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Presented by: 
Dr. Yogender Singh 
Under the guidance of: 
Dr. H S Grover & Faculty
CONTENTS 
• INTRODUCTION 
• DEFINITIONS 
• HISTORY 
• EPIDEMIOLOGY 
• CLASSIFICATION 
• DIAGNOSIS 
• INSULIN & DIABETES 
• CLASSICAL SIGNS, SYMPTOMS & COMPLICATIONS OF DM 
• DIABETES AND PERIODONTAL DISEASE 
• DENTAL THERAPY CONSIDERATIONS 
• CONCENSUS REPORT- EFP/AAP JOINT WORKSHOP 
• CONCLUSION 
• REFRENCES
INTRODUCTION 
• Diabetes mellitus represents a spectrum of metabolic 
disorders and has emerged as a major health issue 
worldwide. 
• It is a complex metabolic disease characterized by: 
 Chronic hyperglycemia, 
 Diminished insulin production, 
 Impaired insulin action, or a combination of both 
• Result in the inability of glucose to be transported from 
the bloodstream into the tissues, which in turn, results 
in high blood glucose levels and excretion of sugar in 
the urine. 
 Alteration in lipid and protein metabolism.
DEFINITIONS 
• International Diabetes Federation (IDF) describes 
Diabetes as a chronic disease that arises when the 
pancreas does not produce enough insulin, or when 
the body cannot effectively use the insulin it produces. 
• According to Carranza, DM is defined as a complex 
metabolic disorder characterized by chronic 
hyperglycaemia, diminished insulin production, 
impaired insulin action or a combination of both result 
in the inability of glucose to be transported from the 
blood stream into the tissues, which in turn results in 
high blood glucose levels and excretion of sugar in the 
urine.
HISTORY 
• Diabetes is one of the first diseases described with an Egyptian 
manuscript from 1500 BC mentioning “too great emptying of 
the urine.” 
• The term diabetes was probably coined by Apollonius of 
Memphis around 250 BC, which literally meant “to go 
through” or siphon as the disease drained more fluid than a 
person could consume. Later on, the Latin word “mellitus” 
was added because it made the urine sweet. 
5
• Sir Frederick Grant Banting, Charles Herbert Best and 
colleagues purified the hormone insulin from bovine pancreas 
at the University of Toronto. Leading to the availability of an 
effective treatment—insulin injections and the first patient 
was treated in 1922. 
• For this, Banting and laboratory director John MacLeod 
received the Nobel Prize in Physiology or Medicine in 1923. 
6
EPIDEMIOLOGY 
According to International Diabetes Federation (2012), there are more than 371 
million people in world who have diabetes. The number of people with diabetes is 
increasing in every country in which half of people with diabetes are undiagnosed. The 
estimate of the actual number of diabetics in India is around 40 million.
CLASSIFICATIONS 
National Diabetes Data Group(1979)- on the basis of 
age at onset and type of therapy: 
• TYPE I- Insulin dependent DM (IDDM) or Juvenile 
Diabetes 
• TYPE II- Non insulin dependent DM (NIDDM) or Adult 
onset Diabetes
American diabetic 
association 
(1997) 
DM is classified on the 
basis of pathophysiology 
of DM into 4 categories: 
1. Type 1 
2. Type 2 
3. Other Specific types of 
DM 
4. Gestational diabetes
CARBOHYDRATE METABOLISM, INSULIN AND DIABETES
BLOOD GLUCOSE HOMEOSTASIS
ACTIONS OF INSULIN
Characteristics of Type I and Type II 
Diabetes
OTHER SPECIFIC TYPES 
• Those associated with diseases that involve the pancreas and 
destruction of insulin producing cells. 
• Endocrine diseases such as acromegaly, tumors, 
pancreatectomy and drugs or chemicals are included.
GESTATIONAL DIABETES 
• Under normal conditions insulin secretion is increased by 
1.5 to 2.5 fold during pregnancy reflecting a state of insulin 
resistance 
• Gestational diabetes develops in 2% to 5% of all 
pregnancies but disappears after delivery. 
• Women who have had gestational diabetes are at increased 
risk of developing type 2 diabetes later in life. 
• It usually has its onset in the third trimester of pregnancy 
and adequate treatment will reduce perinatal abnormality.
LABORATORY DIAGNOSIS 
BLOOD TESTING 
1. GLUCOSE
LABORATORY DIAGNOSIS 
2. Glycated Hemoglobin
URINE TESTING 
1. GLUCOSE 
Testing the urine for glucose with dipsticks is a common screening 
procedure for detecting diabetes. 
2. KETONES 
Ketone bodies can be identified by the nitroprusside reaction, 
which measures acetoacetate, using either tablets or dipsticks. 
3. PROTEIN 
Standard dipstick testing for albumin detects urinary albumin at 
concentrations > 300mg/L
CLASSICAL SIGNS 
& SYMPTOMS 
It includes polydypsia, 
polyphagia, polyuria, pruritis, 
weakness & fatigue. (More 
common on type 1) occur in 
varying degree in type 2 DM. 
Type 1 DM may associated 
with Weight loss, Ketoacidosis 
Restlessness, irritability & 
apathy may become evident.
