Diabetes mellitus- Dr Sanjana Ravindra

Diabetes
mellitus
Seminar -5
Dr.Sanjana.Ravindra
Rajarajeswari Dental college
Bangalore

Contents
 Introduction
 History
 Epidemiology
 Anatomy of Pancreas
 Synthesis & Secretion of
Insulin
 Action of Insulin
 Homoeostasis of
Metabolic Fuels
 Pathophysiology of
Diabetic mellitus
 Risk factors
 Classification
 Clinical features
 Oral Manifestations
 Acute complications
 Chronic
complications
 Laboratory Findings
 Management
 Dental Management
Of Diabetic Patients
 Prevention of Diabetic
mellitus
 Conclusion
 References

Introduction
Diabetes mellitus (DM) is a clinically and genetically heterogeneous metabolic
disease characterized by:
 Abnormally elevated blood glucose levels (hyperglycemia)
and
 Dysregulation of carbohydrate, protein, and lipid metabolism.
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine:
Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.

Glucose cannot enter cells and, without energy, weakness results
Hyperglycaemia
Glucosuria, polyuria, polydipsia
 Fat and protein stores are metabolized with weight loss, peripheral
muscle wasting, production of ketone bodies (acetoacetate, β-
hydroxybutyrate and acetone)
 Ketonaemia, ketonuria
 Metabolic ketoacidosis  Hyperventilation
Introduction
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine:
Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.

Chronic
hyperglyc
emia
Defect in
insulin
secretion
from
pancreas
Resistance of
body’s cells
to insulin
action
Both
Introduction
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
Scarcity
in plenty

History
The earliest known record
of diabetes was written on
3rd Dynasty Egyptian
papyrus by physician
Hesy-Ra.
He stated recurring
urination as a sign of this
illness
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.

The Indian physician
Sushruta in the 6th
century B.C. noticed
the sweet nature of
urine in such patients
and termed the
condition
Madhumeha.
History

Aretaeus of Cappadocia, a Greek physician who lived during
120-200 AD
Mentioned a condition associated with unquenchable thirst,
excessive drinking of water and excessive passing of urine.
The word "Diabetes" signifies a greek word meaning a siphon,
appropriately describing how fluid cannot be retained in the
body.
Arateus described Diabetes as "the melting down of flesh and limbs" into
urine.
History

 Greek physicians and ancient Hindu physicians, used to taste the
patient's urine to detect abnormal constituents.
 This unpleasant practice perhaps enabled them to detect diabetic
patients.
History

Thomas Willis, in 1764,
observed that the urine
of a diabetic patient
was sweet and he
concluded that it
contained either sugar
or honey.
History

Diabetes
mellitus
Greek word
"diabainein"
meaning "to siphon
or pass through"
Latin word
"mellitus" meaning
"sweetened with
honey"
"to pass through sweetened with honey"

Definition
Gaw et al(1955)-
defined as syndrome
characterized by
hyperglycemia due to
an absolute or relative
risk of insulin or insulin
resistance.
Maline(1968)- defined
as chronic disorder of
carbohydrate
metabolism
characterized by
hyperglycemia and
glycosuria.
National diabetes data
group(1979) defined
diabetes mellitus as a
genetically and
clinically heterogenous
group of disorders that
shared glucose
intolerance in common.
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Med J 2012; 27(4): 269-273

Bennet (1994)- defined as a syndrome characterized by
hyperglycemia and disturbances of carbohydrate, fat and
protein metabolism associated with absolute or relative
deficiencies in insulin action and secretion.
Definition

Globally
382 million people had diabetes in
2013
By 2035, this number will rise to 592
million
In India
65.1 million people had diabetes in
2013
By 2035, this number will increase by
70.6%
Epidemiology
Guariguata L, Whiting DR, Hambleton I, Beagley J, Linnenkamp U, Shaw JE. Global estimates of diabetes prevalence for 2013 and projections for 2035.
Diabetes Res Clin Prac 2014; 103: 137-149

Courtesy: 2015 International Diabetes Federation
Epidemiology

Courtesy: IDF Diabetes atlas, 6th Edition
Epidemiology

Almost half of all people with
diabetes live in just three
countries
• China
• India
• USA
Epidemiology
Wang C, Li J, Xue H, Li Y, Huang J, Mai J, et al. Type 2 Diabetes Mellitus incidence in Chinese: contributions of overweight and obesity. Diabetes Res
Clin Prac 2014.

Prevalance (%) of people with diabetes by age and sex, 2015
IDF Diabetes Atlas. 6th ed. 2015

Wang C, Li J, Xue H, Li Y, Huang J, Mai J, et al. Type 2 Diabetes Mellitus incidence in Chinese: contributions of overweight and obesity. Diabetes Res
Clin Prac 2014.

EXOCRINE secretion
pancreatic juice enzymes promote the digestion of carbohydrates,
proteins and fats
ENDOCRINE secretion
Insulin and glucagon- enter portal vein – transported directly to
the liver – regulate metabolism of carbohydrates, proteins and fats
Normal adult: 50-75 gm (1 gm – islet tissue)
0.5- 1.5 million Islets of Langerhans[ 75 – 175 micrometer]
Pancreas
B D Chaurasia.Human Anatomy Regional and Applied Dissection and Clinical Vol.3 CBS Publishers & Distributers;2004.

Pancreas
15-20%, α cells synthesize and secrete
GLUCAGON
70- 80% β cells synthesize and secrete
INSULIN
1-8% δ cells synthesize and secrete
STOMATOSTATIN and GASTRIN
1-2% F- cells secrete PANCREATIC
POLYPEPTIDE which decreases the
absorption of food from the GIT
B D Chaurasia.Human Anatomy Regional and Applied Dissection and Clinical Vol.3 CBS Publishers & Distributers;2004.

Glucagon
Mobilizer of
glucose
Normal fasting
glucagon levels:
100-150 pg/ml
Blood glucose level
plasma
concentration of
glucagon

Insulin
Polypeptide
hormone
produced by β-
cells of islets of
Langerhans of
pancreas
ANABOLIC
HORMONE
STRUCTURE OF INSULIN
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.

