)

Type 1 diabetes mellitus beta cell destruction usually

leading to absolute insulin deficiency

Immune mediated

Idiopathic

Type 2 Diabetes mellitus insulin resistance with relative

insulin deficiency


Other specific types of Heterogeneous group in which etiology

diabetes mellitus is established or partially known

Genetic defect of beta cell function

Genetic defect in insulin action

Diseases of exocrine pancreas

Endocrinopathies

Drugs or chemical induced

Infections

Uncommon forms of immune mediated

diabetes

Other genetic syndromes sometimes

associated with diabetes

Gestational Diabetes Any degree of glucose intolerance with

mellitus onset or first recognition during

pregnancywww.indiandentalacademy.com

Type 1 diabetes mellitus

It is characterized by idiopathic autoimmune destruction of

pancreatic beta cells, usually leading to absolute insulin

deficency.

Type 1 DM occurs before the age of 25 yrs in 95% of

affected persons, it may occur at any age & affects both

sex equally. The risk of developing type 1 DM is increased

by a family history of type 1 DM gluten enteropathy or

endocrine disease.www.indiandentalacademy.com

There are two distinct subclasses of type 1 DM.

The immune-mediated form of type 1 DM is chronic disease

with a subclinical prodromal period characterized by cellular-

mediated autoimmune destruction of the insulin-producing

beta cells in pancreatic islets.

This may be triggered by an environmental event such as

viral infection but may be associated with autoimmune

diseases such as Hashimoto’s thyroditis, Addison’s disease,

vitiligo or pernicious anemia.


The risk of type 1 DM is reflected by high risk of human

leukocyte antigen (HLA) alleles among ethinic groups in

different geographic location

Patient with type 1 diabetes are highly susceptible to

diabetic ketoacidosis.

The accumulation of ketones in the body fluids, decreased

pH, electrolyte loss and dehydration from excessive

urination, and alteration in bicarbonate buffer system result

in diabetic ketoacidosis. Untreated patients can result in

coma and death.


Type 2 DM Is more common type, comprising 90 to 95% of DM cases.

It is characterized by insulin resistance in peripheral tissue

and defective insulin secretion by the pancreatic beta cells.

The etiology of type 2 DM is multifactorial, including genetic

predilection, advancing age, obesity and lack of exercise.

The underlying pathophysiologic defect in type 2 DM does

not involve autoimmune beta cell destruction but

characterized by the following three disorders:

1) peripheral resistance to insulin, especially in muscle cells;

2) increased production of glucose by the liver

3) insulin secretory defect of the beta cell www.indiandentalacademy.com

Increased tissue resistance to insulin generally occurs first,

followed by impaired insulin secretion.The pancreas produce

insulin, yet insulin resistance prevents its proper use at

cellular level.Glucose cannot enter target cells and

accumulates in the bloodstream resulting in hyperglycaemia.

Risk factors include advancing age, obesity, high caloric

intake, sedentary life style. People with impaired glucose

tolerance, impaired fasting glucose and gestational DM have

high risk of developing type 2 in the future, these conditions

are considered preclinical stages of type 2.

Hyperosmolar Nonketotic Acidosis


Other specific types

These are relatively uncommon. Possible causes include genetic defects of beta-cell function or insulin action, diseases of the exocrine pancreas, endocrinopathies, drug or chemical use, infections and certain genetic syndromes.

Excess amounts of cortisol, glucagon, epinephrine and growth hormone can cause DM in people with pre-existing defects in insulin secretion.

Drugs such as glucocorticoids, thiazides, dilantin and interferon-α can impair insulin secretion.

Certain viruses, have also been associated with beta cell destruction.


Gestational DM

It includes development of type 1 DM or discovery of

undiagnosed type 2 during pregnancy.

It does not include women with DM before pregnancy which

is referred to as pregestational diabetes mellitus.

Pathophysiology of gestational DM is associated with

increased insulin resistance. High incidence of gestational

DM is found in older women, overweight, women of minority

ethnic age group.


Most patients gestational DM return to normoglycemic state

after parturition however, about 30 to 50% of women with a

history of gestational DM will develop type 2 DM within 10

years.

It usually develops during the third trimester and significantly

increases perinatal morbidity and mortality.

The proper diagnosis and management of gestational

diabetes improves pregnancy outcomes.


Signs and Symptoms of Diabetes mellitus

The various manifestations of diabetes mellitus are developed

due to three major setbacks of insulin deficiency.

i. Increased blood sugar level due to reduced utilization by

the tissue

ii. Mobilization of fats from the adipose tissue for energy

purpose, leading to elevated fatty acid content in blood. T

iii. Depletion of proteins from the tissues


1. Loss of glucose in urine

When the blood glucose level rises above 180mg/dl, glucose

appears in urine. This is the renal threshold level for glucose.