THE CLASSIC COMPLICATIONS OF DM 
1. Diabetic Retinopathy 
2. Diabetic Neuropathy 
3. Diabetic Nephropathy 
4. Atherosclerosis 
5. Impaired wound healing 
6. Periodontal disease (Loe H 
1993)
DIABETES & PERIODONTIUM 
ORAL MANIFESTATIONS: 
• Diminished salivary flow 
• Burning mouth & tongue 
• Enlargement of parotid gland (Alteration in basement mem.) 
• Cheilosis 
• Alterations in flora of oral cavity (Predominance by Candida 
albicans) 
• Increase rate of dental caries
PERIODONTAL MANIFESTATIONS 
Hirchfeld I (1934) 
• Tendency towards 
enlarged gingiva. 
• Sessile/pedunculated 
gingival polyps. 
• Ploypoid gingival 
proliferations 
• Abscess formation 
• Periodontitis 
• Loosened teeth
Factors Potentially Contributing to 
Development of Periodontal Disease 
Polymorphonuclear 
leukocyte function 
Collagen Metabolism and 
Advanced glycation end 
products 
Infections in 
patients with 
diabetes 
Wound 
healing 
Bacterial 
Associations
Polymorphonuclear leukocyte 
function 
• Impaired Chemotaxis & adherence 
• Defective Phagocytosis 
 Diminished primary defense against 
periodontal pathogens.
Collagen Metabolism 
Reduced synthesis of 
collagen & 
glycosaminoglycans 
Hyperglycemic state 
Reduced 
collagen 
maturation 
Collagen 
homeostasis- 
Affected 
GCF collagenase 
activity increased
ADVANCED GLYCATION END PRODUCTS (AGEs) 
Hyperglycemic state 
Non enzymatic 
Glycosylation of 
proteins and 
matrix molecules
AGEs 
 Plays central role in diabetic complications . 
 Alter functions of extracelluar matrix . 
 Affects collagen stability and vascular integrity. 
AGEs formation on collagen 
 Increased crosslinking between collagen molecules 
 Reduced solubility . 
 Decreased turn over rate .
AGEs + Macrophages & Monocytes 
Hyper-cellular state changes 
Increased Secreation of IL-1, IGF, 
TNF ἀ 
AGEs 
AGEs + Endothelial cells 
Pre-coagulatory 
•Focal thrombosis 
•Vasoconstriction
AGEs AND PERIODONTIUM
2- WAY RELATIONSHIP BETWEEN PERIODONTAL 
DISEASE AND DM
PATHOGENESIS OF PERIODONTITIS IN DIABETES 
Taylor JJ. JOP 2013
LINKAGE BETWEEN INFECTION,HYPERLIPIDEMIA 
& INSULIN RESISTANCE
INFECTIONS IN PATIENTS WITH 
DIABETES 
Mainly due to: 
• Impaired defence mechanism 
1. Defects in PMN function 
2. Induction of insulin resistance 
3. Vascular changes 
Hyperglycemic state 
Glycosylation of basement 
mem, proteins 
• Thickning of gingival 
capillaries, 
• Disruption of BM 
Swelling of Endothelium 
Impeded 
1. Oxygen diffusion 
2. Metabolic waste elimination 
3. PMN Migration 
4. Diffusion of serum factors
WOUND HEALING 
Wound Healing is Affected as cumulative effect of: 
•Altered cellular activity 
•Decreased collagen synthesis 
•Glycosylation of existing collagen 
•Increase collagenase production 
Readily degrade newly 
synthesized, less completely 
cross linked collagen 
•Reduced Collagen solubility 
•Delayed remodelling of wound site 
Defective Healing
BACTERIAL ASSOCIATION 
• Glucose content of GCF & blood is higherin diabetics. 
• Results in changed environment fo the microflora 
• Presence of higher levels of specific microorganisms such as 
Actinobacillus actinomycetemcomitans and Capnocytophaga . 
(Mashimo et al 1983) 
• The proportion of P gingivalis was reported to be higher in non-insulin- 
dependent diabetes mellitus patients with periodontitis. 
• This may be due to the abnormal host defense mechanisms in 
addition to hyperglycemic state can lead to the growth of 
particular fastidious organisms. (Zambon et al,1988)
EFFECT OF DIABETES ON PERIODONTITIS 
Data of multiple studies reveal 
strong evidence 
•Diabetes is a risk factor for gingivitis & 
periodontitis. 
•The level of glycemic control appears to be an 
important determinant in this relationship. 
Cianciola et 
al 
1982 In children with type 1 diabetes, the prevalence of gingivitis was greater than in 
non-diabetic children with similar plaque levels. 
Sastrowijot 
o S et al 
1990 Improvement in glycemic control may be associated with decreased gingival 
inflammation. 
Papapanou 
PN 
1996 Majority of the studies demonstrate a more severe periodontal condition in 
diabetic adults than in adults without diabetes. 
Tsai C et al 2002 In a large epidemiologic study in the United States, adults with poorly controlled 
diabetes had a 2.9-fold increased risk of having periodontitis compared to non-diabetic 
adult subjects; conversely,well-controlled diabetic subjects had no 
significant increase in the risk of periodontitis. 
Salvi GE et 
al 
2005 Rapid and pronounced development of gingival inflammation in relatively well-controlled 
adult type 1 diabetic subjects than in non-diabetic controls, despite 
similar levels of plaque accumulation and similar bacterial composition of plaque, 
suggesting a hyperinflammatory gingival response in diabetes.