Gluconeogenesis : The synthesis of glucose from non-
carbohydrate precursors( e.g. amino acids, glycerol)
Glycogenesis: The formation of glycogen from glucose.
Glycogenolysis : The breakdown of glycogen to
glucose

Synthesis &
secretion of
insulin

The synthesis of insulin involves two
precursors, namely preproinsulin with 108
amino acids (mol . wt . 11,500)and
proinsulin with 86 amino acids (mol. wt.
9,000).
They are sequentially degraded to form the
active hormone insulin and a connecting
peptide (C-peptide).
Insulin and C-peptide are produced in
equimolar concentration. C-peptide has no
biological activity, however its estimation in
the plasma serves as a useful index for the
endogenous production of insulin.
Synthesis & secretion of insulin

Synthesis & secretion of
insulin

Factors regulating islet-cell secretion

Regulation of insulin
secretion
Factors stimulating insulin secretion :
 Glucose
 amino acids
 gastrointestinal hormones
Factors inhibiting insulin secretion
 Epinephrine

Glucose is the most
important stimulus for
insulin release. The effect
is more predominant
when glucose is
administered orally (either
direct or through a
carbohydrate-rich meal).
Arise in blood glucose
level is a signal for insulin
secretion.
Amino acids induce the
secretion of insulin. This is
particularly observed after
the ingestion of protein-
rich meal that causes
transient rise in plasma
amino acid concentration
Among the amino acids,
arginine and leucine are
potent stimulator of
insulin release.
Gastrointestinal hormones
(secretin, gastrin,
pancreozymin) enhance the
secretion of insulin. The GIT
hormones are released after
the ingestion of food.
Factors stimulating insulin secretion
secretion

• Epinephrine is the most potent inhibitor of insulin
release.
• In emergency situations like stress, extreme exercise and
trauma, the nervous system stimulates adrenal medulla
to release epinephrine.
• Epinephrine suppresses insulin release and promotes
energy metabolism by Mobilizing energy-yielding
compounds-glucose from liver and fatty acids from
adipose tissue
Factors inhibiting insulin secretion
secretion

Actions of insulin
Stimulation of the activity of glycolytic enzymes
Reduces the activity of the enzymes of gluconeogenesis
Increased synthesis of glycogen
Increased uptake of of glucose by resting skeletal muscles
Reduction of blood glucose level
Reduction of lipolysis and stimulation of lipid synthesis

Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.

Homoeostasis
of metabolic
fuels

Glucose homeostasis

Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Homoeostasis of metabolic fuels

Pathophysiology
of diabetes
mellitus

Hormonal regulation of blood glucose
Hormone Main site of hormone
production
Effect on blood glucose
levels
Insulin
Glucagon
Growth hormone
Thyroid hormone
Catecholamines
(Epinephrine)
Glucocorticoids
Pancreas (beta cells)
Pancreas (alpha cells)
Pituitary gland
Thyroid gland
Adrenal gland (medulla)
Adrenal gland (cortex)
Decrease
Increase
Increase
Increase
Increase
Increase

Classification
Hereditary, primary or idiopathic diabetes
Prediabetes
• Subclinical, latent or stress diabetes
• Chemical diabetes
• Overt, or clinical diabetes
• Juvenile, or early-onset diabetes
• Maturity, adult or late-onset diabetes
Nonhereditary, secondary diabetes
• Damage to or removal of pancreatic islet tissue
• Disorders of other endocrine glands
• Drugs or chemicals
Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000. p. 251-274.
Prior
classification
of diabetes by
the American
Diabetes
Association,
1975

Classification
Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-145.

Classification

Type Ketosis Islet cell
antibodies
Human
lymphocyte
antigen
association
Treatment
Insulin Dependent-
type I
Present Present at
onset
Positive Insulin (mixtures of rapid
acting and intermediate
acting insulin at least twice
daily) and diet
Non-insulin
dependent- type II
Non-obese
Absent Absent Negative Eucaloric diet alone
Or
Diet plus insulin or
sulfonylureas
Obese Absent Absent Negative Weight reduction and
Hypocaloric diet plus
sulfonylureas or insulin for
symptomatic control only
Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000. p. 251-274.
Classification

The American Diabetes
Association provided the
most recent classification
of diabetes mellitus
(1997).
Classification
Cumming CG. Diabetes. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and Treatment. 9th
ed. USA: JB Lippincott
Company; 1994. 607-614

1. Type 1 DM
 It is due to insulin deficiency
and was formerly known as:
 Type I
 Insulin Dependent DM
(IDDM)
 Juvenile onset DM
2. Type 2 DM
It is a combined insulin resistance
and relative deficiency in insulin
secretion and is frequently known
as:
Type II
Noninsulin Dependent DM
(NIDDM)
Adult onset DM
Classification

What goes wrong in
diabetes?
Multitude of mechanisms
 Insulin
 Regulation
 Secretion
 Uptake
 Beta cells
 Damage Type 1 DM
Type 2 DM
Company; 1994. 607-614

Risk factors
Family history: risk of
developing diabetes rises
if a close relative such as a
parent or sibling has the
disease
Overweight individuals
Inactivity
Age: the risk of developing
type 2 diabetes increases
with age especially after
45 years
Race: Type 1 diabetes is more
common in Caucasians and in
European countries, such as Finland
and Sweden. Type 2 diabetes is
especially common in people of
African heritage, Asians.
Genetics: The HLA
haplotypes DR3 and/or
DR4 are associated with
increased susceptibility to
type 1 diabetes in
Caucasians.
Company; 1994. 607-614

Type 1 DM
Autoimmune
destruction of
pancreatic
beta cells.
Individual has
an absolute
insulin
deficiency and
no longer
produces
insulin.
Such patients
are absolutely
dependent on
exogenously
administered
insulin for
survival.
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice of Medicine. 20th ed. India: Elsevier;
2006. p. 805-848..

It comprises 5 to 10% of all DM cases.
Sudden onset
Develops over a period of a few days to weeks.
Type 1 DM occurs before the age of 25 years in
95% of affected persons but may occur at any age.
Affects both sexes equally
More prevalent in Caucasians.
Most type 1 diabetic individuals are of
normal weight or are thin in stature.
Type 1 DM
Company; 1994. 607-614

T cell-mediated autoimmune disease destruction of the
insulin-secreting β cells; 70–90% of β cells
Islet cell antibodies  variable predictive value as a marker
Glutamic acid decarboxylase (GAD) antibodies  latent
autoimmune diabetes in adults (LADA)
Associated with other autoimmune disorders thyroid disease,
coeliac disease, Addison’s disease, pernicious anemia and
vitiligo
Type 1 DM
2006. p. 805-848..

Genetic factors  one-third of the
susceptibility to type 1 diabetes
20 different regions of the human genome; human
leucocyte antigen (HLA) region, major histocompatibility
complex on the short arm of chromosome 6  IDDM 1
HLA haplotypes DR3 and/or DR4 
Caucasians
Other genes implicated  CD25, PTPN22, IL2RA
Type 1 DM
2006. p. 805-848..

