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 considerationwww.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.

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.

 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 cellwww.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.

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.

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.

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