This appearance of glucose in urine is called glucosuria

2. Osmotic diuresis

The excess of glucose in the renal tubules develops osmotic

effects. This osmotic effect causes reduction in the

reabsorption of water in the renal tubules. So, diuresis

occurs. And this type of diuresis called osmotic diuresis.

3. Polyuria

The increased urinary output is called polyuria. This is due to

osmotic diuresis caused by increased blood sugar level.

Following are the various features of diabetes melliutus


4. Polydypsia

The increased water intake is called polydipsia. The

excessive loss of water causes stimulation of thirst center

in hypothalamus.

5. Polyphagia

Polyphagia means excessive intake of food. This is very

common in diabetes mellitus.

6. Asthenia

The loss of strength is called asthenia. The body becomes

very weak. There is loss of weight and energy. This is

because of lack of insulin. Which causes decrease in

protein synthesis and increase in protein breakdown.


7. Acidosis

In severe cases acetone is expired in the expiratory air,

giving the characteristic smell and this is known as acetone

breathing.

8. Kussmaul’s breathing

Because of acidosis rate and depth of breathing and depth

of respiration are increased. This is known as Kussmaul ‘s

breathing. This occurs in severe conditions.

9. Circulatory Shock

The osmotic diuresis leads to dehydration, which causes

circulatory shock.


10. Coma

Due to Kussmaul breathing excessive carbon dioxide is lost

in expiration. This leads to drastic reduction in the

concentration of bicarbonate causing severe acidosis and

coma. It occurs in severe cases of diabetes mellitus.

Sometimes, the increased plasma levels of glucose results

in coma by developing hyperosmolarity of plasma. This is

called hyperosmolar coma.


Chronic diabetes is associated with some other conditions

which are mentioned below-

1. Degenerative changes in retina- diabetic retinopathy

2. Renal disease- diabetic nephropathy

3. Loss of function of autonomic and peripheral nerves-

diabetic neuropathy


Diagnosis

Criteria for diagnosis of diabetes are, in adults,

1. Unequivocal elevation of plasma glucose concentration

(greater than 140mg/dl) together with clinical symptoms

of diabetes., or

2. Elevated fasting plasma glucose concentration(greater

than 140 mg/dl ) on more than one occasion, or

3. Elevated plasma glucose concentration (greater than 200

mg/dl) 2 hours after a 75-g oral glucose challenge on

more than one occasion.

Diagnosis of diabetes in children requires either 1 or 2

described above and 3.


Urine Sugars

Urine sugars are often misused in diagnosis of diabetes and

are both insensitive and nonspecific.

If test for urinary glucose is not a glucose oxidase test and

therefore not specific for glucose, the presence of other

reducing sugars in urine such as lactose in lactating mother

may also give a false positive result.

False negatives can occur in early diabetes when patient

has only transient glucosuria, which when diluted with

normal urine gives a negative test or conversely, with

advanced diabetic nephropathy

wherein the renal threshold for

glucose is markedly elevated.


Blood glucose there is controversy as to whether a blood

test for glucose should be performed in fasting state or in

postprandial state.

The fasting plasma glucose is a more specific test in that

patients who have significantly elevated fasting plasma

glucose levels with no other cause almost always turn out to

be diabetic; however to meet diagnostic criteria, an

elevation of plasma glucose greater than 140mg/dl must be

demonstrated on more than one occasion.

Blood glucose


On the other hand, a 2- hour postprandial determination

of the plasma glucose is more sensitive test, because some

diabetics who have normal fasting glucose levels early in

disease will exhibit hyperglycaemia only when challenged

with an oral glucose load.


Glucose tolerance test

The test should be performed in the morning after at least

3 days of unrestricted diet containing usual amount of

carbohydrates and normal physical activity.

The patient should fast for 10 to16 hours before the test is

performed. A standardized oral 75g dose of glucose is

given, and the plasma glucose is measured at the

beginning and at 30 minutes intervals for up to 2 hours.

The test is interpreted as positive if the 2 hour level and

any other sample taken between time 0 and 2 hours is

equal to or greater than 200 mg/dl.


Haemoglobin A1c levels

Haemoglobin A1c is a postsynthesis modification of

haemoglobin molecule produce by an addition of glucose

molecule to the N-terminus of the beta chain of Hb A.

It is synthesized at constant rate throughout the life span.

It is a useful index of control of hyperglycaemia and blood

glucose levels during the 2-3 months immediately prior to

measurement.