Hygiene
hypothesis Viral infection-
mumps,
Coxsackie B4,
retroviruses,
rubella (in
utero),
cytomegaloviru
s, Epstein–Barr
virus
Stress
Dietary factors

nitrosamines
Bovine serum
albumin
Type 1 DM
2006. p. 805-848..

Pathogenesis of type 1
diabetes mellitus
2006. p. 805-848..

Type 1 DM
2006. p. 805-848..

Fats
Lipolysis
Glycerol Free fatty acids
Glucose Ketones
Company; 1994. 607-614

NORMALLY In THE
BODY
DIABETES TYPE 2

Type 2 DM
 Most common type
 Comprises 90 to 95% of DM cases
 Multifactorial etiology  genetic
predilection, advancing age,
obesity and lack of exercise.
• The genetic influence in type 2 DM
is greater than that seen in type 1
DM.
• More prevalent in African
Americans, Native Americans,
Hispanics, and Paciﬁc Islanders than
in Caucasians.
Company; 1994. 607-614

Most type 2
DM patients
are
overweight,
and most are
diagnosed as
adults.
Slow
onset
Approximate
ly half of the
patients are
unaware of
their disease
The insidious nature of the
disease allows prolonged
periods of hyperglycemia to
begin exerting negative
effects on major organ
systems
By the time many
type 2 diabetic
patients are
diagnosed,
diabetic
complications
have already
begun.
Type 2 DM

Peripheral
resistance to
insulin, especially
in muscle cells
Increased
production of
glucose by the
liver
Insulin secretory
defect of the beta
cells
• Obesity contributes greatly to insulin resistance
• Insulin resistance generally decreases with weight loss
Type 2 DM
The underlying pathophysiologic defect in type
2 DM is characterized by the following three
disorders:

 The high blood
glucose levels often
stimulate an increase
in insulin production
by the pancreas
 Excessive insulin
production  Hyper
insulinemia
Type 2 DM
Company; 1994. 607-614

Complex condition  resistance to the actions of insulin in liver and muscle +
impaired pancreatic β-cell function  ‘relative’ insulin deficiency
Type 2 DM

Type II Diabetes Mellitus-
Insulin resistance
Intra-abdominal adipose tissue  Free Fatty
acids
Compete with glucose for oxidation +
Releases a number of hormones
(adipokines- IL-6, TNF α, leptin, adiponectin )
Adipose tissue drains into the portal vein
potent influence on insulin sensitivity in the liver
2006. p. 805-848..

Insulin resistance
 Physical inactivity  downregulation of insulin-sensitive kinases
 Promote accumulation of FFAs within skeletal muscle
 Sedentary people > active people
 Physical activity  non-insulin-dependent glucose uptake into
muscle
 Deposition of fat in the liver  non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis and cirrhosis

2006. p. 805-848..
Insulin resistance syndrome / Reaven’s
syndrome /Syndrome X

Type II Dm
Genetic predisposition
 Marked differences in susceptibility in different ethnic groups
 Genome-wide Association studies  20 genes or gene regions;
TCF7L2
 Altered regulation of β-cell mass  primary predisposing factor
2006. p. 805-848..

William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition

Type II Dm
Environmental and
other risk factors
Diet and Obesity:
 Overeating Obesity + underactivity
 BMI > 30 kg/m2  risk increases tenfold
 Obesity diabetogenic factor; genetically predisposed both to
insulin resistance and to β-cell failure
 Constituents of the diet and the style of eating  Sweet foods rich
in refined carbohydrate consumed frequently may increase the
demand for insulin secretion, while high-fat foods may increase
FFAs and exacerbate insulin resistance
2006. p. 805-848..

Type II Dm
Environmental and
other risk factors
Age:
 Prevalence increases with age; ~10% over 65 years
 Renal threshold for glucose rises with age  Glycosuria
Pregnancy:
 Insulin sensitivity is reduced through the action of placental
hormones
 Insulin-secreting cells of the pancreatic islets  unable to meet
this increased demand
 “Gestational diabetes” 80% of women develop permanent
diabetes
2006. p. 805-848..

Metabolic disturbances in
type II diabetes
 Slow onset of ‘relative’ insulin deficiency
 Lipolysis and proteolysis are not unrestrained and weight loss and
ketoacidosis
 Polyuria and polydipsia  degree of glycosuria
 Rise in renal threshold for glucose
 Large number of cases remain undetected
2006. p. 805-848..

Obesity & insulin resistance
The risk for diabetes increases as the
body mass index (a measure of body
fat content) increases. It is not only
the absolute amount but also the
distribution of body fat that has an
effect on insulin sensitivity .
Central obesity (abdominal fat) is
more likely to be linked with insulin
resistance than are peripheral
(gluteal / subcutaneous) fat depots.
2006. p. 805-848..

Gestational DM
Development of type 1 DM or
discovery of undiagnosed
asymptomatic type 2 DM during
pregnancy
Occurs in 2 to 5% of pregnant
women
However, about 30 to 50% of
women will develop type 2 DM
within 10 years.
Seen during the third trimester,
which significantly increases
perinatal morbidity and
mortality
Pathophysiology: Associated with
increased insulin resistance
Risk factors: Older women,
overweight women and women
of minority ethnic groups
Most patients return to a
normoglycemic state after
parturition
2006. p. 805-848..

Other specific
types of DM
Comprises 1 to 2% of
DM cases
Caused by various specific
genetic defects of beta cell
function and insulin
action, diseases of the
exocrine pancreas,
endocrinopathies,
pancreatic dysfunction
induced by drugs,
chemicals, or infections.
Genetic syndromes
sometimes associated with
DM include Turner’s
syndrome, Down
syndrome, Wolfram
syndrome, Klinefelter’s
syndrome, Friedreich’s
ataxia, Huntington’s
chorea, Laurence-Moon-
Biedl syndrome, myotonic
dystrophy, porphyria, and
Prader-Willi syndrome.
2006. p. 805-848..

William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition
Pancreatic β-cell failure

β-cell dysfunction in type2 diabetes manifests as both in qualitative&
quantitative.
Qualitative beta cell dysfunction is initially seen as loss of normal pulsatile,
oscillating pattern of insulin secretion.
Followed by rapid phase of insulin secretion which is triggered by an
elevation in plasma glucose.
Quantitative beta cell dysfunction is reflected by an beta cell mass, islet
degeneration, & deposition of amyloid.
Pancreatic β-cell failure

Impaired Glucose Tolerance
& Impaired Fasting Glucose
Represent
metabolic states
lying between
diabetes and
normoglycemia
Risk factors
for future
diabetes
30 to 40% of
individuals with
IGT or IFG will
develop type 2
diabetes within
10 years after
onset
Pathophysiology
 increased
insulin resistance
whereas
endogenous
insulin secretion
is normal
People with IFG
have increased
fasting blood
glucose levels but
usually have
normal levels
following food
consumption
Those with IGT are
normoglycemic
most of the time
but can become
hyperglycemic
after large glucose
loads
2006. p. 805-848..

Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide to Diagnosis and Management. New Delhi: Jaypee Brothers Medical Publishers
(P) Ltd; 2014.

References
1. IDF diabetes atlas. 6th ed. 2015
2. B D chaurasia. Human anatomy regional and applied dissection and clinical vol.3 CBS
publishers & distributers;2004.
3. Malamed sf. Medical emergencies in the dental office. 5th ed. Noida: mosby; 2000.
4. Warnakulasuriya s, tilakaratne wm. Oral medicine and pathology A guide to diagnosis and
management. New delhi: jaypee brothers medical publishers (P) ltd; 2014.
5. Frier BM, fisher M. Diabetes mellitus. In: boon NA, Colledge NR, Walker BR eds. Davidson’s
principles and practice of medicine. 20th ed. India: elsevier; 2006. P. 805-848..
6. Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-
145.
7. Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral
medicine: diagnosis and treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.
8. Cumming CG. Diabetes. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine:
diagnosis and treatment. 9th ed. USA: JB lippincott company; 1994. 607-614.
9. Mandal AK, Chaudhury S. Textbook of pathology for dental students. 2010.

10. Mealey B. Diabetes Mellitus. Greenberg MS, Glick M eds. Burket's Oral Medicine. 10th ed.
Spain: BC Decker Inc; 2003. 563-577.
11. Joshi SK, Shrestha S. Diabetes mellitus: A review of its associations with different
environmental factors. Kathmandu University Med J 2010; 8(1): 109-115.
12. Wang C, Li J, Xue H, Li Y, Huang J, Mai J, et al. Type 2 Diabetes Mellitus incidence in
Chinese: contributions of overweight and obesity. Diabetes Res Clin Prac 2014. In Press.
13. Guariguata L, Whiting DR, Hambleton I, Beagley J, Linnenkamp U, Shaw JE. Global estimates
of diabetes prevalence for 2013 and projections for 2035. Diabetes Res Clin Prac 2015; 103:
137-149.
14. Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed.
The Association of Physicians, Mumbai; 1097-1136.
15. Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current
Trends. Oman Med J 2012; 27(4): 269-273.
16. Maitra A, Abbas AK. The Endocrine System. In Kumar Abbas Fustao eds. Robbins and Cotran
Pathologic Basis of Disease. 7th ed. Elsevier Saunders, China 2005.
17. William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition.
18. Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds.
Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.
References

Glucose cannot enter cells and, without energy, weakness results
Hyperglycaemia
Glucosuria, polyuria, polydipsia
 Fat and protein stores are metabolized with weight loss, peripheral
muscle wasting, production of ketone bodies (acetoacetate, β-
hydroxybutyrate and acetone)
 Ketonaemia, ketonuria
 Metabolic ketoacidosis  Hyperventilation
Lynch MA. Diabetes Mellitus. In: Lynch MA, Brightman VJ, Greenberg MS eds. Burket's Oral Medicine: Diagnosis and
Treatment. 8th
ed. USA: JB Lippincott Company; 1984. 842-848.

Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd
ed. Uppala Author- publisher, Vijayavada 2008.

Clinical features
The onset of type 1 diabetes is
usually abrupt whereas type 2
diabetes is often present for years
without overt signs or symptoms
When complications of poor glucose control
develop, patients complain of:
• Visual impairment
• Neurologic symptoms: numbness,
dizziness
• Chest pain
• Gastrointestinal symptoms
• Genitourinary symptoms, especially
urinary incontinence
Treatment. 8th

Clinical features
Endocrinology. In: Scully C. Medical problems in dentistry. 6th ed. China: Elsevier; 2010. P. 138-145.

Oral
manifestations
Related to poor glycemic
control
1. Burning mouth syndrome
2. Altered wound healing
3. Increased incidence of infection
4. Candidal infection  Median Rhomboid
glossitis, Angular cheilitis, Acute
pseudomembranous candidiasis of tongue,
buccal mucosa and gingiva
Treatment. 8th

 Bilateral generalized salivary gland enlargement
 Xerostomia
 Gingivitis
 Periodontitis, periodontal abscesses
 Dental caries
Oral manifestations
Treatment. 8th

Related to medications
Salivary hypofunction
Xerostomia
Dry mucosal surfaces
Gets easily irritated
Causing minor mucosal ulcerations,
oral burning sensation, increased
susceptibility of fungal infections
Drug induced lichenoid reactions (Metformin)
Oral manifestations
Treatment. 8th

ORAL CANDIDIASIS
Oral manifestations
POOR ORAL HYGEINe WITH
EXCESS CALCULUS
FORMATION
TENDENCY FOR
PROGRESSIVE
CARIES
Treatment. 8th

Oral manifestations
CHRONIC PERIODONTITIS- multiple abscess, SUPPURATIOn, MOBILITY
Palmer R, Soory M. Modifying factors. In: Lindhe J, Lang NP, Karring T. Clinical Periodontology and
Implant Dentistry. 5th ed. Singapore: Blackwell Munksgaard; 2008. p. 307-311.

In the diabetic patient, the
abnormal host defence
mechanism in addition to
hyperglycemia state can lead
to the growth of particular
fastidious organism.
The most frequently isolated
microrganism are prevotella
intermedia followed by
camphylobacter rectus.
The association of aac &
capnocytophaga is similar to
periodontitis in healthy patient
& periodontitis in diabetic
patient.
Effect on periodontal flora:
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In: Newman MG, Takei HH,
Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China: Elsevier; 2011. p. 285-288.

Effect on periodontal flora:

PERIODONTAL VASCULATURE
Increased thickening of gingival capillary endothelial basement
membrane & the walls of small blood vessels seen in diabetes.
This thickening may impair oxygen diffusion& nutrient
provision across the basement membrane.
Increased thickness of small vessel wall results in narrowing of
the lumen, altering normal periodontal tissue homeostasis.
Klokkevold PR, Mealy BL. Influence of systemic disorders and stress on the periodontium. In: Newman MG, Takei HH,
Klokkevold PR. Carranza’s Clinical Periodontology. 10th ed. China: Elsevier; 2011. p. 285-288.

Radiographic
Features
Preshaw PM. Periodontal diseases. In: Warnakulasuriya S, Tilakaratne WM. Oral Medicine and Pathology A Guide
to Diagnosis and Management. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2014.p. 72.