EFFECT OF PERIODONTAL DISEASE ON 
DIABETES 
• Periodontal diseases can have a significant impact on the 
metabolic state in diabetes. The presence of periodontitis 
increases the risk of worsening of glycemic control over time. 
Williams RC Jr., 
Mahan CJ. 
1960 Type 1 diabetic patients with periodontitis had a reduction in required insulin 
doses following scaling and root planing, localized gingivectomy, and selected 
tooth extraction combined with systemic procaine penicillin G and streptomycin 
Taylor GW et al 1996 In a 2-year longitudinal trial, diabetic subjects with severe periodontitis at 
baseline had a six-fold increased risk of worsening of glycemic control over time 
compared to diabetic subjects without periodontitis 
Rodrigues DC 
et al 
2003 Better improvement in glycemic control in a diabetic group treated with scaling 
and root planing alone compared to diabetic subjects treated with scaling and 
root planing plus systemic amoxicillin/clavulanic acid. 
Promsudthi A 
et al 
2005 In older, poorly controlled type 2 diabetic subjects who received scaling and root 
planing plus adjunctive doxycycline showed a significant improvement in 
periodontal health but only a non significant reduction in HbA1c values.
MECHANISM BY WHICH PERIODONTAL 
DISEASE MAY INFLUENCE DIABETES 
Acute bacterial and viral infections 
Chronic gram-negative periodontal infections have 
significantly higher serum markers of inflammation such 
as c-reactive protein (CRP), IL-6, and fibrinogen than 
subjects without periodontitis. 
Periodontal treatment may reduce inflammation locally and 
also decrease serum levels of the inflammatory mediators 
that cause insulin resistance, thereby positively affecting 
glycemic control
EFFECTS OF DIABETES ON THE 
RESPONSE OF PERIODONTAL THERAPY 
• Many diabetic patients show improvement in clinical 
parameters of disease immediately after therapy, patients with 
poorer glycemic control may have a more rapid recurrence of 
deep pockets and a less favorable long-term response. 
• Further longitudinal studies of various periodontal treatment 
modalities are needed to determine the healing response in 
individuals with diabetes compared to individuals without 
diabetes.
CURRENT MEDICAL MANAGEMENT OF 
DIABETES MELLITUS 
1. DIET : The goals of this intervention include 
weight reduction, improved glycemic control, 
with blood glucose levels in the normal 
range, and lipid control. 
2. Exercise : Regular physical exercise to weight 
reduction, increased cardiovascular fitness, 
and physical working capacity.
3.Pharmacological therapy :
Anti-AGE Therapies 
• It include Aminoguanidine, ALT-946, ALT 711, 
Statins (Cervistatin) 
• Pyridoxamine, the natural form of vitamin B6, is 
effective at inhibiting AGEs at 3 different levels. 
– prevents the degradation of protein-Amadori 
intermediates to protein-AGE products. 
– In diabetic rats, pyridoxamine reduces hyperlipidemia 
and prevents AGE formation. 
– scavenges the carbonyl byproducts of glucose and 
lipid degradation 
– Benfotiamine, a lipid-soluble thiamine derivative, 
inhibits the AGE formation pathway.
DENTAL THERAPY CONSIDERATIONS 
• Patients with well-controlled diabetes can often be treated in 
a similar way to non-diabetic patients. 
• Communicate with patient’s physician to obtain control of 
blood glucose levels 
• Control acute infections. 
• As aggravated glycemic control increases the risk of micro & 
macrovascular diabetic complications like- Stroke, MI, Heart 
Failure.
Timing of treatment 
Patients with well controlled DM can be treated 
similarly to non-diabetic patients for most routine 
dental needs. 
• Keep appointments short, atraumatic, and stress-free 
• morning appointments 
• Use appropriate vasoconstrictor agents 
• For stressful procedures the usual drug regime may 
be altered
ANTIBIOTICS USE 
• Antibiotics are not necessory for routine 
procedures in patients with well-controlled 
diabetes. 
• But considered in the presence of overt oral 
infection. 
• The combination of mechanical debridement+ 
systemic tetracycline provide greater positive 
effect on glycemic control in some DM 
patients.
DENTAL IMPLANT CONSIDERATIONS 
IN THE DIABETIC PATIENT 
• Diabetes-induced changes in 
bone formation: 
• Inhibition of collagen matrix 
formation 
• Alterations in protein 
synthesis 
• Increased time for 
mineralization of osteoid 
• Reduced bone turnover 
• Decreased number of 
osteoblasts and osteoclasts 
• Altered bone metabolism 
• Reduction in osteocalcin 
production 
Possible Diabetic Disturbances in Implant 
Wound Healing Process In Implants
DIABETIC EMERGENCIES 
• Hypoglycemic crisis 
• Hyperglycemic crisis
MANAGEMENT OF HYPOGLYCEMIA 
FACTORS THAT INCREASE THE RISK OF HYPOGLYCEMIA 
Skipping or delaying food intake 
Injection of too much insulin 
Injection of insulin into tissue with high blood flow (eg, injection into thigh after 
exercise such as running) 
Increasing exercise level without adjusting insulin or sulfonylurea dose. 
Inability to recognize symptoms of hypoglycemia 
Denial of warning signs or symptoms 
Past history of hypoglycemia 
Hypoglycemia unawareness 
Low Blood Glucose 
• Sign & symptoms occurs as fall in blood glucose 
level below 60 mg/dl. 
• Severe hypoglycemia refers to fall in blood glucose 
concentration below 40 mg% (2.2-mmol/1) 
requiring help from outside for recovery.