Normal level is 5.5% and in diabetes it generally runs

higher averaging 7% to 10%.

It is particularly useful in the latter instance in that it gives

a long term, chronic measurement of blood glucose levels.


Medical Management

Primary treatment goals for DM are achieving blood glucose

level that are close to normal as possible and prevention of

diabetic complications.

Other goals are normal body weight, avoidance of sustained

hyperglycaemia or symptomatic hypoglycaemia, the

prevention of diabetic ketoacidosis and nonketotic acidosis

and immediate detection and treatment of long term diabetic

complications.

Diet, exercise and weight control and medications are

mainstay of diabetic care. Weight reduction and exercise

improve tissue sensitivity to insulin and allow its proper use

by target tissue.www.indiandentalacademy.com

Diet, exercise and weight control and medications are

mainstay of diabetic care. Weight reduction and exercise

improve tissue sensitivity to insulin and allow its proper use

by target tissue.

The primary medication in type 1 DM is insulin, on which

patients are dependent on survival. Type 2 patients take

oral medications although many use insulin to improve

glycemic control.


All patients with type 1 DM use exogenous insulin, as do

many with type 2 DM. Insulin is taken via subcutaneous

injection, most often with a syringe. Insulin infusion pumps

deliver insulin through a subcutaneous catheter.

Ideally, use of insulin provides an insulin profile similar to

that seen in a nondiabetic individual, with a continuous

basal level of insulin availability following each meal.


Diabetic Care Management Guidelines

American Diabetes Association, Clinical

Practice Recommendations, 2011

The physician should evaluate blood glucose

control and disease complications. The patient with

diabetes (type 1 or 2) should have the following:-


An annual retinal eye exam.

Glycemic control: The A1C goal for patients in general is an

A1C goal of <7%. A Hemoglobin A1C (HbA1c) test two times

a year if stable glycemic control; quarterly in patients whose

therapy has changed or who are not meeting glycemic goals.

An annual LDL screening performed, with a goal of

<100mg/dl as the primary goal of therapy for adults. Very

high-risk patients, LDL <70mg/dl.

Nephropathy screening should be performed annually to test

for the presence of microalbuminuria in type 1 diabetic

patients with diabetes duration of 5 years and in all type 2

diabetic patients, starting at diagnosis and during pregnancy.www.indiandentalacademy.com

Periodontal Diseases

The mechanism by which hyperglycaemia can induce

periodontal destruction is not yet fully understood.

However, there are many theories which propose factors

such as advanced glycation end products, changes in

collagen statue, and altered immune function that causes

impaired polymorphonuclear leukocyte function which may

facilitate bacterial persistence in the tissue.

The increase in collagenase activity together with the

reduction in collagen synthesis will adversely influence

collagen metabolism.


Effect of diabetes on the periodontium:-

1) Greater loss of attachment.

2) Increased bleeding on probing.

3) Increased tooth mobility.

4) Insulin dependent diabetic children tend to have more

destruction around the first molars and incisors.

5) Increased bone loss and retardation of post surgical

healing of periodontal tissues seen.

6) Frequent periodontal abscess is another feature of

diabetes.

7) Type 2 patients have sub gingival flora composed mainly

of anaerobic organisms.

8) Increased susceptibility to infection is seen in these

patients due to leukocyte deficiencies.


Salivary Dysfunction

Symptoms of reduced salivary flow rate and xerstomia were

more frequently reported by patients with diabetes than the

controls, especially by those diabetics who had developed

neuropathy.

An increase in salivary pathogens was also reported in

these patients. The constant dryness of the mouth would

irritate the oral soft tissues, which in turn will cause

inflammation and pain.

Patients with diabetes with xerostomia are more

predisposed to periodontal infection and tooth decay.


It is known that diabetes mellitus is associated with chronic

complications such as neuropathy, microvascular

abnormalities and endothelial dysfunction that lead to

deterioration of microcirculation and this may play a role in

reduction of the salivary flow rate and composition.


Taste Dysfunction

Salivary dysfunction can contribute to altered taste

sensation or elevation of detection thresholds.

Taste dysfunction has been reported to occur more

frequently in patients with poorly controlled diabetes

compared to healthy controls.

Diabetic patients who suffer from neuropathy have a

higher taste threshold.


Oral Infection

Fungal Infection Candidal infection is reported to be more prevalent in

patients with diabetes especially in those patients who

smoke, wear dentures,have poor glycaemic control and use

steroids and broad spectrum antibiotics.

In addition, salivary dysfunction in patients with diabetes can

also contribute to higher carriage of fungi in this group.

