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Introduction
Disease of metabolic dysregulation Hyperglycemia Defects in Insulin secretion or action or both Chronic elevation Why important for a periodontist?
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Type 1 Diabetes
Occurs at young age; can also occur in later life Most frequent chronic disease in children Cell mediated auto immune disorder Destruction of cells of pancreas Destruction rate is variable Multiple genetic predisposition Linked to the presence of Human Leukocyte Antigens (HLA) Environmental factors (Viral infections)also play a role
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Dental caries
Increase caries prevalence in adult with diabetes. (xerostomia, increase saliva glucose) Hyperglycemia state shown a positive association with dental caries.
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Oral Manifestations
Cheilosis
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Oral Manifestation
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Miscellaneous conditions
Pulpitis : degeneration of vessels Neuropathies : may affect cranial nerves. (facial) Drug side-effects : lichenoid reaction may be associated with sulphonylurea. (chlopropamide) Ulcers
Walter et al 1985
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Gingivitis
Higher risk of developing gingivitis ( Jenkins et al 2001 Perio 2000) The prevalence of gingivitis in children and adolescents is nearly twice when compared with non diabetics (DePommereau et al 1998 JCP) Diabetes mellitus- associated Gingivitis Specific entity in the recent classification of gingival diseases ( Holmstrup et al 1999 Ann Periodontol, Issue 4) Several studies show a positive association Normalizing the glycemic levels may significantly reduce the severity and extent of gingivitis in diabetics (Karjalainen et al 1996 J Dent Res )
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Periodontitis
GCF shows an increased glucose level Diabetic status increases the host susceptibility to periodontal infection due to impaired immune response. (Dranchman et al 1966, Crook et al 1998) Increased calculus formation in patients with diabetes, may be due to an increased concentration of serum calcium in both parotid and submandibular saliva (Marder et al.1975 JOP)
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Sub gingival microbiota GCF Glucose levels Periodontal vasculature Host response Collagen metabolism
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Subgingival microbiota
Early studies showed possible differences in subgingival colonization Recent studies, however show very little differences. Periodontally diseased sites in diabetic patients harbor similar species as comparable in non diabetic individuals. ( Christagu et al JCP 1998, Zambon et al JOP 1988, Sastrowijoto et al JCP 1989) Lack of significant differences in the primary bacterial etiological agent in non diabetic and diabetic patients
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Twice amount of glucose in GCF of diabetic patients (Ficara et al JPR 1975) Decreased chemotaxis of periodontal fibroblasts to PDGF in a hyperglycemic environment ( Nishimura et al. 1998 Ann Perio) Thus, affects periodontal wound healing and also host response to microbial challenge. Should also promote a unique hyperglycemic environment, resulting in shifts of the microbial flora.
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Periodontal Vasculature
Periodontal vasculature is also affected like other vessels Basement membrane of the endothelial cells of gingival capillaries are thickened (Frantzis et al. 1971 JOP, Listgarten et al.1974 JOP, Seppala et al.1997 JOP) Leads to impaired oxygen and nutrient supply Two fold increase in AGE in diabetic gingiva ( Schmidt et al 1996) Increased oxidant stress in capillaries Leading to wide spread vascular injury
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Act by Stimulation of arterial smooth muscle proliferation AGE modified collagen inhibits normal degradation leading to thickness of basement membrane AGE modified collagen can bind circulating LDL resulting in atheroma and further narrowing. Thus results in increased severity and progression of periodontitis
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Host Response
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Collagen Metabolism
Increased Collagenase activity ( Ramamurthy et al. 1983 JPR) Collagenases primarily degrade newly formed collagen AGE-modified collagen predominates Net effect is destruction of newer collagen and dominance of older, cross-linked collagen. Leading to impaired wound healing
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Periodontal Abscess
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More susceptible to gingivitis, gingival hyperplasia and periodontitis Increased cytokines in gingival tissues Decreased growth factors interference with the healing of tissues. Increased levels of serum triglycerides may be related to greater probing depths and attachment loss
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Periomedicine
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Urine Tests
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Glycosylated Hemoglobin
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Treatment
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Pharmacological Treatment
Oral Hypoglycemics
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Insulin
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Insulin Syringe
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Insulin Pen
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Insulin Pump
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Diet
Ensure that the patient has eaten normally and taken medications as usual.
Prophylactic antibiotics
Established infection Pre-operation contamination wound Major surgery
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After treatment
Infection control Dietary intake Medications : Salicylates increase insulin secretion and sensitivity avoid aspirin.
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Emergency Management
Emergencies
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Hypoglycemia
Early stage More severe stage Later severe stage
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Emergency management
15 grams of fast-acting oral carbohydrate. Measure blood sugar. Loss of consciousness, 25-30ml 50% dextrose solution iv. over 3 min period. Glucagon 1mg i.m or s.c
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Emergency management
Severe hyperglycemia A prolonged onset Ketoacidosis may develop with nausea, vomiting, abdominal pain and acetone odor. Difficult to different hypo- or hyper-.
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Emergency management
Hyperglycemia need medication intervention and insulin administration. While emergency, give glucose first ! Small amount is unlikely to cause significant harm.
Jenner et al,JADA, 2001
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Acetaminophen Alcohol Anabolic steroids Clofibrate Disopyramide Gemfibrozil Monoamine oxidase inhibitors (MAOIs) Pentamidine Sulfonylurea medications
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Maintanence of Osseointegration
Conclusion
Commonly encountered in dental office Complete medical history to be known by the dentist Dentist should be aware of hypoglycemia and should be in a position to manage it Dentist plays a major role in oral hygiene education Patients should be made aware of the periodontitis-diabetes inter relationship
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