Clinical Diagnosis
Polyuria, Polydipsia, polyphagia with periodontal
problems
Radiological problems
Not specific
Plasma Glucose concentration
Unequivocal elevation of plasma glucose concentration
greater than 140 mg/dl
Diagnosis
Family history
Personal
history
Mealey B. Diabetes Mellitus. Greenberg MS, Glick M eds. Burket's Oral Medicine. 10th
ed. Spain: BC Decker Inc;
2003. 563-577.

Laboratory diagnosis
Urine analysis
Blood chemistry
Immunological Assays
• Glucose
• Ketone
• Microalbuminuria
• Blood glucose estimation
• Glucose tolerance test
• Glycated hemoglobin
measurement
• Lipid profile
Diagnosis
Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians,
Mumbai; 1097-1136.

Mumbai; 1097-1136.

Laboratory test
for diagnosis
Estimation of blood glucose.
Oral glucose tolerance test.
Mumbai; 1097-1136.

Diagnosis
The diagnosis of diabetes is based on the presence of clinical signs and symptoms,
along with specific laboratory findings

Diagnosis
Treatment. 8th

Estimation of
blood glucose
Depending
on time of
collection
Measurement of blood glucose is indicative of
current state of carbohydrate metabolism.
Fasting blood glucose- after
an overnight fast.
Post meal or postprandial
blood glucose-2 hrs after the
subject has taken a normal
meal.
Random blood glucose – Any
time of the day.
Mumbai; 1097-1136.

Total glucose in 100 ml of plasma is about 15% greater
than in 100 ml of whole blood.
Plasma is prefered as whole blood is affected by
concentration of proteins (especially haemoglobin).
In capillary blood the value of blood glucose at rest is
about 5 % higher than venous blood.
diagnosis
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles and Practice
of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848..

Urine analysis
GLUCOSE:
• Dipsticks- common screening procedure
• Urine passed 1-2 hours after a meal
• Disadvantage individual variation in renal threshold for glucose
KETONE BODIES:
• Nitroprusside reaction acetoacetate, using either tablets or dipsticks
• Ketonuria  normal people who have been fasting, exercising strenuously for
long periods, vomiting repeatedly, diet high in fat and low in carbohydrate
Diagnosis
Normally less than
500mg/24 hrs or
less than 15 mg/dl
of glucose is
present in urine.

Urine analysis
 Protein:
 Dipstick > 300mg/L
 Microalbuminuria
specific albumin dipsticks/
laboratory measurement
Diagnosis

 Qualitative test.
 Benedicts.
 Clintest tablet test.
 Reagent strip test
 Quantitative test.
 Benedicts.
Diagnosis
Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials
of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008.

Procedure
Add 8 drops of
urine
Boil for 2
to 3 min
CoolTake 5.0ml of
Benedict’s
reagent
Observe
Benedict reagent : sodium citrate 173 gm, sodium carbonate 100 gm, cupric sulphate
17.3 gm and distill water 900 ml.
Benedicts test
Diagnosis

Observations
Color Sugar
Blue Absent
Green without
precipitate
Present, trace
Green with precipitate 1+ (0.5 g/dl)
Brown precipitate 2+ (1.0 g/dl)
Yellow - Orange
precipitate
3+ (1.5 g/dl)
Brick red precipitate 4+ (≥ 2.0 g/dl)
Benedicts test
Diagnosis

Triglycerides
(mg/dl)
Category
<150 Low risk
150-199 Intermediate risk
≥ 200 High risk
LDL cholesterol
<100 Low risk
≥130 High risk
HDL cholesterol
<35 High risk
>45 Low risk
Diagnosis

Blood analysis
Glucos
e
Enzymatic reaction (glucose oxidase)  random/ fasting
Colorimetric or other testing sticks capillary (fingerprick)
testing to monitor diabetes treatment
Diagnosis of diabetes accurate laboratory method
Glucose venous < arterial/capillary blood
Whole blood glucose concentrations < plasma concentrations
Venous plasma values most reliable for diagnostic purposes
Diagnosis

Blood analysisDiagnosisGlycated haemoglobin:
Accurate and objective measure of glycaemic control over a period of weeks to months
Assessment of glycaemic control by repeated measurements every few months
Slow non-enzymatic covalent attachment of glucose to haemoglobin (glycation) increases the amount in the
HbA1 (HbA1c) fraction relative to nonglycated adult haemoglobin (HbA0); chromatography
Total glycated haemoglobin (GHb), HbA1 or HbA1c
Rate of formation of HbA1c α ambient blood glucose concentration
1% HbA1c 2 mmol/L (36 mg/dL) blood glucose

Indications
 In all diabetics to monitor long term blood glucose level control, index of
diabetic control:-
7% hba₁с – good
10% hba₁с- fair
13-20% hba₁с- poor.
 To monitor patient compliance.
 To predict development & progression of microvascular complication.
 For determining the therapeutic option whether to use oral agents, insulin ,or β
cell transplantation.
 Also increasingly used for primary diagnosis of dm.
Mumbai; 1097-1136.

At what interval should HbA₁с be
determined?
Treatment by time of diabetes Recommended frequency
Type-1 DM( minimal /conventional
therapy)
4 times a year
Type – 1 DM (intensified therapy) Every (1) -2 months.
Type-2 DM Twice a year in stable patients.
Mumbai; 1097-1136.

Another assay that can be
used to determine long-term
glucose control
Not used as widely as the
glycated hemoglobin assay
but is often helpful in
managing women with
gestational diabetes
The fructosamine assay
assesses glycemic control 2 to
4 weeks preceding the test.
The normal range for
fructosamine is 2.0 to 2.8
mmol/L
This test may become more
widely used in the future,
since at-home testing is now
available.
Diagnosis
FRUCTOSAMINE TEST
Mumbai; 1097-1136.

In asymptomatic persons with
sustained or transient glycosuria.
In persons with symptoms of diabetes
but no glycosuria or hyperglycemia.
Persons with family history but no
symptoms or positive blood findings.
In persons with or without symptoms of
diabetes mellitus showing one abnormal
blood findings.
In patients with neuropathies or
retinopathies of unknown origin.
Diagnosis
Indications of Glucose tolerance test
Confirmed diabetics
mellitus.
GTT has no role in
follow-up of diabetics.
The test should not be
done in ill patients
Contraindications of glucose tolerance test

Types of glucose
tolerance test
Standard Oral
glucose
tolerance test
I/V Glucose
tolerance test
Mini Glucose
tolerance test
 Patient should on carbohydrate rich
unrestricted diet for 3 days.
 Patient should be ambulatory with
normal physical activity.
 Medications should be discontinued
on the day of testing.
 Exercise, smoking and tea or coffee
are not allowed during test period.
 OGTT carried out in the morning after
patient has fasted overnight for 8-14
hours.