Both local and systemic predisposing factors might increase

candidal carriage rate and hence increase the risk of oral

candidal infection in patients with diabetes.


Bacterial infections

Patients with diabetes are more susceptible to developing

oral bacterial infections.

They are well known to have an impaired defense

mechanism hence considered to be immuno-compromised.

Diabetics with diabetic complications and poor metabolic

control are more prone to spreading and recurrent bacterial

infection.


Poor Oral Wound Healing

Poor soft tissue regeneration and delayed osseous healing

in patients with diabetes are known complications during

oral surgery.

Therefore, the management and treatment of patients with

diabetes undergoing oral surgery is more complex.

It was reported that delayed vascularisation, reduced blood

flow, a decline in innate immunity, decreased growth factor

production, and psychological stress may be involved in the

protracted wound healing of the oral cavity mucosa in

patients with diabetes.


Non-Candidal Oral Soft Tissue Lesion

Oral lesions that are not caused by candidal infection

have been reported to occur in patients with diabetes

such as fissured tongue, irritation fibroma and traumatic

ulcer.


Oral Mucosal Disease

Both lichen planus and recurrent apthous stomatitis have

been reported to occur in patients with diabetes.

OLP is reported to occur more frequently in patients with

type1 diabetes compared to type 2 diabetes.


Neuro-Sensory Oral Disorder

Oral dysesthesia or burning mouth syndrome (BMS) is a

painful condition affecting the oral cavity (palate, tongue,

throat and gingivae).

Other abnormal oral sensations may co-exist with the

burning mouth sensation such as tingling, numbness,

dryness or sore mouth at the same time.

The exact cause of Diabetic neuropathy could be the

underlying cause of BMS in patients with diabetes. Therefore, it is crucial to screen patients who have

symptoms of BMS for diabetes mellitus.www.indiandentalacademy.com

Dental caries and tooth loss

It is well known that patients with diabetes are susceptible to

oral infections that lead to tooth decay and loss.

Salivary secretion dysfunction, periodontal and sensory

disorders could increase the likelihood of developing new

and recurrent dental caries and tooth loss. The relationship

between diabetes and development of dental caries is still

unclear.

It is well-known that the cleansing and buffering capacity of

the saliva is diminished in patients with diabetes mellitus

resulting in increased incidence of dental caries, especially

in those patients who suffer from xerostomia.www.indiandentalacademy.com

Median rhomboid glossitis

Median rhomboid glossitis, which is a well demarcated,

central, nonulcerated, smooth pink/red area on the middle

third of the dorsum of the tongue, is often associated with

diabetes.


Dry socket (alveolar osteitis) Atherosclerosis is known in diabetes mellitus, so

microvascular changes are seen in alveolar bone bone in

oral cavity.

So the normal blood supply gets hamperred which may

sometimes be precipitated by traumatic extraction and using

LA with epinephrine which again leads to increased risk of

localized osteitis after extraction of tooth.


Dental management

To minimize the risk of an intraoperative emergency,

clinicians need to consider a number of management

issues before initiating dental treatment.

Medical history

It is important for clinicians to take a good medical history

and assess glycemic control at the initial appointment.

They should ask patients about recent blood glucose levels

and frequency of hypoglycemic episodes.

Antidiabetic medications, dosages and times of

administration should be determined. A variety of other

concomitantly prescribed medications may alter glucose

control through interference with insulin or carbohydrate

metabolism. www.indiandentalacademy.com

The hypoglycemic action of sulfonylureas may be

potentiated by drugs that are highly protein-bound, such as

salicylates, dicumerol, β-adrenergic blockers, sulfonamides

and angiotensin converting enzyme inhibitors.

Epinephrine, corticosteroids, thiazides, oral contraceptives,

phenytoin, thyroid products and calcium channel–blocking

drugs have hyperglycemic effects.

Any complications of DM, such as cardiovascular or renal

disease, will have their own effects on dental treatment

planning. If necessary, the dentist should consult with the

patient’s physician.


Scheduling of visits.

In general, morning appointments are advisable since

endogenous cortisol levels are generally higher at this time.

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.

If the patient skips breakfast owing to the dental appointment

but still takes the normal dose of insulin, the risk of a

hypoglycemic episode is increased.

For certain procedures (for example, conscious sedation),

the dentist may request that the patient alter his or her

normal diet before the procedure. In such cases, the

medication dose may need to be modified in consultation

with the patient’s physician.www.indiandentalacademy.com

Depending on the patient’s medical history, medication

regimen and procedure to be performed, dentists may

need to measure the blood glucose level before beginning

a procedure. This can be done using commercially

available electronic blood glucose monitors, which are

relatively inexpensive and have a high degree of accuracy.

