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DIABETES AND PERIODONTIUM

DIABETES AND PERIODONTIUM. 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

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DIABETES AND PERIODONTIUM

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  1. DIABETES AND PERIODONTIUM

  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.

  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.

  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: Type 1 Type 2 Other Specific types of DM Gestational diabetes

  10. CARBOHYDRATE METABOLISM, INSULIN AND DIABETES

  11. BLOOD GLUCOSE HOMEOSTASIS

  12. ACTIONS OF INSULIN

  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 • 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 • Diabetic Retinopathy • Diabetic Neuropathy • Diabetic Nephropathy • Atherosclerosis • Impaired wound healing • 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 MANIFESTATIONSHirchfeld 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

  24. Polymorphonuclear leukocyte function • Impaired Chemotaxis & adherence • Defective Phagocytosis • Diminished primary defense against periodontal pathogens.

  25. Collagen Metabolism • Hyperglycemic state Reduced synthesis of collagen & glycosaminoglycans • Collagen homeostasis- Affected • GCF collagenase activity increased • Reduced collagen maturation

  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 • AGEs + Macrophages & Monocytes AGEs + Endothelial cells Pre-coagulatory changes Hyper-cellular state • Focal thrombosis • Vasoconstriction Increased Secreation of IL-1, IGF, TNF ἀ

  29. AGEs AND PERIODONTIUM

  30. 2- WAY RELATIONSHIP BETWEEN PERIODONTAL DISEASE AND DM

  31. PATHOGENESIS OF PERIODONTITIS IN DIABETES Taylor JJ. JOP 2013

  32. LINKAGE BETWEEN INFECTION,HYPERLIPIDEMIA & INSULIN RESISTANCE

  33. INFECTIONS IN PATIENTS WITH DIABETES • Hyperglycemic state Mainly due to: • Impaired defence mechanism • Defects in PMN function • Induction of insulin resistance • Vascular changes • Glycosylation of basement mem, proteins • Thickning of gingival capillaries, • Disruption of BM • Swelling of Endothelium Impeded • Oxygen diffusion • Metabolic waste elimination • PMN Migration • 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 • Reduced Collagen solubility • Delayed remodelling of wound site Readily degrade newly synthesized, less completely cross linked collagen 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 Actinobacillusactinomycetemcomitansand Capnocytophaga. (Mashimo et al 1983) • The proportion of P gingivaliswas 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 • Diabetes is a risk factor for gingivitis & periodontitis. • The level of glycemic control appears to be an important determinant in this relationship. Data of multiple studies reveal strong evidence

  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.

  38. MECHANISM BY WHICH PERIODONTAL DISEASE MAY INFLUENCE DIABETES

  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 • DIET : The goals of this intervention include weight reduction, improved glycemic control, with blood glucose levels in the normal range, and lipid control. • Exercise : Regular physical exercise to weight reduction, increased cardiovascular fitness, and physical working capacity.

  41. 3.Pharmacological therapy :

  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 appointmentsshort, 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 Possible Diabetic Disturbances in Implant Wound Healing Process In Implants • 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

  47. DIABETIC EMERGENCIES • Hypoglycemic crisis • Hyperglycemic crisis

  48. MANAGEMENT OF HYPOGLYCEMIA • 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. Low Blood Glucose

  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

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