SIGN & SYMPTOMS 
Low Blood Glucose 
The most common emergency related to DM in the 
dental office and a potentially life-threatening situation 
that must be recognized and treated expeditiously. 
MENTAL CONFUSION, SUDDEN MOOD CHANGE 
LETHARGY,….TACHYCARDIA , NAUSEA, 
COLD CLAMMY SKIN, HUNGER, INCREASED 
GASTRIC MOTILITY, HYPOTENTION , 
HYPOTHERMIA. 
Severe hypoglycaemia may result in seizures or loss 
of consciousness.
If patient is 
UNCONSCIOUS 
Low Blood Glucose 
Give 50 ml of 50% intravenous glucose- through a large 
vein to avoid thrombophlebitis. 
As soon as patient recovers consciousness, start oral 
carbohydrate intake, otherwise 5-10% glucose infusion has 
to be continued till patient recovers consciousness. 
Intramuscular injection of 1.0 ml of glucagon may be given 
if hypoglycaemia is insulin induced. It promotes 
glycogenolysis, gluconeogenesis. 
If patient does not regain consciousness inspite of normal 
blood glucose levels, then cerebral oedema is likely 
possibility which should be treated with intravenous 
dexamethasone or mannitol.
ADMINISTRATION OF 15g OF ORAL 
CARBOHYDRATE (JUICE,CANDY) 
Repeated hypoglycaemic episodes are hazardous for 
CNS; hence, one should find out the cause and treat it 
or correct it by adjusting the patient's therapy. 
Low Blood Glucose 
If patient becomes 
CONSCIOUS 
PREVENTION
MANAGEMENT OF HYPERGLYCEMIA 
High Blood Glucose 
It occurs when blood glucose levels over 200mg/dl for 
extended period of time. 
In Type 1 DM- ketoacidosis may occur- Characterized by- 
Disorientation, rapid & deep breathing, hot drying skin & 
acetone breath. 
Type 2 DM- hyperosmolar non-ketotic diabetic acidosis. 
Severe hypotention & Loss of consciousness occurs if left 
untreated. 
• A medical emergency from hyperglycemia is less 
likely to occur in the dental office since it develops 
more slowly than hypoglycaemia.
High Blood Glucose 
Care is initiated by activating the emergency 
medical system, opening the airway, and 
administering oxygen. Circulation and vital signs 
should be maintained and monitored, and the 
patient should be transported to a hospital . 
• Under some instances, severe hyperglycemia may 
present with symptoms mimicking hvpoglycemia. 
• If a glucometer is not available, these symptoms 
must be treated as hypoglycemia.
DIABETES & PERIODONTAL DISEASE: CENSUS REPORT OF THE JOINT 
EFP/AAP WORKSHOP ON PERIODONTITIS & SYSTEMIC DISEASES 
(CHAPPLE LC,GENCO R. J PERIODONTOL 2013)
GUIDELINE- A 
[Suggested Guidelines for physicians and other medical health professions for Use in Diabetes 
Practice] 
• Patients with diabetes should be told that periodontal disease 
risk is increased by diabetes. 
• If they suffer from periodontal disease, their glycaemic control 
may be more difficult, and they are at higher risk for diabetic 
complications such as cardiovascular and kidney disease. 
• Patients with type 1, type 2 and gestational diabetes should 
receive a thorough oral examination, which includes 
comprehensive periodontal examination. 
• For all newly diagnosed type 1 and type 2 diabetes patients, 
subsequent periodontal examinations should occur & annual 
periodontal review is recommended. 
• For children and adolescents diagnosed with diabetes, annual 
oral screening is recommended from the age of 6–7 years by 
referral to a dental professional.
GUIDELINE- B 
[Suggested guidelines for use in dental practice] 
• If periodontitis is diagnosed, manage it properly. If not, patients 
with diabetes should be placed on a preventive care regime and 
monitored regularly for periodontal changes. 
• Patients with diabetes presenting with any acute oral/periodontal 
infections require prompt oral/ periodontal care. 
• Patients with diabetes who have extensive tooth loss should be 
encouraged to pursue dental rehabilitation to restore adequate 
mastication for proper nutrition. 
• Provide oral health education. 
• Patients who present without a diabetes diagnosis, but at risk for 
type 2 diabetes and signs of periodontitis should be informed about 
their risk for having diabetes, assessed using a chair-side HbA1C 
test, and/or referred to a physician for appropriate diagnostic 
testing and follow-up care.
GUIDELINE- C 
[Recommendations for patients with diabetes at the physician’s practice/ office] 
• If your physician has told you that you have diabetes, 
you should make an appointment with a dentist to 
have your mouth and gums checked. This is because 
people with diabetes have a higher chance of getting 
gum disease. Gum disease can lead to tooth loss and 
may make your diabetes harder to control.
GUIDELINE- D 
[Recommendations for patients at the dental surgery/office who have diabetes or are 
found to be at risk for diabetes] 
• People with diabetes have a higher chance of 
getting gum disease. If you have been told by 
your dentist that you have gum disease, you 
should follow up with necessary treatment as 
advised. 
• If you do not have diabetes, but your dentist 
identified some risk factors for diabetes 
including signs of gum disease, it is important 
to get a medical check-up as advised.
CONCLUSION 
• Diabetes mellitus has significant impact on tissues throughout the 
body, including the oral cavity. As research indicates that poorly 
controlled diabetes increases the risk periodontitis. 