Patients with low plasma glucose levels (< 70 mg/dL for

most people) should be given an oral carbohydrate before

treatment to minimize the risk of a hypoglycemic event.

Clinicians should refer patients with significantly elevated

blood glucose levels for medical consultation before

performing elective dental procedures.

Blood glucose monitoring


Specific management guidelines

Use of epinephrine: is not contraindicated in these patients

because it helps to promote better dental anesthesia and

significantly lowers the amounts of endogenous epinephrine

release in response to stress.

Oral candiasis: oral fungal infections can signify

uncontrolled DM and can manifest in presence of salivary

hypofunction.

Management of Recurrent Herpes Simplex Virus

Infection: treatment should be initiated early and if possible

in the prodromal stage, to reduce durations and symptom of

the patient.


Management of burning mouth syndrome: in uncontrolled

DM, xerostomia and candidiasis can contribute to the

symptoms associated with burning mouth. Interestingly

amitriptyline, a drug has also been use to treat autonomic

neuropathy in DM.

Surgical consideration and periodontal management:

prior to any oral surgical procedures, the oral health

practioner must review any previous history of surgical

complications, asses glycemic control, and update concurrent

DM management.

following the oral surgical procedures, it is critical that

patients maintain a normal diet to avoid hypoglycaemia.

well controlled adult DM patient may not require antibiotics

should be considered for orofacial infections and oral surgical

procedures in the poorly controlled DM patient. www.indiandentalacademy.com

If periodontal surgery is necessary, several factors

should be considered depending on extent of the

surgery, anticipated level of postsurgical pain and stress,

and level of glycemic control.

These include use of antibiotics, nutritional counseling

and changes in DM medications.

Supportive periodontal therapy should also provide at

relatively close intervals of 2 to 3 months.


After treatment

Clinicians should keep in mind these postoperative

considerations. Patients with poorly controlled DM are at

greater risk of developing infections and may demonstrate

delayed wound healing.

Acute infection can adversely affect insulin resistance and

glycemic control,which, in turn, may further affect the body’s

capacity for healing. Therefore, antibiotic coverage may be

necessary for patients with overt oral infections or for those

undergoing extensive surgical procedures.


If the dentist anticipates that normal dietary intake will be

affected after treatment, insulin or oral antidiabetic

medication dosages may need to be appropriately adjusted

in consultation with the patient’s physician.

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.


Managing the diabetic emergency in the dental office

The most common emergency related to DM in dental

office is hypoglcaemia, a potentially life-threatening

situation that must be recognized and treated

expeditiously.

Signs and symptoms include confusion, sweating, tremors,

agitation, anxiety, dizziness, tingling or numbness and

tachycardia. Severe hypoglycaemia may result in seizure

or loss of consciousness.

As soon as a patient experiences signs and symptoms of

hypoglycaemia, the patient or dentist should check the

blood glucose with glucometer.

If glucometer is unavailable it should be treated as

hypoglycemic episodes.


Rapidly absorbed oral carbohydrates are preferable,

particularly if the dentist is not trained or adequately

equiped to administer intravenous, intramuscular, or

subcutaneous glucagons or dextrose.

Following the treatment, the signs and symptoms of

hypoglycaemia should resolve in 10 to 15 minutes, and the

patient should be carefully observed for 30 to 60 minutes.

A second evaluation should be done to ensure that that

normal blood glucose level has been achieved before the

patient is released.


A medical emergency from hyperglycaemia is likely to

occur in dental office since it develops more slowly than

hypoglycaemia.

Care is initiated by emergency medical system, opening

the administering oxygen.

Circulation and vital signs should be maintained and

monitored, the patient should be transported to hospital as

soon as possible.


Diabetes mellitus can have a significant impact on the

delivery of dental care. It is important for dentists to be

familiar with the medical management of patients with DM,

and to recognize the signs and symptoms of undiagnosed

or poorly controlled disease.

By taking an active role in the diagnosis and treatment of

oral conditions associated with DM, dentists also may

contribute to the maintenance of optimum health in patients

with this disease

Conclusion


References

Burket’s textbook of oral medicine, eleventh edition.

Essentials of Medical physiology, Sembulingam

Oral Manifestations and Complications of Diabetes

Mellitus-A review SQU Med J, May 2011, Vol. 11, Iss. 2,

pp. 179-186,

Diabetes care, volume 35, supplement 1, january 2012

Diagnosis and Classification of Diabetes Mellitus

American diabetes association.

Dental management considerations for the patient with

Diabetes Mellitus- JADA, Vol. 132, October 2001;1425-32.