Mumbai; 1097-1136.

Test
A fasting venous blood sample is
collected in the morning.
Patients ingest 75 g of anhydrous
glucose in 250-300 ml of water over
5 minutes. ( for children, the dose is
1.75 g of glucose per kg).
• In the classical procedures, the blood and urine
samples are collected at half hourly interval of the
next three hours.
• A curve is plotted with the blood glucose levels on
the vertical axis against the time of collection on the
horizontal axis.
• The curve so obtained is called glucose tolerance
curve.
Standard ogtt

Intravenous Gtt
•This test is undertaken for patients
with malabsorption (Celiac disease
or enteropathies).
•Under these conditions oral glucose
load is not well absorbed and the
results of oral glucose tolerance test
become inconclusive.
•Carried out by giving 25 g of glucose dissolved in
100 ml distilled water as intravenous injection
within 5 minutes.
•Completion of infusion is taken as time zero.
•Blood samples are taken at 10 minutes interval
for the next hour.
•The peak value is reached within a few minutes.
INTERPRETATION
•Normally, blood glucose level returns to normal range
within 60 minutes.
•In diabetes mellitus, this decline is slow.
Zero Hour After 2 Hours
Normal Person < 110 mg/dL < 140 mg/dL
Increase Glucose Tolerance 110 – 126 mg/dL 140 – 199 mg/dL

Gestational diabetes is diagnosed if the woman is at or exceeds any two of the
following four plasma glucose levels during 100 gm test
Fasting – 95 mg/dl
1 hr – 180 mg/dl
2 hr – 155 mg/dl
3 hr – 140 mg/dl
Mumbai; 1097-1136.

Laboratory test for
screening
 Recommended screening test is fasting plasma glucose.
 American Diabetes Association recommends screening for
Type 2 DM in all asymptomatic individuals >= 45 yrs of
age using fasting plasma glucose.
 If fasting test is normal, screening test should be repeated
every three years.
 If fasting blood glucose level is normal but there is strong
clinical suspicion then OGTT.
Mumbai; 1097-1136.

Selective
screening
 High risk individuals ---Obese
Family h/o DM
Hypertension
Dyslipidemia
Impaired glucose tolerance
Screening test is performed at earlier age ( 30 yrs )
and repeated more frequently

Laboratory
test to assess
glycemic
control

Laboratory test to
assess glycemic control
Periodic measurement
of glycated
haemoglobin.
Daily self assessment
of blood glucose.
Others
Mumbai; 1097-1136.

Insulin assay
 Measurement of
insulin level by
radioimmunoassay &
ELISA.
 Crucial for type I DM.
Mumbai; 1097-1136.

Self–blood glucose monitoring (SBGM)
Diagnosis

Affected body part
or condition
Complications
Vascular system Atherosclerosis
Large vessel disease
Microangiopathy
Kidneys Diabetic glomerulosclerosis
Arteriolar nephrosclerosis
Pyelonephritis
Nervous system Motor, sensory, and autonomic neuropathy
Eyes Retinopathy
Cataract formation
Glaucoma
Extraocular muscle palsies
Skin Diabetic xanthoma
Necrobiosis lipoidica diabeticorum
Pruritis
Furunculosis
Mycosis
Mouth Gingivitis, Increased incidence of dental caries and
and periodontal disease, Alveolar bone loss
Pregnancy Increased incidence of large babies, still births,
miscarriages, newborn deaths, and congenital defects
COMPLICATIONS OF DIABETES

COMPLICATIONS OF DIABETES
 Acute complications:
Hypoglycemia
Diabetic ketoacidosis
Non ketotic hyperosmolar diabetic coma
 Late complications :
Retinopathy - blindness
Nephropathy – renal failure
Neuropathy – sensory , autonomic
Macro vascular disease - atherosclerosis, stroke
Altered wound healing
Diabetic foot and ulcers
Frier BM, Fisher M. Diabetes Mellitus. In: Boon NA, Colledge NR, Walker BR eds. Davidson’s Principles
and Practice of Medicine. 20th ed. India: Elsevier; 2006. p. 805-848.

Pathogenesis of complications of
diabetes
Formation of
advanced glycation
end products .
Intracellular
hyperglycemia with
disturbances in
polyol pathways.
Metabolic
pathways appear to
be involved in
pathogenesis of
long term diabetic
complication
Mumbai; 1097-1136.

Protein glycation
leading to AGE is one
of the major cause of
diabetic
complication.
The carbohydrate-containing
proteins which accumulate in
patients with sustained
hyperglycemia are known as
advanced glycosylation
endproducts (AGEs).
Mumbai; 1097-1136.

Hypoglycemia
 Imbalance between food intake and usage, and insulin therapy
 Rapid onset Fainting
 Blood glucose < 3.5 mmol/L (63 mg/dL)
 Non diabetics ‘Spontaneous’ hypoglycemia
 Brittle diabetes – adolescent girls
Acute complications

Acute complications
Endocrinology. In: scully C. Medical problems in dentistry. 6th ed. China: elsevier; 2010. P. 138-145.
Hypoglycemia

• Serious morbidity
• Mortality of upto 4% in
insulin treated patients
• Healthy young patients
(type 1 diabetes) ‘dead-
in-bed syndrome’
Acute complications
Hypoglycemia

 Slow onset over many hours, with deepening drowsiness
 Signs of dehydration (dry skin, weak pulse,
hypotension), acidosis (deep breathing) and ketosis
(acetone smell on breath and vomiting)  Type 1
diabetes
An unconscious diabetic should always be assumed to be
hypoglycemic
Acute complications
Hypoglycemia

Terminate dental procedure
P- position patient supine with legs elevated
slightly
A-B-C- Assess and perform BLS (check
airway, check breathing, check the pulse)
D- initiate definitive care
Emergency medical assistance
Establish IV infusion
Administer oxygen
Transportation to hospital for further
management
Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice
of Medicine. 21st ed. China: Elsevier; 2010. Malamed SF. Medical Emergencies in the Dental Office.
5th ed. Noida: Mosby; 2000.
Acute complications
Hypoglycemia

HYPOGLYCEMIA
UNAWARENESS
 more common in diabetic patients with good
glycemic control
Inability to perceive the warning symptoms of
hypoglycemia
Signs and symptoms most common when
blood glucose levels fall <60 mg/dL
Glucose levels can fall to 40mg/dL or lower
before an individual feels hypoglycemic

Hyperglycaemic coma usually
has a slow onset over many
hours with:
 Drowsiness
 Signs of dehydration (Dry
skin, weak pulse,
hypotension)
 Florid appearance of face
(Bright Red)
 Acidosis (Deep breathing)
 Ketosis (Acetone smell in
breath)
Acute complications

Diabetic
ketoacidosi
s (DKA)
Accumulation
of ketones in
body fluids
Decreased pH
Electrolyte loss
& dehydration
from excessive
urination
Alterations in
the
bicarbonate
buffer system
Untreated DKA can result in coma or death
Acute complications
• Serious cause of morbidity 
type 1 diabetes
• Established diabetes
intercurrent infection  lose
appetite  stop/reduce dose of
insulin
Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current Trends. Oman
Med J 2012; 27(4): 269-273.