• Alteration in host defence and tissue homeostasis appear to play a 
major role. 
• Advances in medical management of DM require a heightened 
awareness by the periodontist in the various treatment regimens 
used by diabetic patients. 
• Familiarity with various medications, monitoring equipments, and 
devices used by diabetic patient allows provision of appropriate 
periodontal therapy while minimizing the risk of complications.
REFERENCES 
• Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for 
pathogenic mechanisms that may link periodontitis and 
diabetes. J Periodontol 2013;84:S113-S34. 
• The position paper on diabetes & periodontal disease. J 
Periodontol 2000;71:664-78. 
• Grossi SG, Genco RJ. Periodontal Disease and Diabetes 
Mellitus: A Two-Way Relationship. Ann Periodontol 1998;3:51- 
61. 
• Periodontal Medicine Rose, Cohen 
• Carranza’s Clinical Periodontology 11th edition 
• Davidson’s Principles and Practice of Medicine 21st edition
THANK YOU

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Diabetes mellitus & Periodontium

  • 1. Presented by: Dr. Yogender Singh Under the guidance of: Dr. H S Grover & Faculty
  • 2. CONTENTS • INTRODUCTION • DEFINITIONS • HISTORY • EPIDEMIOLOGY • CLASSIFICATION • DIAGNOSIS • INSULIN & DIABETES • CLASSICAL SIGNS, SYMPTOMS & COMPLICATIONS OF DM • DIABETES AND PERIODONTAL DISEASE • DENTAL THERAPY CONSIDERATIONS • CONCENSUS REPORT- EFP/AAP JOINT WORKSHOP • CONCLUSION • REFRENCES
  • 3. INTRODUCTION • Diabetes mellitus represents a spectrum of metabolic disorders and has emerged as a major health issue worldwide. • It is a complex metabolic disease characterized by:  Chronic hyperglycemia,  Diminished insulin production,  Impaired insulin action, or a combination of both • Result in the inability of glucose to be transported from the bloodstream into the tissues, which in turn, results in high blood glucose levels and excretion of sugar in the urine.  Alteration in lipid and protein metabolism.
  • 4. DEFINITIONS • International Diabetes Federation (IDF) describes Diabetes as a chronic disease that arises when the pancreas does not produce enough insulin, or when the body cannot effectively use the insulin it produces. • According to Carranza, DM is defined as a complex metabolic disorder characterized by chronic hyperglycaemia, diminished insulin production, impaired insulin action or a combination of both result in the inability of glucose to be transported from the blood stream into the tissues, which in turn results in high blood glucose levels and excretion of sugar in the urine.
  • 5. HISTORY • Diabetes is one of the first diseases described with an Egyptian manuscript from 1500 BC mentioning “too great emptying of the urine.” • The term diabetes was probably coined by Apollonius of Memphis around 250 BC, which literally meant “to go through” or siphon as the disease drained more fluid than a person could consume. Later on, the Latin word “mellitus” was added because it made the urine sweet. 5
  • 6. • Sir Frederick Grant Banting, Charles Herbert Best and colleagues purified the hormone insulin from bovine pancreas at the University of Toronto. Leading to the availability of an effective treatment—insulin injections and the first patient was treated in 1922. • For this, Banting and laboratory director John MacLeod received the Nobel Prize in Physiology or Medicine in 1923. 6
  • 7. EPIDEMIOLOGY According to International Diabetes Federation (2012), there are more than 371 million people in world who have diabetes. The number of people with diabetes is increasing in every country in which half of people with diabetes are undiagnosed. The estimate of the actual number of diabetics in India is around 40 million.
  • 8. CLASSIFICATIONS National Diabetes Data Group(1979)- on the basis of age at onset and type of therapy: • TYPE I- Insulin dependent DM (IDDM) or Juvenile Diabetes • TYPE II- Non insulin dependent DM (NIDDM) or Adult onset Diabetes
  • 9. American diabetic association (1997) DM is classified on the basis of pathophysiology of DM into 4 categories: 1. Type 1 2. Type 2 3. Other Specific types of DM 4. Gestational diabetes
  • 13. Characteristics of Type I and Type II Diabetes
  • 14. OTHER SPECIFIC TYPES • Those associated with diseases that involve the pancreas and destruction of insulin producing cells. • Endocrine diseases such as acromegaly, tumors, pancreatectomy and drugs or chemicals are included.
  • 15. GESTATIONAL DIABETES • Under normal conditions insulin secretion is increased by 1.5 to 2.5 fold during pregnancy reflecting a state of insulin resistance • Gestational diabetes develops in 2% to 5% of all pregnancies but disappears after delivery. • Women who have had gestational diabetes are at increased risk of developing type 2 diabetes later in life. • It usually has its onset in the third trimester of pregnancy and adequate treatment will reduce perinatal abnormality.
  • 16. LABORATORY DIAGNOSIS BLOOD TESTING 1. GLUCOSE
  • 17. LABORATORY DIAGNOSIS 2. Glycated Hemoglobin
  • 18. URINE TESTING 1. GLUCOSE Testing the urine for glucose with dipsticks is a common screening procedure for detecting diabetes. 2. KETONES Ketone bodies can be identified by the nitroprusside reaction, which measures acetoacetate, using either tablets or dipsticks. 3. PROTEIN Standard dipstick testing for albumin detects urinary albumin at concentrations > 300mg/L
  • 19. CLASSICAL SIGNS & SYMPTOMS It includes polydypsia, polyphagia, polyuria, pruritis, weakness & fatigue. (More common on type 1) occur in varying degree in type 2 DM. Type 1 DM may associated with Weight loss, Ketoacidosis Restlessness, irritability & apathy may become evident.
