diabetes mellitus- dr sanjana ravindra

Diabetesmellitus

Seminar -5

Dr.Sanjana.RavindraRajarajeswari Dental collegeBangalore

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

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


Chronic hyperglyc

emia

Defect in insulin

secretion from

pancreas

Resistance of body’s cells to insulin

action

Both

Introduction


Scarcity in plenty

History

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

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 heterogenousgroup 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


Epidemiology

Globally382 million people had diabetes in 2013

By 2035, this number will rise to 592 million

In India65.1 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

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.

Anatomy of pancreas

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



• 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



Actions of insulin

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 glucoseHormone Main site of hormone

productionEffect 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

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 IINon-obese

Absent Absent Negative Eucaloric diet aloneOrDiet 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 DMIt 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


Risk factors

Risk factorsFamily 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.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

Type 1 diabetes mellitus

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


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


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


Hygiene hypothesis Viral infection-

mumps, Coxsackie B4, retroviruses, rubella (in

utero), cytomegalovirus, Epstein–Barr

virus

StressDietary factors

nitrosamines

Bovine serum albumin

Type 1 DM


Pathogenesis of type 1 diabetes mellitus


Type 1 DM


Fats

Lipolysis

Glycerol Free fatty acids

Glucose Ketones


Type 2 diabetes mellitus

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.


Most type 2 DM patients

are overweight, and most are diagnosed as

adults.

Slow onset

Approximately 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


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 veinpotent influence on insulin sensitivity in the liver


Type II Diabetes Mellitus-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



Insulin resistance syndrome / Reaven’ssyndrome /Syndrome X


Type II DmGenetic 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


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

Type II DmEnvironmental 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


Type II DmEnvironmental and other risk factors

Age: Prevalence increases with age; ~10% over 65 years Renal threshold for glucose rises with age GlycosuriaPregnancy: 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


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


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.


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


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.


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

Type II Diabetes Mellitus-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.


Type II Diabetes Mellitus-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


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. 20152. 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 CotranPathologic 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

Diabetesmellitus

Seminar -5

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

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


Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds. Essentials of Biochemistry. 2nd

ed. Uppala Author- publisher, Vijayavada 2008.

Clinical features

Clinical featuresThe 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


Clinical features

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

Oral manifestations

Oral manifestations

Related to poor glycemic control

1. Burning mouth syndrome2. Altered wound healing3. Increased incidence of infection4. Candidal infection Median Rhomboid

glossitis, Angular cheilitis, Acute pseudomembranous candidiasis of tongue, buccal mucosa and gingiva


Bilateral generalized salivary gland enlargement Xerostomia Gingivitis Periodontitis, periodontal abscesses Dental caries

Oral manifestations


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


ORAL CANDIDIASIS

Oral manifestations

POOR ORAL HYGEINe WITH EXCESS CALCULUS

FORMATION

TENDENCY FOR PROGRESSIVE

CARIES


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.

Diagnosis

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


Laboratory test for diagnosis

Laboratory test for diagnosis

Estimation of blood glucose.

Oral glucose tolerance test.


DiagnosisThe diagnosis of diabetes is based on the presence of clinical signs and symptoms,

along with specific laboratory findings

Diagnosis


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.


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


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


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 sulphate17.3 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 risk150-199 Intermediate risk≥ 200 High riskLDL cholesterol<100 Low risk100-129 Intermediate risk≥130 High riskHDL cholesterol<35 High risk35-45 Intermediate risk>45 Low risk

Diagnosis

Blood analysisGlucose

Enzymatic reaction (glucose oxidase) random/ fasting

Colorimetric or other testing sticks capillary (fingerprick) testing to monitor diabetes treatmentDiagnosis of diabetes accurate laboratory method

Glucose venous < arterial/capillary blood

Whole blood glucose concentrations < plasma concentrations

Venous plasma valuesmost 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- fair13-20% 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 βcell transplantation.

Also increasingly used for primary diagnosis of dm.Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians,

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.


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


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.


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/dl1 hr – 180 mg/dl2 hr – 155 mg/dl3 hr – 140 mg/dl


Laboratory test for screening

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.


Selective screening

High risk individuals ---Obese Family h/o DMHypertension DyslipidemiaImpaired glucose tolerance

Screening test is performed at earlier age ( 30 yrs )and repeated more frequently

Laboratory test to assess

glycemiccontrol

Laboratory test to assess glycemic control

Periodic measurement of glycated

haemoglobin.

Daily self assessment of blood glucose.

Others


Insulin assay

Measurement of insulin level by radioimmunoassay & ELISA.

Crucial for type I DM.


Self–blood glucose monitoring (SBGM)Diagnosis

COMPLICATIONS OF DIABETES

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



Acute complications:HypoglycemiaDiabetic ketoacidosisNon ketotic hyperosmolar diabetic coma

Late complications :Retinopathy - blindnessNephropathy – renal failureNeuropathy – sensory , autonomicMacro vascular disease - atherosclerosis, strokeAltered wound healingDiabetic 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


Protein glycationleading 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).