Diabetic Ketoacidosis
Acute complications

 Hyperglycemia osmotic diuresis
 Dehydration & electrolyte loss (Na+ , K+)
 Potassium loss is exacerbated by secondary
hyperaldosteronism as a result of reduced renal
perfusion
 Ketosis  insulin deficiency; elevated catecholamines
and other stress hormones, resulting in unrestrained
lipolysis and supply of FFAs for hepatic ketogenesis
 Accumulate in blood  metabolic acidosis
Acute complications

Courtesy: Colledge NR, Walker BR, Ralston SH. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010.
Acute complications

Investigations
Venous blood
Arterial blood gases severity of acidosis (<12mmol/L)
Urine analysis for ketones
ECG
Full blood count, blood and urine culture, C-reactive protein
Acute complications
Med J 2012; 27(4): 269-273.

Methods to detect
ketone bodies
1. Rothera’s test
2. Reagent strip
3. Gerhardt ferric chloride
test
Rothera test
 Procedure
Take 5.00 ml urine and saturate it with
ammonium sulphate. Add a crystal of sodium
nitroprusside.
Slowly pour concentrated ammonium hydroxide
(1-2ml) by the side of test tube.
Pink-purple ring
Based on nitroprusside reaction

Acute complications

Chronic
Complications
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis and
treatment. 8th ed. USA: JB lippincott company; 1984. 842-848.

VASCULAR COMPLICATIONS
Occurs due to
microangiopat
hy and
atherosclerosis
Changes
seen in
blood
vessels:
Endothelial
proliferation
Thickenin
g of
basement
membrane
Thickening
of walls of
blood vessels
Increase
lipid
metabolis
m
Atheroma
formation
Chronic
Complications

DIABETIC RETINOPATHY
Increases with
increase in
duration of
diabetes and more
common in type I
Dilation
Occlusion
Increase
permeability of
blood vessels
Chronic
Complications

RENAL FAILURE
 35-45% occur in type I and 20% in type II
 Mechanism:
 Mesangium expands, membrane supporting capillary loops
in renal glomeruli expands due to increased production of
mesangial matrix products
 Surface area for capillary glomerular filtration decreases
and gfr declines
Chronic
Complications

 Basement membrane in glomerular thickens and
decrease GFR.
 Earliest sign is microalbuminuria.
 Increase renal blood pressure
 Expanding mesangium, thickening of basement
membrane and renal hypertension and declining of gfr
leads to end stage renal disease.
Chronic
Complications
Med J 2012; 27(4): 269-273.

DIABETIC NEUROPATHY
50% diabetic
individuals
Affect
sensory,moto
r and
autonomic
Peripheral
sensorimotor
is most
common
manifesting
with muscle
weakness,nu
mbness
As neuropathy
worsens
paresthesia
disappears and
replaced by
hypoesthesia, this
reduction in
sensory ability
makes affected
area highly prone
to imjury as there
is absence to
perceive stimuli
Chronic
Complications
Med J 2012; 27(4): 269-273.

Most common cause of death in TYPE
II is MYOCARDIAL INFARCION
Increase intimal thickness and atheroma
formation are hyperglycemic induced tissue
alterations
Increase thickness of walls leads to partial
obstruction and educed blood flow.
Increase thrombus formation along vessel wall
and increase platelet aggregation lead to
intravascular thrombi leading to intermittent
hypercoagulation
Chronic
Complications
Baliga V, Sapsford R. Review article: Diabetes mellitus and heart failure -- an overview of epidemiology and
management. Diabetes Vascular Dis Res 2009; 6: 164.

MEDICAL MANAGEMENT OF DIABETES
1. Educate the patient
2. Diet
a.Obese pt – weight reducing diet,
restrict calorie content
b.Ideal body weight – maintenance diet
Carbohydrates - 55 – 65%
Proteins - 10 – 15%
Fat - 20 – 30%
Abdullah A, Peeters A, Courten M, Stoelwinder J. The magnitude of association between overweight and obesity and
the risk of diabetes: A meta-analysis of prospective cohort studies. Diabetes Res Clin Prac 2010; 89: 309-319.

3. Exercise -Aerobic exercise
- Walking, swimming, cycling
- Brisk walking – 30mins for 5 days /
week
- Evaluate CVS status before advising
exercise
4. Therapy
Type 1 (IDDM) - Insulin
- Combination of long acting and short
acting insulin
- Twice daily
Abdullah A, Peeters A, Courten M, Stoelwinder J. The magnitude of association between overweight and obesity and
the risk of diabetes: A meta-analysis of prospective cohort studies. Diabetes Res Clin Prac 2010; 89: 309-319.

Management
PRIMARY TREATMENT GOALS
 Achieving blood glucose levels that are as close to normal
 Prevention of diabetic complications.
 Normal growth and development
 Normal body weight
 Avoidance of sustained hyperglycemia or symptomatic
hypoglycaemia
 Prevention of diabetic ketoacidosis and nonketotic acidosis
 Immediate detection and treatment of long-term diabetic
complications
Bastaki S. Diabetes mellitus and its treatment. Int J Diabetes & Metabolism 2005; 13:111-134.

Diet, exercise, weight control and medications are the
mainstays of diabetic care
The primary medication used in type 1
diabetes management is insulin, on
which the type 1 diabetic patients are
dependent for survival.
Type 2 diabetic individuals frequently
take oral medications although many
also use insulin to improve glycemic
control.

• The first-generation sulfonylureas have
been replaced with second-generation
agents that are more potent, have fewer
drug interactions, and produce less
significant side effects.
• Sulfonylureas stimulate pancreatic
insulin secretion.
• Relatively long duration of action of 12
to 24 hours
• Taken once or twice per day.
• Hypoglycemia is a major side effect.
• Food intake must be adequate to prevent
glucose levels from falling too low.
Lynch MA. Diabetes mellitus. In: lynch MA, brightman VJ, greenberg MS eds. Burket's oral medicine: diagnosis
and treatment. 8th
ed. USA: JB lippincott company; 1984. 842-848.