  • 20. THE CLASSIC COMPLICATIONS OF DM 1. Diabetic Retinopathy 2. Diabetic Neuropathy 3. Diabetic Nephropathy 4. Atherosclerosis 5. Impaired wound healing 6. Periodontal disease (Loe H 1993)
  • 21. DIABETES & PERIODONTIUM ORAL MANIFESTATIONS: • Diminished salivary flow • Burning mouth & tongue • Enlargement of parotid gland (Alteration in basement mem.) • Cheilosis • Alterations in flora of oral cavity (Predominance by Candida albicans) • Increase rate of dental caries
  • 22. PERIODONTAL MANIFESTATIONS Hirchfeld I (1934) • Tendency towards enlarged gingiva. • Sessile/pedunculated gingival polyps. • Ploypoid gingival proliferations • Abscess formation • Periodontitis • Loosened teeth
  • 23. Factors Potentially Contributing to Development of Periodontal Disease Polymorphonuclear leukocyte function Collagen Metabolism and Advanced glycation end products Infections in patients with diabetes Wound healing Bacterial Associations
  • 24. Polymorphonuclear leukocyte function • Impaired Chemotaxis & adherence • Defective Phagocytosis  Diminished primary defense against periodontal pathogens.
  • 25. Collagen Metabolism Reduced synthesis of collagen & glycosaminoglycans Hyperglycemic state Reduced collagen maturation Collagen homeostasis- Affected GCF collagenase activity increased
  • 26. ADVANCED GLYCATION END PRODUCTS (AGEs) Hyperglycemic state Non enzymatic Glycosylation of proteins and matrix molecules
  • 27. AGEs  Plays central role in diabetic complications .  Alter functions of extracelluar matrix .  Affects collagen stability and vascular integrity. AGEs formation on collagen  Increased crosslinking between collagen molecules  Reduced solubility .  Decreased turn over rate .
  • 28. AGEs + Macrophages & Monocytes Hyper-cellular state changes Increased Secreation of IL-1, IGF, TNF ἀ AGEs AGEs + Endothelial cells Pre-coagulatory •Focal thrombosis •Vasoconstriction
  • 30. 2- WAY RELATIONSHIP BETWEEN PERIODONTAL DISEASE AND DM
  • 31. PATHOGENESIS OF PERIODONTITIS IN DIABETES Taylor JJ. JOP 2013
  • 33. INFECTIONS IN PATIENTS WITH DIABETES Mainly due to: • Impaired defence mechanism 1. Defects in PMN function 2. Induction of insulin resistance 3. Vascular changes Hyperglycemic state Glycosylation of basement mem, proteins • Thickning of gingival capillaries, • Disruption of BM Swelling of Endothelium Impeded 1. Oxygen diffusion 2. Metabolic waste elimination 3. PMN Migration 4. Diffusion of serum factors
  • 34. WOUND HEALING Wound Healing is Affected as cumulative effect of: •Altered cellular activity •Decreased collagen synthesis •Glycosylation of existing collagen •Increase collagenase production Readily degrade newly synthesized, less completely cross linked collagen •Reduced Collagen solubility •Delayed remodelling of wound site Defective Healing
  • 35. BACTERIAL ASSOCIATION • Glucose content of GCF & blood is higherin diabetics. • Results in changed environment fo the microflora • Presence of higher levels of specific microorganisms such as Actinobacillus actinomycetemcomitans and Capnocytophaga . (Mashimo et al 1983) • The proportion of P gingivalis was reported to be higher in non-insulin- dependent diabetes mellitus patients with periodontitis. • This may be due to the abnormal host defense mechanisms in addition to hyperglycemic state can lead to the growth of particular fastidious organisms. (Zambon et al,1988)
  • 36. EFFECT OF DIABETES ON PERIODONTITIS Data of multiple studies reveal strong evidence •Diabetes is a risk factor for gingivitis & periodontitis. •The level of glycemic control appears to be an important determinant in this relationship. Cianciola et al 1982 In children with type 1 diabetes, the prevalence of gingivitis was greater than in non-diabetic children with similar plaque levels. Sastrowijot o S et al 1990 Improvement in glycemic control may be associated with decreased gingival inflammation. Papapanou PN 1996 Majority of the studies demonstrate a more severe periodontal condition in diabetic adults than in adults without diabetes. Tsai C et al 2002 In a large epidemiologic study in the United States, adults with poorly controlled diabetes had a 2.9-fold increased risk of having periodontitis compared to non-diabetic adult subjects; conversely,well-controlled diabetic subjects had no significant increase in the risk of periodontitis. Salvi GE et al 2005 Rapid and pronounced development of gingival inflammation in relatively well-controlled adult type 1 diabetic subjects than in non-diabetic controls, despite similar levels of plaque accumulation and similar bacterial composition of plaque, suggesting a hyperinflammatory gingival response in diabetes.
