DIABETES AND THE PERIODONTIUM

1. DIABETES AND THE PERIODONTIUM

2. Bennet(1994)-defined this 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 . • Gaw et al –(1955) defined diabetes mellitus as a syndrome characterized by hyperglycemia due to an absolute or relative lack of insulin or insulin resistance .

3. Glickman was the first investigator to examine the relationship between diabetes and periodontal destruction . Malins (1968)- defined diabetes as a chronic disorder of carbohydrate metabolism characterized by hyperglycemia and glycosuria .

4. National diabetes data group(1979) defined diabetes mellitus as a genetically and clinically heterogenous group of disorders that shared glucose intolerance in common . Ervasti et al (1985)-defined diabetes mellitus as a metabolic disorder with disturbances in the intrinsicproduction, of insulin leading to an abnormal fat , carbohydrate and protein metabolism .

5. Presently it is defined as a complex metabolic disease ,characterized by hyperglycemia , diminished insulin production ,impaired insulin action or a combination of both ,which results in the inability of glucose to be transported from blood stream into the tissues ,which in turn results in high blood glucose levels and excretion of sugar in urine .

6. Classification-Rifkin and Ross(1975) Nakkey and Halck(1976) 1)Heriditary/primary 2)Non heriditary/secondary a)potential diabetes a)damage or Removal of b)sub clinical diabetes pancreatic islet tissue c)latent diabetes b)disorders of other endocrine glands 2)National Diabetes data group (1979)a)Diabetes Mellitus a)TYPE-1 (IDDM) B)TYPEII-NIDDM 2)Impaired glucose tolerance(IGT) 3)Gestational diabetes(GDM)

7. III)EDWARD C.M et al (1995) 1) Primary TYPE I-IDDM TYPE II-NIDDM 2) Secondary a) pancreatic pathology b) Excessive endogenous production of hormonal antagonists to insulin Growth hormone Glucocorticoids Thyroid hormones

8. C. Medication with corticosteroids , thiazide 3) Associated with genetic syndromes a)Down’s syndrome b)Klenefelter’s syndrome c)Turner’s syndrome

9. CLINICAL FEATURES TYPE I(IDDM)-is caused by a cell mediated autoimmune destruction of insulin producing cells of islets of Langerhans in the pancreas. This results in insulin deficiency and often occurs in children and young adults. It has a marked tendency towards ketosis and coma, and requires injected insulin. This type shows symptoms traditionally associated with diabetes such as polyphagia , polyuria and polydipsia.

10. IDDM appears to be heterogenous in terms of genetic and environmental factors that precipitate the disease. The initiation of pathogenesis however precedes the abrupt clinical onset of diabetes by several years, thus there is a prediabetic period during which the standard biochemical tests for diabetes are of little value. HLA genotyping and detection of complement fixing islet cell antibodies are of greater value .

11. TYPE II- (NIDDM) manifests by minimal or no symptoms of metabolic aberrations of diabetes. They are not prone to ketosis . This is caused by peripheral resistance to insulin action , impaired insulin secretion and increased glucose production in the liver but the insulin producing beta cells are not destroyed.

12. NIDDM is the most common type of diabetes seen in 90 –95% of all cases .It is also called as adult onset diabetes .It generally occurs in obese individuals can often be controlled by diet / oral hypoglycemic agents . This form of diabetes can present with the same symptoms as type I but typically in a less severe form .

13. ORAL MANIFESTATIONS OF DIABETES Numerous oral changes have been described in diabetes. Oral signs and symptoms of diabetes can range from normal to severe . Poor oral hygiene allows for more accentuated reaction of the gingiva leading to hypertrophy,deep red erythema and painful hemorrhagic papilla.(Mascola 1970)

14. Goldman and Cohen in (1973) reported that due to the lowered tissue resistance the infection may quickly advance deeper into the periodontium leading to 1.Granular subgingival proliferations 2.Periodontitis and 3.Multiple lateral periodontal abscesses

16. Burnek in 1975 reported that there may be some possible alterations in the dentition ,from an increased incidence of enamel hypoplasia to hypo calcification An increased incidence of caries was noted due to the decreased salivary flow and increased levels of carbohydrates in saliva .

17. The other oral changes are • Cheilosis • Mucosal drying and cracking • Burning mouth and tongue • Diminished salivary flow • Alterations in the flora of the oral cavity with greater predominance of Candida albicans, hemolytic Streptococci and Staphylococci.