• Repaglinide stimulates pancreatic
insulin secretion
• Rapidly absorbed, reaches peak plasma
levels in 30 to 60 minutes, and is then
rapidly metabolized.
• The drug is taken with meals and
lowers the peaks of postprandial
plasma glucose in type 2 diabetes
and treatment. 8th

• Metformin is a biguanide agent that
lowers plasma glucose mainly by
preventing glycogenolysis in the liver.
• Metformin also improves insulin use,
counteracting the insulin resistance
seen with type 2 diabetes.
• Because metformin does not stimulate
increased insulin secretion,
hypoglycemia is much less common
with this drug.
and treatment. 8th

//www.google.co.in/search?q=met
+of+diabetes+mellitus&biw

• The thiazolidinedione agents act to
increase tissue sensitivity to insulin,
thus increasing glucose utilization
and decreasing blood glucose levels.
• These drugs also decrease hepatic
gluconeogenesis.
• Like metformin, the
thiazolidinediones generally do not
cause hypoglycemia.
and treatment. 8th

• Acarbose is taken with meals, and it
slows the digestion and uptake of
carbohydrates from the gut.
• This serves to lower postprandial
plasma glucose peaks.
and treatment. 8th

Site of actions of drugs in the treatment of type 2 DM

Insulin
 All type 1 diabetic patients use exogenous
insulin, as do many with type 2 diabetes.
 Insulin is taken via subcutaneous injection,
most often with a syringe.
 Insulin infusion pumps deliver insulin
through a subcutaneous catheter.

Side effects of insulin therapy
1. Hypoglycaemia
2. Weight gain
3. Peripheral oedema (insulin treatment
causes salt and water retention in the
short term)
4. Insulin antibodies (animal insulins)
5. Local allergy (rare)
6. Lipodystrophy at injection sites
and treatment. 8th

//www.google.co.in/search?q=drugs+of+diabetes+mellitus&biw

and treatment. 8th

//www.google.co.in/search?q=prevention+of+d
iabetes+mellitus&biw

Cure to Diabetes Using Stem Cells

Dental
management
of diabetic
patients

To minimize the risk of an intraoperative emergency,
clinicians need to consider some issues before initiating
dental treatment.
Medical history: Take history and assess glycemic
control at initial appointment.
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
Dental management
considerations
Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.

Dental management
considerations
Scheduling of visits
• Morning appointment
• Do not coincide with peak activity.
Diet
• Ensure that the patient has eaten normally and taken medications as usual.
Blood glucose monitoring
Prophylactic antibiotics
• Established infection
• Pre-operation contamination wound
• Major surgery

During treatment
• The most complication of DM occur is hypoglycemia episode.
• Hyperglycemia
After treatment
• Infection control
• Dietary intake
• Medications : salicylates increase insulin secretion and sensitivity avoid
aspirin.
Dental management
considerations

Stress reduction
Changes in medication regimens
Management of emergencies
Dental management
considerations

Dental management
of diabetic patients
General management
Assess patient’s level of glycemic
control prior to initiating treatment
Maintain a close working
relationship with patient’s physician
Refer patients with signs & symptoms
suggestive of undiagnosed or
uncontrolled diabetes to physician
Antibiotic prophylaxis
Dentists should have in-office
glucometer and glucose source in
dental office
• If patient’s HbA1c level is >11-12%
• If there are signs of recurrent
intraoral bacterial infections

Specific management
 Use of epinephrine
 Oral candidiasis
 Management of Recurrent herpes simplex virus
 Management of burning mouth syndrome
 Surgical considerations
 Periodontal disease management
 Oral disease management with corticosteroids
Dental management

Use of epinephrine in LA is not contraindicated
 Promotes better anaesthesia
 Lowers amount of endogenous epinephrine released in response to
pain and stress
 Endogenous epinephrine elevate blood glucose levels
Dental management
Specific management

Oral fungal
infections
• Signifies uncontrolled DM
• Treatment is similar to that of standard
regimen except topical antifungals
should be sugar free
• Oral fungal infections uncontrolled
diabetes mellitus
• Recurrent orofacial herpes simplex
infection
Dental management
Specific management

Management of
Recurrent herpes
simplex virus
• Treatment of recurrent cases should be initiated early in the prodromal stage
• If patient has insufficiency or renal failure, nephrotoxic antiviral drugs require dose
modification
Management
of BMS
• In uncontrolled DM, xerostomia and candidiasis can contribute to BMS
• Treatment of xerostomia and candidiasis
• Improve glycemic control
• Counselling and reassurance in mild cases
• Amitryptyline, Doxepin, Clonazepam given for analgesic effect
Dental management
Specific management

Surgical
consideration
• Prior to surgical procedure, review previous h/o surgical complications and
assess glycemic control
• Maintain normal diet after surgical procedure
• Antibiotic administration in poorly controlled DM patients
Periodontal disease
management
• 6th complication of DM
• Primary treatment: Nonsurgical debridement + Systemic Antibiotics
• Tetracycline + Scaling & root planning
• Supportive periodontal therapy at intervals of 2-3months
Dental management
Specific management

Dental management
Specific management
and treatment. 8th

Every dental office should have readily available source of carbohydrate  glucose
powder, fruit juice, hard candy
When patient experiences signs and
symptoms of hypoglycemia, dentist
should check blood glucose level with
a glucometer
If glucometer is unavailable, by default
treat it like hypoglycaemia
Following treatment, signs and symptoms should revert back in 10-15min
Dental management
and treatment. 8th

Treatment of Hyperglycaemia
 Terminate dental procedure
 Position patient supine with legs elevated slightly
 Follow the A-B-Cs
 Open airway
 Administer oxygen
 Maintain and monitor circulation and vital signs
 Transportation to hospital for further management

Dental management

Conclusion
 Diabetes mellitus is a metabolic condition affecting multiple organ
systems.
 The oral cavity undergoes changes that are related to the diabetic
condition, and oral infections may adversely affect metabolic control of
the diabetic state.
 Hence, Oral healthcare professional is a crucial part of the health care
team in screening and monitoring patients with Diabetes Mellitus.

References
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Management. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2014.
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Association of Physicians, Mumbai; 1097-1136.

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Medicine: Diagnosis and Treatment. 8th ed. USA: JB Lippincott Company; 1984. 842-848.
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