  • 37. EFFECT OF PERIODONTAL DISEASE ON DIABETES • Periodontal diseases can have a significant impact on the metabolic state in diabetes. The presence of periodontitis increases the risk of worsening of glycemic control over time. Williams RC Jr., Mahan CJ. 1960 Type 1 diabetic patients with periodontitis had a reduction in required insulin doses following scaling and root planing, localized gingivectomy, and selected tooth extraction combined with systemic procaine penicillin G and streptomycin Taylor GW et al 1996 In a 2-year longitudinal trial, diabetic subjects with severe periodontitis at baseline had a six-fold increased risk of worsening of glycemic control over time compared to diabetic subjects without periodontitis Rodrigues DC et al 2003 Better improvement in glycemic control in a diabetic group treated with scaling and root planing alone compared to diabetic subjects treated with scaling and root planing plus systemic amoxicillin/clavulanic acid. Promsudthi A et al 2005 In older, poorly controlled type 2 diabetic subjects who received scaling and root planing plus adjunctive doxycycline showed a significant improvement in periodontal health but only a non significant reduction in HbA1c values.
  • 38. MECHANISM BY WHICH PERIODONTAL DISEASE MAY INFLUENCE DIABETES Acute bacterial and viral infections Chronic gram-negative periodontal infections have significantly higher serum markers of inflammation such as c-reactive protein (CRP), IL-6, and fibrinogen than subjects without periodontitis. Periodontal treatment may reduce inflammation locally and also decrease serum levels of the inflammatory mediators that cause insulin resistance, thereby positively affecting glycemic control
  • 39. EFFECTS OF DIABETES ON THE RESPONSE OF PERIODONTAL THERAPY • Many diabetic patients show improvement in clinical parameters of disease immediately after therapy, patients with poorer glycemic control may have a more rapid recurrence of deep pockets and a less favorable long-term response. • Further longitudinal studies of various periodontal treatment modalities are needed to determine the healing response in individuals with diabetes compared to individuals without diabetes.
  • 40. CURRENT MEDICAL MANAGEMENT OF DIABETES MELLITUS 1. DIET : The goals of this intervention include weight reduction, improved glycemic control, with blood glucose levels in the normal range, and lipid control. 2. Exercise : Regular physical exercise to weight reduction, increased cardiovascular fitness, and physical working capacity.
  • 42. Anti-AGE Therapies • It include Aminoguanidine, ALT-946, ALT 711, Statins (Cervistatin) • Pyridoxamine, the natural form of vitamin B6, is effective at inhibiting AGEs at 3 different levels. – prevents the degradation of protein-Amadori intermediates to protein-AGE products. – In diabetic rats, pyridoxamine reduces hyperlipidemia and prevents AGE formation. – scavenges the carbonyl byproducts of glucose and lipid degradation – Benfotiamine, a lipid-soluble thiamine derivative, inhibits the AGE formation pathway.
  • 43. DENTAL THERAPY CONSIDERATIONS • Patients with well-controlled diabetes can often be treated in a similar way to non-diabetic patients. • Communicate with patient’s physician to obtain control of blood glucose levels • Control acute infections. • As aggravated glycemic control increases the risk of micro & macrovascular diabetic complications like- Stroke, MI, Heart Failure.
  • 44. Timing of treatment Patients with well controlled DM can be treated similarly to non-diabetic patients for most routine dental needs. • Keep appointments short, atraumatic, and stress-free • morning appointments • Use appropriate vasoconstrictor agents • For stressful procedures the usual drug regime may be altered
  • 45. ANTIBIOTICS USE • Antibiotics are not necessory for routine procedures in patients with well-controlled diabetes. • But considered in the presence of overt oral infection. • The combination of mechanical debridement+ systemic tetracycline provide greater positive effect on glycemic control in some DM patients.
  • 46. DENTAL IMPLANT CONSIDERATIONS IN THE DIABETIC PATIENT • Diabetes-induced changes in bone formation: • Inhibition of collagen matrix formation • Alterations in protein synthesis • Increased time for mineralization of osteoid • Reduced bone turnover • Decreased number of osteoblasts and osteoclasts • Altered bone metabolism • Reduction in osteocalcin production Possible Diabetic Disturbances in Implant Wound Healing Process In Implants
  • 47. DIABETIC EMERGENCIES • Hypoglycemic crisis • Hyperglycemic crisis
  • 48. MANAGEMENT OF HYPOGLYCEMIA FACTORS THAT INCREASE THE RISK OF HYPOGLYCEMIA Skipping or delaying food intake Injection of too much insulin Injection of insulin into tissue with high blood flow (eg, injection into thigh after exercise such as running) Increasing exercise level without adjusting insulin or sulfonylurea dose. Inability to recognize symptoms of hypoglycemia Denial of warning signs or symptoms Past history of hypoglycemia Hypoglycemia unawareness Low Blood Glucose • Sign & symptoms occurs as fall in blood glucose level below 60 mg/dl. • Severe hypoglycemia refers to fall in blood glucose concentration below 40 mg% (2.2-mmol/1) requiring help from outside for recovery.
  • 49. SIGN & SYMPTOMS Low Blood Glucose The most common emergency related to DM in the dental office and a potentially life-threatening situation that must be recognized and treated expeditiously. MENTAL CONFUSION, SUDDEN MOOD CHANGE LETHARGY,….TACHYCARDIA , NAUSEA, COLD CLAMMY SKIN, HUNGER, INCREASED GASTRIC MOTILITY, HYPOTENTION , HYPOTHERMIA. Severe hypoglycaemia may result in seizures or loss of consciousness.