18. All these changes are less likely to be observed in well controlled diabetes. The other changes are 1.Tendency towards enlarged gingiva 2.Sessile or pedunculated gingival polyps 3.Polypoid gingival proliferations 4.Abscess formations 5.Periodontitis and loosened teeth

20. The most striking change in uncontrolled diabetes is the reduction in the defense mechanism and the increased susceptibility to infection leading to destructive periodontal disease . Periodontitis in Type I diabetes appears to start after 12 years .The prevalence of periodontitis has been reported as being 9% in 13- 18 years old to 39% in 19 years and older.

22. It’s noted that periodontal disease in diabetes follows no consistent or distinct pattern . . a) Children with type I diabetes tend to have more destruction around the first molars and the incisors than elsewhere. b) Some investigators have reported that the rate of periodontal destruction appears to be similar for those with or without diabetes upto 30 years after which there will be greater destruction in diabetic patients.

23. This may be due to disease destruction overtime and also due to the diminished tissue integrity that continues to deteriorate. The majority of well controlled studies show a higher prevalence and severity of periodontal disease in individuals with diabetes than those without. With similar local factors, there is greater loss of attachment , increased bleeding on probing and increased tooth mobility in diabetics.

24. Diabetes does not directly cause gingivitis or periodontal pockets, but there are indications that it alters the response of the periodontal tissues to local factors thus hastening boneloss and retarding post surgical healing of periodontal tissues.

25. MICROBIOLOGY Mashimo (1983)found that it was composed of Capnocytophaga species and anaerobic Vibrios with few pigmented Bacteroids Actinobacillus actinomycetemcomitans were cultivated from the subgingival pockets of these patients.

26. Zambon (1988) found more of Bacteroid species in severe Periodontitis with type 2 diabetes mellitus . Sastrowijoto et al (1989) found that the pockets in poorly controlled diabetic patients harbored more A.actinomycetemcomitans .

27. BACTERIAL PATHOGENS The glucose content of the gingival fluid and blood is higher in individuals with diabetes, than those without ,with similar plaque and gingival index scores.This increased glucose ,changes the environment of the microbial flora, inducing qualitative changes in the bacteria that could account to the severity of periodontal disease.

28. PATHOGENESIS According to Cheraskin (1962), Burket ( 1972) ,Baskar(1977). The progression may follow a definite course. The blood glucose level is maintained by a balance between insulin secreted by the islets of Langerhans in the pancreas and hypophyseal and adrenocortical hormones.

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30. Insulin converts blood sugar into glycogen which is stored in liver and muscles and in reverse it aids in the oxidation of glucose . Adrenalin mobilizes sugar from liver glycogen and then adrenocortical hormones convert aminoacids into sugar instead of protein . Insulin increases the rate of glucose , lipid and protein synthesis and decreases the rate of glycogenolysis and lipolysis

31. In diabetes mellitus, due to a lack of available insulin for cells, there is a decrease in anabolism and increase in catabolism resulting in an abnormal accumulation of glucose in blood. This glucose is not reabsorbed from the urinary filtrate and hence glucose appears in the urine. This inturn increases the production of ketone bodies which results in ketoacidosis. Thus the patient will have an acetone odour in the breath with dehydration and electrolyte depletion leading to shock and coma .

32. In the insulin dependent pts the plasma insulin concentration is consistently reduced or totally lacking . In non insulin dependent pts the plasma insulin concentration is normal or higher but there may be an increased resistance due to the abnormalities at the level of insulin receptors - insulin antagonicity,

33. RELATIONSHIP OF DIABETES AND PERIODONTAL DISEASE- Most of the connective tissue destruction taking place in periodontal disease results from interaction of bacteria and their products with mononuclear phagocytic cells and fibroblasts trigerring activation and local secretion of catabolic inflammatory mediators like IL-1B , PGE2, TNF- AND IL-6

34. One biologic mechanism why diabetics have more severe periodontal disease is due to the formation of AGE. In the hyperglycemic state numerous proteins and matrix molecules undergo a non enzymatic glycosylation resulting in formation of advanced glycation end product (AGE) The formation of the AGEs can occur at normal glucose levels but in hyperglycemic environments AGE formation is excessive.