Acute complications

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



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 infusionAdminister 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/dLGlucose 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

Diabetic ketoacidosis

Acute complications

• Serious cause of morbidity type 1 diabetes

• Established diabetesintercurrent 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

Diabetic ketoacidosis 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 catecholaminesand 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 complicationsDiabetic ketoacidosis


Methods to detect ketone bodies

1. Rothera’s test

2. Reagent strip

3. Gerhardt ferric chloride test

Rothera test

ProcedureTake 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

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.

http://www.sghhealth4u.com.sg/health4u/endocrinology/Eye_disease_in_Diabetes_mellitus.html

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http://www.sghhealth4u.com.sg/health4u/endocrinology/Kidney_disease_in_diabetes_mellitus.html




VASCULAR COMPLICATIONS

Occurs due to microangiopat

hy and atherosclerosis

Changes seen in blood

vessels:

Endothelial proliferation

Thickening of

basement membrane

Thickening of walls of

blood vessels

Increase lipid

metabolism

Atheroma formation



DIABETIC RETINOPATHY

Increases with increase in duration of

diabetes and more common in type I

Dilation

OcclusionIncrease

permeability of blood vessels



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





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 gfrleads to end stage renal disease.



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



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


Baliga V, Sapsford R. Review article: Diabetes mellitus and heart failure -- an overview of epidemiology and management. Diabetes Vascular Dis Res 2009; 6: 164.

Management

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.

ManagementPRIMARY 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 glycemiccontrol.


• 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.



• 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


• 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.


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• 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.


• 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.


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 therapy1. Hypoglycaemia2. Weight gain3. 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


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

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Cure to Diabetes Using Stem Cells

http://www.amyshah.com/stem-cells/the-cure-to-diabetes/

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 levelsFrequency of hypoglycemic episodesMedication, dosage and times.Consultation

Dental management considerations

Malamed SF. Medical emergencies in the dental office. 5th ed. Noida: Mosby; 2000.


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.



Stress reduction

Changes in medication regimens

Management of emergencies



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



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


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


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


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


Specific management



Specific management


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



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


Prevention

Conclusion

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.

References1. IDF Diabetes Atlas. 6th ed. 2014.2. Malamed SF. Medical Emergencies in the Dental Office. 5th ed. Noida: Mosby; 2000. 3. Davidson’s Principles and Practice of Medicine. 21st ed. China: Elsevier; 2010. 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. Frier BM, Fisher M. Diabetes mellitus. Colledge NR, Walker BR, Ralston SH. Davidson’s Principles

and Practice of Medicine. 21st ed. China: Elsevier; 2010. p. 795-835.7. Endocrinology. In: Scully C. Medical problems in dentistry. 6th ed. China: Elsevier; 2010. p. 138-

145.8. 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.

9. Ramachandran A, A.K Das. Diabetology. In Shah SN eds. API Textbook of Medicine. 7th ed. The Association of Physicians, Mumbai; 1097-1136.

10. 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.

11. 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.

12. Mealey B. Diabetes Mellitus. Greenberg MS, Glick M eds. Burket's Oral Medicine. 10th ed. Spain: BC Decker Inc; 2003. 563-577.

13. 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.

14. 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.

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

16. William Boyd A Textbook of Pathology- Structure and Function in Disease; 8th edition.17. Insulin, Glucose homeostasis, and diabetes mellitus. In Satyanarayan U, Chakrapani U eds.

Essentials of Biochemistry. 2nd ed. Uppala Author- publisher, Vijayavada 2008. 18. Olokoba AB, Obateru OA, Olokoba LB. Type 2 Diabetes Mellitus: A Review of Current

Trends. Oman Med J 2012; 27(4): 269-273

References

19. Joshi SK, Shrestha S. Diabetes mellitus: A review of its associations with different environmental factors. Kathmandu University Med J 2010; 8(1): 109-115.

20. 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.

21. 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.

22. Baliga V, Sapsford R. Review article: Diabetes mellitus and heart failure -- an overview of epidemiology and management. Diabetes Vascular Dis Res 2009; 6: 164.

23. 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 ClinPrac 2010; 89: 309-319.

24. Vasiliadis I, Kolovou G, Mavrogeni S, Nair DR, Mikhailidis DP. Sudden cardiac death and diabetes mellitus. J Diabetes Complications 2014; 28(4): 573-579.

25. Oliveira C, Simoes M, Carvalho J, Ribeiro J. Combined exercise for people with type 2 diabetes mellitus: A systematic review. Diabetes Res Clin Prac 2012; 98: 187-198.

26. Bastaki S. Diabetes mellitus and its treatment. Int J Diabetes & Metabolism 2005; 13:111-134.

References

Thank you

diabetes mellitus- dr sanjana ravindra

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