  • 50. If patient is UNCONSCIOUS Low Blood Glucose Give 50 ml of 50% intravenous glucose- through a large vein to avoid thrombophlebitis. As soon as patient recovers consciousness, start oral carbohydrate intake, otherwise 5-10% glucose infusion has to be continued till patient recovers consciousness. Intramuscular injection of 1.0 ml of glucagon may be given if hypoglycaemia is insulin induced. It promotes glycogenolysis, gluconeogenesis. If patient does not regain consciousness inspite of normal blood glucose levels, then cerebral oedema is likely possibility which should be treated with intravenous dexamethasone or mannitol.
  • 51. ADMINISTRATION OF 15g OF ORAL CARBOHYDRATE (JUICE,CANDY) Repeated hypoglycaemic episodes are hazardous for CNS; hence, one should find out the cause and treat it or correct it by adjusting the patient's therapy. Low Blood Glucose If patient becomes CONSCIOUS PREVENTION
  • 52. MANAGEMENT OF HYPERGLYCEMIA High Blood Glucose It occurs when blood glucose levels over 200mg/dl for extended period of time. In Type 1 DM- ketoacidosis may occur- Characterized by- Disorientation, rapid & deep breathing, hot drying skin & acetone breath. Type 2 DM- hyperosmolar non-ketotic diabetic acidosis. Severe hypotention & Loss of consciousness occurs if left untreated. • A medical emergency from hyperglycemia is less likely to occur in the dental office since it develops more slowly than hypoglycaemia.
  • 53. High Blood Glucose Care is initiated by activating the emergency medical system, opening the airway, and administering oxygen. Circulation and vital signs should be maintained and monitored, and the patient should be transported to a hospital . • Under some instances, severe hyperglycemia may present with symptoms mimicking hvpoglycemia. • If a glucometer is not available, these symptoms must be treated as hypoglycemia.
  • 54. DIABETES & PERIODONTAL DISEASE: CENSUS REPORT OF THE JOINT EFP/AAP WORKSHOP ON PERIODONTITIS & SYSTEMIC DISEASES (CHAPPLE LC,GENCO R. J PERIODONTOL 2013)
  • 55. GUIDELINE- A [Suggested Guidelines for physicians and other medical health professions for Use in Diabetes Practice] • Patients with diabetes should be told that periodontal disease risk is increased by diabetes. • If they suffer from periodontal disease, their glycaemic control may be more difficult, and they are at higher risk for diabetic complications such as cardiovascular and kidney disease. • Patients with type 1, type 2 and gestational diabetes should receive a thorough oral examination, which includes comprehensive periodontal examination. • For all newly diagnosed type 1 and type 2 diabetes patients, subsequent periodontal examinations should occur & annual periodontal review is recommended. • For children and adolescents diagnosed with diabetes, annual oral screening is recommended from the age of 6–7 years by referral to a dental professional.
  • 56. GUIDELINE- B [Suggested guidelines for use in dental practice] • If periodontitis is diagnosed, manage it properly. If not, patients with diabetes should be placed on a preventive care regime and monitored regularly for periodontal changes. • Patients with diabetes presenting with any acute oral/periodontal infections require prompt oral/ periodontal care. • Patients with diabetes who have extensive tooth loss should be encouraged to pursue dental rehabilitation to restore adequate mastication for proper nutrition. • Provide oral health education. • Patients who present without a diabetes diagnosis, but at risk for type 2 diabetes and signs of periodontitis should be informed about their risk for having diabetes, assessed using a chair-side HbA1C test, and/or referred to a physician for appropriate diagnostic testing and follow-up care.
  • 57. GUIDELINE- C [Recommendations for patients with diabetes at the physician’s practice/ office] • If your physician has told you that you have diabetes, you should make an appointment with a dentist to have your mouth and gums checked. This is because people with diabetes have a higher chance of getting gum disease. Gum disease can lead to tooth loss and may make your diabetes harder to control.
  • 58. GUIDELINE- D [Recommendations for patients at the dental surgery/office who have diabetes or are found to be at risk for diabetes] • People with diabetes have a higher chance of getting gum disease. If you have been told by your dentist that you have gum disease, you should follow up with necessary treatment as advised. • If you do not have diabetes, but your dentist identified some risk factors for diabetes including signs of gum disease, it is important to get a medical check-up as advised.
  • 59. CONCLUSION • Diabetes mellitus has significant impact on tissues throughout the body, including the oral cavity. As research indicates that poorly controlled diabetes increases the risk periodontitis. • Alteration in host defence and tissue homeostasis appear to play a major role. • Advances in medical management of DM require a heightened awareness by the periodontist in the various treatment regimens used by diabetic patients. • Familiarity with various medications, monitoring equipments, and devices used by diabetic patient allows provision of appropriate periodontal therapy while minimizing the risk of complications.
  • 60. REFERENCES • Taylor JJ, Preshaw PM, Lalla E. A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Periodontol 2013;84:S113-S34. • The position paper on diabetes & periodontal disease. J Periodontol 2000;71:664-78. • Grossi SG, Genco RJ. Periodontal Disease and Diabetes Mellitus: A Two-Way Relationship. Ann Periodontol 1998;3:51- 61. • Periodontal Medicine Rose, Cohen • Carranza’s Clinical Periodontology 11th edition • Davidson’s Principles and Practice of Medicine 21st edition