35. AGE formation crosslinks collagen , making it less soluble and less likely to be normally repaired or replaced . As a result ,collagen in the tissues of poorly controlled diabetics is aged and more susceptible to breakdown . AGEsplay a central role in the classic complication of diabetes . Poor glycemic control and increased AGEs render the periodontal tissues more susceptible to destruction

36. Cellular migration through the cross linked collagen is impeded ,and perhaps more importantly ,tissue integrity is impaired as a result of damaged collagen remaining in the tissue for longer periods . The cumulative effect of altered cellular response to local factors ,impaired tissue integrity and altered collagen metabolism undoubtedly play a significant role in susceptibility of individuals with diabetes to infection .

37. The increased prevalence and severity of Periodontitis commonly seen in pts with diabetes led to the designation of periodontal disease as a sixth complication of diabetes The other five classic complications are 1)Retinopathy2)Nephropathy3)Neuropathy4)Macro vascular disease5)Altered wound healing 6)Periodontal disease(Loe. H, periodontal disease diabetes care 1993)

38. In diabetic pts with periodontitis , periodontal therapy may have beneficial effects on glycemic control. A more recent evaluation of Scaling and Rootplaning combined with systemic doxycycline therapy for 2 weeks in type1(insulin dependent) diabetic pts improved periodontal health and also had a significant improvement in glycemic control ,

39. Conversely, those individuals who demonstrated little beneficial clinical effect from periodontal treatment had no change in glycemic control. Studies suggest that combination of sub gingival mechanical debridement and systemic doxycycline may result in short term improvement in glycemia in diabetic pts with severe periodontitis and poor metabolic control.

40. The mechanism by which adjunctive antibiotics may induce positive changes in glycemic control when combined with mechanical debridement are unknown.But systemic antibiotics may eliminate bacteria following scaling and root planing thus decreasing the bacterial challenge to the host . • Tetracyclines are also known to suppress glycation of proteins and decrease the activity of matrix metalloproteinases. These changes may contribute to improvement in metabolic control of diabetes .

41. Systemic infections increase tissue resistance to insulin thus preventing glucose from entering target cells.This in turn leads to elevated blood glucose levels . • It is possible that chronic gram – ve periodontal infection may also result in increased insulin resistance and poor glycemic control .This mechanism explains the worsening of glycemic control associated with severe periodontitis

43. The maturation and gradual transformation of the sub gingival flora into an essentially a gram –ve flora triggers infection mediated pathway of cytokine up regulation with secretion of TNF and IL-1 and a state of insulin resistance effecting glucose utilizing pathway.

44. Hence it is proposed that periodontal infection mediated cytokine synthesis and secretion may amplify the magnitude of the AGE mediated cytokine response and vice versa. The relationship between the diabetes mellitus and periodontal disease has become 2- way .This proposed dual mechanism of tissue destruction suggests that control of periodontal infection is essential to achieve long term control of diabetes mellitus

45. HISTOLOGY- a) Frantiz BrownA.L(1971)noted significant thickening of the vascular basement membrane in diabetics b) Listgarten M.N et al (1974) noted gingival angiopathies(due to compromised delivery of nutrients to the surrounding tissues and poor elimination of metabolic waste )

46. C) Kalpan .R. et al (1982) reported defective collagen metabolism in diabetics. IMMUNOLOGY- Manouche pour(1981) suggested that the abnormal polymorphonuclear leukocyte chemotaxis might contribute to the increasing severity of periodontal disease in diabetes pts .

47. GENETICS Todd J. A(1987) reported that diabetes mellitus is a genetically heterogenous condition. Insulin dependent diabetes mellitus is an organ specific autoimmune disease and there exists evidence for autoimmune diseases to be associated with a particular HLA specificity.

48. HLA class IIgenes that determine imm une responsiveness have been mapped to specific regions of chromosome 6 at residue 57 of the HLA- DQ beta chain. Auto immune response against insulin producing islet cells is specified and it is here that an inherited predispostion to diabetes mellitus is determined.

49. Heterozygotes for the haplotype DR3 AND DR4have demonstrated an increased risk of developing insulin dependent diabetes mellitus.

50. MANAGEMENT The diabetic pts require special precautions before the periodontal therapy .Over the last decade the medical management of diabetes has changed significantly in an effort to minimize the debilitating complications associated with the disease . If the clinician detects intra oral signs of undiagnosed or poorly controlled diabetes